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Dyslipidemia It is an abnormal increase in cholesterol or Triglyceride LDL is the main cause of atherosclerosis HDL is good lipoprotein and does not cause atherosclero%Risk factors: Endocrine: Hypothyroidism, Cushing's syndrome, DM,Obesity Renal: CKD, Glomerulonephritis Liver disease Sedentary fifestyle and alcohol Drug use: OCP, Steroid, Diuretic in high dose Signs: Atherosclerosis: blood vessels plaque (CAD, PAD, Renal artery stenosis) Skin manifestations: o Tendinous xanthoma: associated with familial hypercholesterolemia o Eruptive xanthoma: associated with hypertriglyceridemia Investigations: Fasting Lipid profile (LDL, HDL, Total cholesterol, TG) TFT, KFT, LFT, Serum glucose Assessment of CAD Cases in which statin should be used (CAD equivalents): Peripheral arterial disease (PAD) Carotid disease Aortic artery disease Management: Lifestyle modifications Statins (HMG CO-A inhibitors) o The best treatment for a high LDL level o The lipid-lowering agent with the strongest mortaüt Y o They have an antioxidant effect on the endothefial o E. g., Atorvastatin, Simvastatin, Lovastatin, Rosuvastoff o Side effects: Myositis, hepatotoxicity, warfarin potentiation p b-gels/ | INTERNAL1-17AFEEF-MERGED-1.pdf |
Niacin: o Excellent drug to add the statino Niacin is stronger than statin, exercise, and smokingcessation to raise HDL o Associated with Glucose intolerance, elevation of uricacid, and itching Fibrates (lipoprotein lipase stimulators):o E. g., Gemfibroil, fenofibrate o Lower TG level more than statino The combination with a statin increases the risk of Myositis Cholestyramine: o Bile acid Sequestrant o Has significant interaction with other medications inthe gut (decrease their absorption)o Side effects include constipation and Flatus. Ezetimibe (Cholesterol absorption inhibitor): o Lowers LDL but with no benefit o Not better than placebo in the clinical endpoint Protein Convertase Subtilisin Kexin type 9 (PCSK9) inhibitors:o E. g., Evolocumab, Alirocumab o Injectable medication that can decrease LDL strongly o Used if the patient is not responsive or cannot tolerate statin Page 189 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Metabolic syndrome Also known as insulin resistance syndrome or syndromex A cluster of metabolic and pathophysiologic disordersconfer increased cardiovascular disease and DM risk. Components: Central obesity (waist circumference) High triglycerides (> I. 7 mmol/l) Low HDL 1. 0 mmol/l) HTN T2DM or impaired glucose tolerance (IGT) Women with PCOS are at increased risk of developing insulin resistance, hyperlipidemia, and metabofic syndrome LDL and total cholesterol may be below average in patients with metabolic syndrome. Therefore, they do not exclude CVD risk and are not a part of this cluster. Management: Lifestyle modifications (diet, physical activity) Treatment of dyslipidemia Blood pressure control Diabetic control pogelß | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pulmonology CHAPTER 3 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 191 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pulmonary Function Test (PFT) Spirometry and Lung volumes PFT is used to determine the nature of the pulmonary disease(Obstructive V. S restrictive) Spirometry is used to differentiate obstructive vs. restrictivelung diseases. Components of Lung volumes and spirometry: Tidal volume (TV): o The volume of respiration at rest o Normally 20 ml in newborn 0 350 ml in adult female 0 500 ml in adult male Residual volume (RV): o The remaining volume which cannot be exhaled o Normally 1200 ml in adults o This volume cannot be measured by the spirometry Total Lung Capacity (TLC): o Equal to FVC + RV = normally 6200 ml o Increased in case of Emphysema Forced Vital capacity (FVC): o The volume of forced inspiration to forced expiration o VC ml o It will be reduced in case of restrictive lung disease FEVI : o Forced expiratory volume in I second o It is significantly reduced in the case of obstructive lung disease FEVI/FVC ratio: o Significantly reduced in case of obstructive lung disease o Normal or increased in restrictive lung disease Inspiratory capacity (IC) = TV + IRV Vital capacity (VC) = TV + IRV + ERV Forced resedual capacity (FRC) = ERV + RV Total lung capacity (TLC) = RV + ERV + TV + IRVs påge192 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Lung volumes E 2200 Time Lung capacities Figure 10.-The normal lung volumes for a healthy 70 kg male(1-Tidal volume, 2-inspiratory reserved volume, 3-residual volume, 4-expiatoryreserved volume, 5-inspiratory capacity, 6-vital capacity, 7-functional residual FEVI NC FEVI/FVC Example:capacity, 8-total lung capacity) Obstructive diseases Significantly reduced Reduced or normal Reduced Asthma COPD Bronchiectasis Cystic fibrosis Restrictive diseases Reduced Significantly reduced Normal or increased Pulmonary fibrosis, Asbestosis, Sarcoidosis, ARDS, RDS, Kyphoscoliosis, Neuromuscular disorders Table 37: Obstructive vs. Restrictive lung diseases Page 193 | INTERNAL1-17AFEEF-MERGED-1.pdf |
TLco (DLco) Diffusing capacity or transfer factor of the lung for CO gas It describes the rate of gas diffusion from alveoli to blood. In COPD, DLco differentiates emphysema from chronic bronchitis In restrictive lung diseases, DLco differentiates intrinsic vs. extrinsic restrictive lung diseases. Causes of increased DLco Causes of decreased DLco Asthma Fibrosis Polycythemia Pneumonia Pulmonary hemorrhage PE Male gender Pulmonary edema Exercise Anemia Left to right shunt Emphysema Low cardiac output Table 38: causes of high vs. low DLco A-a gradient It measures the efficacy of gas exchange between alveoli (A) and the artery (a) How to calculate: A —a gradient = PA02 — Pa02 Pa02 is measured by ABCs PA02 = Fi02 * (760-47) (1. 25 * Pa C02) The normal A-a gradient = 0. 3 * age in years Interpretation: An abnormal A-a gradient suggests the lungs as a possible cause for hypoxemia The normal A-a gradient suggests causes external to the lung as a cause for hypoxemia Hypoxia with wide Aa gradient Hypoxia with narrow Aa gradient Pulmonary edema (CHF, ARDS) Hypoventilation Lobar pneumonia Atelectasis Pulmonary embolism COPD and Asthma Pneumothorax Central nervous system disorders High altitude Hemoglobin defect (Anemia) Table 39: Causes Of hypoxia according to the A-a gradient Page 194 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Obstructive lung diseases Asthma Asthma is a chronic disease that causes inflammation with reversible & variable narrowing of the airways (The main difference between asthma and COPD is reversibility and variability) Asthma is usually associated with a history or family history of other Ig E-related diseases like atopic dermatitis (eczema) and atopic rhinitis (hay fever) 70% of asthmatic patients are sensitive to Aspirin and other NSAl Ds. Triggers are: dust, smoking, air pollution, Drugs — NSAID, Beta-blockers, exercise, emotions, sudden changes in air temperature Types of asthma: Occupational asthma: chemicals at work worsen asthma, and the patient is better at weekends. Cough variant asthma: asthma presented with cough exclusively. Exercise-induced asthma: asthmatic attack triggered by exercise. Pathophysiology: Exposure to allergen bronchospasm, airway edema, increased m UCUS and goblet cells airway obstruction-4 hypoxemia-+ hyperventilation —+ Decreased Pa C02-4 respiratory alkalosis respiratory muscle fatigue decreased ventilation-+ increase C02+ respiratory acidosis + respiratory failure Diagnosis: CXR shows a hyperinflated chest:o Horizontal ribso Wide spaces between ribso Low set, flat diaphragmo Vertical hearto Hyperlucent lung field Pulmonary function test (PFT) (The most accurate test):o Will show decreased FEVI/FVC ratioo Increase in FEVI > 12% and 200 ml after use of SABA (reversibility)o FEVI also used for staging Page 195 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Increased DLCO Peak expiratory flow and ABCs (the best initial tests in acute asthma) Other tests: o CBC: eosinophilia o Skin testing: to identify the specific allergen The main clinical features of asthma: Symptoms usually worsen at night and vary over time Cough (the most common symptom) Dyspnea, expiratory wheezing, tachypnea, tachycardia, chest tightness PUISUS paradoxus Reversible obstruction on PFT Associations: o Asthma is frequently associated with nasal polyps and sensitivity to aspirin o History or family history Eczema and atopic dermatitis are usually present. Classification of asthma: Class of asthma Mild intermittent Mild persistent Diurnal attacks Nocturnal attacks FEVI% < 2/week < 2/month 280 > 2/week > 2/month 280 Moderate persistent Every day > I per week 60-80 Severe persistent Every day Every day < 60 Table 40: Asthma classification according to the severity Page 196 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Asthma manaaement The following table shows the stepwise approach to treating asthma Step up or step down in medications according to the patient's symptoms. The patient's compliance with his inhaler and technique should be checked before changing the medications. very severe ersistent Oral steroids Severe persistent LABA LABA Moderate persistent LABA Mild persistent ICS ICS ICS ICS high dose high dose Mid intermittent Low dose Low dose SABA + ICS as requiered for symptomatic relief Figure J l: A stepwise approach to asthma control Short-acting beta-agonist: Used as needed (reliever) Side effects: hypokatemia, tachycardia, and tremor SABA alone has more risk of exacerbation compared to SABA + ICS use. Therefore, according to the recent guidelines, ensure the patient will adhere to ICS therapy before prescribing SABA. Inhaled corticosteroids (ICS) Used as add on if asthma is not controlled on SABA alone Example: beclomethasone, fluticasone Used as a controller (preventer) but (not used as a reliever inacute asthma) Side effects include dysphonia and oral candidiasis Long-acting beta 2 agonists (LABA) Used as controller, not reliever Example: Salmeterol Formoterol is a fast-acting LABA used as a reliever. it is not used as monotherapy in asthma patients Page 197 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Leukotriene receptor antagonist (LTRA) Oral medication (not inhaler) is used to control asthma but not as a reliever Example: Montelukast Long-acting muscarinic antagonist (LAMA) Used as controller, not reliever Example: Tiotropium It can be used alone or in combination as ICS-LABA-LAMA Acute exacerbation of asthma It is also called Status asthmaticus it is defined as acute or subacute worsening of symptoms and lung function in a patient with asthma. Asthma exacerbation is classified as moderate, severe, and life-threatening asthma. Parameter Moderate PEFR General Condition Pulse Chest ABGs Pa C02 02 sat. 50-75% Conscious Normal speech < 25/min < 110/min Resp. alkalosis Low 92%Severe33-Conscious Can't complete a sentence > 25/min > 110 Wheezy Resp. alkalosis Low Life-threatening < 33% Cyanosed Confusion Coma Bradycardia Hypotension Silent chest Resp. acidosis Normal or high < 92% Table 4 1: classification of acute asthma exacerbation Assessment of acute asthma exacerbation: If the patient has an 02 saturation of < 92%, ABCs test is mandatory Chest x-ray is recommended in the following cases: o Life-threatening asthma o When pneumothorax is suspected o If the patient is not responding to the usual treatment Page 198 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Indications for admission: All patients with life-threatening asthma Severe asthma attack not responding to the initial treatment Previous near-fatal asthma attack Pregnant women An attack despite the use of oral steroids Treatment: The first step: o Oxygen: For all hypoxic patients, given by venturi mask o SABA: 5— 10 puffs by MDI and spacer (SABA nebulizer is indicated in severe cases)-can be repeated up to 3 doses in 1 hour. o Early administration of systemic Steroid (40 — 50 mg oral prednisolone) The second step: Nebulized SAMA (Short-acting muscarinic antagonists, e. g., Ipratropium) The third step: Magnesium sulfate IV (l. 2 — 2 g over 30 minutes) o Not routinely used o Only if the previous measures fail to improve the patient-Intubation and mechanical ventilation should be done in any patient with life-threatening or near-fatal asthma. Earty administration of intramuscular adrenaline is indicated in a patient with acute asthma exacerbation and anaphylaxis Aminophylline and theophylline have poor efficacy and safety profile, so they are not recommended in the treatment of acute asthma exacerbation anymore High-dose ICS-formoterol combination is similar to SABA in refieving asthma, but this will need more studies to be adopted officially. Avoid sedatives in asthma exacerbation because theyfurther suppress respiration and worsen the condition. Page 199 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Asthma controllers (preventers) Inhaled steroids (ICS) Oral steroid (OCS) LTRA, IABA, ICS-formoterol Cromoglycate Ketotifen Asthma relievers Oral steroids (OCS) I. V steroids SABA, SAMA, ICS-LABA Magnesium sulfate Atropine, Adrenaline Ephedrine sulfate Table 42: Asthma controllers and relievers medications COPD COPD is a chronic obstructive lung disease that causes progressive inflammation and narrowing of the airways. Patients have irreversible and non-variable (fixed) narrowing of the airways and loss of elasticity of the lungs. Causes: Smoking: o It is the most common cause o Tobacco destroys Elastin fibers in the lung o The most effective mortality benefit is to stop smoking Alpha-I-Antitrypsin deficiency: o The most common cause in young and non-smokers. Other causes (pollution, occupational exposure) Clinical picture: there are two clinical types of COPD: Chronic bronchitis: o Cough and sputum on most days for at least 3 months in 2 consecutive years o Cyanosis, peripheral edema (due to Cor pulmonale), prolonged expiration. Emphysema: o Enlargement of distal airway spaces and obstruction of alveoli, the AP diameter (pigeon chest), and increased TLC o Pink skin, barrel chest, hyper-resonant to percussion o Lung compliance is increased in emphysema Stage 1 Stage 2 Stage 3 Stage 4 FEVI 50-79% 30-49% FEVI/FVC < 0. 7 < 0. 7 < 0. 7 < 0. 