Cardiology Flashcards
These can be heard in mitral stenosis, except for:
A) apical holosystolic murmur radiating towards the axilla
B) low-frequency apical diastolic murmur
C) opening snap
D) loud first heart sound
A) apical holosystolic murmur radiating towards the axilla
EXPLANATION
Holosystolic heart murmurs that radiate towards the axilla and are best heard at the apex are characteristic of mitral regurgitation, therefore they cannot be heard in mitral stenosis. Severe mitral stenosis might be accompanied by tricuspidal insufficiency that can cause a holosystolic, apical murmur, but it never radiates towards the axilla. The pathomechanism behind the low-frequency, diastolic murmur is the fast, turbulent flow through the stenotic mitral valve. The opening snap (o.s.) is heard as the mitral leaflets buckle in their attempt to open and it cannot be heard when the valve is severely calcified. The loud, tapping first heard sound is especially easy to notice when the heart is in sinus rhythm and when it is introduced by a presystolic murmur.
All of the following statements about nitroglycerine are true, except for:
A) it increases intracellular cGMP levels
B) it is primarily metabolised in the liver
C) it can induce significant reflex tachycardia
D) it significantly prolongs AV-conduction
E) it can lead to postural hypotension
D) it significantly prolongs AV-conduction
EXPLANATION
Nitrates don’t alter atrioventricular conduction.
The typical features of Prinzmetal angina: A) ST segment depression during angina B) negative T waves during angina C) pathologic Q waves during angina D) elevated necroenzymes E) ST segment elevation during angina
E) ST segment elevation during angina
EXPLANATION
Prinzmetal angina is a unique type of angina pectoris that is caused by coronary spasm which can affect healthy and stenotic arteries, too. Chest pain is accompanied by ST segment elevation indicating subepicardial or transmural ischemia. ST segment depression during chest pain means subendocardial ischemia, while negative T waves are non-specific features. Pathologic Q waves and elevated necroenzymes are signs of myocardial infarction.
The most important risk factor of atherosclerosis:
A) elevated serum LDL-cholesterol level
B) elevated serum HDL-cholesterol level
C) elevated serum triglyceride level
D) elevated serum cholesterol level
A) elevated serum LDL-cholesterol level
EXPLANATION
Chronic hypercholesterolemia and changes in the LDL/HDL ratio play key roles in the pathomechanism of atherosclerosis. LDL is released into the bloodstream and the toxic metabolites of its oxidation propagate the mechanism that eventualy leads to plaque formation. Elevated LDL concentration is the most significant proatherogenic risk factor. HDL cholesterol has protective qualities. Elevated triglyceride levels are less significant but they are proatherogenic, too.
The ideal target value of serum LDL-cholesterol in a diabetic patient after myocardial infarction: A) < 1,8 mmol/l B) > 2,6 mmol/l C) < 3,5 mmol/l D) > 3,5 mmol/l
A) < 1,8 mmol/l
EXPLANATION
Total serum cholesterol and HDL/LDL ratio are main factors of atherosclerosis. The target level of LDL in very high-risk patients is below 1.8 mmol/l, lower than in primary prevention.
Upon the physical examination of a 45 year old man without any symptoms a soft systolic murmur and ejection click can be heard in 2L2. These have been known since he was a child. What is the most likely diagnosis? A) patent ductus arteriosus B) coarctation of the aorta C) ventricular septal defect D) Ebstein’s anomaly E) pulmonary valve stenosis
E) pulmonary valve stenosis
EXPLANATION
‘An organic heart disease that has been known since childhood and doesn’t cause any symptoms is most likely a mild pulmonary stenosis. Based on the physical examination and the mild signs and symptoms patent ductus arteriosus (its typical feature is a continuous murmur), coarctation of the aorta (elevated blood pressure on the upper limbs), ventricular septal defect (very loud systolic murmur) or the very rare Ebstein’s anomaly are highly unlikely diagnoses.
Correct statements about aortic stenosis, except for:
A) it causes pulsus parvus et tardus
B) it can cause syncope
C) it can cause anginalike chest pain
D) Austin-Flint murmur can be heard upon auscultation
E) it causes concentric left ventricular hypertrophy
D) Austin-Flint murmur can be heard upon auscultation
EXPLANATION
The patients’ pulse in aortic stenosis is usually parvus et tardus (slow-rising and anacrotic). A hemodynamically significant aortic stenosis might cause exercise-related syncope. The chest pain that is typically associated with ischemic heart disease might occur in significant aortis stenosis. The increased preload of the heart induces concentric left ventricular hypertrophy. Its severity can be measured with echocardiography. Severe left ventricle might cause strain signs on the ECG. The Austin-Flint murmur can be heard in aortic regurgitation and not in aortic stenosis.
