Cardio-Vascular System Sheet 2024-2025 PDF

INTERNAL MEDICINE 2024– 2025 DR. MOHCEN AL.HAJ DR. MOHCEN AL. HAJ 1   INTRODUCTION: Anatomy of the Heart: Histology of the Heart : The Heart Consists of 4 Chambers The Heart...

INTERNAL MEDICINE 2024– 2025 DR. MOHCEN AL.HAJ DR. MOHCEN AL. HAJ 1   INTRODUCTION: Anatomy of the Heart: Histology of the Heart : The Heart Consists of 4 Chambers The Heart Consists of 3 Layers: 2 Atria & 2 Ventricles. 1- Inner Layer: Endocardium Include the Valves. Those 4 Chambers are Separated By 4 Valves; 2- Middle Layer: Myocardium Containing Conductive System of the Heart. Two Right Valves: Two Left Valves: 3- Outer Layer: Pericardium (Visceral & Parietal).  Tricuspid Valve:  Mitral Valve: Between Right Atrium Between Left Atrium & Right Ventricle. & Left Ventricle.  Pulmonary Valve:  Aortic Valve: Blood Supply of the Heart : Between Right Ventricle Between Left & Pulmonary Artery. Ventricle & Aorta. Arterial Supply of the Heart Arises From: Right & Left Coronary Arteries. Please Remember  Left Vent Thickness 10mm While Right Vent 3mm. Right Coronary Artery: Left Coronary Artery: Pressure in Lt Vent 4 Times More Than Rt Vent. Supply Mainly Posterior Divided Into: & Inferior Wall of the 1. Left Anterior  Stroke Volume (SV) Amount of Blood That Left Ventricle (80%). Descending (LAD) Ejected By Ventricles Each Beat. Supply Mainly Antero-  Cardiac Output (COP): Amount of Blood That Supply SA Node (60%). Septal Wall of the Heart. Ejected By Ventricles Each Minute. 2. Left Circumflex (LCX)  Ejection Fraction (EF): Percentage of Blood Supply AV Node (90%). Supply Mainly Lateral That Ejected From Ventricles, Normally > 55%. Wall of the Left Ventricle. Conductive System of the Heart: Innervations of the Heart: 1. Sino-Atrial Node (SAN): Known as Peace Maker Autonomic Nerve Supply, Include: Situated in Right Atrium Near to the Site of SVC.  Sympathetic Innervations: By β1 & β2 Receptors It is Generate Impulse  Called Pulse Generator, Increase Heart Rate (Chronotropoic) and It Can Generate 60 to 100 Beat Per Minute. Increase Contractility & COP (Inotropic). 2- Atrio-Ventricular Node (AVN): It's the Only Please Remember  Window Between Atria & Ventricles. Stimulation of β2 Receptors Lead to Vasodilatation Its Function is Physiological Delay of Pulse. of Coronary Blood Vessels. 3- Bundle of His.  Parasympathetic Innervations: Vagal Stimulation 4- Right & Left Bundle Branch. (Only For Atrium Not Ventricles) By M2 Receptors. 5- Purkinje Fibers. Decrease Heart Rate & Increase Function of AV Node DR. MOHCEN AL. HAJ 2   HEART FAILURE (HF): Definition: Pathophysiology: It is a Clinical Syndrome Develop When Heart Can’t According to Definition; in Case of Heart Failure COP Maintain Adequate Cardiac Out Put (COP Less Will Be Decreased Less Than Normal, Than Tissue Requirement). Decreasing of COP Lead to Decrease of Renal Perfusion Affect 10% of People Above 75 Years Old. & That Will Activate Sympathetic Nervous System and Renin Angiotensin Aldosterone System (RAAS): Renin Convert Angiotensinogen to Angiotensin I, COP Depend On Starling Low: Angiotensin I Converted Into Angiotensin II By  Venous Return (Pre-Load): If; COP. Angiotensin Converting Enzyme (ACE).  Arterial Resistant (After-Load): If; COP.  Myocardial Contractility: If; COP.  Angiotensin II (Ag II) Will Do:  Vasoconstriction Which Lead to  After-Load.  Stimulate Secretion of Aldosterone That Will Lead to Salt & Water Retention and Result Into Please Remember  Increasing of Venous Return Lead to  Pre-Load. If COP Decreased; Myocardial Contractility  Sympathetic Nervous System Will Do: Will Be Increased Because;  Stimulation of Cardiac Contractility. Decreasing of COP Lead to Decreasing of  Vasoconstriction. Carotid Sinus Activity Which Will Lead to Increasing of Sympathetic Activity and it is This Mechanism Called: Neuro-Hormonal Called Sympathetic Firing, Activation That Occur in Case of Decrease of COP, This Sympathetic Firing Lead to Increase Heart Which is Physiological in Case of Healthy Heart Contractility & Increasing of Heart Rate. But Pathological in Case of Diseased Heart, Because It Will Lead to Deterioration of Heart Function & Remodeling of the Heart. Classification: According to According to According to According to Involved Chamber: Cardiac Out Put: Cardiac Cycle: Onset of Clinical Picture: 1. Right Side Heart 1. High Cardiac Output 1. Systolic Heart Failure 1. Acute Heart Failure. Failure. Heart Failure (Due to (More Common). 2. Left Side Heart Hyperdynamic Due to Decrease 2. Chronic Heart Failure. Failure. Circulation). Myocardial Contraction. 3. Congestive Heart 2. Low Cardiac Output 2. Diastolic Heart Failure 3. Acute On Top of Failure (Biventricular). Heart Failure. (Less Common). Chronic Heart Failure. Due to Decrease Ventricular Filling. DR. MOHCEN AL. HAJ 3   New York Heart Association (NYHA) Classification of Heart Failure: Class I: No Limitation of Physical Activity. Class II: Slight Limitation of Physical Activity. Class III: Marked Limitation of Physical Activity. Class IV: Symptoms Occur Even at Rest; Discomfort with Any Physical Activity. Symptoms: Signs:  Right Side Heart Failure:  Right Side Heart Failure: 1. Right Hypochondrial Pain & Jaundice. 1. Raised Jugular Venous Pressure (JVP). (Cardiac Cirrhosis). 2. Right Hypochondrial Tenderness with Jaundice, 2. Abdominal Distension, Dyspepsia, Ascites & Hepatomegaly. Malabsorption & Sever Weight Loss. 3. Bilateral Lower Limb Edema / Sacral Edema. (Cardiac Cachexia). 4. Generalized Edema (Anasarca); Develop Only 3. Bilateral Lower Limb Edema. In Severe Cases. 4. Generalized Edema (Anasarca); Develop Only In Severe Cases.  Left Side Heart Failure:  Left Side Heart Failure: 1. Dyspnea, Orthopnia, Paroxysmal Nocturnal 1. Gallop Rhythm (in Acute Lt Side Heart Failure). Dyspnea (PND). 2. Bilateral Basal Crackles of Lungs, Pleural 2. Cough & Wheeze (Cardiac Asthma). Effusion (Decrease Air Entry By Auscultation & 3. Dizziness, Fatigue, Weakness, Chest Pain, Dull By Percussion). Palpitation, Syncope, Cold Periphery, Oliguria, 3. Pallor, Cold Periphery, Sweating, Tachycardia, Low Blood Pressure, Oliguria, Confusion Insomnia, Headache & Intermittent Claudication & Memory Impairment. Precipitating Factors of Heart Failure: FAILED HEART F: Failure to Take Medications A: Arrhythmia I: Infection L: Lung Diseases E: Endocrine Problem (Pheochromocytoma) D: Drugs (Verapamil, Diltiazim, NSAIDS, Steroid & IV Fluid) H: Hypertension E: Endocarditis A:Anemia & Alcohol R: Rheumatic Fever T: Thyrotoxicosis All Those Factors Cause Firing of Chronic Heart Failure & Lead to Acute On Top of Chronic Heart Failure Because They Responsible to Change State of Patient with Heart Failure From Compensated to Uncompensated  So... All Patients with Heart Failure Should Avoid All Those Risk Factors. DR. MOHCEN AL. HAJ 4  Please Remember  Left Side Heart Failure Cause Left Ventricular Dilatation & The Dilatation Lead to Functional Mitral Regurgitation Right Side Heart Failure Cause Right Ventricular Dilatation & The Dilatation Lead to Functional Tricuspid Regurge. Prolonged Chronic Left Side Heart Failure Cause  Pulmonary Hypertension, Prolonged Pulmonary Hypertension Cause  Right Side Heart Failure. - But Right Side Heart Failure Doesn’t Cause Left Side Heart Failure. Causes: Investigations : Causes Related to Causes Related to 1. Echocardiography: (Diagnostic) Myocardial Ventricular Outflow Transthoracic Echocardiography (TTE) Dysfunction: Obstruction: Measure Ejection Fraction [EF]; (Normally >50%) 3 M: AS 3P: (EF in Sever Heart Failure Less Than 35%). 1.Myocardial Infarction 1.Aortic Stenosis. Detect Valve Lesions (Stenosis or Regurgitation). (Most Common). 2.Systemic Hypertension. Detect Cardiomyopathy & Cardiac Tamponade. 2.Myocarditis. 3.Pulmonary Hypertension 3.Myopathies (Dilated 4.Pulmonary Stenosis. 2. 12 Lead Electro Cardiography (ECG): Cardiomyopathy DCM). 5.Pulmonary Embolism. Detect Ischemic Heart Disease & Arrhythmias. 3. Blood Workup For: Level of B-Type Natriuretic Peptide (BNP) or N-Terminal ProBNP (NT-ProBNP)  Causes Related to Causes Related to Elevated Due to Ventricular Dilatation. Ventricular Inflow Ventricular Volume Level of Atrial Natriuretic Peptide (ANP)  Obstruction: Overload: Elevated Due to Atrial Dilatation. MT Stenosis: All Valves Regurgitation: 1.Mitral Stenosis. 