CARDIOLOGY Sherif EL Hawary, MDCopyright © 2010, Sherif EL Hawary, MD Text copyright © 2010, Sherif EL Hawary, MD Figures, tables, illustrations and images copyright © 2010, Sherif El. Hawary, MD [All rights reserved. No patt of this book may be translated, reprinted, used or reproduced inany form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the author.INDEX HEART FAILURE TTT of HEART FAILURE SYMPTOMS OF CARDIAC DISEAS! Dyspnea Cough Hemoptysis Ocdema Syncope Chest pain GENERAL EXAMINATION CARDIAC EXAMINATION THE CARDIAC CYCLE VALVULAR HEART DISEASES Mitral stenosis Mitral regurge MVP Aortic stenosis Aortic regurge Tricuspid stenosis Tricuspid regurge CONGENITAL HEART DISEASES DISEASES OF THE PERICARDIUM Dry pericarditis an Pericardial effusion Constrictive pericarditis Adhesive pericarditis RHEUMATIC FEVER INFECTIVE ENDOCARDITIS ANATOMY OF THE CORONARIES ISCHEMIC HEART DISEASE Angina Pectoris Acute Myocardial Infarction SYSTEMIC HYPERTENSION PULMONARY HYPERTENSION PULMONARY EMBOLISM AND NOW ARRHYTHMIAS CARDIOMYOPATHIES 120 121 125 138 151 162 164 175 227““ My doctor is nice; every time I see him, I'm ashamed of what I think of doctors in general...” ~ Mignon McLaughlin “ Doctors are men who prescribe medicines of which they know little, to cure diseases of which they know less, in human beings of whom they know nothing...” ~ Voltaire [Francois-Marie Arouet] “ The recommendation for a healthy heart may one day be: exercise, eatright and laugh a few times a day...” ~ Michael Miller, MDNORMAL CIRCULATION Low Pressure Highest Pressure Right VentricleHEART FAILURE DEFINITION Itis a CLINICAL SYNDROME tesulting from inability of the heart to pump enough blood sufficient to meet the metabolic needs of the body. ETIOLOGY |. LEFT-SIDED HEART FAILURE 1. Left atrial failure: > Mitral valve disease: MS. © Left atrial myxoma: rare cause. 2. Left ventricular failure: 0 Pressure overload: * SYSTEMIC HYPERTENSION. * Valvular disease: Aortic stenosis. * Congenital disease: Coarctation of aorta. 0 Volume overload: » HYPERDYNAMIC CIRCULATION. + Valvular disease: Aortic regurge & Mitral regurge. + Congenital disease: e.g. VSD © Impaired cardiac contractility: + CAD: Myocardial infarction | Segmental disease + CardioMyopathy. - evita } Global disease © Impaired cardiac filling: + Pericardial disease: Cardiac tamponade, Constrictive pericardit + Myocardial disease: RCM.ll. RIGHT — SIDED HEART FAILURE 1. Right atrial failure: © Tricuspid valve disease: Tricuspid stenosis. © Right atrial myxoma: very rare cause, 2. Right ventricular failure: © Pressure overload: + PULMONARY HYPERTENSION: - LVF (the most common cause of RVF). - Pulmonary disease, e.g. COPD (cor — pulmonale). Acute pulmonary embolism (causes acute RVF). + Valvular disease: Pulmonary stenosis. + Congenital disease: Pulmonary stenosis. © Volume overload: * HYPERDYNAMIC CIRCULATION. + Valvular disease: Pulmonary regurge & Tricuspid regurge. + Congenital disease: eg. ASD © Impaired cardiac contractility: + CAD: Myocardial infarction | Segmental disease + CardioMyopathy. + Myocarditis. © Impaired cardiac filling: + Pericardial disease: Cardiac tamponade, Constrictive pericarditis. + Myocardial disease: RCM. Global disease - The most common causes of LVF are: o CAD. o SYSTEMIC HYPERTYENSION. - Them mmon ses of _RVF are: o LVF. o PULMONARY DISEASE.PRECIPITAT TORS) - Inpatient with compensated HF, these factors may decompensate the heart - During ttt of HF, if these factors are not removed, HF will not improve (refractory HF). y Infections: esp. infective endocarditis, rheumatic activity & chest infection. v Latrogenic: © Corticosteroids & Calcium — channel blockers. © Discontinuation of anti-failure treatment. o Excessive salt intake & IV fluids. y Acute myocardial infarction. v Arrhythmias. vy Anemia, thyrotoxicosis & other causes of hyperdynamic circulation. ¢ Physical & emotional stress. y Pregnancy & late labor. ¢ Pulmonary embolism. PATHOPHYSIOLOGY 1. The clinical manifestations of HF result from: > Forward Failure: Failure of the heart to eject a sufficient CO: - This gives rise to manifestations of low CO. > Backward Failure: Failure of the heart to accept the VR: - This gives rise to manifestations of congestion. © Pulmonary congestion: in case of Left—sided HF. © Systemic congestion: in case of Right - sided HF2. Compensatory mechanisms (Cardiac reserve): + These mechanisms try to restore the cardiac output. * They are beneficial within limits. + If they exceed these limits, they will aggravate HF. > TACHYCARDIA: 1. Mechanism sympathetic stimulation mediated by: - Marey’s law: HR is inversely proportional to BP. - Bainbridge reflex: Increased RA pressure causes increased HR. 2. Effect: It increases the CO. - Ifitis marked (>160 / min): it will | the diastole, | the ventricular filling & thus | the CO. > DILATATION: * Increased LENGTH of cardiac muscle fibre: in VOLUME overload. + It increases the force of contraction (according to Starling’s law). * If it exceeds certain limits, it will lead to diminished contraction. > HY! * Increased THICKNESS of cardiac muscle fibre: in PRESSURE overload. TROPHY: + It increases the force of contraction. * If it exceeds certain limits, the hypertrophied muscle cannot get its adequate blood supply (becomes ischemic) —> diminished contraction. > REDISTRIBUTION OF BLOOD FLOW: * There is diversion of blood: - From less vital organs (eg. skin & muscles), = To more vital organs (eg. brain & heart). > HYPERVOLEMIA: (due to salt & water retention) + Itincreases the preload & force of contraction. * Ifit exceeds certain limits, it will aggravate HF.VENTRICULAR DILATATION Normal Heart Dilated Heart VENTRICULAR HYPERTROPHY Left Atrium Right Ventricle Normal Heart Hypertrophied Heart3. Neurohormonal changes in HF: Some of these changes are beneficial, others are harmful: a) Activation of the RAAS + Beneficial effect: maintains BP & perfusion of vital organs. + Harmful effects: © The increased angiotensin II: results in vasoconstriction. © The increased aldosterone: __ results in salt & water retention. b) Activation of the SNS * Beneficial effect: increases the ventricular contractility. + Harmful effects: © Increases the afterload. © Induces arrhythmias. © Causes direct myocardial damage. c) The Natriuretic peptide system (ANP) * Beneficial effect: produce natriuresis & peripheral VD (A & V). 4. Asynchronus ventricular contraction: ~ In approximately 30% of patients with heart failure due to cardiomyopathy: There is an abnormality in the heart's electrical conducting system (called an “intraventricular conduction delay" or bundle branch block). - This problem causes the 2 ventricles to beat in an Asynchronous fashion: therefore, instead of beating simultaneously: © The 2 ventricles beat slightly out of phase. © Also: segmental asynchrony within the LV may occur. This asynchrony greatly reduces the efficiency of the ventricles in patients with heart failure, whose hearts are already damaged.RAAS Angiotensinogen Renin——_* Angiotensin | cotnayme ——m| (ACE) Angiotensin II Stimulation of ’ aldosterone secrection Constriction Aldosterone of vascular smooth muscle Increased water and sodium retention Increased Afterload Increased Preloa teCLINICAL PICTURE I. LEFT — SIDED HEART FAILURE Symptoms 1) Ss of low CO: forward failure. 2) Ss of pulmonary congestion _ backward failure. 3) When RVF oceurs: mptoms of pulmonary congestion improve Signs 1) General: a) RESPIRATION: Tachypnea (shallow rapid respiration), b) PULSE: © Tachycardia: except in patients receiving digitalis or B-blockers, o Small volume: except in conditions of high CO. © Pulsus alternans: * alternating strong & weak regular beats detected by palpating the pulse or using the sphygmomanometer. c) SKIN: — Coldness of the skin & Peripheral cyanosis. d) CHEST: Pleural effusion & Bilateral basal crepitations. * 2) Cardiac: a) Precordial examination: Signs of LV.enlargement. b) Auscultation: © Over the mitral area: - Left ventricular gallop (S3): due to flabby myocardium, - Pansystolic murmur of functional MR: due to LV dilatation. 0 Over the pulmonary area: ~ Signs of pulmonary hypertension. Manifestations of the cause e.g. Typical chest pain in Myocardial infarction.ll. RIGHT — SIDED HEART FAILURE Symptoms 1) Symptoms of low CO (forward failure). 