Question 1

What is the triad for treatment principle for AF?

Accepted Answer

Rate control +rhythm control + prevention of thromboembolism Rate control = blocking the AVN to slow conduction through the AVN

Question 2

What is non pharmacological rhythm control for AF?

Accepted Answer

Direct current (DC) cardioversion Indications: haemodynamically unstable patients, refractory to pharmacological cardioversion, rapid control of ventricualr rate during AF is required Delivery of electrical shock synchronized with QRS complex to avoid inducing VF which can occur by a shock applied during ventricular repolarization of T wave AF<48 hours of duration: pre and post cardioversion anticoag required only in patients with high risk of thromboembolism AF >48 hours of duration or unknown duration: precardioversion anticoagulation > 4 weeks. Post cardioversion anticoagulation >4 weeks Urgent cardioversion: need for restoration of SR takes precedence over need for protection from thromboembolism. Can be anticoagulated acutely with heparin and proceed directly to anticoagulation if no atrial thrombus seen on pre-cardioversion TEE Catheter ablation Indicated in patients with symptomatic paroxysmal/ persistent/long standing persistent AF who are refractory or intolerant to >1 class I or III anti arrhythmic drugs when a rhythm control strategy is desired RFA and cryoballoon ablation. Anticoag required for RFA ablation. Complications: cardiac tamponade (most common), stroke, TIA or pulmonary veins tenosis Surgical maze procedure (surgical ablation): indicated in selected patients undergoing cardiac surgery for another indication such as valvular replacement or CABG

Question 3

What are the types of heart failure?

Accepted Answer

Low output heart failure (more common): decreased CO but increased filling pressure High output heart failure: increased SV and normal or even increased CO, body responds by increasing fluid retention and preload e.g. sepsis/anemia, thyrotoxicosis/AVF or shunting Left vs right heart failure Left heart failure (increased left heart filling pressure) Symptoms: orthopnea, paroxysmal nocturnal dyspnea, dyspnea on exertion, nocturnal cough, palpitation Signs: tachycardia, presence of S3/S4, cardiomegaly, lung crepitations RHF Symptoms: abd distension, ankle swelling Signs: elevated JVP, hepatojugular reflex, pleural effusion, hepatomegaly, ascites, bilateral ankle pitting edema HF with reduced ejection fraction <40%: decreased LVEF due to impaired systolyc function, increased LV dilatation HF with preserved ejection fraction >50%: increased filling pressure but anormal LV filling due to impaired diastolic function. No or niminal LV dilatation Heart failure according to haemodynamic profile Presence of congestion = wet vs dry Adequacy of peripheral perfusion = warm vs cold

Question 4

What is clinical, CXR and ECG findings of pressure overload in heart failure

Accepted Answer

Primary response is ventricular hypertrophy (increased myocardial O2 consumption) but not ventricular dilatation. Imbalance between myocardial O2 demand and coronary flow results in relative myocardial ischemia and myocardial fibrosis. Fibrotic ventricles will eventually dilate (volume overload). Clinical o LV hypertrophy = Strong apical impulse but NO displacement of apex beat o RV hypertrophy = Left parasternal impulse Radiological (CXR) o LV hypertrophy = NO abnormality seen o RV hypertrophy = Uptilting of cardiac apex Radiological (ECG) o LV hypertrophy = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern) o RV hypertrophy = Right axis deviation/ Tall R wave in V1/ Deep S wave in V6

Question 5

What is clinical, CXR and ECG findings of volume overload in heart failure

Accepted Answer

Increased end diastolic volume of ventricles. LV or RV dilates to accomodate the increased amounnt of blood Clinical o LV overload = Strong apical impulse/ Displaced apex beat o RV overload = Left parasternal impulse Radiological (CXR) o LV overload = Cardiomegaly with apex extending laterally and downwards o RV overload = Cardiomegaly with apex displaced laterally and tilting upwards Radiological (ECG) (similar to hypertrophy) o LV overload = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern) o RV overload = Incomplete RBBB (rsR’ pattern) (common)/ Right axis deviation/ Tall R wave in V1/ Deep S wave in V6

Question 6

What are the symptoms of HF in adults?