Correct statements about aortic insufficiency, except for:
A) it causes pulsus celer et altus (Corrigan’s pulse).
B) it can be acute and chronic, too.
C) it usually doesn’t lead to left ventricle dilation.
D) it can be congenital.
E) it predisposes to infective endocarditis.
C) it usually doesn’t lead to left ventricle dilation.
EXPLANATION
The patients’ pulse in aortic insufficiency is usually celer et altus (rapidly increasing and suddenly collapsing). It might have a rapid onset (e.g. infective endocarditis, aortic dissection), but its chronic form is the most common. In young adults it is usually predisposed to by congenital bicuspid aortic valve. Aortic regurgitation increases the risk of infective endocarditis because the blood forcefully, turbulently regurgitates from the aorta into the left ventricle. Hemodynamically significant, chronic aortic insufficiency leads to substantial left ventricle dilation through volume overload
A regular wide QRS complex tachycardia can not be:
A) ventricular tachycardia
B) supraventricular tachycardia with bundle branch block
C) atrial fibrillation with bundle branch block
D) antidromic atrioventricular reentry tachycardia (WPW-syndrome)
E) atrial flutter with bundle branch block
C) atrial fibrillation with bundle branch block
EXPLANATION
Atrial fibrillation might have narrow and wide QRS complexes, too, but it is always an irregular rhythm. Monomorphic ventricular tayhcardia (most common in patients after myocardial infarction) has a regular rhythm with wide QRS complexes. Antidromic atrioventricular tachycardia has a regular rhythm, too. The ventricular activation happens through an accessory pathway which results in pre-excited, wide QRS complexes. Supraventricular tachycardia with (either right or left) bundle branch block always creates wide QRS complexes and has a regular rhythm. Atrial flutter might appear as regular tachycardia if it has a fixed conduction or as an irregular rhythm if the AV-block is variable.
A regular wide QRS complex tachycardia can not be:
A) ventricular tachycardia
B) supraventricular tachycardia with bundle branch block
C) atrial fibrillation with bundle branch block
D) antidromic atrioventricular reentry tachycardia (WPW-syndrome)
E) atrial flutter with bundle branch block
C) atrial fibrillation with bundle branch block
EXPLANATION
Atrial fibrillation might have narrow and wide QRS complexes, too, but it is always an irregular rhythm. Monomorphic ventricular tayhcardia (most common in patients after myocardial infarction) has a regular rhythm with wide QRS complexes. Antidromic atrioventricular tachycardia has a regular rhythm, too. The ventricular activation happens through an accessory pathway which results in pre-excited, wide QRS complexes. Supraventricular tachycardia with (either right or left) bundle branch block always creates wide QRS complexes and has a regular rhythm. Atrial flutter might appear as regular tachycardia if it has a fixed conduction or as an irregular rhythm if the AV-block is variable.
A patient was admitted to the Emergency Department because of a palpitation that started three hours earlier. On his ECG an atrial fibrillation with rapid (150 bpm) ventricular response was seen. His blood pressure was 130/90 Hgmm. In the patient’s history there wasn’t anything that indicated structural heart disease. What is the best first step in this situation?
A) pharmacological cardioversion
B) immediate electrical cardioversion
C) coronarography
D) immediate anticoagulation to prevent thromboembolism
E) cardiac stress test
A) pharmacological cardioversion
EXPLANATION
The patient is hemodynamically stable, doesn’t require immediate electrical cardioversion and long-term anticoagulation is not needed in atrial fibrillation that is only a few hours old. Exercise testing and coronarography are later diagnostic steps if ischemic heart disease is suspected. Pharmacological cardioversion is the logical first step.
Which one is the most common permanent arrhythmia? A) ventricular extrasystoles B) atrial fibrillation C) ventricular tachycardia D) supraventricular tachycardia E) junctional escape rhythm
B) atrial fibrillation
EXPLANATION
The prevalence of atrial fibrillation is 0.4-14% depending on the age, which means that it the most common permanent (longer than 30 seconds) arrhythmia. Everyone has ventricular extrasystoles but they are not permanent. The other arrhythmias aren’t nearly as common as atrial fibrillation.
A patient who has been taking amiodarone for a long time was prescribed a fluoroquinolone antibiotic because of a respiratory infection. She had recurring, short-term syncopes that had never occurred before. Which one is the most likely cause of the syncopes?