2) Symptoms of systemic congestion (backward failure). Signs 1) General a) PULSE: 0 Tachycardia: except in patients receiving digitalis or B-blockers © Small volume: except in conditions of high CO. b) SKIN: Coldness of the skin & Peripheral cyanosis. c) CHEST: Pleural effusion. d) PROMINENT SIGNS OF SYSTEMIC CONGESTION: © Neck veins: Congested pulsating neck veins. ©. Liver: Enlarged, tender, pulsating, + Hepato-jugular reflu © Lower Limbs: Oedema of lower limbs & later on ascites. e) CARDIAC CACHEXIA: With severe chronic HF, cachexia occurs due to: © | caloric intake: due to Anorexia, N, V & | absorption (GIT congestion © fealoric loss: due to } metabolic rate (1.2 needs of the failing heart’ 2) Cardi a) Precordial examination: © Signs of RV enlargement. b) Auscultation: ( Over the triscupid area ): © Right ventricular gallop (Ss): due to flabby myocardium, © Pancystolic murmur of functional TR: due to RV dilatation. Manifestations of the cause e.g. Chronic cough, dyspnea & wheezes in COPD.CLINICAL CLASSIFICATION) « ctinicat categories” 1. LVF versus RVF. (also Biventricular failure). 2. Acute versus chronic HF: Maintained BP + Most causes produce chronic HF: LL oedema Ventricular enlargement + Some causes produce acute HF as: - LYFE: AMI, Acute MR (after AMI or SBE). BP RVF: ae Acute pulmonary embolism. See ear : ‘ No ventricular enlargement - Biventricular failure: Acute myocarditis. 3. Forward versus backward heart failure. a) Forward failure: - There are: manifestations of Low CO. - Response to ttt: positive inotropics, _ arteriodilators. b) Backward failure: - There are: manifestations of congestion. - Response to ttt: diuretics, _ venodilators. 4. Systolic versus diastolic failure: a) Systolic Failure: | cardiac contractility, e.g. AMI, DCM. b) Diastolic Failure: | cardiac filling, eg. CP, RCM, systemic HTN.5. Low versus high CO failure: a) Low CO failure: ~ There is reduction of CO below normal. - This type occurs in MOST CASES of HF. b) High CO failure: - There is usually peripheral VD & | peripheral resistance, leading tot VR & ultimately + CO - There is t CO, however, it is insufficient for the metabolic needs of tissues. = This type occurs in cases of HYPERDYNAMIC_ CIRCULATION: o Anemia, AR, Axteriovenous fistula. o Beriberi, PDA, Paget’s disease. © Thyrotoxicosis, Liver failure. 6. Etiological classification: “see before” FUNCTIONAL CLASSIFICATION ~ A classification was developed by the New York Heart Association (NYHA) to assess the SEVERITY of heart failure: CLASS I: Nolimitation of physical activity on ordinary effort. CLASS II: Slight limitation of physical activity on ordinary effort. CLASS II; Marked limitation of physical activity on less than ordinary effort. CLASS IV: Symptoms occur even at rest.INVESTIGATIONS) I. ECG: - Chamber enlargement, - Cause of HF may appear eg. CAD, BBB. - Precipitating factor may appear e.g. arrhythmias. II. IMAGING: 1. CXR: - Chamber enlargement. - Pulmonary congestion in left-sided HF, or Pleural effusion. 2. Echocardiography: - Chamber enlargement. - Cause of HF may appear e.g. valvular lesions. - CONTRACTILITY STATE OF THE MYOCARDIUM: o SHORTENING FRACTION (SF) o EJECTION FRACTION (EF) 3. Cardiac catheterization & angiocardiography: - Chamber enlargement. - Cause of HF may appear eg. CAD. III. Other investigations for the cause & ppt factor: - Cardiac enzymes: for myocardial infarction. - CBC: for anemia. - Thyroid functions: for thyrotoxicosis.(TREATMENT OF HEART FAILURE GUIDELINES for TTT (PLAN of TTT) 1. Treatment of the underlying etiology... @.g... 2. Treatment of the precipitating factors....... @.g... 3. Treatment specific to the syndrome of HF: * Decreasing the cardiac load: a) Rest: Physical & emotional. b) Reduction of preload: o Diet control, especially salt restriction. o Diuretics. o Vasodilators (Venous). c) Reduction of afterload: o Vasodilators (Arterial). = Decreasing the myocardial damage: - B-blockers. « Increasing the myocardial contractility: a) Digitalis. b) Other inotropic agents: 0 Sympathomimetic amines: dopamine & dobutamine. 0 Phosphodiestrase inhibitors: amrinone & milrinone. = Resynchronizing the ventricles: “CRT” = In patients with cardiomyopathy who have the problem of: "intraventricular conduction delay" or bundle branch block. = Symptomatic treatment: a) For hypoxemia: oxygen administration. b) For cardiac dyspnea: aminophylline administration. 4. Treatment of refractory HF. 5.. Treatment of acute pulmonary oedema.PHYSICAL REST - BENEFITS: Bed rest reduces the metabolic needs of the body & the cardi i - POSITION: Semisitting position is preferred to decrease the venous return. - COMPLICATIONS of prolonged bed rest: * DVT & PULMONARY EMBOLISM. + Pneumonia. * Constipation & retention of urine. * Muscle wasting & — osteoporosis. + Bed sores. + Psychoneurosis. EMOTIONAL REST SEDATION may be achieved b Diazepam 2-5 mg tds orally. DIET * Salt restriction: decreases blood volume & thus decreases the preload. * Fluid restriction: only needed in severe cases of HF. * Small frequent meals: to decrease the work of the heart. * Reduction of body weight in obese patients. VASODILATORS) Action 1, Reduction of preload by: veno ~ dilatation. 2. Reduction of afterload by: arteriolar dilatation. Types VASODILATOR Site of action Mode of administration Nitrates (Isosorbide dinitrate) | Venous i 20-40 mg/8h «- orally Hydralazine Arterial 50mg /6h_- ~ orally Na nitroprusside Arterial & venous _| 0.5 - 10 #g/kg/ min, IV infusion Prazosin (0.— blocker) __| Arterial _& venous orally ACE inhibitors: Arterial & venous Short acting: Captopril 6.25 —25 mg/ 8h orally Long acting: Ramipril 1.25 -2.5 mg/day orally ARBs: Arterial & venous Candesartan Initially 4, target 32 mg / day orallyImportant points - Inchronic HF, ACE -I is the most useful, esp. in LY systolic failure. - Contraindications to ACE ~1 in HF: 1. Intolerance due to the presence of side effects, e.g. dry cough. 2. HYPERKALEMIA: serum potassium > than 5.5 mEglliter. 3. Hypotension: SBP <90 mm Hg. 4. Bilateral renal artery stenosis: because they will cause renal failure. 5. Caution in renal failure with serum creatinine > 3.0 mg/dL & stop the drug if: serum creatinine rises by more than 30 % of the base-line level. - When ACE ~I is contraindicated in HF, alternative good VDs are: 1. Combination of Nitrates (venodilator) & Hydralazine (arterio dilator). 2. ARBs: especially Candesartan, (in case of intolerance to ACE - 1). DIURETICS - They are very useful in the treatment of HF. ~ They promote loss of salt & water, thus: | blood volume & | preload. - Types: 1. Thiazides. 2. Loop diuretics. 3. Potassium sparing diuretics. 4. Others diuretics. - Action: 1. Thiazides onthe distal tubules, to | reabsorption of: Na, H,0, K, Cl. - Preparations: 1 2. oe 4. 5. 6. 7 8. Hydrochlorothiazide: 50 — 100 mg/day. Chlorothalidone: 50 — 100 mg/day. le effects: Hypo kalemia: which may precipitate digitalis toxity. Hypo chloremic alkalosis: _ which may lead to tetany. Hypo natremia. ‘Hypo magnesemia. Hyper uricemia. Hyper glycemia. Hyper lipidemia. Hyper calcemia.2. Loop diuretics Action: on the ascending limb of loop of Henle, to | reabsorption of: Na, HO, K, Cl. THEY ARE THE MOST POTENT DIURETICS. Preparations: + Frusemide (Lasix): 40 ~ 200 mg/day (orally or IV). + Ethacrynic acid: 50 — 100 mg/day (orally or IV). Side Effects: + Same as Thiazides (but without hypercalcemia). 3. Potassium sparing diuretics Action: on the distal tubules to | reabsorption of: Na, & HO, BUT: _ they have the advantage of retaining K (they | the secretion of K). THEY ARE WEAK DIURETICS: * Used to potentiate the action of Thiazide or loop diuretics. * Used to avoid the potassium losing effect of Thiazide or loop diuretics. Prey + Spironolactone (aldosterone antagonist): 100-400 mg / day. + Triametrine. + Ameloride. Side effects: + Hyperkalemia & Metabolic acidosis. + Gynecomastia with prolonged use. 4. Other diuretics Natriuretic peptides: - Infusions of recombinant NP have been shown to cause: o Afferent arteriolar dilation & efferent arteriolar constriction > GFR. o Natriuresis. © Peripheral VD (A & V). Carbonic anhydrase inhibitors: - Diuretics: | reabsorption of: NaHCO3 in the proximal tubules. - Also: correct the metabolic alkalosis that occur due to thiazide diuretics.DIGITALIS “ Digitalis is no longer extensively used in the management of HP, although it is an effective positive inotropic agent.” ACTIONS > It increases the myocardial contractility: through: Competitive inhibition of sodium-potassium ATPase —> { intracellular Na. Then, Na-Ca exchange occurs & this increases the intracellular Ca, High intracellular Ca promotes sliding of actin & myosin. This leads to increased force of myocardial contractility; which causes: - Increased cardiac output.. - Decreased venous congestion. - Decreased cardiac size. > It slows the heart rate: through: - Vagal stimulation. - Direct inhibition of the SAN. > It increases the excitability of the atria & ventricles: - In digitalis toxicity, arrhythmias may occur. > It inhibits the conduction of the AVN: ~ In digitalis toxicity, AV block may occur. - Digitalis can be used to protect the ventricle in atrial arrhythmias. through: - Increased renal blood flow. > On ECG: Sagging depression of ST. segment, Flat or imertedT. wave. = Digitalis toxicity: Different ypes of artythmias. INDICATIONS 1. Heart Failure. 