7 Table 43: Staging of COPD Page1100 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: CXR (best initial test) o Hyperinflation, Bulla, Flat diaphragm, horizontal ribs (air trapping) o Increased anteroposterior diameter PET (the most accurate test) 0 Low and low FVC, low FEVI/FVC ratio 70%) Rversibility of < 12% and < 200 m L in the FEVI after SABA administration. DLCO (decreased in emphysema) ABCs (for acute exacerbations), hypoxia, and high C02 ECG: RVH or MAT may be present Echocardiogram: pulmonary HTN, RVH, RAH (a) (b) Figure 12: (a) normal chest X-Ray, (b) Hyperinflated chest Complications: Polycythemia Bulla rupture leading to pneumothorax Respiratory failure (Type Il in chronic bronchitis but Type I in emphysema) Cor-pulmonale (Right ventricular heart failure) Treatment: Measures to reduce mortality:o Smoking cessation (the most important)o H. Influenza and pneumococcal vaccineo Long-Term Oxygen Therapy (LTOT). Measure to reduce symptoms:o SABA (More rapid onset)o SAMA (Most effective in COPD but slower than SABA)o LABA (More sustained effect)o ICS + LABA (ICS is not used as monotherapy in COPD) Page 1101 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Sucd (both o Volume reduction o Lung transplant COPD exacerbation: 02 therapy:and symptomatic benefits): 0 02 saüation target is 88--92% until ABGs aeable o If there is no C02 retention, make the target 94— 98% Bronchodilator (SABA+SAMA) with a back-to-back nebl-fiæ Give prednisolone 40 mg dally for 5 days Oral antibiotics (Amo)öa Tln, Tetracyc Ene, or clarittvornydn) only if there are pcm-dent sputum Other importa N points about COPD: The most common bacteria in COPD exacerbation is H. Influenzae. then streptococcus pneumonia. Do not use 100% oxygen (If 100% 02 is used in a patient with C02 retention, 02 will inhibit the resgfratoty center leading to hypoventilation and respiratory failure) Indcafions for LTOT: Pa02< 55 mm Hg (resting or exercise) 02 saturation < 88% (resting or exercise) Pa02 < 60 mm Hg with heart disease or potycythemia 02 saturation < 90% with heart disease or polycythenia Instrucfiors for LOTO usage: Maintain 02 saturation > 90% and Pa02> 60 mm Hg Devices used: Nasal cannula or venturi mask Duration: at least 15 hours per day Signs and symptoms of hypercapnia (C02 retention): Headache Tremor (asteri)ös) Large pube volume Warm extremities (due to vasodilatation) Papilledema (due to high ICP) Decreased LOC Indications for admission of COPD exacerbation patients: Life-threatening exacerbation For ventilator support (NIV, or conventional mechanicd ventilator) Table 44: Indications for LTOT P age 1102 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Alpha-I-antitrypsin deficiency æficiency of alpha-I-antitrypsin due to a genetic problem Autsomal recessive condition (located on chromosome 14) o Normally, Pi MM o Homozygous Pi SS (50% normal AIAT levels) o Homozygous PIZZ (10% normal AIAT levels)-antitrypsin is a protease inhibitor protein synthesized by the Ever Al AT defidency presents with a combination of COPD and Ever cirrhosis COPD (usualty emphysema) in young (< 40 years) and non-smoker patients is considered AIAT deficiency until proven otherwte Chest X-Ray: findings of COPD Low albumin, high PT time (caused by fiver cirrhosis) PFT: fixed obstruction AIAT level (low) Genetic testing Treatment: No smoking Intravenous AIAT Treat as COPD if it occurs Page 1103 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Bronchiectasis Dilatation of the airways due to chronic lung infection in childhood (anatomic defect) Usually affects medium-sized airways The most common infectious pathogen is Pseudomonas aeruginosa Causes: Cystic fibrosis is the most common cause of bronchiectasis Obstruction: tumor, foreign body Chronic or Recurrent Infection Kartageneds syndrome (ciliary dysfunction) Hypogammaglobulinemia Symptoms: Episodes of lung infection with a high volume of foul-smelfing SPUtum. 4 Hemoptysis Clubbing Recurrent infections Diagnosis: High-resolution CT scan (signet ring appearance) Chest X-Ray (tram-track appearance) PFT Obstructive pattern Investigations of the cause Treatment: Treatment of the cause Antibiotics Chest physiotherapy ICS Page 1104 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Interstitial lung diseases (ILD) The main presentation in these patients is progressive shortness of breath or nonproductive coughs. They present with decreased lung compliance, a restrictive pattem on PET, hypoxia, and decreased DLco, VC, and TLC. However, FEVI/FVC ratio is increased or normal. Classification of ILD Classification based on the major underlying histopathology: Infiammatory and fibrotic ILDs Idiopathic pulmonary fibrosis Asbestosis Drug-induced Radiation-induced Connective tissue disorders Granulomatous ILDs Hypersensitivity pneumonitis Sarcoidosis Granulomatous with polyangiitis Churg-strauss syndrome Classification based on the most commonly affected lung zone: Lower lobe fibrosis Upper lobe fibrosis Idiopathic pulmonary fibrosis Silicosis Drug-induced ILDHypersensitivity pneumonitis Asbestosis Ankylosing spondyfitis Most connective tissue diseases Tuberculosis Sarcoidosis Table 45:causes of Upper vs. Lower lobe lung fibrosis Page 1105 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Idiopathic Pulmonary Fibrosis (IPF) Also known as cryptogenic fibrosing alveolitis An idiopathic progressive disease of an Irreversible process Symptoms: Exertional dyspnea and non-productive cough Late expiratory crackles (Velcro-like crepitations) Clubbing Diagnosis: Chest x-ray: o Early: reticulonodular pattern o Late: honeycombing A restrictive pattern on PFT High-resolution CT scan (Best): ground glass appearance Biopsy (the most accurate but rarely needed) Treatment: Oxygen Supportive measures Lung transplant for end-stage (definite treatment) Sarcoidosis Unknown etiology usually occurs in young and black patients A multi-system disease characterized by non-caseating granuloma More common in non-smokers Clinical picture: It could be asymptomatic, but cough, SOB, and fatigue may present Facial nerve involvement is the most common neurological manifestation Skin manifestations: o Erythema nodosum (Good prognosis) o Lupus pernio (purplish lesion of the facial skin) (poor prognosis) Anterior uveitis Hepatosplenomegaly Non-deforming arthritis Hypercalcemia: (macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)) Page 1106 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Syndromes of sarcoidosis: Lofgren's syndrome is an acute form of sarcoidosis characterized by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever, and polyarthralgia. It usually caries an excellent prognosis Heerfordts syndrome (uveoparotid fever) there is parotid enlargement, fever, uveitis, and facial palsy secondary to sarcoidosis Diagnosis: Chest x-ray (best initial test) Non-specific (high ESR, Hypercalcemia... ) Bronchoalveolar lavage: increased lymphocytes (T-helper cells) (CD4/CD8> 4) Spirometry: restrictive pattern Biopsy of lung or lymph nodes showing non-caseating granuloma (the most accurate) The ACE level may be elevated, but it is not specific, not sensitive, and has a minor role in diagnosis. However, it can be used for monitoring the disease activity Stages of sarcoidosis according to Chest X-Ray: Stage I: Bilateral Hilar Lymphadenopathy (BHL)Stage 2: BHL + interstitial infiltrates Stage 3: diffuse interstitial infiltrates only Stage 4: diffuse fibrosis Poor prognostic factors in sarcoidosis: Insidious onset, symptoms > 6 months An absence of erythema nodosum Extra-pulmonary manifestations: e. g., lupus pernio,splenomegaly Chest X-Ray: stage Ill-IVBlack people and Older ages Treatment: Stages 1 spontaneous resolution Steroids may be needed If:o Stages > 2 with progressive symptomso Hypercalcemiao Eye-heart or CNS involvement Page 1107 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Extrinsic Allergic Alveolitis (EAA) Also known as (hypersensitivity pneumonitis) Inhalation of organic substances leads to the destruction of alveoli and pulmonary fibrosis Involves type 3 or type 4 hypersensitivity reaction (Type 3 more prominent) Examples of EAA: Farmer's Lung (Thermophilic Actinomycetes) Bird Breeder's/Bird Fancier's Lung (Chlamydia psittaci in bird droppings) Humidifier Lung (Aureobasidium pullulans) Sauna Taker's Lung (Aureobasidium) Clinical features: Acute EAA: o Dyspnea, cough, fever, chills, malaise (lasting 18-24 h) o CXR: diffuse infiltrates o Type Ill (immune complex) reaction Chronic EAA: o Insidious dyspnea, cough, anorexia, weight loss o PET: progressively restrictive o Chest X-Ray: upper lobe lung fibrosis. o Type IV (cell-mediated, delayed hypersensitivity) o Chronic changes are irreversible Diagnosis: Chest x-ray: (Upper zone fibrosis) Bronchoalveolar lavage (Lymphocytosis) Blood-NO EOSINOPHILIA Treatment: Avoid exposure Steroid Drug and radiation-induced ILD Drug-induced ILD examples: Bleomycin, Cyclophosphamide, Amiodarone, Procainamide, Illicit drugs (heroin, methadone), Antibiotics (nitrofurantoin, penicillin, sulfonamide), Anti-inflammatory Agents (methotrexate, penicillamine), Gold salts, Rituximab, anti-TNF agents (Infliximab, Etanercept, Adalimumab). Page 1108 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Radiation-Induced fibrosis: Early-onset fibrosis: (before 6 weeks) Late-onset fibrosis: (6-12 months post-exposure) Infiltrates conform to the shape of the radiation field Adult Respiratory Distress Syndrome (ARDS) ARDS: is a respiratory failure from lung injury or due to systemic disease Presented with Secondary hypoxia + distress + non-cardiogenic pulmonary edema Prognosis is Poor, Mortality 30-40% Causes: ARDS is idiopathic, but a large number of illnesses and injuries are associated with alveolar damage; examples are: Aspiration Sepsis Near drowning Pneumonia, PE, COVID19 Burn, Shock, Trauma Diagnosis: Chest X-ray shows bilateral infiltrates and air bronchogram. ABCs: 0 Pa02/F102< 300: mild ARDS 0 Pa02/F102< 200: moderate ARDS 0 Pa02/F102< 100: severe ARDS Nofe: on room air, the Fi02 is 21% (0. 21 so if the patient has Pa02 of 105 on room air, then the Pa02/Fi02 = 105/0. 21 = 500 Example: Patient on 50% oxygen has Pa02 of 80 mm Hg, calculate the Pa02/fi02 ratio: Pa02/fi02 ratio = (80/0. 5) = 160 (160 means moderate ARDS) Treatment: Mechanical ventilation with the following settings o Low Tidal volume 6ml/kg (best support) o High PEEP to keep alveoli open A prone position of the patient's body Steroids may be used in the late stage if fibrosis occurs. Treatment of the underlying disorder Page 1109 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Respiratory infections Pneumonia Introduction and classification Pneumonia is defined as an infection of the lung, which can be bacterial, viral, or fungal Risk factors: Low Immunity Low ciliary movement (e. g., smoking, CF, and Kartagener's syndrome) Decrease protective mechanisms like gag and cough reflex Aspiration pneumonia usually presents in the Right middle or lower lobe, Due to the vertical direction of the right Bronchus Pneumonia classification: Community-acquired (CAP): pneumonia that occurs before or within 48 hours after hospital admission o Typical CAP (high fever, productive cough, unwell toxic patient) usually shows lobar consolidation on chest X-Ray. o Atypical CAP is caused by organisms that are not detectable on gram stain and not culturable on standard blood agar, usually with milder symptoms with no SPUtum and diffuse patchy infiltration on chest X-Ray. Hospital-acquired pneumonia (HAP): o It started 48 hours after admission. o Staphylococcus aureus is the most common cause o Pneumonia developed in the first 48 hours post-admission is CAP, not HAP. Page 1110 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Most common cause Presentation Chest x-ray Other causes Typical pneumonia Pneumococci Fever, productive cough Lobar consolidation H influenza type B Staph aureus Pseudomonas E coli Klebsiella Atypical pneumonia Mycoplasma Myatgia, arthralgia Patchy infiltration Viruses (e. g., CMV) Fungi Legionella Chlamydia Table 46: Typical vs. atypical pneumonia Differential diagnoses of pneumonia The clinical scenario Typical pneumonia Pneumonia after recent influenza Alcoholism and DM. Cavity lesion on chest x-ray. Poor dentition, aspiration Atypical pneumonia Young, Healthy patients Associated Cold AIHA Associated erythema multiform Contaminated water sources. Air conditioning systems. Diarrhea, Hyponatremia. HIV positive patients Pneumonia in COPD patient CF or bronchiectasis patient The most likely organism Strep pneumonia (80%) Staph aure US Klebsiella pneumonia Anaerobic bacteria Mycoplasma pneumonia Legionella pneumocystis jiroveci (PCP) Hemophilus influenzae Pseudomonas Table 47: Differential diagnosis of pneumonia | INTERNAL1-17AFEEF-MERGED-1.pdf |
Typical pneumonia The most common cause is streptococcus pneumonia Streptococcus pneumonia is characterized by rapid onset, higher fever, rusty sputum, and the activation of herpes labialis. Clinical picture: Cough with sputum Fever or hypothermia Dyspnea (if severe infection) Hemoptysis can be a feature Pleuritic chest pain Signs of consolidation (Bronchial breathing, Egophony) Can cause Atrial fibrillation Diagnosis: Chest X-ray (best initial test) Leukocytosis (non-specific marker) ABGs and Pulse oximeter to assess the severity Gram stain and Culture (best to determine etiology) Treatment: Supportive (02, IV fluids, Analgesia) Salbutamol nebulizer or MDI Antibiotics Hospitalize if needed according to CURB65 criteria (1 point for each element) c 65 Confusion Urea>7 RR < 90/60 Age O-1 point: Treatment at home 2 — 3: admission to the hospital 4 — 5: ICU admission Table 48: CURB65 score for pneumonia prognosis page 1112 | INTERNAL1-17AFEEF-MERGED-1.pdf |
