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Cardiology PANCE (uworld) Latest
Exam |Complete Version 2025/2026|
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cardiac drug which blocks sympathetic activity? beta blockers (decrease in rate of impulse generation at the AV node and increases the refractory period at the AV node). Does not increase QRS interval this drug increases intracellular sodium and thus reduces sodium calcium exchange activity. enhances vagal tone and decreases conduction through the AV node? digoxin drug which is occasionally used in the treatment of atrial fibrillation. This drug acts by blocking sodium channels and inhibits the initial depolarization phase of the action potential. This drug has a slow rate of dissociation from the sodium channel (where it blocks), thus, then a patient has increased heart rate they may experience prolongation of the QRS? class I arrhythmia drugs (flecainide) wide a fixed splitting of the second heart sound? atrial septal defect is frequently seen in marfan syndrome? mitral valve prolapse (mid to late systolic murmur)
opening snap heard in early diastole? mitral stenosis. is normal in young healthy peoples? third heart sound (low frequency diastolic sound) but is a bad sign if the patient has dilated ventricles. (mitral valve prolapse resulting in regurgitation and heart failure may produce a third heart sound) A complication of aortic dissection? aortic regurgitation (presents with an early diastolic murmur)
**- pulsatile tinnitus
- stroke/TIA
- flank pain
- recurrent headache
- subauricular systolic bruit
- abd bruit affects renal and internal carotid arteries* fibromuscular dysplasia 90% of pts are women. causes hypertension and headache. Patient may be young. tx: ACE and ARBS are first line HTN is caused by renal artery stenosis in these patients. syncope with activity? aortic stenosis these patients will also have pulsus parvus et tardus (slow rising and low amplitude pulse) hypotension, tachycardia, distended jugular veins, and respiratory variation in systolic blood pressure (pulses paradoxus) are consistent with? cardiac tamponade: compression of the heart by fluid in the pericardium. >20mmhg systolic between arms? aortic dissection acute treatment is labetolol. or intravenous like esmolol. give morphine for pain control. sodium nitroprusside if SBP>120mmhg. urgent surgical repair.
what happens to patients who have systolic CHF? in patients with congestive heart failure, activation of the renin-angiotensin-aldosterone system (RAAS) and production of angiotensin II causes preferential vasoconstriction of efferent arterioles, which increases intraglomerular pressure to maintain adequate glomerular filtration rate (GFR). what is an early finding in patients with autosomal dominant polycystic kidney disease? hypertension and is often present before any significant decline in kidney function. tx: ultrasound to confirm. initiate ACE inhibitors. traumatic injury to the thigh (or trauma in general) with resultant development of tachycardia, left ventricular hypertrophy (pt of maximal impulse is displaced left slightly/will have soft systolic murmur)? this is high output heart failure. the increased preload is dilating left ventricle. This is due to a arteriole venous fistula AVF which has formed in the thigh. extremities lack oxygen causing the heart to work extra hard. (this is also see congenitally). *the shunting of the blood from the arterial to the venous side causes increased cardiac preload. Patient then develops heart failure because the circulation is unable to match tissue demand for O2. primary orthostatic hypotension is caused by? decreased baroreceptor responsiveness. and is defined as postural decrease in systolic of 20mmhg OR 10mmhg diastolic what are some causes of pericarditis?
- cardiac surgery
- radiation therapy
- idiopathic or viral pericarditis
- tuberculous pericarditis (traveler) impairs ventricular filling during diastole, causing patients to experience symptoms related to decreased cardiac output (fatigue and dyspnea on exertion), and signs of venous overload (elevated JVP, ascites, pedal edema) constrictive pericarditis *low voltage QRS on ECG or atrial fibrillation
wide split S2? pulmonary hypertension which often occurs in COPD and pulmonary emboli patients. (cor pulmonale) prolonged expiration with wheezing indicates? bronchoconstriction *aspirin and beta blockers are common triggers for bronchoconstriction in asthma patients. what beta blockers are considered somewhat safe in asthma patients? beta 1 blockade/cardioselective (safe): metoprolol atenolol bisoprolol nebivolol unsafe/beta 1 & 2 blockade: propranolol nadolol sotalol timolol sharp pleuritic chest pain which is relieved by leaning forward? acute pericarditis (pericardial friction rub may be present on cardiac auscultation) dyspnea and bronchoconstriction are not common.