2. Rapid atrial arrhythmias: - Atrial fibrillation (AF). - Atrial flutter. = Supraventricular tachycardia.Digitalis is highly indicated in: * Patients with HF & rapid atrial arrhythmias, esp. AF. * Patients with HF not responding to: Vasodilators, BB & Diuretics. CONTRAINDICATIONS « ABSOLUTE CONTRAINDICATIONS: - Digitals toxicity. - Ventricular tachycardia (Digitalis may change it to fatal VE). ¢ RELATIVE CONTRAINDICATIONS: “ Tt is better avoided: ” - Incomplete heart block. - Nodal rhythm. - Hypertrophic cardiomyopathy. PREPARATIONS & ADMINISTRATION 1. Oral: A Itis the usual route of administration: - Digoxin: excreted mainly by the kidney (tab = 0.25 mg). - Digitoxin: metabolized mainly by the liver (tab = 0.1 mg). A Dose: - Initial dose: 2 tablets daily for 5 days. - Maintenance dose: 0.5 —2 tablets daily. 2. Intravenous: A Indicated in: “ Acute pulmonary oedema_& rapid atrial arrhythmias ”. - Digoxin (amp. = 0.5 mg). - Cedilanid. - Ouabain, A. Dose: - 0.5—1 mg in 5% glucose over 30 min, 0.5 mg /6h till a therapeutic response appears, THEN: - Continue with oral digitalis. E E IZ IZ20 DIGITALIS TOXICITY ical Picture: A Gastrointestinal: = Anorexii usually the first symptom. - Nausea & vomiting. A Cardiovascular: “Different types of arrhythmias_& heart block” - Premature beats, especially occurring in bigemini or trigemini. - Paroxysmal atrial tachycardia: with heart block. - Paroxysmal ventricular tachycardia: most serious. A Neurological: - MENTAL disturbances, e.g. _ psychosis - PAIN: headache & — neuralgias. - VISION: Blurring of vision & coloured vision (yellow or green). ellaneous: = Increased blood coagulability. - Gynecomastia, with prolonged use. 2. Treatment: = Stop digitals. = Correct hypokalemia, if present: = Stop drugs causing hypokalemia e.g. loop diuretics. Give potassium : Orally or IV. = Digitalis antibodies. = TTT of the manifestations of digitalis toxicity: - For vomiting: Anti-emetic drugs, e.g. metoclopramide. - For arrhythmias: 1. Anti-arrhythmic Drugs: especially epanutin & lidocaine. 2. Atropine: for heart block & bradycar 3. DC: Avoided because it may induce more serious arrhythmias Allowed ONLY. in case of the fatal arrhythmia: VF. 2021 BETA - BLOCKERS 3Xe - In the past: they were absolutely contraindicated in HF due to their - ve inotropic effect. - Recently: they are used to treat HF because they were found to: Decrease the direct myocardial damage induced by catecholamines in HF. © Improve the prognosis. - INDICATIONS: o Chronic HF. o Moderate HF (NYHAclasses Il & Ill). - CONTRA — INDICATIONS: o Acute HF (eg. shortly after AMD. o Severe HF (NYHA lass IV). - ADMINISTRATION: o TYPES: * Only: Second generation 8, blockers (e.g. Metoprolol), or: Third generation 8, blockers (e.g. Carvedilol). o DOSE: “Gradually increasing doses” - We start with extremely low doses (one-eighth of the target dose). - We gradually + the dose every 1-2 weeks to reach the target dose. - Target dose: 25-50 mg of carvedilol daily. 2122 (freatment of Refractory Heart Failure Etiology of refractory HF: 1. Presence of a mechanical factor hindering the cardiac function: e.g. + Severe valvular disease. + Pericardial effusion or constrictive pericarditis. 2. Persistence of the cause: e.g. Uncontrolled Hypertension, 3. Presence of a precipitating factor: e.g. Chest infection. 4, Improper management: eg. + Inadequate rest. * Inadequate salt restriction. + Inadequate digitalis. 5, Terminal cases of HF: with advanced myocardial damage, e.g. Massive myocardial infarction. Treatment: 1, Removal of the mechanical factor: — e. surgical ttt of valvular disease. 2. TIT of the cause: e.g. proper control of Hypertension. 3. Removal of the precipitating factor: e.g. proper antibiotics for chest infec 4, Proper management: © Adequate rest. * Adequate salt restriction (<1gm/ day) & fluid restriction in severe cases + Adequate digitalis. 5, For Terminal cases of HF: a) Diuretic use combinations e.g, loop diuretic & potassium-sparing dius b) Vasodilators: use combinations of IV vasodilators such as Na nitropruss! and a potent IV inotrope such as dopamine or dobutai c) Mechanical measures: = Mechanical removal of fluid using phlebotomy or dialysis. * Mechanical assistance of circulation using intra-aortic balloon counterpulsatic “Balloon is inflated in diastole & deflated in systole ”. d) Cardiac transplantation: in patients below the age of 60. 22[Treatment of Acute Pulmonary Oedemal . Hospitalization in ICU: bed rest in sitting position. 2. Oxygen administration: 6-8 litres / min , 3. Morphine IV 5 mg, torelieve the anxiety and decrease the sympathetic stimulation, thus causing VD.|_ | ia, >a imartant measures 4. Frusemide IV 40 mg, to correct the hypervolemia, to be repeated every 4 hour until relief. 5. Vasodilators IV: - Na nitroprusside: IV infusion (0.5 - 10 yg /kg/ min). = Nitroglycerine: IV infusion. 6. Positive inotropics IV: - Digitals, esp. in cases associated with AF. - Dopamine or Dobutamine. 7. Aminophylline IV (250-500 mg), slowly, to relieve the bronchospasm. 8. Treatment of the cause & the precipitating factor. 9. In refractory conditions: - Mechanical removal of fluid using phlebotomy or dialysis. ~ Mechanical assistance of circulation using intra-aortic balloon counterpulsation. - Mechanical ventilation Resynchronizing the ventricles: “CRT” Indication - In patients with cardiomyopathy who have the problem of: “intraventricular conduction delay" or bundle branch block: * As evidenced by wide QRS > 0.12 sec in ECG. * In patients with severe symptoms (NYHA class III, IV) despite proper ttt. Method - Biventricular pacing or - LV pacing CRT = Cardiac Resynchronization Therapy 2324, CARDIAC RESYNCHRONIZATION THERAPY “CRT” Left subclavian vein Coated wires called leads carry electrical energy from the CRT device to the heart. ‘This energy helps the RV and LV to pump at the same time (Synchronized).25 Important points in Heart failure CAD is the most common cause of LVF. LVF is the most common cause of RVF. Symptoms of LVF improve when RVF develops. <<¢«<«< Pulsus alternans is an important sign of LVF. ¥ SF is an important echocardiographic indicator of the cardiac function & is measured as follows: SF = LVDD-LVSD LVDD - LVDD is the LV diastolic diameter - LVSD is the LV systolic diameter ¥ The 3 main lines of treatment are : - To decrease: the preload. - To decrease: the afterload. - To decrease: the myocardial damage. - To INCREASE: _ the myocardial contractility. ¥ B-blockers are recently considered: - An effective measure in the treatment of HF. 2526 Clinical manifestations of Cardiac Disorders Symptoms of cardiac disorders 1. PULMONARY CONGESTION SYMPTOMS: - These occur in left sided heart failure due to failure of the heart to accept the pulmonary venous return: + Dyspnea. * Cough. + Hemoptysis. 2. SYSTEMIC _ CONGESTION SYMPTOMS: - These occur in right sided heart failure due to failure of the heart to accept the systemic venous return: * Confusion & insomnia. + Right hypochondrial pain. + Anorexia, nausea, vomiting, dyspepsia & epigastric pain. * Oedema of dependent parts (LLs or sacrum). + Abdominal swelling due to ascites. 3. Low CARDIAC OUTPUT SYMPTOMS: - These occur in left or right sided heart failure or in both due to failure of the heart to eject a sufficient CO: + BRAIN: Dizziness, headache & syncope. + EYES: Blurring of vision. + HEART: — Angina pectoris. + KIDNEYS: Oliguria. + MUSCLES: Easy fatiguability & Intermittent claudication. + SKIN: Pallor & coldness; peripheral cyanosis in severe cases 264. PALPITATIO! 