A) hypotension induced by the medications
B) torsade de pointes ventricular tachycardia induced by the medications
C) sinus bradycardia induced by the medications
D) her symptoms are not induced by her medications, it is just a coincidence
E) AV block induced by the medications
B) torsade de pointes ventricular tachycardia induced by the medications
EXPLANATION
Both Class III antiarrhythmic agent amiodarone and fluoroquinolone antibiotics can prolong the QT interval (long QT syndrome). Their concomitant administration increases the chance of polymorphic ventricular tachycardia (torsade de pointes), syncope because of ventricular arrhythmia and sudden cardiac death. At the onset of these symptoms the therapy or therapies should be immediately discontinued.
These could be the first ECG findings in the acute phase of myocardial infarction, except for: A) pathologic Q waves B) inverted T waves C) ventricular fibrillation D) ST segment elevation E) ST segment depression
A) pathologic Q waves
EXPLANATION
ST segment elevation with lasting chest pain are characteristic of ST Segment Elevation Myocardial Infarction. However, in Non-ST-Segment Myocardial Infarction the ECG findings range from ST segment depression to T wave inversion. Sometimes the first ECG recording of a severe myocardial infarction already shows ventricular fibrillation. The manifestation of pathologic Q waves takes hours, sometimes days.
Pathologic Q wave in leads II, III and aVF with isoelectric ST segment and positive T waves indicate:
A) acute ischemia
B) acute phase of a progressing myocardial infarction
C) previous myocardial infarction
D) aneurysm after myocardial infarction
E) subendocardial ischemia
C) previous myocardial infarction
EXPLANATION
The typical ECG findings of acute myocardial ischemia are ST segment elevations and depressions. ST segment depression and T wave abnormalities (changes in amplitude, inversion) indicate subendocardial ischemia. During the progression of a myocardial infarction these changes are accompanied by a decrease in R wave amplitude, the appearing of pathologic Q waves and T wave inversion. In the recovery phase of the myocardial infarction the ST segment becomes isoelectric and in most cases the T wave normalizes, too. The pathologic Q wave is permanent. If the ST segment stays elevated for more than 2-3 weeks after the onset of the symptoms, a left ventricle aneurysm is likely.
In the diagnostic workup of a 60 year old patient with a history of smoking who has chest pain at exertion the first step should be: A) stress echocardiography B) exercise test C) stress perfusion scintigraphy D) Holter ECG monitoring E) stress MRI
B) exercise test
EXPLANATION
The patient’s symptoms are most likely to be caused by significant coronary artery disease. Unless stress testing is contraindicated, an exercise test should be the next step. If significant ST segment changes appear during the test, then an invasive diagnostic procedure is necessary. If the results of the stress test are questionably or the symptoms are atypical, diagnostic imaging tests (echocardiography, coronary CT angiography) or stress tests with imaging (stress echocardiography, stress MRI) should be considered. Holter ECG is not suitable to detect significant coronary artery disease, this test is only recommended if we need additional information (e.g. the duration of ischemic burden, possibility of Prinzmetal angina).
The best first-choice drug for bradycardia during myocardial infarction is: A) isoproterenol B) theophyllin C) atropine D) dobutamine
C) atropine
EXPLANATION
Myocardial infarction, especially posterior wall infarction often induces bradycardia. These usually respond well to atropine since they are partially caused by an increase in vagal tone. Sympathomimetic drugs should be avoided because they raise the myocardial oxygen demand which is unfavorable in ischaemia. Although diaphyllin elevates the heart rate but it should be avoided in myocardial infarction because of its proarrhythmogenic effect.
Which disease(s) cause(s) systolic hypertension?
1) aortic insufficiency
2) thyreotoxicosis
3) beriberi
4) atherosclerosis
A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
E) All four answers are correct
EXPLANATION
Patients with aortic insufficiency have increased cardiac output because of the regurgitated volume. In thyreotoxicosis the thyroid hormone accelerates the circulation which also leads to a higher cardiac output. Beriberi (vitamin B1 deficiency) can induce a special form of dilated cardiomyopathy with extremely high cardiac output, so all of these conditions can lead to systolic hypertension. Arteriosclerosis causes systolic hypertension through the increased vascular resistance.
Aortic aneurysm can be caused by: 1) arteriosclerosis 2) Marfan’s syndrome 3) vascular syphilis 4) giant-cell arteritis A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All of the answers are correct
A) Answers 1, 2 and 3 are correct
EXPLANATION
Arteriosclerosis, Marfan’s snydrome and vascular syphilis can all cause aortic aneurysm. All of these diseases damage the arterial wall’s tunica media that leads to its weakening, the loss of its elastic elements and the consequent dilation (aneurysm). Aneurysm formation is unusual in giant-cell arteritis, its characteristic feature is the throbbing pain of the temporal arteries.