1.Mitral & Aortic Regurge BNP Used Mainly For: 2.Tricuspis Stenosis. 2.Tricusp & Pulm Regurge Diagnosis, Prognosis & Follow Up of Heart Failure. 3. Hyperdynamic Circulation Differentiate Between Cardiac & Non Cardiac Dyspnea 4. Chest X Ray (CXR): Causes Related to Causes Related to Detect Pulmonary Venous Congestion. Diastolic Dysfunction: Cardiac Rhythm: CRP: Sever Tachycardia & 5. Other Blood Workup 1.Constrictive Pericarditis. Sever Bradycardia: Arterial Blood Gas (ABG) For Hypoxia. 2.Restrictive Cardiomyopthy. 1.Ventricular Tachycardia Complete Blood Count (CBC) For Anemia & Infection 3.Pericardial Tamponade. 2.Ventricular Fibrillation Thyroid Function Test (TFT) For Thyorotoxicosis. 3.Third Degree Heart Block Renal Function Test (RFT) For Complications. Liver Function Test (LFT) For Liver Congestion. Cor-Pumonale Means Any Chronic Lung Parenchymal or Chest Wall Diseases Lead to Isolated Right Ventricular Hypertrophy with or without Heart Failure. DR. MOHCEN AL. HAJ 5  Treatment:  Non Pharmacological Treatment: Patient Education About Life Style Control Which are: Decrease Body Weight + Regular Aerobic Exercise + Regular Vaccinations + Salt Free Diet + Fluid Restriction + Small Frequent Meals + Stop Smoking + Stop Alcohol + Avoid Some Drugs as Ca Channel Blockers & NSIDS.  Pharmacological Treatment: 1. Diuretics: 2. Angiotension Converting Enzyme Inhibitor (ACE I): Mechanism of Action: Mechanism of Action: Decrease Preload (Main Action) Also Afterload Decrease Afterload (Main Action). Types: They Improve Survival Rate & Decrease Hospitalization -Loope Diuretics (furosemide = Lasix): 1st Line Types: -Thiazide (Metolazone, Bendroflumethiazide). Captopril (Capotin): Has Rapid Action. -Potassium Sparing Diuretic: Spiranolactone & Enalapril, Lisinopril, Ramipril, Quinapril. Eplerenone (Which Improve Survival Rate).  ACE I Improve Survival Rate. 3. Angiotension II Receptors Blockers (ARBs): 4. β– Blockers Mechanism of Action: Mechanism of Action: Decrease Afterload (Main Action). Moderate Afterload Reduction & Slight Preload Reduction Types: But the Main Action is Protect the Heart Against Candisartan, Valsartan, Irbesartan, Losartan Sympathetic Stimulation & Inhibit Remodeling & Decrease Risk of Arrhythmias (VT) So Reduce Risk of 5. Vasodilators: Sudden Death & Decrease Hospitalization. Given When the Patient Stabilized By Other Medications Mechanism of Action: Types: Decrease Preload & Afterload. Carvidolol, Metopolol, Bisoprolol, Nebivolol. Types:  β– Blockers Improve Survival Rate. Nitrate, Hydralazine, Nitroprosside Sodium 6. Digoxin: 7. Amiodaron: Mechanism of Action: It is a Strong Anti-Arrhythmic Drug which has Little Increase Intracellular Calcium That Lead to Negative Inotropic Effect and May Be Valuable in Increase Myocardial Contractility. Patients with Poor Left Ventricular Function. *Also Increase Vagal Activity Leading to Only Effective in Treatment of Symptomatic Arrhythmias Decrease Conduction of Impulse Through AVN & Should Not Be Used in Asymptomatic Patient.  Digoxin Doesn’t Improve Survival Rate. 8. New Drugs: Ivabradine (Regulate Heart Rate & Decrease Hospitalization), Neprilysin Inhibitor (Sacrubitril) Better If It Used with ARBs (Valsartan) Known as Entresto (Reduce Risk of Death & Hospitalization) SGLT-2 Inhibitors Which are: Empagliflozin, Dapagliflozin & Sotagliflozin (Reduce Risk of Death & Hospitalization)  Interventional Treatment in Patient with Heart Failure: 1. Implantable Cardiac Defibrillator (ICD): Indicated in Patients with Heart Failure Who Have Had, or Who are at High Risk of Ventricular Arrhythmia. 2. Cardiac Resynchronization Therapy Device (CRT): Indicated in Patients with Marked Conduction System Disease, Especially Left Bundle Branch Block. 3. Coronary Revascularization (PCI & CABG): For Selected Patients with Heart Failure & Coronary Artery Disease. 4. Heart Transplantation: It is the Last & Definitive Surgical Intervention. DR. MOHCEN AL. HAJ 6  About Heart Failure Medications: About Heart Failure Medications:  Side Effect of Furosemide: Side Effect of Ag II Receptors Blockers: 1. Hypotension (Hypovoleamia) 2. Hypocalceamia, Same Side Effects of ACE I, Except: No Cough. 3. Hypokaleamia, 4. Hyponatreamia 5. Hypomagneseamia, 6. Hyperglyceamia, Please Remember  7. Hyperureceamia. ARBs Improve Survival & Decrease Mortality In Patients with Heart Failure (Similar to ACE I)  Side Effect of Thiazide: & They are a Useful Alternative For Patients Same as Side Effects of Furosemide Except: Who Can’t Tolerate ACE I Side Effects 1. Hypercalceamia (Not Hypocalceamia), as Cough. 2. Hyperlipideamia. Please Remember  furosemide & Thiazide Improve Symptoms But  Side Effects of β–Blockers: Doesn’t Improve Survival. 1. Peripheral Vasoconstriction. 2. Mask Symptoms & Signs of Hypoglyceamia.  Side Effect of Spironolactone: 3. Bronchospasm. Hyperkaleamia & Gynecomastia. 4. Depression & Nightmares. 5. Acute Heart Failure. Please Remember  Spironolactone Improve Survival Rate. Contraindications of β–Blockers: (BADR Heart Failure) 1. Bradycardia.  Side Effect of ACE Inhibitors: 2. Asthma. 1. Dry Cough (Most Common Side Effect) in 10%-15%. 3. Diabetes Mellitus. 2. Firs Dose Hypotension: So In the First Day Should 4. Reynaud’s Phenomenon. Be Given at Bed Time with Half Dose. 5. Heart Failure Grade 4  (NYHA Class IV). 3. Hyperkaleamia So Don’t Give It with Spironolactone. 6. Active Heart Failure (Acute Symptoms). 4. Renal Impairment In Patient with Bilateral Renal Artery Stenosis: So Renal Function Test Should Be Checked 1-2 Weeks After Starting Treatment.  Side Effect of Digoxin: 5. Angioedema. 6. Skin Rash & Leukopenia (Rare). Digoxin Toxicity (Digoxin Not Given to Patient with Hypokaleamia; Because It Lead to Toxicity). Please Remember  Indication of Digoxin Use: ACE I are Given to All Patients with Heart Failure, 1. Heart Failure with Atrial Fibrillation. Because ACE I Inhibit Remodeling of the Heart & Improve Survival (Prognosis) & Decrease Mortality 2. Marked Systolic Dysfunction (Severe HF). Rate In Patients with Heart Failure. 3. Persistent of Symptoms Even After Optimal Dose of Diuretics & ACEI. DR. MOHCEN AL. HAJ 7  Complications: 1. Cardiac Arrhythmias:  Very Common and Related to Electrolytes Disturbance, Include:  Atrial Fibrillation (Occur in 20%).  Ventricular Tachycardia.  Ventricular Fibrillation.  Ventricular Ectopic. 2. Organ Failure:  Renal Failure:  Due to Poor Renal Perfusion & May Exacerbated By Diuretics, ACE I & ARBs.  Liver Failure:  Due to Hepatic Venous Congestion & Poor Arterial Perfusion. 3. Thrombo-Embolism:  Due to Blood Stasis Which Occur Due to Low COP or Patient Immobility, Which Include:  Deep Venous Thrombosis (DVT).  Pulmonary Embolism (PE). 4. Electrolytes Disturbance:  Mostly Due to Medications Side Effects:  Hyperkaleamia Due to ACE I & Spironolactone.  Hypokaleamia Due to Furosemide & Thiazide (Also Due to Activation of RAAS).  Hyponatreamia Due Diuretics and Also Due to Severe Heart Failure and It is a Poor Prognostic Feature. 5. Sudden Death:  Occur in 50% of Patients with Heart Failure and Most Often Due to Ventricular Fibrillation. DR. MOHCEN AL. HAJ 8   ACUTE PULMONARY EDEMA: Definition: Causes: Most Common Cause  Myocardial Infarction. It is an Acute Left Side Heat Failure. Also Caused By Atrial Fibrillation with Mitral Stenosis Pathophysiology : Sudden Left Ventricular Failure Lead to  Increase of Left Ventricular Pressure, Raised Left Ventricular Pressure Lead to  Sudden Increasing of Pressure In Left Atrium, Raised Left Atrial Pressure Lead to  Sudden Increasing of Pressure in Pulmonary Capillaries, Raised Pulmonary Capillaries Pressure Lead to  Sudden Pulmonary Congestion, Pulmonary Congestion Cause  Movement of Fluid From Pulmonary Capillaries To Alveoli & Lung Interstitium, Movement of Fluid From Pulmonary Capillaries To Alveoli Cause  Alveolar Edema & Fluid Moves From Pulmonary Capillaries To Lung Interstitium Cause  Interstitial Edema This Known as  Acute Pulmonary Edema. Please Remember  Alveolar Edema: Interstitial Edema: Accumulation of Fluid In Alveolar Space. Accumulation of Fluid In Lung Interstitium (More at Base).  