27 - This is an unpleasant awareness of the heartbeat. - This occurs due to: * Change in rate: + Change in rhythm: + Change in force: 5. CHEST PAIN: + Psychoneurosis. e.g. Tachycardia or Bradycardia. Arrhythmia. Forceful cardiac contraction. - Pain of cardiac origin may arise from: Myocardium: Pericardium: Endocardium: Aorta: Pulmonary: eg. eg. eg. eg. eg. angina pectoris or AML pericarditis or pericardial effusion. mitral valve prolapse. dissecting aortic aneurysm, acute pulmonary embolism. 6. PRESSURE SYMPTOMS: - These occur due to pressure of enlarged cardiac chambers on the surrounding structures. - Ancnlarged left atrium, aortic aneurysm or pericardial effusion may compress: Oesophagus: Tracheobronchial tree: Left RLN: Spine: sve: 7. CYANOSIS: dysphagia. dyspnea & cough. hoarseness of voice. back pain. swelling of the face & puffiness of eye lids. - Bluish discolouration of skin & may be mucous membranes due to the presence of more than 5 gm reduced (unoxygenated) Hb / 100 cc of blood. 2728 28 DYSPNEA ~ It is a subjective distress associated with difficulty in breathing. TYPES 1. Exertional: S grades (American thoracic society scale) * Grade 0: none no dyspnea. + Grade 1: mild dyspnea on Marked — exertion. + Grade 2: moderate dyspnea on Moderate exertion. * Grade 3: severe dyspnea on Mild _ exertion. * Grade 4: very severe dyspnea on Minimal exertion. 2. Dyspnea at rest. 3. Orthopnea: - What happens ?? © Itis dyspnea on recumbency that is relieved by sitting up. - Pathogenesis: recumbency results in: 0 TVR tothe heart — more pulmonary congestion & more dyspnea. © Elevation of the diaphragm & improper use of chest wall muscles. 4. Paroxysmal nocturnal dyspnea: PND - What happens ?? Classic PND: ~ The patient is aroused 1-2 hours after sleeping with: o Severe dyspnea, Sweating, Cyanosis, Cough, © Expectoration: frothy blood-tinged. - The patient sits up in bed or stands beside a window to get more air. Cardiac asthma: - Generalized wheezes: due to bronchial oedema & bronchospasm. ‘Acute Pumonary oedema: - Generalized bubbling crepitations: due to intra-alveolar oedema.29 - Pathogenesis: © Recumbancy increases the VR to the heart —> more pulmonary congestion. © Decreased sympathetic activity during sleep — reduction of inotropism. - Incidence: * PND occurs more commonly in acute LVF as it is an acute process, + PND occurs less commonly in MS because it is a gradual process allowing time for protective mechanisms to take place to | further pulmonary congestion. a. Reflex vasoconstriction of pulmonary arteries: This will decrease the pulmonary congestion, but on the other hand it will lead to development of pulmonary hypertension. > Anastomosis between pulmonary & bronchial vein: This will cause shunting of high pressure & congestion from the pulmonary veins to the bronchial veins. This may lead to formation of BRONCHIAL VARICES which may rupture on coughing or straining causing severe hemoptysis. . Development of interstitial pulmonary barrier: Chronic pulmonary congestion — to haemosiderosis & fibrosis. This will decrease transudation of fluid from pulmonary capillaries. d. Thickening of the walls of pulmonary vessels, ° Differentiation between Cardiac & Bronchial asthma CARDIAC BRONCHIAL | Age ‘Any age Usually young age Past history Cardiac symptoms _| Chest symptoms Duration Short Long Time of the attack | 1-2 hours after sleep _ Early in the morning Sputum Frothy, may be blood — tinged | Thick pellets Chest examination | Generalized wheezes, Generalized wheezes Bilateral basal crepitations Heart examination _| Gallop & murmurs Normal ECG Abnormal Normal DRUGS Adrenaline Contraindicated Improves the condition Morphine Improves the condition Contraindicated Aminophylline _ | Improves the condition [Improves the condition 2930 ACUTE PULMONARY OEDEMA DEFINITION - Rapid accumulation of fluid in the interstitial & intra-alveolar spaces of the lung. ETIOLOGY| 1. CARDIOGENIC PULMONARY OEDEMA: Sudden increase in the_ pulmonary venous pressure: * Acute left sided heart failure (LSHF): e.g. AML. * Acute exacerbation of chronic LSHF: e.g. MS witha ppt. factor as AF, 2. NON - CARDIOGENIC PULMONARY OEDEMA: (ARDS) Sudden incr in the pulmonary capillary permeability: * SEPTICEMIA, Pneumonia (severe), Pancreatitis. * STROKES, Head injuries. * SHOCK. * TRAUMA, Burns. * TERMINAL Liver & renal failure. * INHALATION of gases (e.g. chlorine), Aspiration of gastric contents. * DIC. 3. OTHER CAUSES: * Sudden expansion of a collapsed lung.e.g. rapid aspiration of massive pleural eftsion © Severe hypoalbuminemia. (CLINICAL PICTURE 1. Manifestations of the cause: eg. 0 Typical chest pain in AMI (Cardiogenic pulmonary oedema), © Neurological manifestations in STROKE. (Non - Cardiogenic pulmonary oedema). 3031 2. Typical Manifestations of Acute Pulmonary Oedema: Severe dyspnea at rest & orthopnea. Sweating & marked irritability. Central cyanosis. Cough with expectoration of excessive frothy blood-tinged sputum. Generalized BUBBLING CREPITATIONS, Generalized wheezes. coo cco [INVESTIGATIONS 1. Investigations of the cause: eg. © BCG & Cardiac enzymes for AMI (Cardiogenic pulmonary oedema). © Brain imaging (CT scan) for STROKE (Non - Cardiogenic pulmonary oedema). 2. CHEST X — Ray: Exaggerated pulmonary vascular markings especially in upper lung zones. © Haziness of lung fields, o Kerley B lines. ARTERIAL BLOOD GASES (ABG): o PO: Decreased. o PCO; Decreased at first, then, —_ Increased lately in severe cases. TREATMENT 1. Treatment_of the cause: eg. 0 Reperfusion (revascularization) for AMI (Cardiogenic pulmonary oedema). © General care, Antiplatelets for STROKE (Non - Cardiogenic pulmonary oedema). 2. Treatment of Cardiogenic pulmonary oedema: o Refer to the section of HEART FAILURE. 3. Treatment _of Non - Cardiogenic pulmonary oedema: o Mechanical ventilation. o IV Corticosteroids. 3132 COUGH - Inthe cardiac patient, cough is usually due to: * Pulmonary congestion. * Pulmonary infection. © Pulmonary infarction. HEMOPTYSIS - Inthe cardiac patient, hemoptysis is usually due to: ¢ Pulmonary congestion. + Pulmonary infection. * Pulmonary infarction. ¢ Rupture of bronchial varices. * Rupture of aortic aneurysm. OEDEMA - Pathogenesis of cardiac oedema: 1. Increased capillary hydrostatic pressure: A) Increased venous pressure: due to stagnation of blood in systemic veins. B) Salt & water retention due to; 1. Decreased GFR: due to | renal blood flow, due to | CO. 2. Increased Aldosterone: due to: = renin release due to: reduced renal blood blood flow. = J stimulation of: volume receptors of Aldosterone. = | hepatic catabolism of: Aldosterone. 3. Increased ADH: due to: stimulation of: volume receptors of ADH. - | hepatic catabolism of: ADH. 2. Increased capillary permeability: due to hypoxia of the capillary walls. 3. Decreased plasma oncotic pressure due to: o Decreased protein intake due to: anorexia & vomiting. o Decreased protein absorption due to: _ intestinal congestion. o Decreased protein formation due to: liver congestion. 32- Characteristics of cardiac oedema: 1. Occurs in the dependant parts of the body: © Ankle oedema: in ambulant patients. © Sacral oedema: in. bed ridden patients. 2. Bilateral: but one side may be affected more due to: 0 Deep venous thrombosis. o Postural, in patients sleeping on one side. 3. Pitting. 4. Associated with other features of cardiac disease. 5. Oedema of lower limbs always precedes appearance of ascite: except in two conditions in which ascites occurs first “Ascites precox”: @) Pericardial effusion & constrictive pericarditis: ~ Kinking of hepatic veins causes early liver congestion & ascites. - Obstruction of lymphatics passing through the central tendon of the diaphragm causes accumulation of lymph in the peritoneum. b) Tricuspid regurge: - Regurgitation of blood causes liver congestion & ascites. - Differential diagnosis of cardiac oedema: 1. Renal Oedema: Itoccurs in GN, ¢.g. Nephrotic or Nephritic syndrome. Oedema occurs first in eye lids & is associated with features of renal disease. 2. Hepatic Oedema: Oedema of LLs occurs after ascites & is associated with features of liver disease. 3. Nutritional Oedema: It occurs in severe nutritional deficiency & is associated with other features of nutritional deficiencies. 4. Angioneurotic Oedema: - This allergic oedema occurs with constant relation to certain factors, e.g. eating certain food, or _ inhaling certain substances. - Acute onset especially in: Lips, Lids, Larynx, but may be generalized. ~ There is usually +ve family history of: _ oedema or other forms of allergy. - The patient himself may have: other forms of allergy. - There is characteristic rapid response to: anti-allergic measures. 