The choice of antibiotic in typical pneumonia treatment: Outpatient cases: o If previously healthy with no antibiotic use in the past 3 months, use macrolides (azithromycin or clarithromycin) or Doxycycline o If there are comorbidities or use of antibiotics in the past 3 months, use respiratory fluoroquinolones (Levofloxacin or Moxifloxacin) Inpatient cases: Respiratory fluoroquinolone (Levofloxacin or Moxifloxacin) or o Ceftriaxone with Azithromycin Indications for the pneumococcal vaccine: Everyone above the age of 65 years Chronic (heart, liver, lung, or kidney) diseases Functional or anatomical asplenia Hematologic malignancies (leukemia, lymphoma)Immunosuppression (DM, alcoholics, steroid use, HIV)CSF leak and cochlear implantation recipients If the vaccine was given before the age of 65 for anothercondition, it should be repeated 5 years after the first dose Table 49: indications for the pneumococcal vaccine Klebsiella pneumonia It is classically in alcoholics and DM patients Presented with Red-Current jelly SPUtum (hemoptysis fromnecrotizing disease)Present with aspiration pneumonia A common cause of Lung Abscess and cavitating lesion onchest x-ray Mycoplasma pneumonia The most common cause of atypical pneumonia Present with a dry cough, rarely severe Associated with:o Bullous myringitis (eardrum infection)o Cold agglutinin hemolytic anemia o Erythema multiform (rash with typical target lesion) o Splenomegaly This bacterium has no cell wall, so it is resistant to antibiotics that inhibit cell wall like penicillin Treatment: Erythromycin, clarithromycin Page 1113 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Legionella pneumonia Commonly in air-conditioning systems, workers Associated with: o Gl symptoms (abdominal pain and diarrhea)o CNS symptoms (e. g., headache and confusion)o Hyponatremia Lymphopenia is a feature Diagnosis by Urine antigen test Treatment: Macrolides (e. g., Erythromycin) Pneumocystis Carinii Pneumonia (PCP) It is caused by yeast-like fungus pneumocystis jiroveci Usually seen in patients with cancer, chemotherapy, HIV, and drug abusers It is the most common cause of pneumonia in HIV patients (with CD4 < 200) Pneumothorax is a common complication Clinical features: dyspnea, cough, fever, and Few chest signs Diagnosis: LDH level is always elevated The most accurate test is bronchoalveolar lavage Treatment: Cotrimoxazole (best initial for treatment and prophylais) Steroids are used if hypoxia is present (decrease mortality) IV pentamidine for severe cases Ventilator-associated pneumonia (VAP) Mechanical ventilation interferes with normal protective mechanisms (cough, mucociliary clearance) The most common pathogen is Acinetobacter Present with fever, new infiltration, and purulent secretions come from the endotracheal tube A sputum culture is the best test Treatment: (three-drug combination) Anti-pseudomonas agent (cephalosporin or penicillin, or Carbapenem) Another antipseudomonal agent (aminoglycoside or fluoroquinolone) MRSA agent (vancomycin, or linezolid) Page 1114 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Tuberculosis (TB) It is an infection caused by Mycobacterium Tuberculosis (an Acid-fast bacilli bacterium that can cause caseating granuloma) Can be latent in 95% and primary active disease in 5%, or secondary active disease (activation of latent infection) It can be pulmonary, extrapulmonary, or both. Transmission of TB Airbome (droplet nuclei) that remain suspended in the air for several hours before inhaled TB bacteria invade the immunity, survive and replicate in the macrophages Classification: Primary infection: o More common in children and immunocompromised patients o Not associated with high-level transmissibility Secondary (post-primary) infection: o More, if the infection is acquired later in lifeo Because of the frequent cavitation, it is more often infectious. Risk factors for TB reactivation: HIV infection (the most potent risk factor)Silicosis (silica is toxic to macrophages)Chronic renal failure and hemodialysis Diabetes mellitus Intravenous drug use Immunosuppressive treatment Smoking Features of pulmonary TB: Primary infection: o More common in children than adultso Usually asymptomatic unless progressed or immune-suppressed patients. o Cough, hemoptysis, upper lobe consolidation, fever,and pleuretic chest pain with no response to usualantibiotics Page 1115 | INTERNAL1-17AFEEF-MERGED-1.pdf |
o Constitutional symptoms (night sweating, weight loss, anorexia) o Ghon's complex is a lesion seen in the lung caused by tuberculosis. The lesions consist of a calcified focus of infection and an associated lymph node Post-primary (secondary): o More common in adults (called Adult-type) o Mainly in the apical zones (higher oxygen tension compared to the lower zones) o The lesion varies from small infiltration to extensive cavitation Features of extrapulmonary TB: Lymph nodes: the most common (35% of extrapulmonary cases) Genitourinary TB TB potyserositis: pleuritis, peritonitis, and pericardifis Pott's disease: TB infection of the vertebrae Hepatitis, meningitis, osteomyefitis. Intestinal TB most commonly occurs in the ileocecal region, causing intestinal obstruction. Adrenal involvement: Hypoadrenafism can manifest. Features of miliary TB: Widespread hematogenous dissemination of TB to the lung, abdominal organs, CNS, etc. The lesions are usually yellowish granulomas of 1 — 2 mm in diameter Fever, night sweats, anorexia, weakness, and weight loss are presenting symptoms in the majority of cases Diagnosis of active TB: Chest —X-Ray: upper zone lesion, Hilar lymphadenopathy, or miliary TB. Sputum or tissue smear for acid-fast bacilli (AFB) Nucleic acid amplification technology o Rapid to confirm TB in AFB-positive patients o Real-time nucleic acid amplification technology simultaneously detects TB and rifampin resistance in less than 2 hours Mycobacterial culture: o Sputum stain and Culture for acid-fast bacilli (done 3 times to exclude TB) o Modern cultures require 2—3 weeks to confirm the presence of TB Page 1116 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis of latent TB: PPD test is indicated. Tuberculin purified protein derivative (PPD) test Also called Mantoux skin test or tuberculin skin test (TST) The test measures the response to antigenic stimulation by T cells that reside in the skin. It will not differentiate between active and latent TB Once the PPD test is positive, it remains positive for life Mantoux test is considered positive in the following conditions: Induration 2 15 mm induration (for any patient) Induration 10 mm induration and one of the following : o A recent arrival from a high prevalent country o I. V drug user o Child < 4 years Induration 5 mm induration and one of the following: o HIV positive o Recent contact with TB patient o Typical TB changes on chest x-rayo Organ transplant Table 50: Mantoux test interpretation Prevention: BCG vaccination Provided for all infants within 45 days of life A booster dose can be provided for those who are travelingto endemic areas Isolation of TB cases should be done Treatment: Rifampin, Isoniaid (INH), Pyrazinamide, Ethambutol (RIPE):o Give 4 drugs (RIPE) for 2 months, then,0 2 drugs (RI) for 4 months If bacteria are sensitive to all drugs, no need for Ethambutol If previously treated, add streptomycin For a patient with latent TB, INH for 9 months. Treatment is extended to 9 months if (osteomyefitis, miliary TB, or pregnancy)Steroids can decrease neurogenic complications in TBmeningitis. All Anti-TB are bactericidal except Ethambutol which is a bacteriostatic Page 1117 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Drug Rifampicin Isoniazid Pyrazinamide Ethambutol Adverse effects Red-colored body secretions Peripheral neuropathy Hyperuricemia Hepatotoxicity Optic neuritis/ color vision Streptomycin Ototoxic, nephrotoxic Treatment No need for treatment Prophylactic with pyridoxine (Vit B6) Treat if symptomatic only Adjust dose in renal failure Dose adjustment. Table 51: the side effects of Anti-TB medications Lung abscess Locafized collection of pus in the lung occuräng in patients with large-volume aspiration not adequately treated Predisposing factors are processes that interfere with swallowing or coughing (e. g., stroke, Intoxication) Clinical features: Cough with a large volume of foul-smelling sputum Fever, Weight loss, clubbing fingers Diagnosis: Cavity with Air fluid level appears on imaging A lung biopsy is the best to determine the pathogen A sputum culture is not beneficial (all people have normal flora of anaerobes in their mouth) Figure 13: A chest X-ray showing Air fluid level (Lung abscess) Treatment: Clindamycin or penicillin Surgical drainage is used only if failed medical therapy. Page 1118 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pleural diseases Pleural effusion Pleura: is a serous membrane covering the lungs. It has 2 parts: parietal pleura (outer) and visceral pleura (inner) Pleural space: is the space between parietal and visceral pleura and normally contains 25 ml of fluid called serous fluid Pleural effusion is an abnormal collection of fluids within the pleural space Pleural fluids can be Transudates or exudates Pneumothorax: air in the pleural space Hemothorax: blood in pleural space Chylothorax: lymphatic fluid in pleural space Empyema: Pus in the pleural space Causes: Transudative Pleural effusion CHF (most common) Liver cirrhosis Nephrotic syndrome Peritoneal dialysis Myxoedema Constrictive pericarditis Exudative Pleural effusion Infection, Empyema Malignancy Inflammation Trauma Oesophageal perforation Asbestosis Superior vena cava syndrome Meigs t Syndrome Pulmonary embolism can cause both exudates and transudates but can cause exudates more often Table 52: Causes of Exudative and Transudative pleural effusion Clinical picture: Can be asymptomatic Dyspnea, chest pain Stony Dullness to percussion + Decreased TVF + tracheashifted away Decreased or absent breath sounds, bronchial breathingabove effusion. Signs and symptoms of the cause Page 1119 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: Chest X-ray (best initial test) o PA view will show the effusion if > 250 m L (Loss of costophrenic angle, meniscus sign) o A lateral view will show the effusion if > 50 ml in amount. o Lateral decubitus will show a shifting of fluids (now replaced by chest ultrasound and paracentesis) CT scan (more informative than chest x-ray) Thoracentesis (most accurate test): differentiate exudates from Transudates ' 'Alf,. Figure 14: chest X-Ray showing bilateral pleural effusion How to differentiate exudate from transudate: Check for pleural fluid protein: If > 30 g/l, consider exudates If < 20 g/l, consider transudates If 20 30 g/l and one of the light's criteria are found, consider exudates Modified Light's criteria: Pleural/serum protein ratio > 0. 5 Pleural/serum LDH ratio > 0. 6 Pleural fluid LDH > two-thirds the upper limit of normal serum Table 53: Modified lights criteria Page 1120 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatmen F. Small effusion needs no treatment Treat the cause Cardiogenic pleural effusion is highly responsive to diuretics Thoracentesis (therapeutic and diagnostic) If refractory and recurrent, pleurodesis (intrapleural bleomycin or talcum powder) If empyema develops, a chest tube, antibiotics, and surgical drainage may be needed Asbestos-related lung diseases Can be asymptomatic for 20 — 30 years (latency period) Pleural exudative effusion and hemoptysis may develop Several diseases occur due to asbestos exposure: Pleural plaques are the most common asbestos-related lung disease (Benign with no malignant transformation) Asbestos may cause pleural thickening Asbestosis (lower lobe fibrosis) Lung cancer: Asbestosis and smoking together increase therisk by 50 times Mesothelioma is a malignant asbestos-related disease of thepleura Diagnosis: Calcified pleural plaques found on chest x-ray Biopsy (best) Treatment: Extra-pleural pneumonectomy (rarely successful) Page 1121 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Other respiratory disorders Sleep apnea syndromes It is defined as a repetitive period of apnea during sleep leading to distorted sleeping, snoring, daytime sleepiness, and hypertension A period of more than 10 seconds without breathing is considered an apneic episode Causes: Obstructive steep apnea (OSA): o Obesity (the most common cause) o Other causes include macroglossia, Large tonsils, Marfan's syndrome, etc. o The chest wall and abdominal movements are present during the apneic episode Central sleep apnea: o CNS disorder o Drug-induced respiratory center suppression o The chest wall and abdominal movements are absent during the apneic episode. Mixed apnea: both central and obstructive. Clinical features: Daytime somnolence, headache, impaired memory Loud snoring (usually noted by a sleep partner) Diagnosis: Epworth Sleepiness Scale (questionnaire by the patient) Polysomnography (Sleep study) is the most accurate test: a pulse oximeter, EEG, airflow, and thoracoabdominal movements may be monitored during sleep. The severity can be determined by the AHI o Mild: AHI 5— 14 events per hour o Moderate: AHI 15 —29 events per hour o Severe: AHI 30 events per hour ABCs show compensated respiratory acidosis Apnea hypopnea index (AHI) is the number of apneas plus hypopneas per hour of sleep Page 1122 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Obstructive sleep apnea: Weight loss C-PAP (continuous positive airway pressure) (first line) o Uvulopalatopharyngoplasty (surgical widening of the airways) o Intra-oral devices (if C-PAP is not tolerated) Central sleep apnea: o Avoid alcohol and sedatives. o Acetazolamide may be effective by causing metabolic acidosis and stimulating respiration o Medroxyprogesterone (a central respiratory stimulant) Complications: Respiratory failure Pulmonary HTN Cor-pulmonale Pulmonary arterial HTN (PAH) Mean pulmonary arterial pressure > 25 mm Hg at rest or Systofic pulmonary pressure > 40 mm Hg The mean arterial pressure (MAP) = systolic + 2(diastolic) / 3 Causes: Primary pulmonary HTN, also known as idiopathic pulmonary arterial HTN (PPH or IPAH) Any form of chronic lung disease can cause Pulmonary HTN: (COPD, Chronic pulmonary emboli, Polycythemia Vera, Interstitial lung disease, Fibrosis, Hypoxia) Clinical features: Dyspnea, Fatigue, Syncope, Chest pain Wide splitting S2 (due to delayed RV emptying), loud S2, raised JVP, RVH Raynaud's phenomenon Tricuspid regurgitation Diagnosis: Chest X-Ray (best initial test): the pulmonary arteries will bedilated proximally and narrowed distally Echocardiography: estimates the pulmonary blood pressureusing Doppler ultrasound Right heart (Swan-Ganz) catheter (the most accurate test)ECG: RAD, right side hypertrophy Page 1123 | INTERNAL1-17AFEEF-MERGED-1.pdf |