Clinically Patient Presented with Symptoms:  Clinically Patient Presented with Sign: 1. Cough with Frothy Sputum, 2. Wheeze. Bilateral Basal Fine Crackles. 3. Dyspnea, 4. Orthopnea, 5. PND. Symptoms: Signs: 1. Agitation & Distressed. 1. Dyspnea. 2. Orthopnia. 3. PND. 2. Pale Periphery & Central Cyanosis. 4. Cough with Frothy Sputum. 3. Hypotension & Tachycardia. 5. Heamoptysis. 6. Wheeze. 4. Bilateral Basal Crackles. 5. Raised Jugular Venous Pressure. DR. MOHCEN AL. HAJ 9  Investigations: Treatment: It is an Emergency Case: 1. Chest X Ray (to Detect Pulmonary Edema).  Call For Help + Admission In Coronary Care Unit 2. Echocardiography (to Confirm Diagnosis). Patient On Sitting Position + Full Monitoring and Give High Flow Oxygen. 3. Cardiac Enzyme (to Detect MI). MODN: 4. Arterial Blood Gas (to Detect Hypoxia). 1. Morphine  (5-10mg IV) Best Choice to Decrease Anxiety & Agitation of the Patient. Also Morphine Decrease Dyspnea & Can Lead to Vasodilatation. (Morphine Given with Metolopramide 10mg IV). Please Remember  2. Oxygen  Continuous Positive Airway Pressure Features of Pulmonary Edema in (CPAP) of 5–10 mmHg By Tight-Fitting Mask. Chest X Ray  (ABCDE): 3. Diuretics  Furosemide (50-100mg IV) is the A  Alveolar Edema: Best Choice, Because It Has Rapid Action. Butterfly Opacity. B  B- Line (Kerley-B Lines): 4. Nitrate  IV GTN (10-200Mcg/Min) or Buccal Due to Interstitial Edema. Given Only If Patient Blood Pressure More C  Cardiomegaly. Than 110 mmHg. D  Dilated Upper Lobe Vessels. Nitrate is Vasodilator Drug (Veno-Dilator) Lead to Dilation of Veins & Decrease Venous Return So E  Pleural Effusion. Improve Pulmonary Congestion. 5. If Previous Measures Failed;  Give Positive Inotropic Drug (Doputamine2.5Mcg/kg/min). DR. MOHCEN AL. HAJ 10   SYSTEMIC HYPERTENSION (HTN): Definition: Types: 1ry HTN (Essential HTN) 2ry HTN It is a Condition in Which Arterial Blood Present in 95% of People, Present in 5% of People, Pressure is Clinically Elevated More Than Unknown But May Related to Caused By: RED COPA; 139/89 mmHg Based on 2 or More Reading in 2 Genetic Factor (Most Renal, Endocrine, Drugs, or More Occasions. Common) & Life Style. Coarctation of Aorta, OSA, Pregnancy, Alcohol Causes: Target Organs in HTN: Primary HTN:  Genetic (Most Common 60%).  Blood Vessels:  Life Style, Stress, DM Type II. Atherosclerosis & Aneurysm. Secondary HTN: RED COPA  Heart:  Renal: Renal Artery Stenosis, Atrial Fibrillation, Left Ventricular Hypertrophy, IHD. Glomerulonephritis, Polycystic Kidney Disease.  Nervous System:  Endocrine: Hypothyroidism, Thyrotoxicosis, Stroke, Subarachnoid Heamorrhage (SAH), TIA. Hyperparathyroidism, Cushing Syndrome, Conn’s  Kidneys: Syndrome, Pheochromocytoma, Acromegaly. Chronic Kidney Disease, Hypertensive Nephropathy.  Drugs: OCP, Steroids, NSAIDs.  Retina:  Coarctation of Aorta. Hypertensive Retinopathy.  Obstructive Sleep Apnea (OSA) + Obesity.  Pregnancy.  Alcohol. Treatment:  Non Pharmacological Treatment: Patient Education About Life Style Control Which are: Decrease Body Weight + Regular Aerobic Exercise + Salt Free Diet + Stop Smoking + Stop Alcohol + Low Saturated Fat in Diet + Increase Vegetables, Fruits and Omega 3 in Diet.  Pharmacological Treatment: Diuretics, ACE Inhibitors (ACEI), Angiotensin II Receptors Blockers (ARBs), Calcium Channel Blockers (CCBs), β–Blockers, Vasodilators. Calcium Channel Blockers Classified Into: Dihydropiridine: Nifedipine & Amlodipine (Cause Reflex Tachycardia) Rate Limiting: Verapamil & Diltiazem (Cause Bradycardia So Considered Also as an Anti-Arrhythmic Drugs). In Patient > 55 Years or White: In Patient > 55 Years or African or Caribbean: Step I: Give ACEI or ARBs. Step I: Give CCBs. If Not Respond; Go to Step II & Add CCBs. If Not Respond; Go to Step II & Add ACEI. If Not Respond; Go to Step III & Add Diuretics. If Not Respond; Go to Step III & Add Diuretics. If Not Respond; Go to Step IV & Add β–Blockers or If Not Respond; Go to Step IV & Add β–Blockers or Add Other Diuretic. Add Other Diuretic. DR. MOHCEN AL. HAJ 11   ATHEROSCLEROSIS: Definition: Risk Factors: It is a Progressive Inflammatory Disorder  Non-Modifiable:  Modifiable: of Arterial Wall, Characterized by Focal 1. Age (Most Common). 1. Alcohol. 2. Smoking. Lipid-Rich Deposits of Atheroma. 2. Sex (Male > Female). 3. DM. 4. HTN. 5. Diet. 3. Positive Family 6. Hyperlipidemia. 7. Obesity. History. 8. Sedentary Life. 9. Stress.  Atheroma It is Yellow Swelling Results From Collections of Fat, Smooth Muscle Cells in Sub-Intimal Surface of the Artery. Please Remember  Atheroma May Become Large in Size & Cause  Atherosclerosis It Can Affect Any Artery But the Impairment of Arterial Perfusion (Ischemia) Most Common Arteries: or May Rupture & Leads to Platelets Coronary Arteries Causing  Ischemic Heart Disease. Accumulation Forming Thrombus That Cause Cerebral Arteries Causing  Ischemic Stroke. Partial or Complete Obstruction of Artery. Peripheral Arteries Causing  Intermittent Claudication.  ISCHEMIC HEART DISEASES (IHD): Cause: Types: Atherosclerosis (Atheroma) in Coronary 1. Stable Angina (or Called Angina Pectoris). Artery. 2. Unstable Angina. 3. Myocardial Infarction (Partial + Full Thickness). Classification of Ischemic Heart Diseases: Chronic Coronary Artery Disease Acute Coronary Syndrome (CAD): (ACS): Stable Angina. 1. Unstable Angina. 2. Partial Thickness Myocardial Infarction. 3. Full Thickness Myocardial Infarction. DR. MOHCEN AL. HAJ 12   STABLE ANGINA (ANGINA PECTORIS): Definition: Clinical Pictures: It is a Clinical Syndrome of Chest Pain Due to Sudden Onset Retrosternal Chest Pain, (Heaviness or Transient Myocardial Ischemia Caused By Pressure or Squeezing in Character), Aggravating By Narrowing of Coronary Artery Lumen Due to Exertion, Heavy Meal, Exposure to Cold & Emotional Stress, Atheroma Formation (Atherosclerosis). Relieving By Rest & Glyceril Tri-Nitrate (GTN), Radiating to the Jaw, Neck, Left Shoulder, Left Arm & Epigastium, Lasting For Less Than 10 Minutes (1-5 Minutes). Investigations: 1. Stress ECG (Exercise ECG): Confirmatory Investigation After Typical History. Done Via  Bruce Protocol By Using Treadmill or According to Bruce Protocol Positive If: Bicycle & During Exercise Monitor ECG & Blood Pressure ECG Shows Arrhythmia or ST Depression. & Observe the Patient Clinically for Any Pain or Dyspnea. Blood Pressure Decrease More than 10mmHg. Clinically Patient Has Pain or Dyspnea. Stress ECG Sensitivity is 75%  So Negative Stress ECG Does Not Exclude Stable Angina. It Can Be False Positive in Left Ventricular Hypertrophy, Digoxin Effect, Left Bundle Branch Block & WPW. Please Remember  Please Remember  Stress ECG Contraindicated in: The Usual ECG That Known as: 1. Acute Coronary Syndrome (ACS). 12 Lead Resting ECG Not Favor in Case of 2. Recent ACS Within 6 Days. Stable Angina; 3. Sever Aortic Stenosis. Because the Result Will Be Normal Due to 4. Sever & Uncontrolled Hypertension. Patient in Rest Stat 5. Decompensated Heart Failure. It Can Be Abnormal If ECG Done and Patient 6. Hypertrophic Cardio-Myopathy. Had Attack of Chest Pain. 2. CT Coronary Angiography is the Imaging Investigation of First Choice: It Clarifies the Diagnosis and Guides the Use of Anti-Anginal Therapies & Excellent Guides the Use of Invasive Cardiac Catheterization. Please Remember  CT Coronary Angiography Help in: 1. Diagnose the Cause of Coronary Artery Narrowing. 2. Reveal the Site & Extent Size of Coronary Lesion. 3. Determine the Way of Treatment. DR. MOHCEN AL. HAJ 13 3. Stress Echocardiography: Done For Patients Which Already Has Coronary Atherosclerosis Disease. Do Echocardiography at Rest, Then Give Patient Dobutamin (Pharmacological Stress) and Repeat Echocardiography; Echocardiography During Rest Show  Normal Myocardial Contractility, But Echocardiography After Pharmacological Stress (Dobutamin) Show  Abnormal Myocardial Contractility. Please Remember  Stress Echocardiography is the Best Choice For Patient Who Can Not Tolerate Exercise & Highly Sensitive (78%) & Highly Specific (86%). Stress Echocardiography Need Good Expert in Echocardiography Machine (Operator Depended). 