Accepted Answer

Dyspnea (fluid accumulation) Orthopnea: quanity with number of pillows used (redistribution of fluid from splanchnic circulation and LL into central circulation during supine with increase in pulmonary capillary pressure leading to pulmonary congestion Paroxysmal nocturnal dyspnea (PND) Cheyne-Stokes respiration: cyclic breathing in which apnea is followed by gradual increase in RR and TV and then gradual increase in RR and TV until next apneic period. Apenic phase decreases arterial pO2 and increases pCO2 which stimulates the respiratory center resulting in hyperventilation and hypocapnia followed by recurrence of apnea Nocturnal cough Edema (decreased CO --> activation of RAAS, sympathetic nervous system) Fatigue Night sweats Decreased excercise tolerance (decreased CO) Other associateing symptoms: RUQ discomfort (acute hepatic congestion), palpitations, anorexia (poor perfusion of splanchnic circulation)

Question 7

What is the diagnostic criteria for congestive heart failure?

Accepted Answer

Framingham criteria  Diagnosis of CHF requires Presence of ≥ 2 major criteria (OR) Presence of 1 major criteria and 2 minor criteria  Major criteria Orthopnea or PND Lung crepitations Pulmonary edema Elevated JVP Hepato-jugular reflux V enous distension Weight loss in response to treatment  Minor criteria Exertional dyspnea Nocturnal cough Pleural effusion Tachycardia Hepatomegaly Ankle edema

Question 8

What is the PE for heart failure?

Accepted Answer

Vital signs: BP, RR, HR, pulse (pulsus alternans) General exam: diminished peripheral pulse, delayed capillary refill, cold, pale or cyanotic extremities Volume assessment: elevated JVP, peripheral edema: ankle, hepatosplenomegaly Resp examination: wheezing, basal crepitations (LHF), signs of resp distress: grunting with nasal flaring (infants), insucking of intercostal and subcostal muscles, use of accessory muscles for breathing CVS exam: presence of S3 (systoloc HF) or S4 (diastolic HF) S3 = early part of ventricular diastole, when there is rapid ventricular inflow into distended ventricles, the distended and tauted ventricular wall vibrates producing S3 S4 = late part of ventricular diastole, if ventricle is stiff and hardened in ventricular hypertrophy or in patients with MI, the ventricles do not expand properly --> atrium has to contract more strongly than normal to push the blood into ventricles. When atrium strains the blood into stiffed ventricle it will cause S4 (stiffened ventricles vibrate due to strong atrial contraction) Pulmonary hypertension signs Single and loud S2: loud P2 (pulmonary component of S2) Functional PR murmur: early diastolic murmur at left upper sternal border

Question 9

What is the PE for heart falure in children?

Accepted Answer

General inspection: body weight, height and head circumference (standard growth charts) Short stature: turner syndrome (associated with coaraction of aorta and bicuspid aortic valve) Tall stature: Marfan (associated with MVP, aortic root dilatation and AR) Dysmorphic features: down syndrome, turner syndrome, diGeorge syndrome General exam Cyanosis Abnormalities of limbs Marfan syndrome: arachnodactyly (long slender fingers) + hyperextensible fingers Down syndrome = clinodactyly + increased space between 4th and 5th finger Finger and toe clubbing Subcutaneous edema Signs of IE: splinter hemorrhage, janeway lesions, osler nodes CVS BP and pulse (rate + rhythm +volume + character): radio-radio delay/pulse volume discrepancy) Respiratory distress: tachypnea (increased RR) Surgical scars Chest wall deformities: pectus excavatum and carinatum (features of Marfans syndrome) Visible cardiac pulsation (volume overload or pressure overload) Cardiac apex Presence of thrills (palpable murmur: at least 4/6) Abnormal cardiac impulse: strong apical impulse (LV pressure or volume overload), left parasternal impulse = RV pressure or volume overload Heart sounds S2: pulmonic valve closes Loud S2: pulmonary hypertension (large left to right heart shunt) Single S2. Inaudible A2 = critical AS/HLHS, inaudible P2 = PA/critical PS/TGA Wide fixed splitting of S2: hallmark of ASD Presence of S3: dilated ventricles (large VSD/PDA/ dilated and hypertrophic cardiomyopathy) Presence of S4: occurs in decreased ventricular compliance Heart murmurs Ejection click in AS or PS Mid systolic click in MVP Opening snap in MS

Question 10

What are biochemical Ix for heart failure?

