Cardiovascular Exam Notes PDF

Themes to Cardiology, angiology Exam William Marrow Mnemonic for the bundle branch block appearance on the ECG: LBBB (Left Bundle Branch Block): - W in V1: Look for a Wide and notched QRS complex resembling a "W". - M in V6: Look for an M-shaped QRS complex. RBBB (Right Bundle Bra...

Themes to Cardiology, angiology Exam William Marrow Mnemonic for the bundle branch block appearance on the ECG: LBBB (Left Bundle Branch Block): - W in V1: Look for a Wide and notched QRS complex resembling a "W". - M in V6: Look for an M-shaped QRS complex. RBBB (Right Bundle Branch Block): - M in V1: Look for an M-shaped QRS complex (RSR' pattern) in V1. - W in V6: Look for a Wide S wave resembling a "W". CARDIOLOGY 1. Diastolic heart murmurs. Heart sounds. 2. Systolic heart murmurs. Heart sounds. 3. Risk factors, primary and secondary prevention.  4. Dilated cardiomyopathy. Cradiomyopathy-myocardial disorder in which the heart muscle is structurally and functionally abnormal, in the absence of: - coronary artery disease, - hypertension, - valvular disease, - congenital heart disease or the degree is not su cient to cause the observed myocardial abnormality. Etiology: - Familial (25%): most commonly autosomal dominant - Idiopathic: unknown etiology - Secondary: myocarditis, chronic alcohol disease, endocrine disorders, chronic tachyarrhythmia etc. Morphology: Reversible/irreversible damage of the myocardium, increased interstitial brosis, decreased systolic function, dilated cavities, thin ventricular walls Symptoms and diagnostics Symptoms: Progressive disease: asymptomatic in early stage, symptoms of heart failure: e.g. fatigue, dyspnea As the disease progresses all signs of left and right ventricular heart failure can appear Diagnostics: - ECG: left bundle branch block, atrial brillation, ventricular arrhythmias - Imaging: echocardiography, CMR: dilated cavities, di use hypokinesia, functional mitral/ tricuspid regurgitation - Coronary angiography, laboratory tests. (eg. NTproBNP) etc. Complications: - Intracardiac thrombus (left ventricle, LA appendage) - Arrhythmias incl. Atrial brillation, malignant arrhythmias (ventricular tachycardia, ventricular brillation) - Progression of heart failure, decompensation Therapy: Aims: to slow the progression, reduce HF symptoms, reduce mortality incl. prevent SCD Depends on the etiology and stage, elimination of myocardium damaging factors, pharmacological and non-pharmacological treatment of heart failure (HF lecture) ICD is recommended Secondary prevention: haemodynamically not tolerated VT/VF Primary prevention: symptomatic heart failure and an ejection fraction 14yo (in the absence of the RBB) 2. Ventricular arrhythmias Major: epsilon wave, non- sustained or sustained VT - histological ndings: brofatty replacement of the myocardium - Family history (genetic test): ARVC in a 1st degree relative who meets current criteria ARVC con rmed pathologically at autopsy/surgery Identi cation of the pathogenic mutation fi fi fi fi fi  Imaging criteria: Echocardiography, CMR: - reduced right ventricular function or dilated RV - +regional walll motion abnormality Therapy-prevention of the SCD, HF: 1. Avoidance of the competitive sports 2. Beta-blockers titrated to the DTM as the 1st line therapy to improve symptoms in patients with non- sustained VT (lasts for less than 30 sec and usually self terminates, brief episodes that may not cause signi cant symptoms and hemodynamic instability) 3. Pharmacological and non-pharmacological therapy of the HF 4. ICD implantation - 1ry prevention: may be considered in patients with the risk factors for ventricular arrhythmias - 2ry prevention: recommended in th patients with a history of the aborted SCD and hemodynamically poorly tolerated VT Restrictive cardiomyopathy Etiology, forms: - Amyloidosis: Heridatory/associated with the other diseases (eg. Multiple myeloma-overproduction of the Ig light chain/ production of the acute phase proteins in the chromic in ammation) Systemic and localised forms-common cardiac manifestation Morphology: amyloid deposits in between the cardiac myocytes, concentric hypertrophy, hypertrophic appearance of the LV, RV, intertribal septum, dilated atria Cardiac symptoms: reduced physical capacity, fatigue, dyspnea, oedema (qscvites, pleural uid) Speci c ECG signs of the amyloidosis: ECG low voltage in limb leads, QS-wave in precordial leads, I-II-III degree AV-block, aspeci c intraventricular conduction disorders, atrial brillation, ventricular arrhythmia - sarcoidosis, - hemochromatosis, - endomyocardial disease EMF, Lö er endocarditis: - Etiology: Complex pathomechanism: toxic e ect of eosinophils - necrosis, endomyocarditis, thrombus formation, brosis - Morphology: Endocardial brosis in the apical and subvalvular region of left and/or right ventricle with thrombus formation - Diagnosis,therapy: Thorough investigation (history, lab test, imaging etc) Elimination of triggering factors, pharmacological treatment, surgical treatment - idiopathic Morphology: Intense rigidity of myocardium !diastolic dysfunction, dilated atria, normal or decreased ventricular volumes Diastolic dysfunction mostly caused by myocardial brosis, in ltration or endomyocardial brosis Symptoms: Reduced physical capacity, fatigue, dyspnea, oedema (ascites, pleural uid) ffl fi fi fi fi fi ff fi fi fl fi fl fi fl  Diagnosis: Physical examination, lab tests, ECG, echocardiography, CMR, biopsy((endomyocardial or extracardiac (eg. abdominal fat, gingiva): detection of amyloid deposits), thorough internal medical -echo: Concentric hypertrophy, diastolic/systlic dysfunction, dilated atria, pleural uid -cardiac MR: Di use Myocardial Enhancement: Amyloid deposits cause a di use, subendocardial to transmural enhancement pattern. “Ground Glass" Appearance: The myocardial enhancement appears as a “ground-glass” or “glassy” texture. Therapy: - In some forms speci c pharmacological therapy, - pharmacological treatment of heart failure, - in case of AA type treatment of the primary disease, - chemotherapy in case of AL type, - autologous stem cell transplantation, - heart transplantation Un-classi ed: noncompaction cardiomyopathy Etiology: Hereditary cardiomyopathy with autosomal dominant gene transmission-Disturbed compaction process during early development of the myocardium Morphology: „Spongy myocardium” LV trabeculae and intertrabecular recessus formation Symptoms, therapy: - progressive heart failure - thrombembolic complications - malignant ventricular arrhythmias - see DCM Un-classi ed: Tako-tsubo „cardiomyopathy”/apical balloning, broken heart syndrome Reversible left ventricular dysfunction of postmenopausal women after emotional or physical stress Etiology: - epicardial coronary spasm, - microcirculatory dysfunction, - cardiotoxic effect of catecholamines Signs, Symptoms: - chest pain, - ST-elevation, - cardiac biomarker positivity (suspicion of ACS), - consequence: heart failure, thrombus, arrhythmia Morphology, function: - Typically apical (and midventricular) wall motion abnormality Therapy: treatment of acute heart failure (avoid cathecholamines) fi fi ff fi ff fl 6. Acute heart failure, cardiogenic shock - etiology, symptoms, diagnostics. 7. Treatment of acute heart failure. 8. Chronic heart failure - etiology, symptoms, diagnostics. 9. Treatment of chronic heart failure. 10. Infective Endocarditis. 11. Pericarditis, pericardial e usion. 12. Aortic valve stenosis. Diagnosis of aortic valve insu ciency. 13. Mitral valve stenosis.Diagnosis of mitral valve insu ciency. 14. Atrial and ventricular septal defects, congenital heart disease. 15. Hypertension I. Etiology, diagnosis. 16. Hypertension II. Treatment. Hypertensive Heart Disease. 17. Anticoagulant treatment and indications. 