4. Myocardial Perfusion Scan: Done For Patients Which Already Has Coronary Atherosclerosis Disease. Give the Patient Thalium TI-201 or Technetium 99, Then Do Isotope Scan at Rest, Then Give the Patient Dobutamin (Pharmacological Stress) and Repeat Isotope Scan; Isotope Scan During Rest Show  Good Perfusion of Myocardium. But Isotope Scan After Dobutamin Show  Abnormal Perfusion Defect of Myocardium. Please Remember  Myocardial Perfusion Scan is Highly Specific (83%) & Highly Sensitive (77%) But It is Expensive. 5. Coronary Angiography (Diagnostic Cardiac Catheterization): It is an Invasive Test, Done When Other Non-Invasive Tests Have Failed to Find the Cause of the Chest Pain. Indications of Coronary Angiography: 1. Heart Failure with Angina. 2. Post MI or Unstable Angina. 3. MI or Angina in Patient Less Than 50 Years. 4. ECG Changes After Doing Stress ECG. 5. Symptomatic Patient Even After Medications. Risk Stratification of Stable Angina: Risk Stratification Help to Determine Prognosis & Treatment: Low Risk If: High Risk If: 1. Predictable Exertional Dyspnea. 1. Post Myocardial Infarction. 2. Stress ECG Shows Ischemia at High Workload. 2. Stress ECG Shows Ischemia at Low Workload. 3. Echocardiography Good Ejection Fraction. 3. Echocardiography Low Ejection Fraction. 4. Coronary Angiography Shows Single Vessel 4. Coronary Angiography Shows Left Main Coronary Involvement or Involvement of 2 Vessels. Artery Involvement or Involvement of 3 Vessels. 5. DM & Comorbidity. DR. MOHCEN AL. HAJ 14  Treatment:  Non Pharmacological Treatment: Patient Education About Life Style Control Which are: Stop Smoking + Control DM + Control HTN + Control Serum Cholesterol + Decrease Body Weight Regular Exercise + Low Saturated Fat in Diet + Increase Vegetables, Fruits and Omega 3 in Diet.  Pharmacological Treatment: 1. Nitrates: 2. β– Blockers: Mechanism of Action:  Coronary Vasodilatation So;  Heart O2 Supply. Mechanism of Action:  Venodilatation So;  Heart O2 Demand.  Decrease Oxygen Demand By Reducing  Arteriolodilatation So;  Heart O2 Demand. Heart Rate, Blood Pressure and Myocardial Types: Contractility. 1. Sublingual Glyceryl Tri Nitrate (GTN): Types: Has Rapid Action (2-3Min) & Short Duration (10-30Min). Metoprolol (50-200mg), Bisoprolol (5-15mg) 2. Transdermal GTN (GTN Patch): 5-10mg Daily. Nebivolol, Carvidolol, Atenolol, Propranolol. 3. Oral Iso-Sorbid Mono-Nitrate (ISMN): 20-60mg Daily Has Long Duration of Action. β – Blockers Should Not Be Withdrawn Sudden; 4. Iso-Sorbid Di-Nitrate (ISDN): 10-20mg 3 Times Daily Because this Lead to Worsening of Angina, Has Long Duration of Action. Arrhythmias & Myocardial Infarction. Side Effects: 1. Severe Headache. Side Effects: 2. Hypotension. 1. Peripheral Vasoconstriction. 3. Tolerance (Avoided By 6-8 Hours Free of Drug). 2. Mask Symptoms of Hypoglyceamia. 3. Bronchospasm. 3. Calcium Channel Blockers: 4. Anti-Platelets: Mechanism of Action: Prevent Thrombus Formation By Inhibiting  Arteriolodilatation So;  Myocardial O2 Demand. Platelets Aggregation.  Decrease Cardiac Contractility. Include:  Decrease Heart Rate Because They Act On SA Node.  Aspirin 75mg: (Inhibit COX). Types:  Clopidogril (Plavix) 75mg: (Inhibit ADP Dihydropyridine: Amlodipine, Nifedipine, Nicardipine. Binding to Platelet Receptors). Rate Limiting: Verabamil, Diltiazem (Cause Bradycardia).  Ticagrelor (Brilinta): Act Like Plavix But More Rapid & Effective. 5. Other Drugs Can Be Used: 1. K Channel Activator: Nicorandil (Vasodilator). 2. IF Channel Antagonist: Ivabradine (Decrease Heart Rate). 3. Ranolazine: Reducing Angina Symptoms. DR. MOHCEN AL. HAJ 15   Interventional Treatment of Stable Angina (Revascularization): 1. Percutaneous Coronary Intervention (PCI): Indications of PCI: Use Balloon Dilatation Then Stent. 1. Failed Medical Treatment. It Relieve Symptoms But Not Prolong Survival. 2. Single or Two Vessels Disease. 3. Stenosis After CABG. Please Remember  4.Acute Myocardial Infarction as Primary Treatment of Choice (in 1st Two Hours). * Post PCI Give Strong Anti-Platelets Drugs to Decrease Risk of Re-Stenosis: 1. Statin Long Life. Complications of PCI: 2. Aspirin + Clopidogrel (Plavix) 75mg or Brilinta 90mg 1. Re-Occlusion of the Vessel: Occur in (Ticagrelor) For 12 Months Then Continuo with Aspirin Only. Third of Patients & Prevented By Stent 2. Spasm of the Vessel Due to Irritation New Antithrombotic Drug: Monoclonal Ab Abciximab of Arterial Wall. (Glycoprotein IIB/IIIA Antagonist).  2. Coronary Artery Bypass Graft (CABG): Indications of CABG: Use Graft From Great Saphenous Vein 1. Failed PCI. or Radial Artery or Internal Mammary Artery. 2. All Three Coronary Arteries. It Relieve Symptoms & Prolong Survival. 3. Left Main Coronary Artery.  Grafting From Artery Better Than Vein; Because Stay Longer. Complications of CABG: Please Remember  1. Angina: Early or Late. 2. Infection: After Surgery. * Post CABG Give: 1. Statin. 2. Aspirin + Clopidogrel (Plavix) 75mg or Brilinta 90mg Post CABG Surgery: (Ticagrelor) For 6 Months Then Continuo with Aspirin Only. 90% of Patient Free From Angina For 1 Year They All Improve Graft Patency. 60% of Patient Free From Angina For 6 Years New Antithrombotic Drug: Monoclonal Ab Abciximab 50% of Vein Grafts Patent For 10 Years. (Glycoprotein IIB/IIIA Antagonist). 80% of Artery Grafts Patent For 10 Years. DR. MOHCEN AL. HAJ 16   UNSTABLE ANGINA (CRESCENDO ANGINA) &  PARTIAL THICKNESS MYOCARDIAL INFARCTION (NON ST ELEVATION MI = Non-STEMI): Definition: Clinical Pictures: It is a Clinical Syndrome of Chest Pain Due Sudden Onset Retrosternal Chest Pain On Minimal to Myocardial Ischemia Caused By Exertion or Even at Rest, Heaviness in Nature, Narrowing of Coronary Artery Lumen Due Radiating to the Left Shoulder & Left Arm, Lasting to Thrombus Formation. For More Than 20 Minutes. Investigations: 1. 12 Leads Resting ECG: Show ST Depression and/or T-wave Inversion, No Pathological Q wave. Don’t Forget ECG Findings Appear in Two Third of Cases & ECG Appear Normal in One Third. 2. Cardiac Enzyme Troponin I & CK MB: Elevated in NSTEMI, But Not in Unstable Angina. Treatment: It is an Emergency Case:  Call For Help + Admission In Coronary Care Unit + Full Monitoring + Bed Rest. Immediately Give the Patient GTN 500μg Sub-Lingual as First Aid + Serial ECG Every Half Hour. If There is No Bradycardia; Metoprolol Can Be Given 50 -100mg Orally (Reduce Arrhythmia & Improve Mortality).  Give Patient 4 Anti (Anti-Pain, Anti-Platelets, Anti-Coagulants, Anti Anginal Drugs): Anti-Pain Anti-Platelets: Anti-Coagulant: Anti Anginal Drugs: (Analgesia): Aspirin 300mg Orally + IV Un Fractionated Heparin or IV β– Blockers Morphine 10mg IV Plavix 300mg Orally LMW Heparin S/C (Best: Enoxaprine) (Atenolol 5-10mg) + Or Diamorphine 5mg Given in 1st 12 Hours. or Fondaparinux 2.5mg Daily S/C IV Nitrate Given with Anti Emetic Decrease Mortality Rate 1. Prevent Thrombus to Increase. (GTN 0.6-1.2mg/Hr) in 25% of Patients. 2. Prevent Formation of New One. Calcium Channel Blockers Reduce: Blood Pressure, Continuo Aspirin 75 + 3.  Risk of Thrombo-Embolism. (Nifidipine or Amlodipine) Infarction Size & Risk of Plavix 75mg For 12 Moths. Continuo 8 Days or Until Discharge. Given If β– Blockers are Ventricular Arrhythmias. Contraindicated. Please Remember  Don’t Use Thrombolytic Therapy in Patients with: Unstable Angina & Non STEMl.  After Stabilizing the Patient; Do Risk Stratification Via Grace Score: In Case of Low Risk: (Risk of Death < 1%) In Case of High Risk: (Risk of Death > 9%)  Patient Should Do Stress ECG After 4-6 Weeks;  Patient Should Do Early Coronary Angiography If Stress ECG Negative  Good Prognosis. Followed By Revascularization (PCI or CABG) within If Stress ECG Positive  Do Coronary Angiography First 48 Hours & Give Glycoprotein IIb/IIIa Followed By Revascularization (PCI or CABG). Receptor Antagonists (Abciximab) IV Infusion. DR. MOHCEN AL. HAJ 17   FULLL THICKNESS MYOCARDIAL INFARCTION (ST ELEVATION MI = STEMI): Definition: Clinical Pictures: It is a Clinical Syndrome of Chest Pain Due Same as Non-STEMI + Associated with: to Myocardial Ischemia Caused By Dyspnea, Nausea, Vomiting, Sweating, Palpitation, Persistent & Complete Occlusion of Syncope, Epigastric Pain Lasting More Than 30 Mint Coronary Artery.  