**- dullness to percussion of the chest wall
- decreased breath sounds
- decreased movement of the ipsilateral chest wall** pleural effusion **- chest pain
- tachypnea (abnormally rapid breathing)** pulmonary embolism **- hypotension
- JVD
- clear lung feilds** right ventricle myocardial infarction how do you manage ST segment elevation? STEMI ST segment myocardial infarction: (most likely anterior descending coronary artery).
- oxygen
- chewed aspirin
systolic stenosis. In order to differentiate the systolic murmur of aortic stenosis from that of hypertrophic cardiomyopathy you should have the pt squat (doing so increases the amount of blood in the left ventricle and aortic stenosis murmur with be more loud due to more blood flowing across the abnormality ). Hypertrophic cardiomyopathy lessens with squating (more filled chameber/can't hear walls hitting each other) and increases with standing (chamber is less full and you hear the slapping of the walls). early diastolic murmur? aortic regurgitation which is associated with water hammer pulse because the blood falls back into the chamber during diastole. a fall of systemic blood pressure by more than 10mmhg during inspiration? pulses paradoxus and is associated with cardiac tamponade what drug causes hypokalemia and hypomagnesemia? furosemide. these electrolyet abnormalities may lead to wide complex tachycardia. if the patient is also on digoxin then hypokalemia may potentiate side effects of digoxin which also includes tachycardia. pt has resistant hypertension defined as 3 htn drug regimen with at least one diuretic at maximum tolerated dose. check for a secondary cause of HTN expecially if the pt has wide-spread atherosclerosis. systolic-diastolic abdominal bruit has a high specificity for renovascular hypertension
**- life threatening arrythmias
- anorexia, nausea, vomiting
- abdominal pain
- color vision alterations** digoxin toxicity what drug increases the serum levels of digoxin and can lead to digoxin toxicity if given concurrently with digoxin? amiodarone or (verapamil, quinidine, and propafenone) it is recommended that digoxin be reduced by 25 - 30% when starting amiodarone severe periumbilical abd pain? mesenteric ischemia (these findings will be out of proportion to exam findings) **- HTN
- Marfan syndrome
- cocaine use all cause?**
aortic dissection
20mmg Hg difference in systolic blood pressure in arms what is a common complication of ascending aortic dissection? aortic regurgitation from retrograde extension of the tear into the aortic valve. (early decrescendo diastolic murmu) When an aortic dissection propgates into the pericardial space and causes bleeding the patient will develop? cardiac tamponade:
- hypotension
- pulsus paradoxus
- elevated jugular venous pulses with clear lung fields
- cardiogenic shock how do nitrates help angina pectoris? systemic vasodilation of the arteries and veins. by doing this, veins dilate and thus preload reduces; this then lowers left ventricular end diastolic volume. this reduces wall stress and thus there is less myocardial oxygen demand. arteries are also affected by nitrates but to a lesser degree then veins. infact, relaxation of the arteries results in reduced afterload but not to the same extent as reduced preload caused by vein dilation. (administering nitrates may result in reflex tachycardia and thus you should give beta-blockers to help with this) what are the common etiologies of cor pulmonale?