Accepted Answer

CBC: anemia and infection (leukocytosis) can exacerbate HF Serum electrolytes: HypoNa (indicator of severe HF) LFT: hepatic congestion RFT: increased serum BUN and creatinine level Urinanalysis TF Fasting blood glucose cTnT/cTnI: for acute decompensated HF or suspected acute coronary syndrome Plasma BNP level and NT-pro BNP BNP >400 pg/ml suggestiv eof HF BNP <100pg/mL is a strong -ve predictor for HF NT-proBNP (should be similar to BNP): NT-pro BNP is 4x higher than BNP in LV dysfunction

Question 11

What are the ix for heart failure (apart from biochemical)?

Accepted Answer

CXR: heart size (CT ratio >0.5), upper lobe blood diversion (cephalization--> pulmonary venous hypertension)), kerley B lines (periphery of lungs just above costophrenic angle --> edema of interlobular septa), Bat wings appearance (pulmonary edema --> alveolar shadowing from hilum), peribronchial cuffing (edema: interstitial fluid accumulates around bronchi causing thickening of wall --> doughnut like densities in lung parenchyma) ECG Echocardiography Excericse test (risk stratification and determing prognosis) evaluate potential candidates for cardiac transplantation or mechanical circulatory support Cardiac catheterization with angiography (indications --> patients with angina or positive excericse test/CAD is likely to be present) Cardiac MRI: distinguish ischemic heart disease from cardiomyopathy/ identify types of cardiomyopathy

Question 12

What is general management of HF?

Accepted Answer

Positioning: prop up the head, sitting up with legs dangling overside of bed. Decrease venous return and thus preload oxygen supplemenetation: treat hypoxemia only as defined as sO2 <90% Morphine: reduces anxiety but also induces nausea and respiratory depression Preload: venodilation which decreases LV filling pressure, afterload = anxiolytic and decrease work of breathing resulting in diminished central sympathetic outflow leading to arterial and venous dilatation

Question 13

What is medical treatment for acute heart failure?

Accepted Answer

Loop diuretics: indications for volume overload, acute cardiogenic pulmonary edema MoA: preload (fluid removal by diuresis reduces preload), preload = initial morphine like effect that induces transient venodilation leading to a fall in cardiac filling pressures and decreased pulmonary congestion prior to onset of diuresis mediated by enhanced release of prostaglandins. Furosmide/bumetanide/torsemide. AE: symptomatic hypotension, hypokalemia, metabolic alkalosis, acute kidney injury Nitrates: for afterload reduction. Patients with hypertensive emergency, acute MR or AR Contraindications: hypotension, suspected RV infarcito, HOCM, constrictive pericarditis, intake of PDE5 inhibitors within 24 hours Nitroglycerin (TNG): venodilation --> arterial vasodilation. Nitroprusside: balanced and venous dilation Inotropes: indicated for patients with LV systolic dysfunction and low CO. Patients with cardiogenic shock to maintian systemic perfusion and preserve end organ performance until definitive therapy is instituted Contraindications: not indicated for AHF with HFpEF Dopamine: D1 receptor. low dose = splanchnic and renal dilatation which improves renal function by increasing renal blood flow and reducing venous pressure. High dose = stimulates alpha-receptors which leads to vasoconstriction Dobutamine (B1 selective agonist): increase SV and HR and thus CO. Mild decrease in SVR and pulmonary capillary wedge pressure Milrinone (PDEi): increase myocardial inotropy by inhibiting degradation of cyclic adenosine monophosphate

Question 14

What is management of chronic heart falure (HFpEF):

Accepted Answer

Treatment for HFpEF has limited and unsatisfactory data Control of pulmonary congestion and peripheral edema BP control (prevention of hypretension) HR control (prevention of tachycardia especially AF) Management of ischemia (coronary revasuclarization in CAD with ischemia) Medical MRA Diuretics: for LV diastolic dysfunction

Question 15

What is treatment of chronic heart failure (HFpEF) in children?

Accepted Answer

Correct unerlying precipitating factors: infection, electrolyte disturbance and cardiac arrhythmias Mechanical circulatory support for potentially reversible pump failure due to myocardial dysfunction: IABP, ventricular assist device Medical treatment Diuretics: furosemide + spironolactone Furosemide is potent and effective for preload reduction, spironolactone added to maintain normoK by reducing K+ in urine MoA = preload reduction which reduces the volume load on heart and the congestion of systemic and pulmonary circulations Furosemide = hypoNa/hypoK, metabolic alkalosis, hyperuricemia Spironolactone = hyperK/metabolic acidosis/endocrine abnormalities Inotrope: digoxin (enhance myocardial contractility by increasing intracellular Ca2+ as well as neurohumoral effect through decreasing central sympathetic outflow to the heart Vasodilators (ACEI/nitrates) ACEI (captopril, enalapril0 Nitrates (IV nitroprusside/nitroglycerine) Inodilators: amrinon/milrinone inhibits PDEIII which prevents inactivation of cAMP, increased cAMP elevates Ca2+ and augments contractility. Increased cAMP inactivates protein kinase in vascular smooth muscle leading to vasodilation and afterload reduction B blockers: improve cardiac contractility, increase excercise tolerance. Myocardial shielding from toxic effects of catecholamines, afterload reduction due to vasodilation