Chest Pain May Be Asymptomatic in DM + Old Age Investigations: 1. 12 Leads Resting ECG: (Confirm Dx) It Shows ST Elevation, Pathological Q wave, Left Bundle Branch Block. Within 1st 12 Hours: ST Elevation, Within 1st Days: ST Elevation + Pathological Q Wave + Inverted T Wave, After Months or Years: Pathological Q Wave Only. ECG Findings Appear in Two Third of Cases & Appear Normal in One Third ;So Normal ECG Doesn’t Exclude STEMI Myocardial Infarction May Occur in Right Ventricle Which Detected By  Right Sided ECG. 2. Cardiac Enzyme (Troponin I/T & CK MB): Troponin I: Most Sensitive, Release in 3-6 Hours, Reach the Peak in 36 Hours, Return Normal After 14 Days. Creatinin Kinase MB (CK MB): Release in 3-6 Hours, Reach the Peak in 16-30 Hours, Return Normal in 2-3 Days. 3. Echocardiography: Normally Performed Before Discharge to Asses Ventricular Function & Complications. 4. Other Investigations: Chest X Ray, CBC (WBC), CRP + ESR (Elevated), Blood Sugar, Lipid Profile. Treatment: It is an Emergency Case:  Call For Help + Admission In Coronary Care Unit + Full Monitoring + Bed Rest. Immediately Give the Patient GTN 500μg Sub-Lingual as First Aid + Serial ECG Every Half Hour. If There is No Bradycardia; Metoprolol Can Be Given 50 -100mg Orally (Reduce Arrhythmia & Improve Mortality).  Give Patient 4 Anti (Anti-Pain, Anti-Platelets, Anti-Coagulants, Anti Anginal Drugs): Anti-Pain Anti-Platelets: Anti-Coagulant: Anti Anginal Drugs: (Analgesia): Aspirin 300mg Orally + IV Un Fractionated Heparin or IV β– Blockers Morphine 10mg IV Plavix 300mg Orally LMW Heparin S/C (Best: Enoxaprine) (Atenolol 5-10mg) + Or Diamorphine 5mg Given in 1st 12 Hours. or Fondaparinux 2.5mg Daily S/C. IV Nitrate Given with Anti Emetic. Decrease Mortality Rate 1. Prevent Thrombus to Increase. (GTN 0.6-1.2mg/Hr) in 25% of Patients. 2. Prevent Formation of New One. Calcium Channel Blockers Reduce: Blood Pressure, Continuo Aspirin 75 + Plavix 3.  Risk of Thrombo-Embolism. (Nifidipine or Amlodipine) Infarction Size & Risk of 75mg For 12 Moths. Continuo 8 Days or Until Discharge. Given If β– Blockers are Ventricular Arrhythmias. Contraindicated. DR. MOHCEN AL. HAJ 18   Specific Treatment of STEMI (Reperfusion): To Restore Coronary Patency, Improve Survival & Decrease Mortality (25%–50%) Which Include: Primary Percutaneous Coronary Intervention: Thrombolytic Therapy: Known as (1ry PCI), It’s the Treatment of Choice. Done If 1ry PCI Cannot Achieved Within 1st 2 Best Time Within 1st 2 Hours (120 Minutes). Hours of Diagnosis, Done in 1st 12 Hours. Effective More Than Thrombolytic Therapy. Thrombolytic Therapy Include: 1. Alteplase, Tenecteplase & Reteplase: Decrease Mortality Rate By 50%. Best Choices, Not Allergic. One Year Survival Rate is More Than 95%. 2. Streptokinase: Not Favor, Allergic. Successful PCI May Associated with Transient Arrhythmias All Patients Who Have Received Successful If 1ry PCI Achieved; Give Glycoprotein IIb/IIIa Receptor Thrombolysis Should Be Considered For Early Antagonists IV (Abciximab IV Bullos 0.25mg 10 Min Before PCI) Coronary Angiography with a View to Coronary In Hospital Continuo S/C LMW Heparin or Fondaparinux & Revascularization (PCI) Within the First 24 Hours Oral Aspirin + Plavix 75mg, β– Blockers, and ACE I Therapy Contraindications of Thrombolytics: Absolute Contraindication: Relative Contraindications: 1. Active Internal Bleeding. 1. Uncontrolled HTN. 2. Active Peptic Ulcer. 2. Previous Hemorrhagic Stroke. 3. Previous Ischemic Stroke. 4. Pregnancy. 3. Suspected Aortic Dissection. 5. Recent Surgery & Recent Trauma.  Rehabilitation Post STEMI: If There is No Complications; Patient Can Mobilize After 2nd Day, Return Home After 2-3 Days, Resume Car Driving After 1-4 Weeks, Return in Work After 4 Weeks.  Secondary Prevention Post STEMI: Non Pharmacological Prevention: Pharmacological Prevention: Control DM, HTN, Serum Cholesterol 1. Aspirin & Plavix or Aspirin & Brilinta For 1 Year, Then After Year Stop Smoking, Regular Exercise, Continuo with Aspirin Only Long Life. Decrease Weight, 2. ACE Inhibitors Long Life ( Risk of Remodeling,  Risk of Heart Failure). Increase Vegetables, Fruits 3. Statin (Atrovastatin or Simvastatin) For Long Life. and Omega 3. 4. β–Blockers For at Least 2 Years: ( Risk of Remodeling). Complications: Immediate Complications: Early Complications: Late Complications: 1. Arrhythmias: Common But 1. Early Pericarditis: 1. Late Pericarditis: Also Known: Often Transient, Include: Occur 2nd-3rd Hour Relieved By Opiate Dressler’s Syndrome; Ventricular Fibrillation (in 5- NSAIDs & Steroid Not Given It is as Autoimmune Event Occur 10% of Patients), Ventricular (Because Risk of Vent Aneurism) Within Weeks to Months, Tachycardia, Ventricular 2. Acute Heart Failure (Poor Prognosis) Relived By NSAIDs or Steroid. Ectopic, Atrial Fibrillation & 3. Left Ventricular Failure. 2. Thrombo-Embolism. Atrial Flutter. 4. Acute Pulmonary Edema. 3. Myocardial Ischemia. 2. Heart Block. 5. Cardiac Rupture: Occur 2nd-5th Day 4. Ventricular Remodeling. 3. Cardiogenic Shock. Rupture of Wall, Ventricular Septum, 5. Ventricular Aneurysm (10%): Papillary Muscles. Characterized By Persistent ST Elevation. DR. MOHCEN AL. HAJ 19   ACUTE RHEUMATIC FEVER: Definition: Pathophysiology: It is an Immune Mediated Delayed Group A β-Hemolytic Streptococcus Has M-Protein That Inflammatory Disease That Result From Look Similar to Some Proteins in the Heart, Joints, Brain Recurrent Untreated Pharyngitis & Tonsillitis By and Skin, Group A β-Hemolytic Streptococci. Some Antibodies Synthesized Against Bacterial Antigens Can Affect Heart, Joints, Brain & Skin. (M-proteins) May Cross React with of Heart Muscle Cause Develop After 2 – 3 Weeks From Infection Inflammation of All Heart Layers, Usually Affect Children (5 – 15 Years). Also Cause Inflammation in Joint, Brain & Skin. It's Histologically Presence of Aschoff's Nodules Only in the Heart Seen in Subacute or Chronic Phase of Rheumatic Fever. Clinical Pictures: Please Remember  First All Patients Have Streptococcal Pharyngitis, Joints are the Most Common Site Affected and Then After 2-3 Weeks Patients Develops: By Rheumatic Fever  75%. 1. Chest Pain, Dyspnea & Palpitation (Due to Pan-Carditis) While All Layers of Heart  60%. 2. Joint Pain with Redness & Swelling (Due to Poly-Arthritis) Basal Ganglia  30%. 3. Erythema Marginatum, Sydenham’s Chorea & Fever Skin  10%. But Don’t Forget It May Be Asymptomatic. Pan-Carditis: Poly-Arthritis: Its Incidence Declines with Increasing Age, Most Common Presentation (75% of Patients); Occur in 60% of Patients Include: It is an Acute, Painful, Migratory (Fleeting), 1. Pericarditis: Causing Pericardial Effusion. Asymmetrical Polyarthritis Affect Large Joints of 2. Myocarditis: Causing Heart Failure. Extremities (Knee, Ankle, Elbow & Wrist) Present with 3. Endocarditis: Involve Valves of the Heart, Redness, Swelling & Tenderness Between 1 Day & 4Weeks Causing Mainly Valves Regurgitation. Please Remember  Affect Mainly: Mitral & Aortic (> 50%) This Type of Arthritis Has Dramatic Response to But Tricuspid & Pulmonary are Rare. Salicylates (Aspirin), If Not Improve to Aspirin; the Diagnosis is Doubt. Sydenham’s Chorea: Erythrma Marginatum: Known as  St Vitus Dance. Non-Tender, Non-Pruritic, Migratory, Redness, with It is Purposeless, Involuntary Movements of Face & Raised Margin & Pale Center, Mainly On Trunk & Proximal Extremities Occur in 20-30%, More in Female Extremities, But Not in Face Occur in Less Than 5%. It is Late Neurological Manifestation Due to Inflammation of Basal Ganglia. Sub-Cutaneous Nodules: It Appears 3-6 Months After Pharyngitis Firm, Painless, Mobile Nodules Common in Extensor Surface Spontaneous Recovery Occur Within Few Months. Appear After 3-6 Weeks of Pharyngitis, Occur in 5-7%. DR. MOHCEN AL. HAJ 20  Investigations: 1. Blood Workup: CBC (WBC), ESR (Elevated) & CRP (Elevated). 2. Throat Swab For Culture: Positive in 10-25% of Patients Only. 3. Serology (Best): High Anti-Streptolysin-O (ASO) Antibody Titer (>200U in Adult & >300U in Children). 