3334 SYNCOPE DEFINITION Loss of consciousness “ SUDDEN & TRANSIENT ” due to acute cerebral hypoxia. There is inability to maintain postural tone & is followed by spontaneous recovery. ETIOLOGY ae Vasomotor syncope A) Vasovagal syncope —_(Neurocardiogenic syncope ): ~ It results from severe vagal stimulation which leads to: Severe bradycardia, hypotension, pallor & — sweating. - Itresults from: Sudden severe fear, pain, trauma (e.g. to testicles). ~ Itis the most common cause of syncope & is known as simple fainting B) Carotid sinus syndrome: ~ It results from pressure on hypersensitive carotid sinus baroreceptors: eg. During shaving. 2. Cardiac syncope (any cause of low CO) _ especially: - Aortic stenosis (or any other valvular obstruction) - Acute heart failure (eg. AMD. - Arrhythmias (whether tachy- or brady — arrhythmias). - Adams-stokes attacks. 3. Cerebral syncope (reduced cerebral blood flow) - Vertebrobasilar TIAs. 4. Hypoxic syncope ({ O2 content of the cerebral blood flow) - Fallot’s tetralogy & other cyanotic diseases or severe anemia, 3435 5. Postural syncope (Orthostatic syncope) - Normally, reflex VC of blood vessels of LLs occurs on standing to prevent pooling of blood in LLs. - This effect is mediated through sympathetic stimulation. - If this mechanism is defective, BP will be markedly lowered in the standing position (postural hypotension) & syncope may occur. - Causes include: * Autonomic neuropathy, e.g. DIABETES. * DRUGS: sympatholytic drugs (e.g. Ganglion blockers), VD. * Lumbar sympathectomy. * Hyponatremia. * Prolonged recumbency. * Elderly patients. 6. Situational syncope - Rare syncope caused by a variety of activities in susceptible individuals: * Cough syncope _(Tussive syncope). * Micturition syncope (more common in old men especially at night). * Defecation syncope. - Underlying mechanism: Straining + decreased VR —> decreased CO — Syncope. DIFFERENTIAL DIAGNOSIS 1. Anxiety attacks: (panic attacks with feeling of faintness or dizziness): © They are not relieved by recumbency. o They are associated with: anxiety, palpitaion & hyperventilation. 2. Hypoglycemic attacks: o History: of DM with overdose of insulin or missed meal. o Features: of sympathetic overactivity as sweating & palpitaion. 3. Epileptic attacks (Seizures): refer to Neurology. 3536 CHEST PAIN CARDIOVASCULAR CAUSES OF CHEST PAIN: Myocardium: CAD: angina or AMI. - Pericardium: Pericarditis or pericardial effusion. - Endocardium: Mitral valve prolapse. - Aorta: Dissecting aortic aneurysm. - Pulmonary: Acute pulmonary embolism. - Type of patient: neurotic patients especially young 9. = Site & Reference: Left inframamary, Localized. - Character & Duration: Stitching, of variable duration. - Precipitating factors: No relation to exertion. - Relieving factors: Not relieved by rest. - Associations: o Features of neurosis: _ especially sighing respiration. 0 Normal cardiac examination. - Huge cardiomegaly: Rarely causes retrosternal heaviness. 36Signs of cardiac disorders I. GENERAL EXAMINATION The general examination of the cardiac patient includes looking for the following signs: 1. [Decubitus 1. Orthopnea: left-sided heart failure. 2. Prayer’s position (sitting up and leaning forward): pericardial effusion. 3. Squatting: the Tetralogy of Fallot. 2. [Pallor| In cardiac disease, pallor may be due to: 1. Anemia. 2. Rheumatic activity. 3. Infective endocardi 4 5. . Low cardiac output. . Shock. 3. { ‘yanosis| 1. Central cyanosis, occurs in: © Congenital heart disease. © Hypoxic cor pulmonale. 2. Peripheral cyanosis, occurs in: © Venous stagnation, eg. Right sided HF. © Venous obstruction. 4. [Jaundice In cardiac disease, jaundice may be due to: 1. Severe right sided heart failure. 2. Pulmonary embolism. 3738 38 6. disease, fever may be due to: . Rheumatic activity. Myocardial infarction. Pulmonary infaretion. Pulmonary infection. Infective endocarditis 2. Cyanotic cardiac conditions (cyanotic clubbing). NECK VEINS) Pressure: © It should not exceed 3 em vertically above the level of the sternal angle. (Clubbing of digits In cardiac disease, it occurs in: 1. (pale clubbing). They should be examined for: (Congested or not ??) o Normally, the neck veins are not congested. Pulsations: © Normally, © Normally, ™ a-waye: = x-descent: = c-wave: = y-wave: * y-descent: (Pulsating or not ?? the neck veins are pulsating with systolic collapse. the pulsations are wavy & consist of: right atrial contraction. right atrial relaxation. transmitted from adjacent carotids. upward bulge of tricuspid valve into right atrium. RA filling. RA emptying.39 ICAL SIGN! ICANCE OF NECK VEIN: 1. Normally: - They are non congested, & are pulsating with systolic collapse. 2. Abnormally: 1) Abnormal pressure: “ Congested neck veins ” Pulsating: ©. Right sided HF. © Pericardial effusion & constrictive pericarditis. © Hypervolemia. + Non-pulsating: © SVC obstruction (SVC thrombosis or Mediastinal syndrome). 2) Abnormal Pulsations: “* Abnormal waves ”” fave: o Absent : AR. © Giant: Pulmonary hypertension, PS, TS. o Cannon waves: - Regular: Nodal rhythm. - Occasional: A-V dissociation. > x-descent: + Obliterated (systolic expansion of neck veins): * TR. * AR, - Prominent: * Constrictive pericarditis. * Pericardial effusion. y-descent: - Prominent: * Constrictive pericarditis. 3940 8. (Oedema of lower limbs o Right sided HF. © Pericardial effusion & constrictive pericarditis. 9. |Abdome 1. Hepatamegaly: - Enlarged tender: Right sided HF & pericardial disease. - Enlarged tender & pulsating: TR & TS. - Enlarged tender & sharp: Cardiac cirrhosis. 2, Splenomegaly: ~ Infective endocarditis (tender). ~ Right sided HF & pericardial disease. 3. Ascites.Il. Cardiac Examination A) AIM OF CARDIAC EXAMINATION: To detect: 1. Evidence of generalized cardiac enlargement: * Shift of the apex outwards lateral to the MCL. 2. Evidence of right ventricular enlargement: aa) Apex beat: ( outermost lowermost impulse ) * Diffuse * Shifted outwards * Shows systolic retraction : accompanied by reciprocal left parasternal uplift (right ventricular rocking ) b) Left parasternal & epigastric pulsations, c) Dullness over the lower half of the sternum. 3. Evidence of left ventricular enlargement: a) Apex beat: + Localized * Shifted outwards & downwards + Shows systolic bulge: accompanied by reciprocal left parasternal retraction (left ventricular rocking ) b) Apex impulse: + Heaving ( forcible , sustained ): pressure overload, + Hyperdynamic ( forcible , non-sustained ): volume overload. + Hypodynamic ( weak ): myocardial disease 4. Evidence of great vessel dilatation: a) Dilated pulmonary artery: + Dullness & pulsations in the second left space. b) Dilated aorta: * Dullness & pulsations in the second right space 5. Evidence of endocardial affection (valvular affection): * Presence of specific murmurs & thrills, 6. Evidence of myocardial affection: * Presence of S3 gallop over the mitral or tricuspid areas in LV or RV affection respectively. 7. Evidence of pericardial affection: * Refer to the chapter of “ Pericardial disease” 4142 8. Evidence of pulmonary hypertension: a) Precordial examination: = Pulsations , diastolic shock & dullness in the second left space. b) Auscultation: + S2 is accentuated. + Systolic ejection click. + Systolic ejection murmur, + Soft early diastolic murmur due to functional pulmonary regurge (Graham Steel). + S4 over the tricuspid area, 9. Evidence of arrhythmias: = Change in the rate or rhythm of the heart beats. B) TECHNIQUE OF CARDIAC EXAMINATION: “ Refer to the Clinical notes ”. 4243 THE CARDIAC CYCLE First Heart Sound: The cardiac cycle starts by contraction of the ventricles resulting in the closure of the mitral & tricuspid valves producing the {first heart sound (Si). Isometric Contraction Phase: The Yentricles continue to contract while the 4 valves of the heart are closed, so the pressure inside the ventricles rises rapidly without change in the volume. Ejection Phase: - When the pressure in the ventricles exceeds the pressure in the aorta & pulmonary artery, the aortic & pulmonary valves will open (normally with no sound). - Then the blood rushes from the ventricles to the aorta and pulmonary artery, first rapidly “maximum ejection phase”, then slowly “reduced ejection phase”. Second Heart Sound: After evacuation of blood, the ventricles relax, so the pressure in the aorta and pulmonary artery will exceed the pressure in the ventricles resulting in closure of aortic & pulmonary valves producing the second heart sound (S,). Isometric Relaxation Phase: The ventricles continue to relax while the 4 valves of the heart are closed, so pressure inside the ventricles falls rapidly without change in the volume. 