Question 16

Differentiate cardiogenic and non cardiogenic pulmomary edema

Accepted Answer

Cardiogenic pulmonary edema: increased transudation of protein poor fluid into pulmonary interstitium and alveolar space leading to decreased diffusing capacity, hypoxemia and dyspnea High pulmonary capillary pressure is responsible for abnormal fluid movement. Rise in pulmonary capillary pressure results from an increase in pulmonary venous and LA pressure Non cardiogenic pulmonary edema: presence of radiographic evidence of alveolar fluid accumulation in the absence of elevated pulmonary capillary wedge pressure (PAWP <18mmHg) Most common mechanism for rise in transcapillary filtration is an increase in capillary permeability

Question 17

When is CABG indicated over PCI for stable CAD (SIHD)?

Accepted Answer

3 vessel disease of significant stenosis >70% 2 vessel disease involving proximal LAD of significant stenosis >70% Unprotected left main disease with significant stenosis >50% --> CABG prefferred/ PCI alternative Survivors of sudden cardiac death with presumed ischemia-mediated VT --> CABG/PCI both are preferred

Question 18

What are the causes of mitral stenosis?

Accepted Answer

Rheumatic heart disease (>95%): fish mouth opening and shortening of chordae tendineae due to repetitive valve scarring. Leaflet thickening and calcification due to stress of chronic turbulent flow through a deformed valve Mitral annular calcification Congenital heart disease Rheumatological diseases (SLE, RA) Miscalleneous: infective endocarditis, carcinoid syndrome

Question 19

What are SS of mitral stenosis?

Accepted Answer

Exertional dyspnea (most common): pulmonary venous hypertension --> reduced compliance of lungs and decrease in vital capacity Decreased excercise tolerance Hemoptysis: increased pulmonary pressure and vascular congestion can lead to haemoptysis. Sudden hemorrhage due to rupture of thin walled and dilated bronchial veins when there is sudden increase in LA pressure Hoarseness: Ortners syndrome which refers to compression of recurrent laryngeal nerve by the LA enlargement Malar flush: pulmonary hypertension Fatigue: reduction of CO

Question 20

What PE findings of mitral stenosis?

Accepted Answer

Inspection: malar flush, JVP (elevated in RHF, loss of a wave if AF is present, prominent a wave (elevtaed RA pressure in pulmonary hypertension), prominent v wave (functional TR in pulmonary hypertension). Pulse: small volume due to low CO, AF due to LA enlargement Palpation Non displaced taping apex beat. Left parasternal heave: RV hypertrophy, pulmonary hypertension Auscultation Loud S1 Loud S2 due to pulmonary hypertension Opening snap Mid diastolic murmur: low pitched rumbling murmur heard maximally over apex. Louder in left lateral decubitus during expiration.

Question 21

What are SS of acute MR What is PE?

Accepted Answer

SS Cardiogenic shock: hypotension Heart failure (pulmonary edema): orthopnea, PND, dyspnea on exertion, reduced excercise tolerance Palpation Pulse: AF Pansystolic thrill Left parasternal heave due to enlarged LA Apex beat: displaced and diffuse apex beat due to LV dilatation, thrusting apex beat due to volume overload Auscultation Soft or absent MI Widely split S2: early A2 due to decreaed LV afterload, late P2 due to pulmonary hypertension Presence of S3 Pan systolic murmur: high pitch blowing holosystolic murmur maximal over apex, radiates to axilla. Louder with handgrip and softer with Valsalvas maneuver

Question 22

What Ix for mitral regurgitation and results?