CTPA and V/Q scan might show PE if it was the cause CBC may show polycythemia (due to hypoxia) Treatment: Treatment of the cause Sildenafil, bosentan, or prostacyclin analogs are the best CCBs, hydralazine, and nitroglycerin are less effective Diuretics for heart failure Oxygen slows the progression (especially in COPD) Definite treatment: heart-lung transplant Eosinophilic lung diseases Diseases that are associated with increased eosinophils in bronchoalveolar lavage and lung biopsy Causes: Loffler's syndrome: pulmonary eosinophilia in response to parasitic infection (e. g., Ascaris, Strongyloides, Dirofilaria) Allergic Bronchopulmonary Aspergillosis (ABPA) Eosinophilic pneumonia (can be viral or bacterial) Churg-Strauss syndrome (vasculitis) Drug-induced (cocaine, Phenytoint some antibiotics, etc. ) Allergic Bronchopulmonary Asperqillosis (ABPA) Hypersensitivity of the lung due to the fungal antigen (Aspergillus fumigatus) Clinical scenario: Patient with asthma or CF presents with infiltration in routine CXR The persistent inflammatory response may lead to bronchiectasis. Clinical features: Cough, Wheezing, Hemoptysis Diagnosis: CBC: eosinophilia Skin test reactivity to Aspergillus antigen High lg E level Imaging: CXR, CT scan (pulmonary infiltration) Aspergillus fumigatus in blood or SPUtum Treatment: Prednisolone (regular low dose) ltraconazole (An anti-fungal agent) may be used If resistant, lg E Monoclonal Antibodies Page 1124 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Aspergilloma: forming fungus ball may be asymptomatic or present with Hemoptysis, treatment by (surgery, Bronchial artery Embolization) Respiratory failure Failure of the respiratory system to maintain normal blood gases Diagnosis: ABCs There are two types: Type 1: Hypoxia without Hypercapnia Type 2: Hypoxia with Hypercapnia Treatment: Intubation and Treatment of the cause Hypoia: P02 < 60 mm Hg, Hypercapnia: Pa C02 > 50 mm Hg Causes of Type 1 Emphysema Moderate asthma Neuromuscular disorders Pneumonia ARDS High altitude Right to left shunt Causes of Type 2 Chronic bronchitis Life-threatening asthma Neuromuscular disorders Chest wall deformities OSA Suffocation Table 54: causes of Type vs. Type 2 respiratory failure Page 1125 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Respiratory neoplasms Small cell lung cancer Also known as Oat cell lung cancer Usually central Usually, metastatic disease by the time of diagnosis Management: Combination of chemotherapy and radiotherapy More extensive disease: palliative chemotherapy Surgery has no rule in the treatment Non-Small Cell lung cancer Three main subtypes of non-small cell lung cancer Squamous cell cancer: Typically, central and can cause a cavitary lesion Strongly associated with finger clubbing Adenocarcinoma: The most common type of lung cancer in non-smokers, although the majority of patients who develop lung adenocarcinoma are smokers Typically, peripheral Large cell lung carcinoma: Poorly differentiated tumors with a poor prognosis Typically, peripheral Paraneoplastic features of lunq cancers Small cell cancer. ADH secretion: SIADH (hyponatremia) ACTH secretion: Cushing's syndrome Antibody formation: Lambert-Eaton-myasthenic syndrome Squamous cell cancer: PTHr P secretion: Hypercalcemia TSH secretion: Hyperthyroidism Hypertrophic pulmonary osteoarthropathy (HPOA) Adenocarcinoma: Gynecomastia H POA Page 1126 | INTERNAL1-17AFEEF-MERGED-1.pdf |
HPOA: a triad of periostitis, digital clubbing, and painful arthropathy of the large joints. Pancoast tumor: is a peripheral tumor that OCCUrs at the apex of the lung, usually spreads to adjacent tissue, usually non-small cell lung cancer, traditionally questioned as a cause of Horner Syndrome Homer syndrome: ptosis, myosis, anhidrosis, and enophthalmos, due to a defect in the sympathetic nervous system, can be caused by Pancoast tumor. Chest wall deformities Kyphosis: abnormal anterior deviation of the thoracic spine Scoliosis: abnormal lateral deviation of the thoracic spine Kyphoscoliosis: mixed with Kyphosis and scoliosis Pectus excavatum (funnel chest): the lower end of thestemum is curved backward Pectus carinatum: (Pigeon chest): outward protrusion of thesternum and rips (caused by severe asthma duringchildhood) Normal Barrel chest scoliosis Pedctl$ camatum Pectus excavaturn Kypho± Figure 15: Different types of Chest deformities Page 1127 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Chest X-Ray lesions Causes of cavitating lesions on chest X-Ray: Lung abscess Squamous cell lung cancer Tuberculosis Wegener's granulomatosis Pulmonary embolism Rheumatoid arthritis Sarcoidosis Aspergillosis, histoplasmosis, coccidioidomycosis Causes of Nodular lesions on Chest X-Ray: Benign tumors, such as hamartomas Infections (TB, histoplasmosis, hydatid cyst) Inflammation (RA-Caplan syndrome, Sarcoidosis, Wegener's granulomatosis) Malignant tumors (primary or metastatic lung cancer) Causes of bilateral hilar lymphadenopathy on Chest X-Ray: Sarcoidosis, EAA Infection: TB, Fungal infections, mycoplasma Malignancy: Lymphoma, carcinoma, mediastinal tumors Page 1128 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cardiology CHAPTER 4 AM JAD K. ALA FEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1129 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diseases of the heart conduction The normal Heart conduction SA node generates impulses that spread through atria, delayed at the AV node, spread down through the HIS bundle, spread to right and left bundle branches, then reach Purkinje fibers Automaticity: cardiac cell's ability to spontaneously generate an electrical impulse (depolarize) — normally at the SA node SA node typically generates impulses at 60 — 100 per minute. AV node typically delays impulse for 0. 08 seconds. AV Node SA Node Left bundle branch htemodal Pathways Right bundle branch Purkinje fibers Figure 16: the heart conduction system On ECG: P wave: represents atrial depolarization (contraction) QRS waves: represents ventricular depolarization (contraction) T wave: represents ventricular repolarization (relaxation) Page 1130 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Basic ECG The essential parts to be assessed on ECG are (Rhythm, Rate, Axis, intervals, and Chamber enlargement) Rhythm: The normal sinus rhythm of the heart, generated from SA node, Regular, Each P wave followed by a QRS complex then T wave If the rhythm is irregular, so you have to determine if it is regularly irregular or irregularly irregular Rate: Normal heart rate is 60 — 100 bpm Rate more than 100 bpm is called Tachycardia A rate of less than 60 bpm is called bradycardia Calculate the rate by dividing 300 by the number of large squares between each QRS complex The Axis deviation: The normal axis is between-30 and +90 degrees Can be determined by examining Leads l, Il, And AVFCauses of RAD (RALPH-W): o Right ventricular hypertrophy (RVH)o Anterolateral Ml o Left Posterior Hemiblock o WPW syndrome Causes of LAD (VILLAH-W):o Ventricular tachycardiao Inferior Mlo Left Anterior Hemiblocko WPW syndrome Axis deviation Lead I Normal Positive Right axis deviation (RAD) Negative Left Axis Deviation (LAD) Positive(v) Extreme axis deviation Negative Leads Il and AVF Positive Positive Negative Negative (v) Table 55: Axis deviation interpretation in ECG Page 1131 | INTERNAL1-17AFEEF-MERGED-1.pdf |
The intervals: PR interval: o Normally 120 — 200 ms (3-5 small squires) o Prolonged in AV block and aortic valve abscess o Short in WPW syndrome The QRS complex: o Normal Q wave (< 40 ms width and < 2 mm depth) o The normal QRS complex is < 120 ms (< 3 ss) (Narrow complex) o Poor R wave progression from V! to V6 is a non-specific sign of infarction The QT interval: o Normal corrected QT (QTc) 380-440 ms (9. 5-11 ss) (QTc = QT/MRR) Chamber enlargement: Left atrial (P mitrale): P wave > 120 ms in lead Il Right atrial (P pulmonale) P wave > 2. 5 mm height in lead Il Left ventricular: S wave in VI + R wave in 35 mm height Right ventricular. RAD with R wave in VI > 7 mm Condition Hyperkalemia Hypokalemia Hypocalcemia Hypercalcemia Hypomagnesemia ECG changes Low or absent P, Prolonged PR interval, Wide QRS. Peaked T wave, Sine wave (severe) High P wave, Depressed ST segment, Broad flat T wave, U wave Intermittent long QT interval, Long ST segment, Torsade de points Short QT interval, Short ST segment, Wide flat T wave, Osborn wave Tall T wave, ST depression Hypermagnesemia Long PR, Wide QRS Hypothermia Long PR, Long QT, Wide QRS, Shivering artifact, Osborn wave, Low voltage Bradyarrhythmia, PVCs Table 56: ECG changes in different conditions page 1132 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Arrhythmias (Abnormal conduction) Sinus Tachycardia Rhythm and rate: regular and fast (HR > 100 bpm) Causes: fever, pain, anxiety, pregnancy, exercise, hyperthyroidism, C02 retention, and drugs Treatment: treat the cause FOwe 17: strep rhythm ECG shovmg shus tachyccrcü) Sinus Bradycardia Rhythm: regular and slow (HR < 60 bpm) Causes: drugs, Myxoedema, heart block, high ICP, hypothyroidism, athletes, and jaundice Obstructive jaundice is often fisted among the causes of bradycardta-It is Usually attributed to the effect of bde salts on the sinoatriai node. Treatment: no need if asymptomatic, atropine ifsymptomatic, but Pacemaker is the definitive treatment insevere cases FOure 1B: strep rhythm ECG showing sinus Wadyccr± Sick Sinus Syndrome (SSS) tt is the most common indication for pacemaker placement Sinus node dysfunction, block/pause, common in theelderfy. It occurs due to age-related degeneration of the cardiacconduction system and fibrosis of the SA node (the most common Cause)It may be associated with tachyarrhythmia, called (Tachy-Brady syndrome)AF and thromboembofism may occur Page 1133 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Can cause intermittent lightheadedness, syncope, or sudden cardiac death Treatment: if symptomatic, cardiac pacing and anticoagulants for AF Figure 19: strep rhythm ECG showing Sick Sinus Syndrome Atrial fibrillation (AF) AF is the most common sustained arrhythmia Re-entrant waves within the atria More in elderly, DM, HTN, and IHD patients Figure 20: a strep rhythm ECG showing Atrial fibrillation Causes: (IHD, pneumonia, HTN, thyrotoxicosis, pericarditis, alcohol) Types: Paroxysmal (less than 7 days, stop spontaneously) Persistent (more than 7 days, stopped by medications or cardioversion) Permanent (do not stop) Signs of Instability in cardiac arrhythmias: Altered mental status Loss of consciousness Hypotension (shock) Pulmonary edema Respiratory distress Increasing chest pain Page 1134 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Managment of Atrial fibrillation (AF) Is the atient stable? o Sunchtonized Is the patient cardioversion old? Is the history of AF Rate > 48 hours? control NO Medical cardioversion Do,TEE or provide anticoagulation for Flecainide,propafenone 3 weeks before cardioversion and 4,amiodarone or sotalol weeks after. Figure 2 J : the approach for Atrial fibrillation treatment The drug of choice for AF with CHF is Digoxin Oral anticoagulants are the first-line anticoagulants in atrial fibrillation patients CA2DS2 VAS score Points Interpretation CHF HTN Age > 75 Stroke or TIA Vascular disease Age > 65 Sex (female)2 2Score O: Aspirin or no anticoagulation Score 1: Aspirin or anticoagulation Score 2 or more: Anticoagulation Table 57: CA2DS2 VAS scoring system Page 1135 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Atrial flutter Figure 22: a strep rhythm ECG showing Atrial flutter Large re-entry circuit in Right Atrium Atrial rate: 300 BPM Ventricular rate: 300 bpm (1:1), 150 (2:1 or 100 (3:1) Rhythm: regular or maybe irregular P waves: saw-tooth appearance, best seen in leads Il, Ill or AVE QRS: normal (less than 120 ms) Treatment: Same as atrial fibrillation Cardioversion guidelines are the same as Atrial fibrillation Multifocal Atrial Tachycardia (MAT) Multiple foci from the atria with re-entrant pathways Associated with COPD, Hypoxia It may be asymptomatic ECG: At least 3 different P wave morphologies Rate > 100 bpm Figure 23: A strep rhythm ECG showing MAT Treatment: Treat as AF but avoid Beta-blockers if lung disease is present Page | INTERNAL1-17AFEEF-MERGED-1.pdf |
Supraventricular Tachycardia (SVT) SVT: regular, no P wave, narrow QRS, and HR > 150 bpm Figure 24: A strep rhythm ECG showing ST Causes: (Hypokalemia, Hyperthyroidism, Excessive alcohol) Treatmen F. For unstable patients: synchronized cardioversion. For stable patients: o Step 1: Vagal maneuvers: (carotid massage, ocular massage, Ice on the forehead, Valsalva maneuver) o Step 2: Adenosine (6, 12, then 12 mg I. V push) o Step 3: I. V verapamil, Diltiazem, or metoprolol. o Step 4: synchronized cardioversion (if unresponsive) Definitive treatment: catheter ablation. Important notes about SVT treatment: Auscultate for bruits before carotid massage (risk of CVA) Adenosine is contraindicated in asthma patients Ventricular Tachycardia (VT) Figure 25: A strep rhythm ECG showing Ventricular tachycardia VT: Regular, wide QRS (> 120 millisecond), no P wave, no Twave Rate > 100 (usually 140-200)Associated with (AV dissociation + capture beats)Can be monomorphic or polymorphic Treatment: For unstable patients: DC cardioversion For stable patients: amiodarone, Lidocaine, procainamide Page 1137 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Torsade de points (Td P) Figure 26: A strep rhythm ECG showing Torsade de points It is also known as (twisting points) It is associated with Long QT syndrome May result in sudden death Treatment: For unstable patients: cardioversion For stable patients: I. V magnesium sulfate Always correct the underlying cause. Hypo-Hypo-K+ Hypo-Ca++ Hypo-Mg++ Hypothermia Anti-Antiarrhythmics (amiodarone, sotalol) Antidepressants (TCA) Antimalarials Antipsychotic (Haldol) Antibiotic (erythromycin)Others Ml SAH Congenital long QT syndrome (Ex: Romano-word-syndrome) Table 58: Causes of long QT syndrome and Td P Premature ventricular contractions (P VCs) Ectopic beats arise from ventricular foci Causes: Hypoxia, fibrosis, Electrolyte disturbances, heart failure, HTN, Digoxin toxicity, hypercalcemia, and hyperthyroidism. Treatment: Treat the underlying cause Avoid alcohol and caffeine If symptomatic, Beta-blockers Figure 27: A strep rhythm ECG showing Bigeminy Page 1138 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Ventricular fibrillation (VF) Figure 28: A strep rhythm ECG showing Ventricular Fibrillation Rhythm: irregular + no clear P, QRS, or T waves, no clear pattern Treatment: DC shock and ACLS protocol Note: the patient with VF never be stable Wolff-Parkinson-White syndrome (WPW) A congenital defect is characterized by the presence of an accessory bundle between the atrium and ventricle. This bundle is called the "bundle of Kenf' Type A (Left Side) or type B (Right Side) Short PR interval and early ventricular depolarization (Delta wave) Figure 29: A strep rhythm ECG showing Delta wave Treatment: Acute arrhythmias (DC shock, amiodarone, orprocainamide) Definitive treatment (electrical ablation of the bundle of Kent) Beta-blockers, CCB, and digoxin are contraindicated in WPW Page 1139 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Heart Block (AV block) Also known as AV block (atrioventricular block) Decreased or absent conduction through AV node It could be first, second, or third-degree Maybe due to RCA-mediated ischemia Types of heart block First degree AV block: long PR interval > 200ms, asymptomatic, need no treatment Second degree AV block (Mobitz type l): progressive prolongation of the PR interval, followed by failure of conduction of P wave, no need for a pacemaker. Second degree AV block (Mobitz type Il): prolongation of the PR interval