Secondary cardiomyopathy can be caused by: 1) hyperthyroidism 2) beriberi 3) amyloidosis 4) glycogenosis A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
E) All four answers are correct
EXPLANATION
Secondary or specific cardiomyopathies can be caused by endocrine disorders, e.g. hyperthyroidism (dilated cardiomyopathy); deficiency diseases, e.g. beriberi (vitamin B1 deficiency) might induce dilated cardiomyopathy while amyloidosis can precipitate restrictive infiltrative cardiomyopathy; and metabolic (storage) diseases, like glycogenosis can lead to hypertrophic-restrictive secondary cardiomyopathy.
ACE inhibitors: 1) decrease blood pressure 2) decrease aldosterone levels 3) increase bradykinin levels 4) stop the deterioration of the left ventricle ejection fraction A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
E) All four answers are correct
EXPLANATION
Due to the inhibition of the ACE the serum level of angiotensin II decreases in parallel with an increase in the production of bradykinin and a reduction in blood pressure. In heart failure the increased pre- and afterload lead to the gradual dilation and remodeling of the left ventricle and its ejection fraction progressively deteriorates. Treatment with ACE-inhibitors decelerates this process.
Which diuretic side effect combination(s) is/are correct? 1) furosemide - hyperuricemia 2) chlortalidone – ototoxicity 3) spironolactone – gynecomasty 4) etacrynic acid - hyperuricemia A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
B) Answers 1 and 3 are correct
EXPLANATION
Furosemide and chlortalidone can occasionally provoke gout by reducing uric acid excretion. Spironolactone can cause gynecomasty through its antialdosterone effect. Etacrynic acid (and furosemide) therapy can lead to temporary, and in some cases permanent hearing loss.
Treatments that reduce morbidity and mortality after myocardial infarction (secondary prevention): 1) beta-blockers 2) antiplatelet drugs 3) HMG-CoA reductase inhibitors 4) ACE inhibitors A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All of the answers are correct
E) All of the answers are correct
EXPLANATION
Heart-rate-lowering beta-blockers reduce both mortality and (through their antiarrhythmic effect) the risk of sudden cardiac death in patients after acute myocardial infarction. They also reduce the oxygen demand of the myocardium, decrease myocardial ischaemia and are especially recommendatory in cases of hypertension and ventricular arrhythmias. It has also been proven that inhibition of platelet aggregation has a favorable effect on survival, microcirculation, vasoconstriction and atherogenesis. Inhibition of HMG-CoA reductase: by lowering serum cholesterol statins mitigate and even reverse atherogenesis. Several clinical trials proved that reducing serum total cholesterol, LDL and triglycerides (all major risk factors of ischaemic heart disease) improve the survival and quality of life of patients suffering from coronary artery disease. 4S (Scandinavian Simvastatin Survival Study) was the first large-scale (n=4444) clinical trial to prove their favorable effect on survival: mortality decreased by 30%, coronary-mortality by 42% and myocardial infarction by 37% during the 8-year follow-up. ACE inhibitors: their most important effect is to stop the postinfarction remodeling, therefore (unless contraindicated) all patients who have suffered a myocardial infarction should be given ACE inhibitors as soon as possible.
Diagnostic options to determine myocardial viability: 1) low-dose dobutamine stress test 2) positron-emission tomography 3) stress perfusion scintigraphy with Tl-201 reinjection 4) Doppler ultrasound A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
A) Answers 1, 2 and 3 are correct
EXPLANATION
Methods to measure the metabolism of the myocardium in vivo: positron-emission tomography (PT) and thallium-201 myocardial perfusion scintigraphy. Low-dose dobutamine stress helps the motion of the viable myocardium walls through its positive inotropic effect. PET is highly sensitive and specific in detecting perfusion-metabolism mismatches. Myocardial perfusion scintigraphy using Tl-201 reinjection is highly sensitive but it is less specific while dobutamin stress testing is very specific but has a slightly lower sensitivity. Conventional Doppler ultrasound isn’t suitable for determining myocardial viability, but the newer tissue Doppler ultrasound seems to be promising.
Diagnostic tests with the ability to detect asymptomatic angina pectoris (silent ischemia): 1) dobutamine stress echocardiogram 2) Holter ECG monitoring 3) exercise test 4) ABPM A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All of the answers are correct
A) Answers 1, 2 and 3 are correct
EXPLANATION
The first-line diagnostic test of ischemic heart disease is exercise testing. If the results are questionable or if the test is contraindicated then the next step is stress echocardiography using dobutamine. Ischemic signs (ST segment depression or wall motion abnormalities) without any symptoms indicate silent ischemia. Holter ECG monitor can be used to detect episodes of angina to determine a silent/symptomatic ratio. Ambulatory Blood Pressure Monitoring, a 24-hour measurement of blood pressure is obviously unable to detect silent ischemia.