4. ECG: For Pericarditis & Heart Block. 5. Echocardiography: For Valve Lesions Mainly Regurgitation & For Pericardial Effusion. Diagnosis: By Revised Jones Criteria Which are:  Major Criteria:  Minor Criteria: Poly-Arthtitis, Pan-Carditis. Arthralgia, Previous Rheumatic Fever. Sydenham’s Chorea, Erythema Marginatum. Fever, Leukocytosis, High ESR or CRP. Sub-Cutenious Nodules. First Degree Heart Block.  Evidence of Previous Streptococcal Infection: Positive Throat Swab Culture or High ASO Antibody Titer.  Rheumatic Fever Diagnosed Clinically in Presence of: Two Major Criteria + Evidence of Previous Streptococcal Infection or One Major + Two Minor Criteria + Evidence of Previous Streptococcal Infection. Treatment:  Bacterial Eradication By Using:  Symptoms Eradication By Using: Single Dose of Benzathine Benzyl Penicillin Injection 1. Aspirin For Poly-Arthritis (Response Within 1.2 Million Unit IM, 24 Hours Which Help to Confirm Diagnosis), Or Phenoxymethyl Penicillin Orally 250mg 4 Times Dose is 100mgxKg/Day & Continuo Until ESR Daily For 10 Days. 2. Steroid For Pan-Carditis or Severe Arthritis. Should Be Given On Diagnosis to Eliminate Any Dose is 2mgxKg/Day & Continuo Until ESR. Residual Streptococcal Infection. 3. Antipyretics For Fever. Please Remember  Recurrence of Infection Prevented By Long-Term Prophylactic Penicillin (Oral Phenoxymethyl Penicillin 250 mg Twice Daily or Benzathine Benzyl Penicillin 1.2 Million Unit IM Monthly), Which Given According to: If Associated with Pan-Carditis with Valve Involvement; Given For 10 Years or Until Age Reach 40 Years Old. If Associated with Pan-Carditis Without Valve Involvement; Given For 10 Years or Until Age Reach 21 Years Old. If There is No Pan-Carditis & No Valve Involvement; Given For 5 Years or Until Age Reach 21 Years Old.  CHRONIC RHEUMATIC FEVER Common in Female, Occur in 50% of Patients with Rheumatic Fever with Pan-Carditis, Causing Valvular Heart Disease Commonly Affect Mitral (90%) Then Aortic Then Tricuspid & Pulmonary Isolated Mitral Stenosis Account For About 25% of All Cases, and an Additional 40% Have Mixed Mitral Stenosis and Mitral Regurgitation. DR. MOHCEN AL. HAJ 21   VALVULAR HEART DISEASES (VHD): Mitral Stenosis: Causes: Pathophysiology: 1. Rheumatic Fever (Almost Always). In Mitral Stenosis Passing of Blood From Left Atrium 2. Senile Degeneration (Heavy Calcification). to Left Ventricle Depending On Atrial Contraction, 3. Congenital (Rare) Which After Long Time It Will Lead to Left Atrial 4. Others: Malignant Carcinoid Disease, SLE, RA. Dilatation & Hypertrophy, Long Time of Dilatation Causes Atrial Fibrillation That Symptoms: Leads to Stasis of Blood & Formation of Thrombus Symptoms Appear When Mitral Orifice is < 2cm Which May Detached Causing Stroke, 1. Fatigue & Cold Periphery (Due to COP). Stasis of Blood in Lt Atrium Lead to Increase of 2. Palpitation (Due to Atrial Fibrillation). Pressure in Lt Atrium Lead to Increase Pressure in 3. Hemiparesis (Due to Stroke). Pulmonary Veins Then Pulmonary Capillaries Which 4. Dysphagia (Due to Compression of Esophagus). Cause Pulmonary Congestion, 5.Hoarseness of Voice (Due to Compression of Recurrent Long Standing Pulmonary Congestion Lead to Pulmonary Laryngeal Nerve Known as Orthner’s Syndrome). HTN That Increase Pressure in Pulmonary Artery and 6. Dyspnea, Orthopnea, PND, Cough with Then Rt Ventricle Causing Rt Ventricular Hypertrophy Heamoptysis & Wheeze (Due to Pulmonary Edema). & Dilatation Leading to Right Side Heart Failure. 7. Bilateral LL Edema & Abdominal Distension (Due to Right Side Heart Failure). Investigations: 1. Echocardiography (Investigation of Choice): Signs: Confirm Diagnosis and Asses Severity & Complications. 1. Irregular Pulse (Due to Atrial Fibrillation). 2. ECG: Atrial Fibrillation (Absent P-Wave) or 2. Bilateral Lungs Crackles (Due to Pulm Edema). Left Atrial Enlargement (P-Mitral). 3. Ascites, Congested Tender Liver & JVP 3. Cardiac Catheterization: Screening For the (Due to Right Side Heart Failure). Presence of Coexisting Coronary Artery Disease. 4. Malar Flushing (Rash). 4. Chest X Ray (Pulmonary Edema, Lt Atrial Dilatation) 5. Loud S1 + Opening Snap + Mid Diastolic Murmur Treatment: If Patient Asymptomatic: Just Follow Up By Echocardiography Every 6-12 Months. If Patient Has Mild Symptoms (Mild to Moderate Stenosis)  Medical Treatment: Diuretics (to Control Pulmonary Edema), If Associated with Atrial Fibrillation Give Anticoagulant with Digoxin or B-Blockers If Patient Has Severe Symptoms (Severe Stenosis): Do Surgical Intervention (Balloon Valvuloplasty, Valvotomy, Valve Replacement)  Balloon Valvuloplasty & Valvotomy are Treatment of Choice in Case If: Isolated Mitral Stenosis, No (or Trivial) Mitral Regurgitation, Mobile & Non-Calcified Valve, Lt Atrium Free of Thrumbus.  Valve Replacement is the Best Choice, There are Two Types Prostatic Valve: Metallic Valve: Tissue Valve (Biological Valve): Stay Long Life. Stay For 7-15 Years. Need Anticoagulant (If Warfarin Target INR 2-3). No Need For Anticoagulant. Mostly Done For Young Patients. Mostly For Old Patients. Click Sound is Heard. No Click Sound. DR. MOHCEN AL. HAJ 22  Mitral Regurgitation: Causes: Pathophysiology: 1. Rheumatic Fever (Most Common). During Contraction of Left Ventricle, Amount of Blood 2. Infective Endocarditis. Will Return Back to Lt Atrium, 3. Mitral Valve Prolapse (Floppy Mitral Valve). This Returned Blood Lead to Left Atrial Dilatation & 4. Post Myocardial Infarction & Cardiomyopathy. Little Increase of Pressure. 5. Lt Ventricular Dilatation (Functional Regurge). Long Time of Dilatation Causes Atrial Fibrillation That Leads to Stasis of Blood & Formation of Thrombus Symptoms: Which May Detached Causing Stroke, 1. Fatigue & Cold Periphery (Due to COP). Stasis of Blood in Lt Atrium Lead to Increase of 2. Palpitation (Due to Atrial Fibrillation). Pressure in Lt Atrium Lead to Increase Pressure in 3. Hemiparesis (Due to Stroke). Pulmonary Veins Then Pulmonary Capillaries Which 4. Dysphagia (Due to Compression of Esophagus). Cause Pulmonary Congestion, 5.Hoarseness of Voice (Due to Compression of Recurrent Long Standing Pulmonary Congestion Lead to Pulmonary Laryngeal Nerve Known as Orthner’s Syndrome). HTN That Increase Pressure in Pulmonary Artery and 6. Dyspnea, Orthopnea, PND, Cough with Then Rt Ventricle Causing Rt Ventricular Hypertrophy Heamoptysis & Wheeze (Due to Pulmonary Edema). & Dilatation Leading to Right Side Heart Failure. 7. Bilateral LL Edema & Abdominal Distension (Due to Right Side Heart Failure). Investigations: 1. Echocardiography (Investigation of Choice): Signs: Confirm Diagnosis and Asses Severity & 1. Irregular Pulse (Due to Atrial Fibrillation). Complications. 2. Bilateral Lungs Crackles (Due to Pulm Edema). 2. ECG: Atrial Fibrillation (Absent P-Wave) or 3. Ascites, Congested Tender Liver & JVP Left Atrial Enlargement (P-Mitral). (Due to Right Side Heart Failure). 3. Cardiac Catheterization: Screening For the 4. Displaced Apex Beat, Soft S1 + S3 + Apical Pan Presence of Coexisting Coronary Artery Disease. Systolic Murmur Radiate to the Axilla. 4. Chest X Ray (Pulmonary Edema, Lt Atrial Dilatation). Treatment: If Mild Mitral Regurgitation: Just Follow Up By Echocardiography Every 6-12 Months. If Moderate to Severe Mitral Regurgitation  Medical Treatment: Give Diuretics & Vasodilators, Digoxin & Anticoagulant Given in Atrial Fibrillation, Also ACE I or ARBs Given in Systemic HTN. If Severe Mitral Regurgitation: Surgical Intervention (Mitral Valve Repair, Valve Replacement).  Valve Repair By Inserting an Annuloplasty Ring, It is a Treatment of Choice For Functional Regurgitation  Valve Replacement is the Best Choice, Done If: 1. Failed Medical Treatment. 2. Progressive Cardiomegaly. 