Accepted Answer

CXR: LA enlargement (straightening of left heart border right double density displaced left mainstem bronchus) cardiomegaly (left ventricular dilatation) pulmonary congestion (enlargement of main pulmonary artery due to pulmonary hypertension) pulmonary vascular congestion or cephalization of pulmonary blood flow to upper lobes ECG P mitrale: broad and bifid P wave (LA enlargement) AF LVH Echocardiography: LV size and function, LA size and pulmonary arter pressure TEE or cardiac MRI indicated when transthoracic echocardiography not sufficiently informative Cardiac catheterization: indicated in primary degenerative MR if there is discrepancy between symptoms and severity of MR

Question 23

What is the most common cause of LV outflow obstruction in children and adults?

Accepted Answer

Aortic stenosis?

Question 24

What are primary causes of aortic stenosis?

Accepted Answer

Rheumatic heart disease Congenital abnormal aortic valve Degenerative calcification

Question 25

What is PE for aortic stenosis?

Accepted Answer

Palpation Carotid and peripheral pulse: small volume and slow rising Apex beat: heaving apex due to pressure overload in LVH Systolic thrill at aortic area Auscultation Presence of S4 Soft, single or reversed spliting S2 Ejection systolic murmur Early peaking murmur is mild to moderate AS, late peaking murmur is severe AS. Maximal over aortic area at right upper sternal border (RUSB), radiates to both sides of carotid artery

Question 26

What are the 5 common signs of severe AS?

Accepted Answer

Slow rising carotid pulse Reduced intensity of S2 Single or reversed splitting of S2 Presence of S4 Late peaking intensity of the murmur

Question 27

What Ix for aortic stenosis and findings?

Accepted Answer

CXR: Cardiomegaly Pulmonary edema Calcification of aortic valve leaflets and aortic root Rounding of the LV apex indicated LVH Dilation of ascending aorta: post stenotic dilatation, tissue abnormalities associated with bicuspid aortic valve ECG Primary findings in AS is the presence of LVH Assess for LA enlargement (LAE), LBBB and AF Echocardiogram Valvular anatomy and structure, maximal aortic jet velocity, mean transvalvular pressure gradient, aortic valve area, left ventricular ejection (LVEF), left ventricular ize Cardiac catheterization: indicated in patients with suspected AS but discrepency between clinical evaluation and echocardiography

Question 28

What SS for TR? What is the PE for tricuspid regurgitation?

Accepted Answer

SS related to RHF: dilated neckveins (elevated JVP), painful hepatosplenomegaly (pulsatile liver), pleural effusion, ascites, sacral edema, bilateral ankle pitting edema PE General exam: pulsatile liver, pleural effusion, ascites, sacral edema, bilateral ankle pitting edema Inspection: elevated JVP (giant v wave due to systolic regurgitation into RA), jugular vein is very pulsatile, jugular venous distension more prominent with inspiration (Kussmauls sign) Palpation: pulse (AF), left parasternal heave (RV heave) Auscultation: presence of S3, pansystolic murmur (maximal over left lower sternal border (LLSB), louder on inspiration, softer on expiration

Question 29

What Ix and findings for tricuspid regurgitation?

Accepted Answer

CXR: pleural effusion, upward displacement of diaphragm due to ascites ECG: right axis deviation, P pulmonale, RVH, RBBB Echocardiography: tricuspid valve motion, dilation of RA and RV, RV function

Question 30

Define syncope Define presyncope

Accepted Answer

Syncope = sudden transient loss of consiousness specifically caused by global cerebral hypoperfusion must often due to abrupt disease in systemic BP and Spontaneously self limited condition with recovery Inadequate cerebral blood flow is tupically of brief duration of 8-10s, loss of postural tone and subsequent gravitationally neutral position generally restores cerebral blood flow Presyncope = prodrome of light headedness without TLOC

Question 31

What is ddx of non syncopal cause of TLOC (not true syncope)?

Accepted Answer

 Neurological causes Seizure/ Epilepsy Traumatic brain injury  Endocrine disturbances Hypoglycemia Hypoxia Hypocapnia  Psychiatric causes Panic disorders Hysteria  Intoxication  Anaphylaxis

Question 32

What is the history taking for syncope?