Treatment option(s) of heart failure: 1) pharmacotherapy 2) heart transplant 3) mechanical circulatory support devices 4) cardiac resynchronization therapy A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
E) All four answers are correct
EXPLANATION
Early stages of heart failure are treated conservatively with medication. However, in severe heart failure non-pharmacologic treatment options (in addition to pharmacotherapy) have recently been given a more important role. Examples are cardiac resynchronization therapy, mechanical circulatory support devices and as a final option, heart transplant.
Drugs that lower serum cholesterol level: 1) rosuvastatin 2) ezetimibe 3) atorvastatin 4) ivabradine A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All of the answers are correct
A) Answers 1, 2 and 3 are correct
EXPLANATION
Statins can reduce serum cholesterol levels. They work by inhibiting the HMG-COA reductase and the intracellular cholesterol production. Currently the most effective statins are rosuvastatin and atorvastatin. Ezetimibe lowers serum cholesterol levels by blocking the absorption of cholesterol in the small intestine. They are mostly used in combination with statins. Ivabradine acts by blocking the If (funny) Na-K channel, it is used to decrease resting sinus heart rate in ischemic heart disease
Characteristic features of Prinzmetal angina:
1) it usually occurs at dawn during rest
2) ST segment elevation can be seen during angina
3) it is caused by coronary spasm
4) it should be treated with calcium-channel blockers
A) Answers 1, 2 and 3 are correct
B) Answers 1 and 3 are correct
C) Answers 2 and 4 are correct
D) Only answer 4 is correct
E) All of the answers are correct
E) All of the answers are correct
EXPLANATION
Prinzmetal angina is caused by coronary vasospasm that can affect healthy and stenotic arteries, too. The symptoms usually present in the early morning at rest and temporary ST segment elevation can be seen on the ECG.
Might mimic the ECG findings of myocardial infarction: 1) pericarditis 2) pancreatitis 3) myocarditis 4) pulmonary embolism A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
E) All four answers are correct
EXPLANATION
ST segment elevation in the precordial leads is not exclusive for myocardial infarction. Pericarditis and myocarditis can cause ST elevation (sometimes in every lead), too. Acute pancreatitis might present with aspecific ST segment and T wave abnormalities. Pulmonary embolism can mimic the ECG findings of a posterior wall myocardial infarction.
Enzyme(s) that is/are elevated in myocardial infarction: 1) creatine kinase (CK-MB) 2) lactate dehydrogenase 3) troponin 4) alkaline phosphatase A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
A) Answers 1, 2 and 3 are correct
EXPLANATION
CK-MB, troponin and LDH serum levels can be used in the diagnostic workup of myocardial damage. Elevated alkaline phosphatase levels indicate gastrointestinal, bone or hematologic diseases.
A 55-year-old patient with a history of hypertension has been rushed to the emergency room because of severe chest pain and ST segment elevation. Possible diagnosis/diagnoses: 1) peptic ulcer 2) acute myocardial infarction 3) mitral valve prolapse 4) aortic dissection A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All of the answers are correct
C) Answers 2 and 4 are correct
EXPLANATION
Chest pain with ST elevation might be the sign of myocardial infarction and aortic dissection, too. Peptic ulcers and mitral valve prolapse can both cause chest pain but they don’t cause ST segment elevation.
A 70-year-old patient had an anterior wall myocardial infarction three weeks ago. He suddenly develops a fever and complains of chest pain. On his ECG there are no new Q waves and his CK-MB level is normal. What is/are the most likely diagnose(s)? 1) myocardial reinfarction 2) pulmonary embolism 3) lobar pneumonia 4) Dressler’s syndrome A) Answers 1, 2 and 3 are correct B) Answers 1 and 3 are correct C) Answers 2 and 4 are correct D) Only answer 4 is correct E) All four answers are correct
D) Only answer 4 is correct
EXPLANATION
The onset of Dressler’s syndrome is typically three weeks after myocardial infarction and it presents with recurring chest pain and fever but cardiac marker levels are usually normal. In reinfarctions and pulmonary embolism cardiac enzymes are often elevated. Although lobar pneumonia can not be ruled out, in the combination of the above-mentioned findings you should always think of Dressler’s syndrome at first instead of other, less likely diagnoses.