4344 ¢ Ventricular Filling Phase: When the pressure in the ventricles becomes lower than the pressure in the atria, blood flows to the ventricles passively, at first rapidly: “maximum filling phase”, then slowly: “reduced filling phase”. ° Atrial Systole: ‘The last amount of blood in the atria is pushed actively by atrial contraction in the late diastole “presystole”. e Ventricular contraction: Occurs again & the cycle is repeated. Cardiac Cycle Maximum ejection phase Reduced ejection phase Opening of A and P Isometric contraction a Closure of M and T. Closure of A and P Isometric relaxation phase Opening of M and T Atrial contraction | Si S2 S1 1 1 1 p— Systole yx __Diastole —> 4445 VALVULAR HEART DISEASES MITRAL STENOSIS ETIOLOGY 1. Rheumatic Fever: the most common cause. 2. Congenital: a rare cause. 3. Relative stenosis: (not an organic stenosis) - Increased blood flow through the mitral valve. - Carey-Coombs murmur in acute rheumatic valvulitis. - Austin flint murmur in severe aortic regurge. PATHOPHYSIOLOGY - In mild cases: The blood flow through the mitral valve remains normal. No symptoms occur. - Insevere cases: (valve area less than 2cm? ): The blood flow through the mitral valve is decreased. Blood stagnates in pulmonary veins (pulmonary congestion). - Later on: Vasoconstriction of pulmonary arterioles occurs to | pulmonary congestion, but this will lead to: pulmonary hypertension. - Finally: RV enlargement & then RVF will occur secondary to pulmonary HTN. 4546 Therefore four stages will occur in patients with MS: ES S OF MITE MITRAL STI AL STENOSIS Stage I: “Mild or asymptomatic mitral stenosis ” ‘The only abnormality is anatomical narrowing of the mitral valve, but the patient is fully compensated (no symptoms). ° Stage Il: “ Mitral stenosis with pulmonary congestion ” The pulmonary venous pressure is elevated. ° Stage MM: “ Mitral stenosis with pulmonary hypertension ” The pulmonary arterial pressure is elevated. ° Stage IV: “ Mitral stenosis with right ventricular failure ” (CLINICAL PICTURE There is a latent period of several years between the initial attack of rheumatic carditis & the development of manifestations of mitral stenosis. Symptoms Does the patient with MS always symptomatize ??? 1. Stage I: No symptoms. 2. Stage II: Symptoms of pulmonary congestion (but pulmonary oedema is not common). Symptoms of low CO. 3. Stage I: Symptoms of pulmonary congestion: __ improve. Symptoms of low CO: increase. 4, Stage IV: Symptoms of systemic congestion. Dyspnea is the most common symptom)47 . Stage I: — no signs. 1 2. Stage I: signs of: pulmonary congestion. 3. Stage III: signs of: low cardiac output, malar flush, giant a-wave. 4 . Stage IV: signs of: — systemic congestion. Cardia A] Precordial examination: Stage I & Stage II: - Apex: normal site & slapping character. - Diastolic thrill: ending in a palpable 8, Stage II & IV: ~The previous findings. - Signs of pulmonary hypertension. - Signs of: right ventricular enlargement. B] Auscultation: > Stage | & Stage II (Over the mitral area): 1. Accentuated first heart sound: due to: - Fibrosis of the mitral cusps. - Forcible closure of the mitral cusps: _ because: © They are displaced downwards due to high LA pressure. NB] Diminished S, in mitral stenosis denotes: © Double mitral lesion (with predominant regurge) or o Calcified mitral valve. 2. Mitral opening snap: - Itis sharp & snapping due to opening of the rigid cusps of mitral valve. Itis heard in the early diastole: © Just after S. (separated from it by the isometric relaxation phase). © Just before the murmur of mitral stenosis. - Its presence denotes non-calcificaton of the mitral valve. 4748 3. Murmur of mitral stenosi = Timing: © Mid-diastolic presystolic with presystolic accentuation. © InAF, _ there is loss of presystolic accentuation (due to loss of atrial contraction). * Character: rumbling. * Site: at or slightly inside the apex. = Propagation: not propagated. = Position: © Best heard with the cone of the stethoscope. © In the left lateral position. 4. Silent Mitral Stenosis (MS with no murmur) — due to: a. High LV pressure: e.g. associated LVF. b. Low LA pressure: eg. * Severe pulmonary hypertension. ° RVF. c. In association with ASD. > Stage Ill = The previous findings. = Auscultatory findings of pulmonary hypertension: a) Over the pulmonary area: = Systolic ejection click. - Systolic ejection murmur. - Soft early diastolic murmur: due to functional PR . (Graham Steel murmur) b) Over the tricuspid area: - Ss > Stage IV - The previous findings. - Auscultation over triscupid area: 0 Pan systolic murmur of functional triscupid regurge. 0 RV gallop (S;) due to RVF. 4849 (COMPLICATIONS 1. In the mitral valve: o Rheumatic activity. © Calcification. © Infective endocarditis. 2. In the left atrium: a) Arrhythmias, especially AF. b) LA enlargement, causing pressure symptoms: - on oesophagus : dysphagia. - on left bronchus : dyspnea & cough. - on left recurrent laryngeal nerve: hoarseness of voice. ©) Thrombo-embolic complications: - Systemic embolization: e.g. cerebral, peripheral, renal. - Ball & valve embolus: leading to syncope & sudden death. 3. In the right ventricle: o RVF. S . In the left ventricl o NoLVF in isolated mitral stenosis. 5. In the lung: o Hemoptysis. © Pulmonary infection. © Pulmonary embolism (secondary to DVT). © Pulmonary oedema is not common in mitral stenosis (see before). a . Complications of surgery. 4950 1. 2. 50 INVESTIGATIONS, CXR: a) Stage I: no abnmormality. b) Stage I: (PA view & lateral view with Barium) © LA enlargement. © Pulmonary congestion. ©) Stage IM & IV: © Right ventricular enlargement & RA enlargement. © Pulmonary hypertension. © May be calcified mitral valve. ECG: a) Stage I: No abnormality. b) Stage II: LAenlargement —_(P mitrale: broad & bifid). c) Stage Ill & IV: - Right atrial enlargement (P pulmonale: tall & peaked). - Right ventricular enlargement. Echocardiography: * The most sensitive & specific non-invasive method diagnosing MS. * Detects the severity of stenosis by measuring: © The valve area. ©. The pressure gradient across the valve. * Detects chamber enlargement. Cardiac catheterization & angiocardiography: - Detects the severity of stenosis by measuring: o The valve area. o The pressure gradient across the valve. - Detects chamber enlargement.SL WHEN DO WE SAY TIGHT MITRAL STEN SIS?? Vv Tight MS is diagnosed: * According to the stage: - Satge II with dyspnea more than grade II, or - Stage III, or - Stage IV. ° According to the echocardiography: - Valve area less than 1 cm’. Y Tight MS is an indication for SURGERY . 1. Medical: a) Prophylaxis against: Rheumatic activity, Infective endocarditis (uncommon). b) Symptomatic for: Complications eg. HF, AF, infection, embolization. 2. Surgical: a) Indications: 1. Tight mitral stenosis (valve area is < 1 cm” ). 2. Marked symptoms not responding to adequate medical treatment. 3. Embolization with no serious deterioration of the condition of the patient. b) Types of operations: 1. Mitral commissurotomy: closed or open. 2. Valve replacement: - Byaprosthesis (tissue or synthetic). - Indication © Calcification . © Associated mitral regurge. o Recurrent stenosis after commissurotomy. 5152 c) Complication: Embolization. Arrhythmias. Mitral incompetence. Restenosis. Post — cardiotomy syndrome: - Pleuro-pericarditis that may occur 10 — 15 days following the operation. ~ It is possibly an autoimmune response to damaged cardiac tissue during surgery. Se eee ete oe 6. Complications of artificial valves: - Infective endocarditis. - Thrombo-embolism. - Mechanical dysfunction. - Hemolytic anemia. 3. Balloon dilatation: - May be performed in some patients indicated for commissurotomy. - Important i “Self — assessment” “What are the changes induced by AF in‘a case of MS” ?? 5253 MITRAL REGURGE [ETIOLOGY A] Organic: 1. Rheumatic fever: the most common cause. 2. Congenital. 3. Prolapse of the mitral valve (MVP). 4. Papillary muscle dysfunction eg. CAD. 5. Infective endocartitis. 6. Iatrogenic: following mitral commissurotomy. B] Relative: - Dilatation of the mitral ring secondary to LV dilatation. PATHOPHYSIOLOGY 1. During systole: A part of blood regurgitates from LV to LA leading to: * LowCo. * LAdilation: due to increased blood volume in LA. 2. During diastole: A large volume of blood —+ LV — LV enlargement which may end in LVF. CLINICAL PICTURE Symptoms 1. No symptoms: in early cases. 