3. Decrease Left Ventricular Function. DR. MOHCEN AL. HAJ 23  Aortic Stenosis: Causes: Pathophysiology: 1. Rheumatic Fever (Most Common in Middle Age). During Contraction of Left Ventricle, to Pump the 2. Congenital (in Infants, Children & Adolescence). Blood to the Aorta; There is a Resistance Through 3. Calcification of Bicuspid Valve (Young,Middle,Old) Aortic Valve, Due to Narrowing of Aortic Orifice, 4. Senile Degeneration (in Middle to Old Age). That Resistance with Time Will Lead to Left Ventricular Hypertrophy. This Left Ventricular Hypertrophy Leads to Symptoms: Increasing of O2 Demand of Myocardium, Patients Remain Asymptomatic For Many Years The Increasing of Myocardial Demand for O2 Lead to (Because Stenosis Develops Slowly), Angina (Angina with Normal Coronary Artery), Fixed Outflow Narrowing Lead to Limit Increasing of Deteriorate Rapidly When Symptoms Develops. COP During Exertion, The Symptoms Develops Due to Exertion Limiting of COP During Exertion Cause Exertional Which are  SAD P.S Syncope + Exertional Angina + Exertional Dyspnea & S: Syncope (Due to Markedly  of COP). Sudden Death. A: Angina (Due to Myocardial O2 Demand). Eventually Left Ventricle Will Fail (Due to Long- D: Dyspnea, (Due to Left Ventricular Failure). Standing Hypertrophy) Leading to Pulmonary Edema. P: Palpitation (Due to Arrhythmia). S: Sudden Death (Due to Ventricular Tachycardia) Investigations: Cardinal Symptoms = SAD (Syncope, Angina, Dyspnea). 1. Echocardiography (Investigation of Choice): Confirm Diagnosis and Asses Severity & Complications. Signs: 2. ECG: Lt Ventricular Hypertrophy, Lt BBB, Down 1. Low Blood Pressure with Narrow Pulse Pressure. Sloping ST & T-Wave Inversion (Strain Pattern). 2. Small Volume Pulse (Palsus Parvus). 3. Chest X Ray: Enlarged Lt Ventricular (Boot-Shape 3. Slow Rising Pulse. Heart), Pulmonary Edema. 4. Bilateral Lungs Crackles (Due to Pulm Edema). 4. Cardiac Catheterization: Screening For the 5. Soft S2 + Harsh Ejection Systolic Murmur Presence of Coexisting Coronary Artery Disease. Radiate to the Neck. Treatment: If Patient Asymptomatic (Mild & Moderate Aortic Stenosis): Just Follow Up By Echo Every 1-2 Years. (In Older Patients & Heavy Calcified Aortic Valve Follow Up Echo Every 3-6 Months). If Symptomatic Severe Aortic Stenosis: Surgical Intervention (Balloon Valvuloplasty, Valve Replacement, Tanscatheter Aortic Valve Implantation = TAVI).  Balloon Valvuloplasty Mainly Done For Congenital Aortic Stenosis (But Not For Old Pts & Calcified Valve).  Tanscatheter Aortic Valve Implantation (TAVI) Done For Older Patients & Pts Not Fit For Replacement.  Valve Replacement is the Best Choice For All Severely Symptomatic Patients. DR. MOHCEN AL. HAJ 24  Aortic Regurgitation: Causes: Pathophysiology: 1. Rheumatic Fever (Most Common). Amount of Blood Return to From Aorta to Left 2. Infective Endocarditis. Ventricle Which Cause Increasing of Blood Volume in 3. Dilatation of Aortic Root (Present in Case of: Left Ventricle, Aortic Dissection & Aneurysm, Aortic Syphilis, Marfan’s Syndrome, Ankylosing Spodylitis). Then in Next Cycle Left Ventricle Bump Large Volume of Blood to Entire Body That Lead to Increasing of COP 2 or 3 Times More Than Before, Symptoms: This High COP Lead to Large Pulsation of Arteries of Patients May Asymptomatic or Just Have the Body, Palpitation Especially in Mild to Moderate Cases. The Symptoms Develops in Severe Cases Recurrence of Returning the Blood From Aorta to Left Which Include: Ventricle Lead to Increasing of Left Ventricular 1. Uncomfortable Awareness of Heart Beat. Pressure, 2. Dyspnea (But PND Sometimes the 1st Symptom) Raised Left Ventricular Pressure Lead to Left 3. Angina (Due to Myocardial O2 Demand). Ventricular Dilatation & Hypertrophy. 4. Head Nodding: Eventually Left Ventricle Will Fail (Due to Long- (Due to Large Pulse of Carotid Artery). Standing Hypertrophy) Leading to Pulmonary Edema. 5. Lately Symptoms of Pulmonary Edema (Orthopnea, PND, Cough with Heamoptysis & Wheeze) Investigations: 1. Echocardiography (Investigation of Choice): Signs: Confirm Diagnosis and Asses Severity & Complications. 1. Wide Pulse Pressure (>100mmHg) with Low 2. ECG: Lt Ventricular Hypertrophy, LT BBB, ST. Diastolic Pressure ( 50 Years. 4. History of Myocardial Infarction. Pathophysiology: Types: Endocardial Damage Occur Due to Abnormal Blood Flow (Due to Septal Defect) Which Act as a Acute Infective Sub-Acute Infective Site That Attract Deposits of Platelets & Fibrin Endocarditis: Endocarditis: Leading to Platelets & Fibrin Aggregation That are Vulnerable to Colonization By Organisms Occurs in Healthy Heart. Occurs in Diseased Heart Leading to Formation of Vegetations. Caused By Strong (VHD, Congenital). Vegetation is Composed of Organisms, Fibrin and Organism. Platelets That Grow and May Become Large. Common at Site of  Fate of Those Vegetations: More Common with IV Pre-Existing Endocardial 1. Valve Destruction (Valve Regurgitation). Drug Abusers & Patients Damage: (at Site of 2. Embolus Formation (Pulm Embolism, Stroke). with Low Immunity. Congenital Anomaly). 4. Abscess Formation (Mainly at Root of Aorta). 3. Immune-Complex Deposition (Vasculitis). Causative Organisms: Streptococci & Staphylococci: Others: Streptococcus Viridance: Coxiella Burnetti (Q-Fever): Normal Flora of Upper Respiratory Tract, Common in Patients with History of Farm Most Common Cause of Sub-Acute Infective Endocarditis Animal Contact (Mostly Involve Aortic Valve). Staphylococcus Aureus: Brucella Normal Flora of Skin, Affect Mainly IV Drug Abusers, Common in Patients with History of Goats & Most Common Cause of Acute Infective Endocarditis. Cattles (Mostly Involve Aortic Valve). Staphylococcus Epidermidis (Coagulase Negative): Candida & Asperogillus (Low Immune Pts). Most Common Cause of Prosthetic Valve Endocarditis, Very Common at First Year of Surgery. Rickettsia, Chlamydia, Klebsiella, Pseudomonas. DR. MOHCEN AL. HAJ 27  Clinical Pictures & Complications: Sub-Acute Infective Endocarditis: Suspected when a Patient with Congenital or Valvular Heart Disease, Include: 1. General Features: 2. Valve Destruction Features (Regurgitation): Fever, Anorexia, Headache, Malaise (FAHM), Cardiac Murmurs. (Persistent Fever, Night Sweating, Weight Loss). 4. Vasculitis Features: 3. Embolisation Features: Splinter Hemorrhage: Hemorrhage Under Nails. Cerebral Vessels: Stroke, Brain Abscess. Roth’s Spots: Retinal Hemorrhage with Pale Center. Retinal Vessels: Sub-Conjunctival Hemorrhage Osler’s Nodule: Small Painful Intra-Cutaneous and Blindness. Nodules in the Tip of Fingers & Toes. Peripheral Vessels: Acute Limb Pain. Glomerular Nephritis: Which Considered as a Cause Coronary Vessels: Retro-Sternal Chest Pain. of Death in Infective Endocarditis. Pulmonary Vessels: Pulmonary Embolism Especially in IV Drug Abusers. 5. Finger Clubbing & Splenomegaly: Late Feature. Mesentertic Vessels: Acute Abdominal Pain. Renal Vessels: Non-Visible Hematuria (Common). (Splenomegaly with Hepatomegaly Common in Coxiella) Acute Infective Endocarditis: Severe Fever, Cardiac Murmurs & Petechiae. Embolic Events are Common, and Cardiac Failure or Renal Failure May Develop Rapidly. If Partially Treated; It Will Behaves Like Sub-Acute Infective Endocarditis. It Can Progress to Death Within Weeks. Investigations: 1. Blood Culture (Identify the Organism): 2. Echocardiography (Vegetations & Valve Lesion): Most Important One, Positive in Most of Cases, Trans-Thoracic Echocardiography (TTE); At Least Take 3-6 Samples Before Giving Antibiotic, Initial Test, Sensitivity  65%. Interval Between Samples 6 Hours or More, Trans-Oseophageal Echocardiography (TOE) First Two Samples Detect 90% of Organism. Can Detect Small Vegetations, Sensitivity  90%. 3. Others: Please Remember  ECG (May Show Heart Block Due to Aortic Root Abscess) Blood Culture May Negative If: ESR & CRP (Elevated). 1. If Patient Taking Antibiotic Before Culture CBC (Leukocytosis, Normoytic Normochromic Anemia). 2. If Organism Was Coxiella Burnetti & Urine Analysis For Glomerulonephritis, Candidal Infection. (Show Proteinuria & Hematuria). Negative Blood Culture Doesn’t Exclude Chest X Ray May Show Evidence of Cardiac Failure & Infective Endocarditis; So Need To Be Cardiomegaly. Followed By Echocardiography. DR. MOHCEN AL. HAJ 28  Diagnosis: By Modified Duke Criteria Which are: Major Criteria: Minor Criteria: 1. Positive Blood Culture: 1. IV Drug Abuser Patient. Typical Organisms From 2 Cultures. 2. Fever > 38.0. 