followed by failure of conduction of P wave, need Pacemaker Third-degree AV block (complete AV block): P and QRS waves are not related to each other, regular P — P intervals and R-R intervals usually come with bradycardia and need Pacemaker Table 59: the ECG changes in the different degrees of AV block Page 1140 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Important to know: Pacemakers (pacer): can be temporary or permanent — the temporary one can help as a bridge until a permanent pacer is inserted. ICD (implantable cardiac defibrillator): a device implanted and used to give DC shock if needed, used in patients who are at risk of sudden cardiac death due to arrhythmias, and severe Heart failure (EF% < 35%) Indications for catheter ablation: AF: ablation at pulmonary vein bifurcation Atrial flutter: ablation of flutter focus at the right atrium WPW syndrome: ablation at the accessory bundle (bundle of Kent) Ventricular tachycardia: usually, the focus is within the right ventricle CPR in adults BLS approach: Indications for BLS use: o Cardiac arrest with no pulse o Bradycardia with poor perfusion The sequence of actions of BLS (C-A-B) o Compression (should be started immediately after no longer than 10 seconds of assessment)o Airway (open the airway after 30 compressions)o Breathing (give mouth-to-mouth breathing)High-quality CPR: Compression quality: In adults, use the heel of one hand with one hand ontop of the other. o Compress over the lower half of the sternum The chest should be depressed 5 — 6 cm in depth witheach compression The compression rate should be 100 — 120 per minute Minimize interruption (less than 10 seconds)Rotate compressor every 2 minutes or sooner iffatigued Page 1141 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Compression to ventilation ratio: o If there is no advanced airway, the compression ventilation ratio should be 30:2 regardless of the number of rescuers. o If advanced airway is present, continuous compression with one ventilation every 5 — 6 seconds o excessive ventilation should be avoided CPR in suspected or confirmed COVID-19: Wear PPE before entering the room Consider using a CPR device for adults and adolescents meeting the height and weight criteria Before intubationt use a bag mask with a tight seal and HEPA filter, if available Intubate early (use a cuffed tube, use video laryngoscopy if available) Pause chest compression to intubate Minimize closed-circuit disconnection Shockable vs. non-shockable rhythms: Asystole and PEA are non-shockable rhythms: start compression, give adrenaline every 3 —5 minutes, reassess the rhythm every 2 minutes Pulseless VT and VF are shockable rhythms: give D/C shock, start CPR for 2 minutes, then start the following cycle: o Shock + CPR for 2 minutes with adrenalin o Shock + CPR for 2 minutes with amiodarone In shockable rhythms, no adrenaline or amiodarone is given after the first shock Adrenaline is given after the second shock, but amiodarone is given after the third shock Compression is done for 2 minutes per cycle, and the patient's rhythm and pulse should be reassessed in less than 10 seconds. Page 1142 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diseases of the myocardium Ischemic Heart Diseases (IHD) Diseases of the heart due to ischemia (decreased blood perfusion) Also known as atherosclerotic heart disease or coronary heart disease The main symptom is (typical chest pain) i' Typical chest pain: Central, retrosternal Heavy, dull, squeezing in character, or pressure-like. Radiated to neck, jaw, epigastrium, shoulders, or back Increased by exercise and relieved by rest or nitrates Types of IHD: Stable Angina, Unstable angina, NSTEMI, and STEMI Types of chest pain and differential diagnosis: Pain changes with exertion: exertional chest pain (IHD) Pain that changes with respiration: pleuritic chest pain (e. g., PE, pleuritis) Pain that changes with position: positional (e. g., pericarditis) Pain that changes with palpation: chest wall tenderness (e. g., costochondritis) Risk factors of IHD: Non-modifiable risk factors: (Old age, male sex, family history(first-degree relatives), Race)Modifiable risk factors:o Diseases: DM, HTN, Dyslipidemia, obesityo Lifestyle and habits: (Smoking, Alcohol, sedentarylifestyle, saturated fatty acid diet) Page 1143 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Notes: Females after menopause will have the same risk as males for CAD Postmenopausal HRT is not protective against CAD The worst risk factor for CAD is DM The most common risk factor for CAD is HTN Only a CAD in a first-degree young family member is a risk factor High LDL is the most dangerous portion of the lipid profile in terms of risk for CAD Smoking cessation has the greatest mortafity improvement in patients with CAD The most common cause of non-ischemic chest pain is Gl causes. Premature CAD: CAD in males < 55 years or females < 65 years old Diagnostic testing: ECG: best initial test for all kinds of chest pain Cardiac enzymes: may be elevated in IHD ECG stress test: to evaluate chest pain when the cause is unclear and the ECG is not diagnostic. Coronary angiography: used to detect the anatomic location of CAD. 24 hours Holter monitor: for rhythm evaluation. Stable angina Stable angina occurs due to stable obstruction of the coronary artery Cholesterol plaque causes narrowing of the blood vessel and leads to a decreased blood supply to the heart muscles (especially during exercise or high demands) In this case, there is no infarction to the heart muscles Symptoms: Symptoms will start after 70% stenosis of the coronary artery Typical chest pain with exertion and relieved by rest 2-10 minutes (Note that ACS pain is 10 —30 minutes) Diagnosis: Just clinical diagnosis Normal cardiac enzymes Normal ECG (maybe abnormal during pain only) Stress Test Page 114 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Treat risk factors (DM, HTN, Dyslipidemia, obesity) and Improve lifestyle (stop smoking, diet, exercise) Beta-blockers (the first-line treatment) Calcium channel blockers (second-line treatment) Nitrates (used in combination with beta-blockers and CCB) Ranolaine (if the patient is still symptomatic despite an optimum dose of beta-blockers, CCB, and nitrates) Cardioprotective medications: Aspirin: reduce the risk of Ml, Stroke o ACEI: reduce the mortality rate in HF, DM, HTN, and old Ml o High-intensity statin: reduce the risk of Ml and death PCI can be done if still symptomatic after drug therapy (notimprove mortality more than drugs) CABG (coronary artery bypass graft) may be needed Coronary Artery Bypass Graft (CABG): Indications: Three vessels disease Left main artery disease Proximal LAD occlusion with EF% less than 50%Chronic disabling angina Graff used: Internal mammary artery (better)A reversed segment of great saphenous vein Table 60: CABG indications and graft used Terminology: ACS: acute coronary syndrome (STEMI, NSTEMI, UA) Stable angina is not a part of ACSST-elevation ACS: ST-elevation Ml Non-ST-elevation ACS: NSTEMI + Unstable angina (UA) CABG: coronary artery bypasses grafting PCI: percutaneous coronary intervention Page 1145 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Stress test: Types of stress tests: Exercise ECG stress test Pharmacological ECG stress test (using Dobutamine) Exercise echocardiogram stress testing Pharmacological echocardiogram stress test Contraindications of ECG stress test: Recent myocardial infarction High-risk Unstable angina Symptomatic severe aortic stenosis Uncontrolled arrhythmias causing hemodynamic instability Uncompensated heart failure Acute pulmonary embolus Acute aortic dissection Malignant hypertension Note: Beta-blockers, CCB, and nitrates should be held 48 hours before the stress test The stress test is not used for low or high-probability patients; it is only used for intermediate probability Table 6 1: Types and contraindications of stress test Notes about nitrates: Nitrates do not decrease mortality but decrease symptoms Nitrates are contraindicated with Viagra (risk of hypotension) Tolerance to nitrate can occur, so nitrate-free intervals should present Notes about beta-blockers: Treat with Beta-blockers to target heart rate of 50-60/m Beta-blockers reduce the heart rate and 02 demand s leading to mortality reduction. Non-selective Beta-blockers are contraindicated with asthma because they can cause bronchospasm Beta-blocker should not be given together with verapamil or diltiazem (risk of cardiac arrest) Page 1146 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Other notes: PCI cannot decrease mortality more than drug therapy in Stable angina but only improve quality of life and decrease symptoms The most anterior chamber of the heart is the right ventricle, while the most posterior chamber is the left atrium. Angina equivalent: exertional shortness of breath Angina decubitus: angina on changing position occurs because gravity redistributes bodily fluids. This redistribution makes the heart work harder. Unstable angina (UA) Unstable angina due to transient obstruction of the coronary' artery The plaque ruptured and mobile, causing transient obstruction of the coronary artery Symptoms: Typical chest pain at rest (central, retrosternal, heavy in character, radiated to neck —jaw-epigastrium or back) Same as stable angina, but the pain comes at rest Unstable angina may be preceded by stable angina for years Diagnosis: Cfinical diagnosis Normal cardiac enzymes (no muscle necrosis)ECG: ST depression or T wave inversion Stable angina Unstable angina (UA)Exertional pain Pain at rest or new-onset pain Crescendo-decrescendo pain Crescendo pain2-10 minutes duration > 10 minutes duration Table 62: Stable vs. Unstable angina Page 1147 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cardiac enzymes Myoglobin: The first cardiac enzyme to appear after MI (1 —4 hours) Not specific CPK (creatinine phosphokinase): Can be high in conditions other than Ml (like a skeletal muscle injury, 1M injections, rhabdomyolysis, CVA, etc. ) Onset: 4 6 hours, and offset at 2— 3 days post-MI CK-MB is useful for diagnosing re-infarction Types of CPK include: o CK-MM (found in skeletal muscles) o CK-MB (mostly found in the heart) o CK-BB (mostly found in the brain) Troponin: It is the most sensitive and specific for myocardial damage Subtypes include Troponin T, l, and C Troponin T and I are sensitive and specific for myocardial damage Onset 4 — 6 hours, offset at 10 — 14 days post-MI Causes of positive troponin other than Ml are (CKD, sepsis, pneumonia, pericarditis 50%, pulmonary embolism, heart failure, atrial fibrillation, rhabdomyolysis with cardiac injury, myocarditis, cardiac injury, and surgery) Other cardiac enzymes: AST can be released by the myocardium in case of Ml The last cardiac enzyme to rise and lasts for the longest period is LDH NSTEMI NSTEMI: infarction of cardiac muscles without ST elevation It affects the partial thickness of the myocardium, so it is called partial thickness Ml Diagnosis: Typical chest pain > 30 minutes associated with sweating and nausea High cardiac enzymes ST depression or T wave inversion (but not ST elevation) page 1148 | INTERNAL1-17AFEEF-MERGED-1.pdf |
STEMI STEMI: complete obstruction of the coronary artery with full-thickness necrosis of the myocardium, also known as full-thickness myocardial infarction. Diagnosis: Typical chest pain Elevated cardiac enzymes ST-elevation ECG changes in Ml: Within hours, peaked T wave and ST deviation (elevation ordepression) Within 24 hours, T inversion and ST-segment resolution Within a few days, pathologic Q wave (> 1/3 the R length or> 40 ms) (persist in 90% of patients and resolute in 10%)Infarction Locations and their relation to ECG: Inferior Ml: o Affected leads on ECG: Il, Ill, AVFo Affected artery: Right Coronary artery (RCA)o Most commonly associated with bradycardia,hypotension, and High JVPo High-fluid volume is recommended as this case ispreload dependent (especially in Right V4involvement)o Nitrates are contraindicated in this case Anterior MI: o Affected leads: V3—o Affected artery: left Anterior descending artery (LAD) Septal Ml: o Affected leads VI— V2o Affected artery: left Anterior descending artery (LAD) Lateral Ml o Affected leads: l, AVL, V5—V6 o Affected artery: left Circumflex artery o Leads I and AVL are high lateral leads Posterior Ml:o ST depression on the anterior and septal leads o Rarely come isolated (usually associated with inferior or lateral Ml) Page 1149 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Arterial supply of the heart: Left aortic sinus left coronary artery (LCA)-+ LAD andcircumflex Right aortic sinus right coronary artery (RCA) posteriordescending RCA supplies SA node in 60%, AV node in 90% Venous drainage of the heart: The coronary sinus drains into the right atrium Thebesian veins (minute veins in the walls of the heart chambers) Aorta RC LCA Circumflex artery LAD Figure 30: anatomy of the coronary artery Treatment of ACS Treatment for all patients with ACS at ER: (MONA-B) Morphine IV for pain relief (not suitable to use in inferior Ml-reduce preload). Oxygen (only if 02 saturation is less than 94%) Nitrates (But contraindicated in inferior Ml risk of severe hypotension) Beta-blockers (Metoprolol IV — reduces mortality) Anti-platelet and Heparin therapy: as follows: o Aspirin: for all types of ACS o If NSTEMI: Ticagrelor or Clopidogrel in addition to Aspirin + Heparin o If PCI is planned: ticagrelor or prasugrel with intravenous GP llb/llla inhibitor Page 1150 | INTERNAL1-17AFEEF-MERGED-1.pdf |