2, Symptoms of low cardiac output: in late cases. 3. Symptoms of pulmonary congestion: in late cases. 4. PALPITATION. Palpitation is the most common s) to) 5354 Signs General: ‘© No signs: in early cases. ©. Signs of low cardiac output: in late cases. © Signs of pulmonary congestion: in late cases. Cardiac: A] Precordial examination: ©. Signs of LV enlargement: with hyperdynamic apex. © Systolic thrill: over the apex. B] Ausculatation: 1. First heart sound: weak (muffled) due to failure of proper mitral closure. 2. Third heart sound: present due to excessive flow of blood from LA to LV. 3, Murmur of mitral regurge: - Timing: pan systolic starting with S, - Character: soft or harsh. - Site: over the apex. - Propagation: © To the axilla. © To the base of the heart & medially in posterior leaflet disease. - Position: heard best in the left lateral position. (COMPLICATIONS Same complications of MS. but: 1. Infective endocarditis is common. 2. Left ventricular failure: occurs. IN STIGATIONS 1. CXR: + No abnormality: in early cases. + Enlarged LA & LV: in late cases. * Pulmonary congestion: in late cases. * Calcified mitral valve especially: _ in late cases. 5455 2. ECG: * Enlarged LA (P mitrale: broad & bifid). * Enlarged LV. 3. Echocardiography: * Detects the severity of mitral regurgitation. * Detects chamber enlargement. * Detects the cause: eg. MVP. 4. Cardiac catheterization & angiocardiography: * Detects the severity of mitral regurgitation. * Detects chamber enlargement. * Detects the cause: eg. CAD. - Same as that of mitral stenosis. 2. Surgical: - Valve replacement. itral Valve Prolapse (Barlow’s syndrome — Floppy mitral valve) - Itis more common in young females. - Mild prolapse is regarded as a normal variant. ETIOLOGY| - Unknown, but there is familial incidence. - Isolated abnormality, but may be associated with: Marfan’s syndrome or ASD. 5556 56 PATHOPHYSIOLOGY During ventricular systole, a mitral valve leaflet (commonly the posterior) prolapses into the LA. This may result in papillary muscle strain & some mitral regurge. Usually the case is not hemodynamically signific: CLINICAL PICTURE Symptoms * ASYMPTOMATIC. + Atypical chest pain: is the most common symptom. * Palpitation. Signs * Mid systolic click. ¢ Late systolic murmur. PLICATIONS * Progressive mitral regurgitation. + Infective endocardi + Arrhythmias. * Systemic embolization. * Sudden death. INVESTIGATIONS - Echocardiography is diagnostic. (TREATMENT * Surgery: mitral valve replacement in cases with severe MR * Prophylaxis against: infective endocarditis. * Anti — arrhythmic therapy. * Propranolol: is effective for chest pain. * Reassurance.57 AORTIC STENOSIS ETIOLOGY 1, Rheumatic fever. 2. Calcific. 3. Congenital: - Itmaybe: valvular, subvalvular or supravalvular. 4. Hypertrophic cardiomyopath: (Idiopathic Hypertrophic Subaortic Stenosis; IHSS): - It produces a subvalvular obstruction in the systole due to: contraction of the hypertrophied interventricular septum. 5. Relative stenosis (not an organic stenosis): a) Dilatation of the aorta: Hypertension, atherosclerosis, aortic aneurysm. b) Increased blood flow across the aortic valve: ‘Hyperdynamic circulation: eg. AR. PATHOPHYSIOLOGY} - During systole, there is obstruction of blood flow from LV to aorta leading to: 1. Low cardiac output. 2. Pressure overload on LV leading to LVH & LVF. - Normally, the aortic valve area is 3-4 cm”, In severe AS, it is less than 0.8 cm”. CLINICAL PICTURE Symptoms 1, No symptoms: in mild cases. 2. Symptoms of low CO: in severe cases. 3. Symptoms of pulmonary congestion: due to LVF. 4, SYNCOPE: especially exertional, 5. ANGINA: due to: Reduced coronary blood flow: due to low CO & shortened diastole. - Left ventricular hypertrophy: increases the myocardial O; demands. Associated coronary atherosclerosis: especially in calcific AS. 5758 Signs General: 1. Pulse: - Pulsus parvus et tardus (plateau pulse): rises slowly, of small volume, returns slowly. - Pulsus bisferiens: bifd pulse occuring in double aortic lesion. 2. Systolic thrill: over the carotid arteries. 3. Signs of low CO: in severe cases (esp. low SBP). 4. Signs of pulmonary congestion: due to LVF. Cardiac: A] Precordial examination: 1. Signs of LVH: with a heaving apex 2. Systolic thrill: over second right space —> apex & carotid arteries. B] Auscultation: - Over the aortic area: 1. Second heart sound: weak. 2. Systolic ejection click: due to opening of the rigid cusps. 3. Systolic ejection murmur: - Midsystolic, harsh. Maximum over second right space —> apex & carotid arteries. - Qver the pulmonary area: Reversed splitting of the second heart sound. - Over the mitral area: Lats, 2. Propagated murmur of AS COMPLICATIONS 1. LVF. 2. Infective endocarditis. 3. Sudden death: usually due to VF. 4. Heart bloc! in calcific AS due to extension of calcification to the AV bundle, 5. Rheumatic activity: in rheumatic AS. 58INVESTIGATIONS 1. CXR: * No abnormality: in mild cases. ° LV: LVH. * Lungs: Pulmonary congestion when LVF occurs. * AORTA: - Small aortic knuckle or post-stenotic dilatation. - Aortic valve calcification may be seen. 2. ECG: - LVH. 3. Echocardiography: - Detects the severity of stenosis by: * Measurement of valve area. * Measurement of pressure gradient across the valve. - Detects the type of stenosis. - Detects LVH. 4. Cardiac catheterization _& angiocardiography: - Detects the severity of stenosis by: * Measurement of valve area. * Measurement of pressure gradient across the valve. - Detects the type of stenosis. - Detects LVH. Congenital Rheumatic Calcific Age Young Young & Middle Old History of RF Absent Present Absent Type Valvular or Subvalvular Valvular Valvular or Supravalvular | Associations | Congenital anomalies} Other valvular | Atherosclerosis lesions. 5960 (TREATMENT) 1. Medical: - Same as that of mitral stenosis. - Anginal attacks: may be relieved by SL nitrates. 2. Surgical: (Aortic valve replacement) Indications: 1. Presence of severe symptoms. 2. Pressure gradient more than 50 mmHg. 3. Valve area less than 0.8 om’. 3. Balloon dilatation: Indications: 1. Children: with congenital AS as an alternative to surgery. 2. Elderly: with severe calcific AS who are too ill to undergo surgery.AORTIC REGURGE ETIOLOGY 1. Rheumatic fever: the most common cause. 2. Infective endocarditis. 3. Congenital. 4. Dilatation of the ascending aorta as in: a) Syphilic aortitis: syphilis produces dilatation of the aortic ring. b) Severe hypertension. c) Ankylosing spondylitis. d) Aortic aneurysm: with dissection. e) Marfan syndrome. PATHOPHYSIOLOGY| - Regurgitation of blood from the aorta to the LV in diastole leads to: 1) Volume overload on the LV leading to LV dilatation & later on LVF. 2) t_ SBP: due to f LV stroke volume. 3) | DBP. 61 - {SBP & | DBP — wide pulse pressure — peripheral signs of AR. CLINICAL PICTURE Symptoms 1. Generalized BODY THROBBING: due to increased arterial pulsations. 2. PALPITATION: due to forcible LV contraction. 3. Symptoms of pulmonary congestion: when LVF occurs. 4. Angina pectoris : wo types of angina occur in aortic regurge - Classic angina of effort: Decreased DBP: reduces coronary filling. - Angina of Lewis: Nocturnal & associated with autonomic disturbances e.g. sweating & tachycardia. 6162 Signs General: “ Peripheral signs of aortic regurge” 1. ign: nodding of the head. 2. : prominent carotid pulsations. 3. Systolic thrill: over the carotid arteries. 4. Water hammer pulse: rises rapidly, of big volume, collapses rapidly. 5. Capilliary pulsations: detected in nail bed, lips or gar lobule. 6. Pistol shots: loud booming sounds heard with each pulse beat over the arteries (especially femoral) due to sudden distension of collapsed arterie a Duroziez’s sign: # It consists of systolic & diastolic murmurs over the femoral artery if it is slightly compressed with the stethoscope. # The systolic murmur is due to the rapid flow of blood to the periphery, while the diastolic murmur is due to rapid regurge of blood to the heart. 8. Blood Pressure: a) Wide pulse pressure: - Exaggerated difference between systolic & diastolic blood pressure. b) Hill’s sign: ~ Exaggerated difference between SBP in LLs & ULs: more than 50 mmHg. - Normally, SBP in LLs is higher than in ULs: by about 10-20 mmHg Cardiac: A] Precordial examination: * Signs of LV enlargement: with hyperdynamic apex. * No thrill over the aortic area: in isolated AR. B] Auscultation: - Over the aortic area: 1. Normal second heart sound. 