3. Embolic Feature. Persistent Positive Blood Cultures Taken > 12 Hours. 4. Vasculitis Feature. 5. Blood Cultures Suggestive Three or More Positive Cultures Taken Over > 1 Hour Organism Grown But Not Achieving Major Criteria. 2. Endocardial Involvement 6. Predisposing Valvular or Cardiac Positive Echocardiographic Findings of Vegetations. Abnormality. New Valve Regurgitation.  Infective Endocarditis Diagnosed in Presence of: 2 Major Criteria or 1 Major Criterion + 3 Minor Criteria or 5 Minor Criteria  Definitive Endocarditis. 1 Major Criterion + 1 Minor Criterion or 3 Minor Criteria  Possible Endocarditis. Treatment: 1. Empirical Antibiotics: Sub-Acute Infective Endocarditis: According to Organism & Natural or Prosthetic Valve Amoxicillin 2g IV 6 Times Daily +/- Gentamycin. Started After Sample & Before Result (Empirical), Acute Infective Endocarditis: Duration of Antibiotic Between 2-6 Weeks IV, Vancomycin 1g IV Twice Daily + Monitored By Clinical Picture & CRP. Gentamycin 1mgxKg Twice Daily. Please Remember  Prosthetic Valve Endocarditis: Prophylactic Antibiotics Before Interventional Vancomycin 1g IV Twice Daily + Procedures (Dental, Genitourinary or Gastrointestinal Gentamycin 1mgxKg Twice Daily + Procedures) No Longer Recommended, Rifampicin Orally 300-600mg Twice Daily. But Considered Only For People With High Risk of IE. 2. Symptomatic Treatment (Antipyretics). 3. Surgical Intervention (Cardiac Surgery with Debridement & Valve Replacement) Indicated in: 1. Failure Medical Treatment. 2. Heart Failure Due to Valve Damage. 3. Prosthetic Valve Endocarditis. 4. Large Vegetation at Lt Side. 5. Valve Abscess. 6. Fungal Endocarditis. 7. Previous Systemic Emboli. DR. MOHCEN AL. HAJ 29   CARDIOMYOPATHIES Hypertrophic Dilated Cardiomyopath Restrictive Cardiomyopathy (HCM): (DCM): Cardiomyopathy (RCM): Definition: Definition: Definition: It is the Most Common Type of Symmetrically Dilatation of Left It is a Rare Condition Cardiomyopathy & It is the Most Ventricle (± Right Ventricle) with Characterized By Myocardial Common Cause of Death in Young Poor Systolic Contractile Function, Stiffness Due to Fibrosis or Athletics, Characterized By Marked (More Common in Male). Myocardial Infiltration Lead to Left Vent- Hypertrophy Which Impairment of Ventricular Filling May: Generalized, Septal, Apical. Dilatation of the Valve Rings Can Lead (Usually Right Ventricle) Septal HCM Lead to Vent- Outflow to Functional Mitral and Tricuspid Which Cause Increase of Atrial Obstruction Known: Regurgitation. Pressures Leading to Atrial Hypertrophic Obstructive Hypertrophy & Dilatation Cardiomyopathy (HOCM). Causes: & Later Cause Atrial Fibrillation Causes: (I AM ASMA) May Lead to Pulmonary Embolism Genetic (Autosomal Dominant). Idiopathic (Most Common), Causes: Alcohol, Muscular Dystrophy, Symptoms: 1. Amyloidosis (Most Common). Autosomal Dominant (25%), SLE, 2. Hemochromatosis. Effort Related Symptoms: SAD P.S Myocarditis (Viral-HIV), Acromegaly 3. Sarcoidosis. S: Syncope A: Angina D: Dyspnea P: Palpitation S: Sudden Death. 4. Idiopathic. Clinical Pictures: Signs: Clinical Pictures: Features of Congestive Heart Failure. Double Carotid Arterial Pulse Known: Features of Congestive Heart Failure. Thrombo-Embolism, Chest Pain, Thrombo-Embolism. Jerky Pulse, Other Signs are Similar Palpitation (Due to Arrhythmia), Palpitation (Due to Arrhythmia). to Signs of Aortic Stenosis. Sudden Death (Due to VT). Sudden Death (Due to VT). Investigations: Investigations: 1.Echocardiography: Diagnostic. Investigations: 1.Echocardiography & Cardiac 2.ECG: Lt Ventricular Hypertrophy. 1.Echocardiography & MRI: Diagnostic MRI are Diagnostic. Treatment: 2.ECG: Low Voltage, Lt BBB. 2.ECG: Low Voltage, Lt BBB. Medications Doesn’t Improve Prognosis 3.Endomyocardial Biopsy (Rare). β–Blockers, Verapamil, Disopyramide Treatment:  Symptoms & Prevent Syncope. 1. Treat Congestive Heart Failure. Treatment: Amiodarone For Arrhythmia. 2. Anticoagulants. Just Symptomatic Treatment; Digoxin & Vasodilators Contraindicated. 3. Ant Arrhythmic Drugs (B-Blockers) Diuretics, Nitrated, Calcium Surgical Intervention; 4. ACE I to Stop Progression. Channel Blockers, Anticoagulants Partial Surgical Resection (Myectomy) Surgical Intervention;  Because It is Poor Prognosis or By Iatrogenic Infarction of Septum. 1. ICD and/or CRT For High Risk. So Definitive Treatment is ICD Done For High Risk. 2. Heart Transplantation (Definitive). Cardiac Transplantation.  MYOCARDITIS Self-Limiting Inflammation of Myocardium That Caused Mainly By Viral Infection (Coxsackie, Influenza A&B, SARS) Other Causes: Bacterial (Mycoplasma Pneumonia), Drugs (Clozapin, Lithium), Autoimmune (SLE, RA, Systemic Sclerosis) Presented as: Fulminant Myocarditis (Follow Viral Infection), Acute Myocarditis (Present with Heart Failure), Chronic Active Myocarditis & Chronic Persistent Myocarditis DR. MOHCEN AL. HAJ 30   PERICARDIAL DISEASES Acute Pericarditis: Pericardial Effusion & Chronic Constrictive Tamponade: Pericarditis: Definition: Definition: Definition: It is an Acute Inflammation of Pathological Accumulation of Fluid or Diffuse, Progressive Thickening, Pericardium Which May Coexist with Blood In Pericardium. Fibrosis & Calcification of Myocarditis. If Effusion Under Tension of Heart Pericardium, Called: Pericardial Tamponade. Then the Heart Become Encased Causes: That Lead to Impaired Filling of in a Solid Shell and Can’t Fill (VIRUS MTM) Cardiac Chambers & Decrease of COP. Properly. 1. Viral (Coxacie B) Most Common. The Calcification May Extend 2. Idiopathic (2nd Common Cause). Causes: Into the Myocardium. 3. Rheumatic Fever (3rd Common). 1. All Causes of Pericardial Effusion. 4. Uremia. 5. SLE. 6. Myocardial 2. Pericardial Metastasis. Causes: Infarction. 7. Tuberculosis. 3. Post MI (Due to Vent Rupture). 1. Tuberculous Pericarditis 8. Malignancy. 4. Cardiac Trauma. (Most Common Cause). 2. Connective Tissue Disease Symptoms: (Rheumatoid Arthritis & SLE). Symptoms: Acute Central Chest Stabbing Pain, 3. Viral Pericarditis. Same Pericardial Effusion Symptoms. Increase By Cough & Deep Breathing, Radiating to Shoulders Symptoms: Signs: Associated with Palpitation & Fever. Fatigue, Fever, Features of Heart 1. Same Pericardial Effusion Signs. Failure (Hall Mark & Mainly Rt Side) Signs: 2. Beck’s Triad: Hypotension +  JVP Palpitation (Because AF is Common) Tachycardia. + Muffled or Absent Heart Sounds. Dyspnea is Not Predominant Muffled Heart Sounds. 3. Pulsus Paradoxus: Dropping of Pericardial Fraction Rub (Diagnostic) Systolic Blood Pressure During Signs: Inspiration >10mmHg. 1. Signs of Rt Side Heart Failure. Investigations: 4.Kussmaul Sign: JVP During 2. Kussmaul Sign: JVP During 1.ECG: ST Elevation in All Leads & Inspiration. Inspiration. PR Interval Depression (Specific). 5. Oliguria. 3. Pulsus Paradoxus: Dropping of 2.Chest X Ray: Pericardial Effusion. Systolic Blood Pressure During 3.Echocardiography For Monitoring. Investigations: Inspiration >10mmHg. 1.Echocardiography: Diagnostic. Treatment: 2.ECG: Low Voltage & Alternate QRS Investigations: NASIDs (Aspirin, Indomethacine, Amplitude (Electrical Alternans). 1.Echocardiography (Diagnostic) Colchicine For 3 Months) Chest X Ray: Flask Shape Heart. 2.ECG: Low Voltage. Viral Pericarditis Resolve Spontaneously 3.Chest X Ray & CT: Calcification. Within Few Days to Weeks. Treatment: 4.Cardiac Catheterization. Steroid No Longer Recommended. Mainly For Cardiac Tamponade: Treatment: Complications: Immediate Pericardial Aspiration Loop Diuretics & Spironolactone. 1. Pericardial Effusion & Tamponade. (Pericardiocentesis) Under Guide of Surgical Resection (Pericardiectomy) 2. Chronic Constrictive Pericarditis Echocardiography + Give Antibiotic. Lead to Dramatic Improvement. DR. MOHCEN AL. HAJ 31  ATRIAL FIBRILLATION (AF): Definition: Classification: 1. Paroxysmal AF: Intermittent Episodes Self- It is a Most Common Sustained Cardiac Arrhythmia Terminate in 7 Days, Most Common 50%. Characterized By Multiple Interacting Re-Entry 2. Persistent AF: Prolonged Episodes Terminated By Circuit in Atrium Leading to Spontaneous, Rapid, Cardioversion. and Ineffective Atrial Contraction. 3. Permanent AF: Prolonged Episodes Difficult to