o Clopidogrel used if patient ineligible for ticagrelor and prasugrel o Prasugrel is contraindicated in those with a history of stroke/Tl A, and a lower dose is recommended for those > 75-year-old Reperfusion choice for STEMI:-If PCI cannot be achieved by 90 minutes in the same hospital or 120 minutes in the nearest PCI-capable hospital, then do thrombolysis If thrombolysis is contraindicated — do PCI If failed thrombolysis, PCI should be done After reperfusion: ACE inhibitors should be used unless contraindicated Dual antiplatelet therapy Continue Statin therapy heparin is indicated during the period of hospitalization TIMI score for UA and NSTEMI: (score from O — 7): Age 65 years old 3 Risk factors for CADKnown case of CAD (> 50% stenosis)Aspirin used in last week2 anginal episodes in the previous 24 hours ST deviation Positive cardiac markers If the score is 3, use LMWH, Glycoprotein IIB/llla inhibitor, and early angiography Table 63: TIMI score for UA and NSTEMI Signs of successful reperfusion after STEMI:Accelerated Idioventricular arrhythmiao Also known as reperfusion arrhythmia o Early (within 6 hours), frequent (> 30 per hour), andrepetitive (> 3 consecutive hours) o Ventricular tachycardia is considered benign if itappears within 24 hours post-reperfusion therapies. Itneeds no treatment. Regression of ST-elevation by 50% Page 1151 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Contraindications to thrombolytics: Absolute contraindications: Prior intracranial hemorrhage (ICH) o Significant closed head trauma or facial trauma within 3 months Intracranial or intraspinal surgery within 2 months Known structural cerebral vascular lesion or malignant intracranial neoplasm o Ischemic stroke within 3 months o Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) o Severe uncontrolled hypertension (unresponsive to emergency therapy) o For streptokinase, prior treatment within the previous 6 months Relative contraindications: o Traumatic or prolonged (> 10 minutes) cardiopulmonary resuscitation (CPR) or major surgery less than 3 weeks previously o History of prior ischemic stroke not within the last 3 months o Recent (within 2-4 weeks) internal bleeding o Pregnancy o Current use of an anticoagulant (e. g., warfarin) with INR > 1. 7 or PT > 15 seconds Page 1152 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Notes: A stent could be inserted during PCI to keep the coronary artery patent Two types of stents are available (drug-eluting and bare-metal stents) Dual antiplatelet therapy should be used with Aspirin and Clopidogrel post-MI Dual antiplatelet therapy lasts for 1 year in the drug-eluting stent and 1 month only in bare metal The most common cause of re-stenosis post PCI is: non-compliance to dual antiplatelet therapy Nifedipine increases cardiac output and heart rate leading to increased oxygen demand (should be avoided in ACS) Avoid NSAl Ds and steroids in periinfarction pericarditis; they interfere with ventricular healing and remodeling but can be used in Dressler's syndrome Antiplatelet and heparin are NOT reperfusion therapy. Reperfusion therapy includes PCI, streptokinase, and TPA Complications of Ml 75% of patients will have arrhythmias, the most commoncause of death during the first hour10-15% will have AF and A. Flutter during hospitalization (poor prognosis) AF and heart block are more common in inferior Ml VT and Ventricular fibrillation in the first 24 hours do not affectprognosis (treated by early DC shock)Ventricular fibrillation is the most common arrhythmia post-MI Page 1153 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Complications of Ml Arrhythmias LV free wall rupture Papillary muscle rupture Ventricular septum rupture LV aneurysm Re-occlusion, stent restenosis Dressler's syndrome (3P's)Features Palpitation, instability, ECG findings Signs of cardiac tamponade-usually occur during the first week Signs of acute Mitral regurgitation Signs of VSD Persistent ST elevation Typical chest pain + high CK-MB and/or new ST elevation 2 10 weeks po;t-Ml, pericarditis, pleuritis, pyrexia treated by NSAl Ds 01 signs of cardiac tamponade: (muffled heart sound + raised JVP + hypotension +pulsus paradoxus + electrical alternans) PI Mitral regurgitation: (soft Sl+split S2+ pan-systoiic murmur-blowing in character, hypotension, acute heart failure) 131 VSD: (pan-systolic murmur-harsh in character) Table 64: Complications of myocardial infarction Conditions like Ml Coronary vasospasm (Prinzmetal angina) Chest pain at rest usually occurs in a young patient Transient ST deviation Absent obstruction on angiogram It can be triggered by drugs like (cocaine and methamphetamine) Aspirin should be avoided (it can aggravate the ischemic attack) Beta-blockers are contraindicated (they can increase the vasospasm) The treatment of choice is CCB with or without long-acting nitrates Takofsubo cardiomyopathy: Typical chest pain + ST-elevation + elevated cardiac enzyme Associated with stress Normal angiogram Echocardiogram shows (octopus pot) Treatment is supportive 95% self-resolution within 7 days Page 1154 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Congestive Heart Failure (CHF) Impaired heart's diastolic filling or Ejection of blood, almost any cardiac disease can cause heart failure Classifications: Systolic (HFr EF) vs. Diastolic (HFp EF) heart failure Right-Sided vs. Left-sided Heart failure (the most common cause of right-side HF is left-side HF) low output HF vs. High output HF The severity of HF according to EF%: Grade I (EF > 60%) (Normal) Grade Il (EF = Grade Ill (EF = 21-39%) Grade IV (EF 20%) NYHA classification of HF: Class l: no limitations on ordinary physical activities Class Il: slight limitation of ordinary physical activities Class Ill: marked limitation of physical activity Class IV: symptoms of CHF present at rest Hyponatremia is an independent predictor of mortality in CHF Symptoms of HF: Symptoms of low cardiac OUt PUt left side (hypotension,syncope, cold extremities... )Symptoms of backward congestion are as the following:o Left-side heart failure: dyspnea, orthopnea, PND,pulmonary edema, pleural effusion, cardiomegaly,left side S3/S4 Gallop rhythm. o Right-side heart failure: peripheral and lower limbedema, liver congestion, hepatojugular reflux, ascites,high JVP, right side S3/S4 gallop rhythm. Terminology: Dyspnea: shortness of breath Orthopnea: shortness of breath on lying flat Paroxysmal nocturnal dyspnea (PND): SOB about a h hour after sleepin Page 1155 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pathology: Heart insult decreases heart function-4 decreases renal perfusion —+ activation of the Renin-angiotensin system and the sympathetic nervous system-+ leads to sodium water retention more load at heart-+ more cardiomegaly and dilation-+ More heart insult. Diagnosis: Echocardiogram measures Ejection fraction and assesses the valvular condition and wall motion abnormalities. Identify risk factors and causes which lead to HF ECG, CXR Blood workup (CBC, U&Es, KFT, LFT, AIC. LIPID profile, TSH) Features of CHF on CXR: (ABCDE) Alveolar edema (Bat's wings) Kerley B lines (interstitial edema) Cardiomegaly Dilated prominent upper lobe vessels Effusion (pleural) Treatment of chronic CHF: Lifestyle measures: diet, exercise, DM control, smoking cessation, decrease alcohol consumption, sodium restriction (no more than 2. 4 sodium or 5 grams salt daily) ACEI/ARB can reduce the mortality rate (Avoid CCB as it can worsen the edema) Beta-blockers (only: carvedilol or bisoprolol) decrease the mortality rate (avoid during decompensated heart failure) Diuretics (Aldactone — reduce mortality, Furosemide — symptomatic treatment) Digoxin has only symptomatic benefits and no effect on mortality Annual influenza vaccine One-time pneumococcal vaccine Page 1156 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Advanced treatment: sacubitril/Valsartan: Angiotensin Receptor Neprilysin Inhibitor (ARNI); it is a new drug that provides mortality and symptomatic benefit for systolic dysfunction Ivabradine: inhibits the "Funny channels" used in a patient with heart failure where heart rate > 70 bpm or when Beta-blockers are contraindicated ICD is indicated if EF < 35%-to decrease the risk of sudden death Left ventricular assist device (LVAD) or Cardiac transplant (last resort for treatment of HF) Treatment tips: HF treatment with mortality benefits are: ACEI/ARB, Beta-blockers, Spironolactone, Eplerenone (hydralazine + Nitrates), ICD, Sacubitril/Valsartan Digoxin and Loop Diuretics have no mortality benefits (only symptomatic) CCB may increase the mortality rate and worsen edema in systolic heart failure but reduces the mortality in isolated diastofic heart failure Digoxin and spironolactone are not beneficial in diastolic heart failure Role of BNP: BNP (brain natriuretic peptide) is an enzyme secreted by heart muscles due to stretching or infarction of these muscles. It acts asa dn.-retic to decrease blood pressure and decrease the load onthe heart; useful to investigate if you are not sure if shortness ofbreath is due to a cardiac or respiratory cause If BNP level is high (> 500 pg/ml), cardiac cause If BNP is not high, non-cardiac cause Causes of high BNP: Heart failure Acute Ml Mitral valve rupture Constrictive pericarditis Lar e pulmonary embolus Table 65: BNP rule in the diagnosis of SOB Page 1157 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pulmonary edema Pulmonary edema is a collection of fluids in the interstitium of the lungs It can be caused by increased orthostatic pressure or decreased oncotic pressure inside the blood vessels leading to fluid leak to the interstitium. Acute pulmonary edema usually presents due to Decompensated Heart Failure (DHF). (associated with high BNP) Other causes include: renal failure, excessive fluid replacement, ARDS, decreased albumin (nephrotic syndrome, liver cirrhosis) Late inspiratory crepitations (unchanged with cough) Treatment of Acute pulmonary edema: keep patient in a semi-sitting position Oxygen Morphine (reduces anxiety and preload) High dose furosemide (40-500mg) Nitrates Non-invasive or mechanical ventilation if indicated. Dobutamine or intra-aortic balloon pump can be used in pulmonary edema and cardiogenic shock. Treatment of the precipitating condition (Ml, arrhythmia Digoxin and digoxin toxicity Digoxin is used in the treatment of HF (positive inotropic) & rate control in the management of atrial fibrillation (rate control) Action: decrease AV node conduction and increase the force Of cardiac muscle contraction Features of toxicity: Fatigue, nausea & vomiting, anorexia, confusion Yellow-green vision Arrhythmias: e. g., AV block, bradycardia, short QT interval Predisposing factors: Hypokalemja (Most Common) Hyperkalemia (less common) Increasing Age Renal Failure Myocardial Ischemia P age 1158 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Hypomagnesaemia, Hypercalcemia, Hypernatremia, Acidosis Hypoalbuminemia Hypothermia Hypothyroidism Treatment. Correct arrhythmia Correct and monitor potassium Digibind (Digifab): is a digoxin-specific antibody used as an antidote to digoxin in case of toxicity In digoxin toxicity, calcium gluconate should be avoided; it may precipitate ventricular fibrillation or ventricular tachycardia. Myocarditis It is an inflammation of the heart muscle that can be acuteor chronic and cause dilated cardiomyopathy. Causes: Could be idiopathic, infectious, toxin, or systemic disease Most common infection = viral infection = coxsackie B virus,other virus: HIV Bacterial: diphtheria, clostridia Lyme disease Autoimmune (SLE, RA... )Chagas disease: American trypanosomiasis can be a cause Drug-induced: Doxorubicin Symptoms: Fever, chest pain, and SOB may present with sudden death Diagnosis: ECG: Non-specific ST-T changes Positive cardiac enzymes High WBC The lab results of the cause Chest X-Ray: dilated heart + silhouette sign Echocardiography: hypokinesia, dilated heart chambers Treatment: Supportive Treatment of complications like arrhythmias Treatment of the cause, if possible complications: DCM, Embolic events, Arrhythmias, and sudden Page 1159 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cardiomyopathies Cardiomyopathy is a Primary myocardial disease with no known cause The new classification: Primary cardiomyopathy: o Hypertrophic obstructive cardiomyopathy (HOCM) o Arrhythmogenic Right Ventricular Cardiomyopathy Mixed cardiomyopathy: o Dilated cardiomyopathy o Restrictive cardiomyopathy Acquired cardiomyopathy: o Peripartum cardiomyopathy o Takotsubo cardiomyopathy Secondary cardiomyopathy: o Infective (coxsackie B virus, HIV, Chagas disease... ) o Infiltrative (Amyloidosis) o Storage (Hemochromatosis) o Toxicity (drugs, Alcohol) o Inflammatory (sarcoidosis) o Autoimmune (SLE) Dilated Cardiomyopathy (DCM) It is the most common form of cardiomyopathies Dilated heart and systolic +/-diastolic dysfunction All 4 chambers affected but LV more than RV Absence of congenital, valvular or ischemic heart disease Causes: Most cases are idiopathic Post-viral Myocarditis (the most common cause) Alcohol or Drugs (e. g., Doxorubicin) Radiation Chagas disease Clinical Features: Features of Congestive heart failure Arrhythmias and sudden death may occur Embolization Mitral regurgitation Page 1160 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Drugs that lower mortality: (ACEI, ARB, Beta-blockers, spironolactone) Digoxin used to control symptoms pacemaker improves both symptoms and survival Implantable Cardioverter Defibrillator (ICD) has mortality benefits in some patients Hypertrophic obstructive cardiomyopathy It is regional hypertrophy of the left ventricle that most commonly involves the interventricular septum HOCM is the most common cause of sudden death in athletes Most cases are inherited as an autosomal dominant disease Due to a mutation in the gene encoding ß-myosin heavy chain protein (sarcomere) Pathogenesis: Left ventricular outflow tract obstruction due to septal and the anterior mitral valve leaflet hypertrophy. Factors affecting the degree of obstruction: o Factors increasing preload and afterload will reduce the obstruction o Factors that reduce the ventricular size (e. g., dehydration, Inotropes, ACEI, ARBs) will worsen the obstruction. Cllnlcal features: The condition is usually asymptomatic It may present with sudden death Chest pain (usually at rest and not related to exercise) Syncope (usually arrhythmogenic during exercise) Features of CHF (usually diastolic — reduced filling) Diagnosis: ECG: o Left ventricular and left atrial hypertrophyo Inverted symmetric T wave in leads V3—V6 (apical) Echocardiogram: (MR SAM ASH)o Mitral Regurgitation (MR)o Systolic anterior motion (SAM) of the anterior ritralvalve o Asymmetric septal hypertrophy (ASH) > 1. 