2. MURMUR of AR: - Timing: early diastolic, decrescendo. - Character: soft blowing. - Site: maximum over the third space. - Propagation: to the apex. - Position: best heard with the diaphragm of the stethoscope, the patient is: * Sitting up. + Leaning forward. + Holding his breath in forced expiration, 3. Soft ejection systolic murmur: = Due to f blood flow across the aortic valve (relative AS), 6263 - Over the Mitral area: 1. Ss 2. Propagated murmur: of AR. 3. Pan systolic murmur: _of functional MR. 4, Austin Flint murmur: —_(mid-diastolic) due to: ¢ Elevation of anterior leaflet of the mitral valve by the regurgitant blood from the aorta causes relative MS. COMPLICATIONS| 1. Rheumatic activity. 2. Infective endocarditis. 3. LVF. INVESTIGATIONS ~ LV enlargement & dilated aorta “Aortic configuration (Boot-shaped heart)”. ~ Lungs: Pulmonary congestion when LVF occurs. 2. ECG: - LV enlargement, 3. Echocardiography: - Detects the severity of the lesion. = Detects LV enlargement. 4. Cardiac catheterization & angiocardiography: - Detects the severity of the lesion. - Detects LV enlargement. ATMENT 1. Medical: - Same as that of mitral stenosis. - Syphilis: anti—syphilitic ttt. 2. Surgical: (Aortic valve replacement) Indications: 1. Presence of severe symptoms. 2. Progressive cardiomegaly. 3. Declining LV functions. 6364 TRICUSPID STENOSIS ETIOLOGY - Rheumatic fever: the most common cause, & is almost always associated with MS. = Carcinoid syndrome: a rare cause. PATHOPHYSIOLOGY, - During diastole, there is obstruction of blood flow from RA to RV leading to: * Systemic venous congestion. + Low Co. (CLINICAL PICTURE Symptoms 1. Systemic venous congestion. 2. Low CO. Signs General: 1. Systemic congestion including: * Congested pulsating neck veins with giant A wave. + Enlarged tender pulsating liver. * Ascites before oedema of lower limbs (ascites precox). 2. Low CO. Cardiac: A] Precordial exa: ation: - RAenlargement (dullness to the right border of the sternum). - RVenlargement (due to frequently associated MS). B] Auscultation: Over triscupid area: Accentrated first heart sound. - Opening snap. - Mid-diastolic murmur that increases by ins] piration, 6465 INVESTIGATIONS 1. CXR: - RA & RVenlargement. 2. ECG: - RA & RVenlargement. 3. Echocardiography: - Diagnostic 4. Cardiac catheterization & angiocardigraphy: - Diagnostic. (TREATMENT 1. Medi - TIT of right sided - HF. 2. Surgical: - Valve replacement. 6566 TRICUSPID REGURGE IETIOLOGY| 1. Functional: the most common cause due to dilatation of the tricuspid ring secondary to RV dilatation, 2. Organic: rare: * Rheumatic fever. © Infective endocarditis. © Congenital. * Carcinoid syndrome. ee uOENYSO! 7 2 systole, blood regurgitates from RV to RA causing: * LowCO. * RA enlargement. * RVenlargement. * RVF (systemic congestion). CLINICAL PICTURE Symptoms 1. Systemic congestion. 2. Low CO. Signs General: 1. Systemic congestion including: © Congested pulsating neck veins: with systolic expansion. o Enlarged tender pulsating liver. © Ascites before oedema of LLs (ascites precox). © Mild jaundice & peripheral cyanosis (cyano — icteric face). 2. Low CO. Cardiac: A] Precordial examination: o RA & RVenlargement. o Rarely: systolic thrill over tricuspid area. 6667 B] Auscultation: “ Over tricuspid area ” 1. Weak muffled S;, 2. Ss, 3. Pan systolic murmur: - Timing: - Character: - Site: - Propagation: = Caravallo’s sign: INVESTIGATIONS 1. CXR: - RA & RVenlargement. 2. ECG: - RA & RVenlargement. 3. Echocardiography: - Diagnostic. pan systolic. soft or harsh. tricuspid area. to the apex, but not to the axilla. murmur increases with inspiration being of right sided origin. 4. Cardiac catheterization & angiocardiography: - Diagnostic. (TREATME. 1. Medical: - TTT of right sided — HF. 2. Surgical: - Valve replacement. 6768 PULMONARY STENOSIS A] Organic: * Congenital: the most common cause. * Carcinoid syndrome: rare. B] Functional: - Pulmonary hypertension. PULMONARY REGURGE A] Functional: - Mostly due to PH which causes dilatation of the pulmonary ring. B] Organic: * Congenital. * Carcinoid syndrome. 6869 Aa aay uopsafiu0o ava ; Teuonouny aL UND}. aval SUIDA 3Joou UT HoIsUBdXD oTJoISKg - beraaeed uonendsu: yim |, pidsnoin eee « wonestdsut oni ava ava sono J Sunjqumns So1seyp-py - aaa onvumnoy SL neA-® IPI ~ ne «200d 19] PAP aUp 10A0 ,, i nee FA 3uvso1q yos oyoiseyp Kueq-| — uonwendyea onmiydks av SAT podeys-oog xode orueuxpiadéy - BuqqosryL opeumarry suBts yexaydueg - ‘uoneIeUp xe onounis-isog TOS 10 4c Pho) — aoeds 14811 puoses 10,0 ,, ¥ jrusfu05 aAT ayyoniy TE 39 7¥ sHo1s&s uonoafa ysTEHy - Ty sv omioe jews xade Buravay-| “dso Q9 MOT AAT aAT SAT ‘eqLxe 0} porededoud xode sono TOPPA Seenneitt aw av1 av1 Tam) 29 FH onorses weg - av ‘ uoisuonadsy Sreuowng-| FaRAST “dso oneuino aqpuoumnd-g | YONSBLOD WINE | ody sono FR Buqums oHeiserp-pIW.-| yonsosu0 ‘wing mre oF open avT Ig porenjuaooy - uais ‘o;duxts asnzy | WOISe7] ae he que zodary soy queyrodan ysoyy | yuejz0dur ysoyy| angen, 69CONGENITAL HEART DISEASES CRITERIA TO SUSPECT CONGENITAL HEART DISEASES: 1. Absence of history of rheumatic fever. 2. Basal or parasternal thrills or murmurs. 3. Cardiac manifestations before the age of 5 years. - Gentral cyanosis or systemic hypertension in infancy or early childhood. ww Dextrocardia without mediastinal shift. THESE DISEASES MAY BE CLASSIFIED ACCORDING TO: 1. The presence or absence of cyanosis. 2. The hypertrophied (overloaded) ventricle. CLASSIFICATION ‘The hypertrophied 5 ade Non-cyanotic Cyanotic 1. Right ventricular | a) Pulmonary stenosis a) Triology of Fallot hypertrophy b) Atrial septal defect b) Eisenmenger’s syndrome 2. Left ventricular a) Aortic stenosis a) Tricuspid atresia hypertrophy b) Coarctation of the aorta c) Patent ductus arteriosus a) Transposition of the 3. Biventricular 'a) Venticular septal defect great arteries hypertrophy b) Truncus arteriosus 4, Absence of a) Any mild lesion a) Tetralogy of Fallot ventricular b) Dextrocardia hypertrophyPULMONARY STENOSIS TYPES 1. Valvular: + The most common type. * Commonly there is post-stenotic dilatation. 2. Subvalvular: infundibular. 3. Supravalvular: the rarest. PATHOPHYSIOLOGY| ince to flow of blood from RV to pulmonary artery causes: * Low CO. + RV hypertrophy then RVF. CLINICAL PICTURE Symptoms 1. LowCo. 2. RVE. Signs General: 1. Signs of low CO. 2. Signs of low RVF. 3. Giant a-wave. Cardiac: A] Precordial examination: = Signs of RV hypertrophy. - Systolic thrill over the pulmonary area. ~ Dullness without pulsations over the pulmonary area in valvular PS (due to post-stenotic dilatation).7 B] Auscultation: - Over the pulmonary area: * Weak S, with wide splitting * Ejection systolic click (in valvular PS). + Ejection systolic murmur. - Over the tricuspid area: » Ss (COMPLICATIONS) 1. Infective endocarditis. 2. RVF. 3. Pulmonary TB due to lung oligemia. INVESTIGATIONS, 1. CXR & screen: - RA & RVenlargement. - Dilated non pulsating pulmonary artery (post-stenotic dilatation) ~ Lung oligemia, 2. ECG: ~ RA & RVenlargement. 3. Echocardiography: ~ Diagnostic. 4, Cardiac catheterization & angiocardiography: = Diagnostic. TREATMENT Medical = Prophylaxis against infective endocarditis. ~ Treatment of RVE. (Insevere cases: pressure gradient more than 50 mmHg ) - Valvular stenosis: Valvotomy. = Infundibular stenosis: Infundibular resection. Valvular stenosis. may be done in: Balloon Valvotomy: 2B ATRIAL SEPTAL DEFECT - A communication between the 2 atria. PATHOPHYSIOLOGY LA pressure is higher than RA pressure, so part of blood is shunted from LA to RA which also receives blood coming from the venae cavae, leading to RA dilatation ( volume overload ). This volume overload will then pass to the RV (RV dilatation), then to the pulmonary artery (pulmonary artery dilatation ), then to the lung ( lung plethora ). - Later on, vasoconstrictive & obliterative changes occur in the pulmonary arterioles to decrease the lung plethora, but this will lead to pulmonary hypertension. Therefore RA pressure will increase till it exceeds the LA pressure causing reversal of the shunt & central cyanosis (Eisenmenger’s syndrome). CLINICAL PICTURE Symptoms 1. Absent in small defects. 2. Dyspnea & recurrent chest infections ( due to lung plethora ). 3. Symptoms of RVF in late cases. 4, Symptoms of low CO in severe cases. Signs General: 1. Giant a-wave due to pulmonary hypertension. 2. Systemic congestion signs due to RVF. 3