18. Anti-platalet treatment and indications. ff ffi ffi  19. Manifestations and evaluation of Ischemic Heart Disease. Forms of the ischaemic heart disease: 1. Asymptomatic (silent ischaemia) 2. CHF 3. Stable angina 4. Acute coronary syndrome - ACS without ST elevation-depending on the time: 1)Unstable angina(without necrosis biomarkers) 2)Non-ST elevation myocardial infarction(TrT is increased, normal40%) - pulmonary cogestion - Cariogenic shock - RVF- impaired lling pressure (CAVE: nitro) THERAPY of the HF: I. vasopressors+inotrops, II. ventilation, III. mechanical circulatory support: A. intraaortic balloon pump(IABP): easy to use, passive augmentation of the cardiac output up to 20%, limited e ect on the survival B. extracorporeal membrane oxygenator (ECMO): relatively easy to use, active support of the CO(100%), 5-7days, bridge to the decision and recovery 5. Mechanic complications: - mitral papillar rapture-acute mitral regurgitation - Ventricular septal rapture - Free wall rapture-tamponade ff fi  20. Angina pectoris. - symptom of the ischaemia Etiology: I. Decreased O2 supply: cardiac: (coronary stenosis, coronary spasm, microvascular diseases), extra cardiac: (anaemia, sickle cell disease, pulmonary disease (eg asthma, COPD, obstructive sleep apnea, pneumonia, pulmonary brosis etc), II. Increased O2 demand: noncardiac: (physical exertion, HT, hyperthyreosis, sympathomimetic toxicity, hyperthermia, arteriovenous stula, shock/sepsis,), cardiac: (structural heart diseases (eg hypertrophy), tachycardia (arrhythmia), aortic stenosis, dilated cardiomyopathy) Diagnostic approach Presentation of the unstable angina: 1. New onset angina: angina of at least CCS class III severity with onset within 2mo of initial presentation 2. Increasing (crescendo) angina: previously diagnosed angina that is distinctly more frequent 3. Angina at rest: usually prolonged for more than 20 min Pathophysiology of the unstable angina: formation of a thrombus around the ruptured plaque, causing the partial occlusion of the vessel ECG manifestation of the unstable angina: normal/ inverted T waves/ ST depression Biochemistry-extracardiac causes: anaemia (Hb), thyroid function (TSH) Risk pro le: DM(HbA1C), hyperlipidaemia(LDL-C) Check x-RAY: extracardiac causes (eg pulmonary diseases) Echocardiography at rest: LV function (if less than 50%-perform the anatomical test (CT angiography) to nd the CAD, wall motion abnormalities fi fi fi fi  Symptom type, age, gender+modifying factors 15% high clinical likelihood 1. Low clinical likelihood-coronary CTA: anatomical information, high “-“ predictive value (optimal for rule out), severe Ca cation causes artefact (limited information in the elderly patients). +exercise ECG (low sensitivity-used for low to intermediate clinical likelihood)-ischaemic ECG signs typically V4-6 St depression, T inversion (DON’T PROVIDE THE EXACT LOCALISATION) 2. High clinical likelihood-testing for the ischaemia-stress 1. MRI/2.stress echocardiography/3.SPECT/PET-areas with reduced or absent radiotracer uptake suggest reduced blood ow, gives information about the perfusion, not coronaries themselves: high sensitivity and speci city, provide localization of the ischaemia, viability of the myocardium, pharmacological stress(dobutamine, dipyridamole (vasodilator that inhibits PDE and adenosine uptake)-mimics increased O2 demand upon the physical exercises 3. Very high clinical likelihood-invasive angiography-additional indications: systolic disfunction (reduced EF) with angina pectoris, positive ischaemic test or CCTA (high event risk) Punction location: - arteria radialis (preferred) - Arteria femoralis - Arteria brachiales Fractional ow reserve can be assessed during the invasive coronary angiography, for the measurement maximal hyperaemia should be reached via using the vasodilator agents (eg. Adenosine, nitrates) FFR=Distal coronary presssure/Proxiaml coronary pressure Should be measured I case of the 40-90% stenosis on the angiography Will determine the e ect of coronary revascularization: optimal value FFR