5 times the thicknes of the posterior wall. Page 1161 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Management Avoid competitive sports (to prevent sudden death) Beta-blockers (first line if ejection fraction 50%) CCB (e. g., verapamil) may be substituted for beta-blockers Warfarin or DOAC, regardless of the CHA2DS2VASc score Septal ablation or surgical myomectomy Cardioverter-defibrillator for high-risk patients Digitalis, Nitrates, positive inotropes, ACEI, and ARBs will worsen the obstruction in HOCM, and they should not be used. Arrhythmoqenic Right ventricular cardiomyopathy (ARVC) Also known as Arrhythmogenic right ventricular dysplasia It is the second most common cause of sudden death in athletes An autosomal dominant pattern that may present with syncope or sudden cardiac death The right ventricular myocardium is replaced by fatty and fibrofatty tissue Implantable-Cardioverter-Defibrillator (ICD) is the treatment of choice and is better than Beta-blockers and other antiarrhythmic agents ECG changes: T wave inversion in Vl-V3. An epsilon wave in 50% of cases (a small positive deflection at the end of the QRS complex) Ep iton Figure 31: One beat ECG showing epsilon wave Page 1162 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Peripartum cardiomyopathy Typical develops between the last month of pregnancy and 5 months post-partum more common in older women, greater parity and multiple gestation Cardiac tumors The most common primary cardiac tumor is atrial myxoma, but the most common cardiac tumors are metastatic (e. g., melanoma, thymoma) The most common site for atrial myxoma is the left atrium The most common site for angiosarcoma is the right atrium Clinical features: Constitutional symptoms: fever, anorexia, weight loss Digital clubbing, Embolization, atrial fibrillation Mid-diastolic murmur Diagnosis: Echocardiography Treatment: Resection to reduce the risk of embolization andcomplications Anticoagulation Figure 32: A sketch showing an Atrial myxoma Page 1163 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diseases of Endocardium Infective Endocarditis (IE) Endocarditis is an inflammation of the endocardium or heartvalves, usually due to bacterial infection. Risk factors: IV drug users — most commonly affect the tricuspid valve Previous Endocarditis Prosthetic valve Congenital heart disease (But not ASD)Valvular heart disease (Mitral prolapse... )Poor dental hygiene Most common bacteria causing endocarditis: The common cause of Native valve Endocarditis:o Health-care associated: Staphylococcus aure US. o Community-acquired: Streptococcus viridans The most common cause of prosthetic valve endocarditis: o In the first 2 months: Coagulase-negative Staphylococcus epidermidis (Co NS) o From 2— 12 months: Staphylococcus aureus o After 12 months: Streptococcus viridans The most common cause in IV drug users: o Staphylococcus aureus The most common cause in patients with colon cancer: o Streptococcus gallolyticus (S. bovis) o Clostridium septicum endocarditis Streptococcus viridans (most in poor dental hygiene) Non-infective endocarditis (sterile vegetation): o Libman-Sacks: due to SLE o Marantic endocarditis: due to malignancy Signs and symptoms: Non-specific symptoms: (fever, rigors, general weakness) Cardiac: (dyspnea, chest pain, clubbing, new murmur, CH F) Embolic phenomena: (petechiae, splinter hemorrhage, Janeway lesion-at sole and palm, CNS or Renal emboli) Immune complex phenomena (Oslets nodes at digits, Glomerulonephritis, Roth's spots at retina) Hemolytic anemia can be caused if there is an infective Endocarditis in a prosthetic valve Page 1164 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Oder nodes Janeway lesiors Roth spots Figure 33: a) Osler nodes, B) Janeway lesions, C) Roth spots Notes: Osler nodes are pathognomonic for infective endocarditis The most common sign of IE is: fever The second most common sign of IE is: Heart murmur Modified Duke Criteria: Pathological criteria: (positive Histology or microbiology ofpathological material obtained at autopsy or cardiac surgery) Major criteria: Positive culture "2 cultures, 48 hours apart, and typicalorganisms" Positive Echo. Minor criteria: Predisposing factors Fever > 38. 5 Embolic phenomena Immune complex phenomena Positive culture but not meeting major criteria Diagnosis: I Pathological criterion, or 2 major criteria, or3 minor criteria and I major, or 5 minor criteria Page 1165 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Supportive treatment Empyrical antibiotics then switch according to culture results The empirical antibiotics for Infective endocardltls: Native valve: amoxicillin, ± Low-dose Gentamicin Penicillin allergic, MRSA, or severe sepsis: vancomycin + low-dose gentamicin Prosthetic valve: vancomycin + rifampicin + low-dose gentamicin Indications for surgery In IE: Severe valvular incompetence Aortic abscess (often indicated by a lengthening PR interval) Infections resistant to antibiotics/fungal infections Cardiac failure refractory to standard medical treatment Recurrent emboli after antibiotic therapy Poor prognostic factors: Staph aureus infection Prosthetic valve (especially early, acquired during surgery) Culture-negative Endocarditis Low complement levels Valvular heart diseases Aortic stenosis Progressive degenerative disease of the normal trileaflet aortic valve is the most common cause (in elderly patients) Congenital bicuspid aortic valve usually occurs in 20-40 years olf patients Clinical features: Chest pain, dyspnea, syncope (usually exertional) Systoüc ejection murmur S4 and muffled S2 Narrow pulse pressure and slow rising pulse Echocardiogram is the most accurate test page 1166 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: If asymptomatic, there is no need for treatment, Medical treatment: diuretics, digoxin, and ACE inhibitors If symptomatic; valve replacement for elderly or balloon valvoplasty in young patients Aortic requrqitation Acute AR is mostly caused by aortic dissection and IE Chronic AR is caused by aortic dilatation, calcification, rheumatic disease, and bicuspid aortic valve. Clinical features: Angina, orthopnea, exertional dyspnea Early diastolic murmur Soft Sl and S2, loud S3 Wide pulse pressure Specific signs of AR: Water hammer pulse Easily palpable popliteal and Dorsalis Pedis pulse Hill's sign: Popliteal systolic blood pressure exceeding brachial systolic blood pressure by 60 mm Hg (most sensitive sign for aortic regurgitation) Quincke's sign: capillary pulsations in nail beds Corrigan sign: Prominent (jerky) carotid pulsation (dancing carotid) De Musset's sign: Head nodding in time with the pulse Muller's sign: Pulsation of the uvula in time with the pulse Rosenbach's sign: Hepatic pulsations Traube's sign: Systolic and diastolic sounds heard over the femoral artery ("pistol shots")Treatment: Indications for surgical replacement of the valve in AR:o Acute aortic regurgitationo Chronic symptomatic ARo Chronic asymptomatic with LVEF < 50%ACEI and CCB are only indicated in symptomatic patients. Page 1167 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Mitral stenosis The most common cause is RF (Rheumatic mitral stenosis is more common in women) Other causes (congenital, calcification, fibrosis) Cllnlcal features: Pulmonary edema, Pulmonary HTN, hemoptysis Malar flush (due to C02 retention) Late-diastolic murmur with opening snap Laud S' Atrial fibrillation (as a complication) Hypoplastic left ventricle Treatment: Surgical repair or replacement Diuretics, long-acting nitrates, beta blockers, and CCB Warfarin for all patients with AF and MS regardless of CHA2DS2VASc score. Mitral regurgitation The most common cause is RF, It can be caused by Ml, Left ventricular dilatation Symptoms: Pulmonary edema, atrial enlargement, Pan-systolic murmur, soft S', split S2, and S3 (if severe) Treatment: o Diuretics 0 ACEI o Surgery (may be needed if severe) Mitral prolapse Can be associated with (Marfan's syndrome, Turner syndrome, Ehlers-Danlos syndrome, polycystic kidney disease) Symptoms: atypical chest pain, palpitation, can cause sudden death Mid-systolic click, late systolic murmur page 114 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Tricuspid valve abnormalities Tricuspid stenosis: Cause endocarditis, RF, congenital Diastolic murmur Tricuspid regurgitation: Cause — Right Ventricular dilatation, RF, pulmonary-HTN, Signs: Pansystolic murmur, pulsatile hepatomegaly Heart SOUnd S The first heart sound (Sl ) is caused by the closure of the Mitral and Tricuspid valves, while the second heart sound (S2) is due to aortic and pulmonary valves closure Head sound first heart sound (Sl) 2nd heart sound (S2) 3rd heart sound (S3) 4th heart sound (S4)Features Closure of mitral and tricuspid valves Soft if mitral regurgitation and Loud in mitral stenosis Closure of aortic and pulmonary valves Soft in aortic stenosis Splitting during inspiration is normal Fixed splitting is seen in the case of ASD Caused by diastolic filling of the ventricle Considered normal if < 30 years old (may persist in women up to 50 years old). Heard in left ventricular failure (e. g., dilated cardiomyopathy), constrictive pericarditis, and severe mitral regurgitation Caused by atrial contraction against a stiff ventricle It may be heard in aortic stenosis, HOCM, hypertension Table 66: Heart sounds and their causes Page 1169 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Type of PLAse PUISUS paradoxus Slow ri Sng pube Collapsing PUISI-S atternars Bisfeiens pulse Jerky pulse Pulses Featl. res and causes Greater than the normal (10 mm Hg) fal in systolic blood pressure during inspiration Causes: Severe asthma, COPD, Cardiac tamponade Aortic Aortic regurgitation Patent d UCt US arteriosus (PDA) Hyperiänetic (anemia, fever, exercise/pregnancy) Regular alternation of the foce of the pube Cased by severe LVF Double pube-bao systofic pecks Caused by Mixed aortic valve dsease Occasionally occurs in HOCM Caused by HOCM Taue 67: Featues and cal-ses of types of Murmur type äection systoüc Pan-systoüc Late 5Ftoüc Earty dast05c Md4ate dastoüc Continuous mac Nne-fike Murmurs Causes Aortic stenosis, Pulmonary stenosis, HOCM. ASD, Fallout's MRf TR (blowing in ch Uacter) VSD (harsh' in character) Mitral valve prolapse Coarctafion of aorta Aortic regur$tafion Grahan Steel murru (PR, blowing rnurn-r) Mtral stenosis ('rumbfing in chcracter) Aust WFEnt murmur (severe AR. rumbüng murmur) Patent ductus (PDA) Tooe 68: Causes of types of heat rncrmz. rs Page 1170 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Effects of some maneuvers on Murmurs Squatting and leg rising: Increased venous return Increased intensity of all murmurs except Mitral prolapse and HOCM, which will be decreased Standing and Valsalva maneuver. Decrease venous return to the heart Decrease the intensity of all murmurs except for MVP and HOCM, which are increased. Handgrip: Decrease left ventricular emptying Decrease loudness of (AS, MVP, and HOCM) murmurs Increase loudness of (AR and MR) murmurs No effect on MS Nhrates. Same effect as ACEI on murmurs Direct arteriolar vasodilator Increased ventricular emptying Increase loudness of (AS, MVP, and HOCM) murmurs Decrease loudness of (AR and MR) murmurs No effect on MS Page 1171 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pericardial diseases Pericarditis Pericarditis is an inflammation of the pericardium If pericarditis is associated with extravasation, pericardial effusion and tamponade can occur If chronic pericarditis, fibrosis, and calcification will result in constrictive pericarditis Causes: Most commonly — idiopathic Infection (viral, bacterial, TB, fungal) o The most common infection is coxsackie B virus Inflammation (SLE, RA, Dressler's syndrome) Metabolic (uremia) Malignancy (Hodgkin's lymphoma, breast cancer, lung cancer) Clinical features: A friction rub is the earliest sign of pericarditis Atypical chest pain (positional; increased by lying back and decreased by bending forward) Fever, General weakness Diagnosis: Clinical picture + friction rub + ECG changes The most specific ECG change is depressed PR interval (elevated on AVR) Other ECG changes: ST elevation in all leads (diffuse ST elevation) (Depression on AVR) Echocardiogram for assessing for pericardial effusion Treatment: Bed-rest, NSAl Ds Colchicine decreased recurrence Steroids for severe or recurrent cases Treatment of the underlying disease Anticoagulant is not safe to use in pericarditis Page 1172 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pericardial effusion It defined as Fluid collection within the pericardium Causes: Can be Transudate due to (CHF, hypothyroidism, or hypoalbuminemia) Exudates due to (same causes of pericarditis) Symptoms: It depends on the amount of fluid and May be asymptomatic Dyspnea, cough, signs of pericarditis, elevated JVP and Ewart's sign, muffled heart sounds Best investigation: pericardiocentesis (determine exudates Vs. Transudate) Treatment: If mild: observation + NSAl Ds If sever. pericardiocentesis Ewart's Sign: Bronchial breathing and dullness to percussion at the lower angle of the left scapula due to effusion. Figure 34: Pericardiocentesis procedure Page 1173 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cardiac tamponade Rapid or massive accumulation of pericardial effusion, or blood collection in the pericardial space It causes decreased venous return, filling, and stroke volume. Diagnosis: Beck's tirade (hypotension, increased JVP, and muffled heart sounds) Other symptoms: dyspnea, pulsus paradoxus, shock, and peripheral edema PUISUS paradoxus (inspiratory fall in systolic BP > 10 mm Hg during quiet breathing) Electrical alternans (high and low voltage of QRS's on ECG alternatively) Treatment: Best: urgent pericardiocentesis Pericardiectomy IV fluids (to increase cardiac output) Treatment: of the underlying cause Note: avoid diuretics in cardiac tamponade because it decreases venous return and worsens the symptoms. Constrictive pericarditis fibrosis, calcification, thickening, and adherence of pericardium that limit the expansion of the heart Kussmaul's sign: a paradoxical rise in jugular venous pressure (JVP) on inspiration, usually present in constrictive pericarditis. (Rarely present in tamponade). Best Treatment: Pericardiectomy Page 1114 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Other cardiology problems Anaphylaxis Anaphylaxis: lg E mediated severe, life-threatening, generalized, or systemic hypersensitivity reaction; the patient must be already sensitized to the antigen Anaphylactoid reaction: Non-lg E related (complement-mediated), similar clinically to anaphylaxis and treated the same way, does not need preceding sensitization to antigen Urticaria: is a part of anaphylaxis (redness of the skin as a result of exposure to an antigen) pathogenesis: Exposure to an antigen —i immune system activation lg E binds to Mast cells histamine, prostaglandins, and leukotrienes release vasodilatation —+ hypotension and shock Common causes of anaphylaxis Food (e. g., Nuts)-the most common cause in children Medications Bites and stings (e. g., Wasp sting)Clinical presentation: Rash (present in all types of anaphylaxis)Hypotension and tachycardia Respiratory symptoms (SOB, wheeing, stridor... )The best investigation is serum tryptase level that remains elevatedfor 12 hours post anaphylaxis Treatment: First-line treatment is adrenalin 1/1,Hydrocortisone: (its action needs up 000 to (best 4 hours)to give 1M) Chlorphenamine (Allerfrin)Nebulized Beta-2 agonist Supportive measures (02, I. V Fluids)Emergent airway protection if required (intubation,cricothyroidotomy) Doses of adrenalin0. 