Accepted Answer

HPI Number, frequency and duration of episodes. Multiple episodes occuring over a short period of time suggests serious underlying disorder such as intermittent high grade heart block or paroxysmal VT Onset of syncope: extended symptoms with classic prodrome associated with vasovagal form of reflex syncope. Duration of syncoep: TLOC is compatible with syncope. Prolonged loss of consiousness may indicate a seizure or conversion reaction Prodromal symptoms: light headedness/ feeling of warm or cold/ pallor/palpitation/ sweating/nausea Position before incident (supine, sitting, standing): reflex syncope commonly occurs when patient is upright and almost never supine. Syncope resulting from orthostatic hypotension occurs when change from supine to erect posture but severeal minutes may pass between arising and the collapse Activity before the incident (trigger factors) Situational syncope: coughing, sneezing, defacation, swallowing, urination, post prandial Vasovagal syncope: emotional stress, fear or intense pain Carotid sinus hypersensitivity: immediately after abrupt neck movements/head turning/shaving Cardiac syncope: during excercise Orthostatic hypotension: standing up, prolonged stanging Medical history DM: orthostatic hypotension secondary to autonomic neuropathy or apparent syncope due to hypoglycemia Hypertension: orthostatic hypotension secondary to antihypertensives Structural heart disease: CAD, VHD, congenital heart disease, cardiomyopathy Neurological disease: seizure disorder/epilepsy, migraine headaches, parkinsons disease, stroke Intoxication: alcoholism, illicit drug use Surgical history: previous cardiac surgery Drug history Diuretics Nitrates (hydralazine/nitroglycerin) Alpha blockers (terazosin) B blockers (propranolol) CCB PDE inhibiotrs (sildenafil) Antidepressants (SSRIs/ TCAs/MAOI) Antipsychotics Antiarrhythmics (Class 3): torsade de pointes Family history Sudden death at a young age <40: brugada syndrome, congenital or acquired long QT syndrome (LQTS) Familial cardiomyopathy: HOCM, arrhythmogenic right ventricular cardiomyopathy Seizure disorders Migraine headaches

Question 33

What are the leading causes of sudden cardiac death in young athletes?

Accepted Answer

 Hypertrophic obstructive cardiomyopathy (HOCM)  Arrhythmogenic right ventricular dysplasia (ARVD)  Congenital anomalies of coronary arteries  Atherosclerotic coronary heart disease (probably homozygous familial hyperlipidemia)

Question 34

What are the histological findings of renal disease induced by hypertension?

Accepted Answer

 Nephrosclerosis Macroscopic o Kidneys are shrunken and scarred Microscopic o Obsolescence of glomeruli o Interstitial fibrosis o Arterial intimal fibroplasia o Hyalinization in small arteries

Question 35

When should you refer to a specialist with hypertensive patient?

Accepted Answer

 Young hypertensive patients (< 40 years old)  Patients with secondary hypertension  Patient with severe hypertension that is difficult to control

Question 36

What combination therapy given for hyperlipidemia?

Accepted Answer

 Highly synergistic combinations Statins + Resins Stains + Cholesterol absorption inhibitors

Question 37

What non invasive invasive and invasive assessment of CAD?

Accepted Answer

Stress testing indications: d of stable ischemic heart disease, risk stratification after acute coronary syndrome, evaluate excercise tolerance, localization of ischemia Excercise tolerance test (with ECG and imaging) Pharmacological stress test (with imaging only) Imaging SPECT Echocardiography Cardiac MRI: viability assessment for patients with significant coronary artery narrowing: assess for viable myocardium in the territory affected which helps to determine if PCI or CABG will lead to an improvement in cardiac function MDCT (multidetector row CT) for coronary artery calcium score: recommended in asymptomatic patients with framingham intermediate risk for screening of CAD. Estimates the plaque burden but not % of coronary stenosis. CAC sc Coronary CT/MR angiography: anatomical assessment of coronary arteries and myocardium. Detects coronary artery stenosis and estimate % stenosis before applying invasive coronary angiography. Indicated in patients with intermedate pre test probability of CAD who are unable to perform or have equivocal result from excercise test, stress echocardiography or nuclear stress test Invasive coronary angiography (gold standard) indications High risk patients after non invasive testing Non invasive testing is contraindicated or inconclusive Survivors of sudden cardiac arrest of life threatening arrhythmia Unacceptable ischemia on guideline directed medical therapy and candidacy for revascularization

Cardiovascular system Flashcards

Atrial fibrillation, Heart failure, CAD, Valvular heart disease, Cardiogenic syncope, Hypertension, Myocarditis, IE, Rheumatic fever, Congential heart diseases, Aortic dissection, DVT, PE

Brainscape's Knowledge GenomeTM

Cardiovascular system Flashcards

Atrial fibrillation, Heart failure, CAD, Valvular heart disease, Cardiogenic syncope, Hypertension, Myocarditis, IE, Rheumatic fever, Congential heart diseases, Aortic dissection, DVT, PE

Brainscape's Knowledge Genome^TM