5 ml for adults Doses of hydrocortisone 0. 3 rnl for children > 6 months25 mg < 6 months 0. 15m for children < 6 months 100 mg 6 years-12 years Table 69: Doses of adrenalin and 200 hydrocortisone mg > 12 years in anaphylaxis Page 1175 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Syncope Sudden impairment of consciousness Should be distinguished from seizures In syncope, no warning symptoms, no abnormal movements during the attack, fast and full recovery in less than 2 minutes, and no symptoms after the attack. Causes: Gradual onset syncope: o Toxic metabolic o Hypoglycemia o Anemia o Hypoxic etiology Sudden onset with a sudden return to consciousness syncope: o Structural heart disease (e. g., valvuiar disease) o Ventricular arrhythmias o Vasovagal attack Diagnosis: Cardiac and neurological examination: o If a murmur is present, echocardiography is indicated o If there is a history of head trauma or focal neurological deficit, a brain CT scan is indicated o If normal cardiac exam and still suspected cardiac cause, Holter monitor is indicated ECG, cardiac enzymes Serum glucose Oximeter CBC Urine and blood toxicology screen Tilt table testing (vasovagal syncope) Only brain stem stroke can cause syncope (lesion in the posterior circulation). The Brain stem is responsible for sleep and awake control Treatment: Treatment of the cause Vasovagal syncope treated with beta-blockers (maintenance) and atropine (for attack) Page 1176 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Gastroenterology CHAPTER 5 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1177 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Introduction to gastroenterology Dysphagia is a Difficulty in swallowing that is present in most esophageal disorders Oropharyngeal dysphagia: o It is difficulty of initiating swallowing o Causes (CVA, Parkinson, MG, ALS) o Diagnosis (Videofluoroscopy with liquid and solid phases) Esophageal dysphagia: o For solid food: esophageal web, Schatzki ring o Progressive for solid food: esophageal cancer or peptic stricture o For liquid only or liquid and solid food: motility disorder (e. g., achalasia) Odynophagia: painful swallowing Alarm symptoms indicating endoscopy: Weight loss Blood in stool Anemia Both dysphagia and odynophagia can lead to weight loss Figure 35: A sketch showing the alimentary tract (l) pharynx. (2) Esophagus, (3) Stomach, (4) descending colon, (5) Sigmoid, (6) Rectum, (7) Duodenum. (8) Transverse colon. (9) Ascending colon. Page 1178 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Disorders of the esophagus Gastroesophageal reflux disease (GERD) Reflux disease: reflux of gastric acidity to the esophagus. Due to inappropriate relaxation of the lower esophageal sphincter (LES) Symptoms of GERD are worsened by alcohol, nicotine, chocolate, caffeine, late-night meals, Hiatus hernia, and obesity. Causes: Transient LES relaxation (Most common cause) Decrease LES tone (e. g., systemic sclerosis) Acid hypersecretion (e. g., Zollinger-Ellison Syndrome) Clinical picture: Heartburn (the most common symptom) Gastric content regurgitation Chest pain may present, especially with esophagitis present Dysphagia is a late symptom Cough, wheezes, and aspiration pneumonia Hoarseness, metallic taste, and dental caries Diagnosis: The clinical picture with improvement after the Trial of PPI(Proton pump inhibitor) is usually diagnostic. (if there are noalarm symptoms) 24-hours PH Monitoring (best investigation)Endoscopy indicated if:o Alarm symptoms o Screening for Barrett's esophagus (after 5-10 years)Treatment: Lifestyle modification:o Weight loss, no late meals, head elevation in bedo Avoid coffee, tea, alcohol, and carbonatedbeverages Medical treatment:o PPI (the best maintenance therapy)o H2 blockers (for mild or intermittent sympto@o Antacids (On demands)Surgical treatment (Nissan's fundoplicafion) indicated if:0 Failed medical treatment o Development of complications Page 1179 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Stepwise treatment for GERD if there are no Alarm symptoms: Order once-daily PPI Order twice-daily PPI if there is no improvement Do Upper endoscopy of no improvement after 8 weeks ifalarm symptoms appear Complications: Barrett's Esophagus Esophagitis: inflammation of the esophagus, ranging fromredness to ulceration and bleeding Motility disturbance Anemia: IDA (due to bleeding if present) Stricture: narrowing of part of the esophagus due to longstanding esophagitis Barrette's Esophagus (BE) The Squamous lining of the lower esophagus is replaced by columnar lining due to chronic exposure to acidity due to GERD (cellular metaplasia) This is a pre-malignant condition "0. 5%/year risk of malignant transformation"; it can cause adenocarcinoma of the esophagus Clinically asymptomatic Diagnosis: biopsy Treatment: symptomatic treatment and endoscopy. For barrette's alone: PPI and endoscopy q3 — 5 years For low-grade dysplasia: PPI and endoscopy q6-12 months or endoscopic ablation For high-grade dysplasia: endoscopic ablation Anti-reflux surgery does not prevent the progression of BE to Adenocarcinoma page 1180 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Esophagitis Esophagitis is an inflammation of the esophagus The most common presenting symptom is Odynophagia The most common cause of infectious esophagitis is Candida albicans, followed by CMV and HSV. Esophageal candidiasis: Candida albicans: is a normal commensal of mouth It can cause oral thrush and esophagitis in immune-suppressed patients (e. g., DM, Steroid users, HIV) In an immunosuppressed patient with oral thrush and odynophagia, treat for candidiasis without doing an upper endoscopy. The absence of oral thrush does not rule out esophageal candidiasis Treatment: o Fluconazole or ltraconazole for candidiasiso Ganciclovir for CMV esophagitis o Acyclovir for HSV esophagitis Drug-induced esophagitis: Potassium supplements, NSAl Ds, tetracycline, andbisphosphonates are known to induce esophagitis Symptoms of severe retrosternal pain with swallowing afterseveral hours of ingesting the pill are characteristic. Treatment is supportive Eosinophilic Esophagitis (EE): The presence of eosinophils in the esophageal biopsy Most commonly occurs in children Young adults with EE will present with severe dysphagia andfood impaction. GERD may be associated with esophageal eosinophilia andmimic EE Treatment: Fluticasone or budesonide swallowing (8 weeks PPI to rule out GERD induced Eosinophilia) Corrosive esophageal damage: Substances that can cause burns in the mouth, pharynx, andesophagus Seen commonly in suicidal attempts Induction of vomiting or NG tube insertion arecontraindicated in corrosive esophageal injuries. Page 1181 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Motility disorders of the esophagus Achalasia Achalasia is the most common esophageal motility disorder It is caused by degeneration of the myenteric plexus leading to hypertonic LES that fails to relax during swallowing Usually, it presents in the middle ages, about 40-year-old Females are more affected than males. Achalasia is a premalignant condition; it can result in squamous cell carcinoma of the esophagus. 2 Figure 36: A sketch showing achalasia. (l) Dilated esophagus, (2) hypertonic LES Causes: Failure of local nerve supply (Vagus nerve): o Weak peristaltic waves of the body of the esophagus o Failure of LES to relax Chagas Disease (Trypanosoma cruzi) is a cause Carcinoma, lymphoma. (Pseudoachalasia) Clinical picture: Longstanding, painless, slowly progressive Dysphagia (to liquid more than solid foods) with periods of remission and relapse (the most common symptom) Some patients developed severe chest pain due to spasms of the esophagus. Non-acidic regurgitation of undigested food Heartburn is usually absent Pulmonary symptoms (night cough, aspiration pneumonia) Page 1182 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis:(wide mediastinum and features of aspiration) Barium swallow (best initial test) will show a fluid level with distal tapering (Bird's beak sign, or rat-tail sign) Esophageal manometry (the most accurate test) Endoscopy to rule out adenocarcinoma (i. e., pseudoachalasia) (in achalasia, mucosa will be normal) For achalasia testing: start with Barium swallow, then do manometry to document the absent peristalsis and then finally do Endoscopy to rule out pseudoachalasia Treatment: Endoscopic pneumatic dilatation of LES (safer than surgery) Botufinum toxin injection to LES (high recurrence rate) Surgical myotomy (Heller Myotomy) (more effective than pneumatic dilatation) Esophageal Spasm It is an abnormally forceful non-peristaltic contraction of the esophagus with normal sphincteric relaxations It may be spontaneous or triggered by cold or hot liquids,stress, or carbonated beverages. Cünical features: Chest pain that is related to food Typical chest pain that is relieved by nitrates may present Dysphagia to solids and liquidsuagnosis: ECG should be done to rule out Myocardial infarction. Barium swallow (Corkscrew appearance)Esophageal manometry (the most accurate test)Treatment: Medical treatment: Nitrates, CCB, and anti-reflux measures Endoscopic botulinum toxin injection Surgery (long esophageomyotomy) (only if refractory) Nutcracker esophagus (Hypertensive peristalsis): Severeesophageal spasm with very high pressure on manometry The most common symptom is chest pain Treatment: nitrates and nifedi ine Page 1183 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Stomach and Small intestine Epigastric pain Epigastrium is the region just below the xiphoid process Pain in the epigastrium is as common as 25% of the population at some point in their lives Non-ulcer dyspepsia is the most common cause of epigastric pain in patients less than 50-year-old (50-90%) Epigastric pain features and association Most likely diagnosis The most important cause The most common cause Pain that increased with food Pain in young with weight loss Pain improved with food, weight gain Pain in elderly with weight loss Radiated to the back with tenderness Metallic taste, cough, and hoarseness Diabetes, bloating, early satiety Myocardial infarction Non-ulcer dyspepsia Gastric ulcer (GU) Gastric ulcer (GU) Duodenal ulcer (DU) Gastric cancer Pancreatitis GERD Gastroparesis Table 70: The differential diagnosis of epigastric pain Non-ulcer dyspepsia (NUD) Also called functional dyspepsia (FD) Epigastric pain with no identified etiology It is the most common cause of epigastric pain Diagnosis is made after endoscopy (will be normal) NUD cause is not known (but NSAl Ds, antibiotics, bisphosphonates, and potassium supplements may be implicated) Treatment: Stop all medications that may be the cause (if possible) If < 60 years old and no alarm symptoms: Test and treat approach for H. pylori If 2 60 years or alarm symptoms: upper endoscopy page 1184 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Acid suppression: o Liquid antacids are as effective as H2 blockers o H2 blockers are effective in 70% of patients with epigastic pain o PPI (proton pump inhibitors) (Best initial): have the best effect on epigastric pain treatment, but no difference in efficacy between different PPIs Antihistamin Histamin Gastrin Acetylcholine Proton Pump Parietal cells Antacid HCl Figure 37: The gastric acid secretion and drugs effect on it Gastritis (Gastropathy) It is an inflammation of the stomach epithelial lining Can be acute or chronic, autoimmune, drug-induced, or infectious Causes: alcohol, NSAl Ds, stress, H. Pylori infection, portal HTN Clinical features: Most chronic gastritis cases are asymptomatic and need notreatment, but acute cases are usually symptomatic. Gastrointestinal bleeding without pain (the most common)Epigastric pain in severe erosive gastritis Diagnosis: Test and treat strategy for H. pylori Upper endoscopy is the only accurate test CBC may show anemia Treatment: H. pylori eradication if positive PPI (proton pump inhibitors) have the best effect onepigastric pain treatment, but no difference in efficacybetween different PPIs Page 1185 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Autoimmune gastritis: Anti-parietal cell antibodies or anti-intrinsic factor antibodies It causes mucosal atrophy and loss of the intrinsic factor leading to B12 deficiency It is associated with other autoimmune diseases Increase the risk of malignancy You cannot distinguish Duodenal ulcer, gastric ulcer, gastritis, and non-ulcer dyspepsia clinically without endoscopy. NSAl Ds have an anti-prostaglandin effect, leading to a loss of protective mechanisms in the stomach mucosa: o Decreased MUCOUS secretion o Decreased bicarbonate secretion o Decreased blood flow Peptic Ulcer disease (PUD) It is an ulceration of the lower esophagus, stomach, or duodenum and can occur in the ileum adjacent to Meckel's diverticulum. The most common site of gastric ulcer (GU) is at the lesser curvature (exactly at the Incisura angularis) Blood Group O is a risk factor Causes: H. pylori: o The most common cause in developing countries o More common in the duodenum than in the stomach NSAl Ds: non-selective COX 1 &2 inhibitors: o The most common cause in developed countries o The 2nd most common cause in developing countries o Inhibit prostaglandins, thus decreasing mucus Stress-induced: any acute illness, RTA, Burn Zollinger Ellison syndrome (Gastrinoma) Crohn's disease Idiopathic page 118b | INTERNAL1-17AFEEF-MERGED-1.pdf |
All patients with peptic ulcer disease should be tested for H. pylori regardless of the use of NSAl Ds Alcohol and smoking are not causing a peptic ulcer, but they can delay healing and increase complications Incisura angularis: is a part of the lesser curvature of the stomach. It is the most common site for H. pylori colonization, atrophy, metaplasia, ulceration, and gastric carcinoma (routine biopsy is taken from it during gastroscopy) Clinical picture: Dyspepsia is the most common symptom Recurrent episodes of epigastric pain, which is related to meal PUD is the most common cause of UGIB, but most ulcers do not bleed Sometimes vomiting may present Diagnosis: Test all patients for H. pylori infection and treat if positive Upper Gl endoscopy is the most accurate test: o If alarm symptoms present o If onset 60-year-old o If no improvement despite adequate treatment o Biopsy from ulcerated mucosa should be done (for assessment of H. pylori and to rule out malignancy) Management: Stop smoking and alcohol Identify and treat the cause (to prevent recurrence)PPI is effective in 95% of cases Surgical treatment is rarely required (gastric resection orvagotomy) Page 1187 | INTERNAL1-17AFEEF-MERGED-1.pdf |