- copd
- interstitial lung disease
- pulmonary vascular disease (thromboembolic)
- obstructive sleep apnea **- peripheral edema
- increased jugular venous pressure with prominent a wave
- loud S
- right sided heave
- pulsatile liver from congestion
- tricuspid regurgitation murmur** cor pulmonale: *the murmur is holosystolic at the lower left sternal border (tricuspid regurgitation) *definitive diagnosis is done with right heart catheterization showing elevated pulmonary artery systolic pressure greater than 25mm hg. **- inciting event, stress or prolonged standing
- prodrome of pallor, nausea, and diaphoresis
- consciousness regained rapidly (less than one minute)**
**- abd distension with ascites
- lower extremity edema** this is tricuspid regurgitation leading to right sided heart failure. *holosystolic murmur will be heard at the lower left sternal border. holosystolic murmur heard at the cardiac apex? this is involvement of the mitral valve. systolic ejection murmur best heard at the upper left sternal border? pulmonic valve stenosis. (congenital defect and is often asymptomatic; however, some patient's develop right sided heart failure). tricuspid regurge is best heard when there is? increased preload causes a palpable thrill and a harsh holosystolic murmur with maximal intensity at the left midsternal border? ventricular septal defect when is renin produced and in response to what? RAAS or renin-angiotensin-aldosterone system can play a significant role in HTN. Renin is produced in response to hypotension (by the juxtaglomerular cells (in the kidney). Renin cleaves angiotensinogen into angiotensin I, which is converted into angiotensin II by angiotensin-converting enzyme (ACE) in the lungs. Angiotensin II is a potent vasoconstrictor that also promotes aldosterone production in the adrenal cortex. Aldosterone acts on the collecting ducts to increase renal sodium and water reabsorption. this will then increase blood pressure, total body sodium and water, and blood volume. Therefore, any drug which blocks the effect of angiotensin II or aldosterone enhances natriuresis. Aliskirne is a direct renin inhibitor (unlike ACE inhibitors which block ACE in the lungs). STEMI treatment? treat with emergency catheterization or thrombolysis NSTEMI treatment? treat with appropriate anticoagulation **chest pain with:
- estrogen therapy
- smoking
- family history concerning for?** acute coronary syndrome ACS. ACS usually presents with retrosternal chest pain radiating to the let arm with associated diaphoresis, nausea, and or vomiting.
*patients with stable ACS should receive aspirin (reduces the rate of MI). Patients with ACS findings on ECG should be treated with heparin. Heparin is used for patients who have positive ECG and cardiac markers for MI/ST seg elevation)
**- peripheral edema
- ascites
- elevated jugular venous pressure JVP
- clear lung fields** right sided heart failure *other features will include hepatic congestion with hepatomegaly and eventual progression to cirrhosis (cardiac cirrhosis) these patients may have a pericardial knock (mid diastole) *this is not cor pulmonale because it refers to right ventricular failure from pulmonary hypertension due to severe lung disease such as COPD, pulmonary vascular disease, or obstructive sleep apnea. (there will be a dilated right ventricle with tricuspid regurge) Large MI involving the left anterior descending coronary artery. what complication will occur 3-5 days post op? hingt: harsh holosystolic murmur with palpable thrill at the left sternal border. interventricular septum rupture *acute cardiogenic shock: pulmonary edema, hypotension, confusion due to poor organ perfusion, jugular venous distension and hepatomegaly. patient has recurrent substernal chest pain elicited by strong emotion and resolving after several minutes?. this eve stable angina workup: do a stress test physically or by pharmacotherapy this therapy allows for evaluation of CAD (use a coronary artery vasodilator like adenosine or dipyridamole for pharm version. if there is a stenotic lesion; there will be a reduction in radioactive isotope uptake compared to wide open blood flow. (appears as a ischemic defect on myocardial perfusion imaging) HTN and schistocytes in a patient with severe hypertension? they have systemic sclerosis (scleroderma). The schistocytes are caused by blood being squeezed through the renal architecture. They will also have tightened skin (HTN symptoms will be blurry vision, headache, nausea). UA will show mild proteinuria. what are the guidelines for a smoker and AAA risk? men aged 65-75 who have smoked cigarettes at any time require a one time abd ultrasound. repair of large AAAs is advised if they are 5.5cm or greater. (men) not women apparently. **- crescendo-decrescendo murmur on inspiration
- systolic ejection click and widened split of S**
- S
**- delayed and diminished carotid pulse (pulsus parvus et tardus)
- single and soft S
- harsh ejection (crescendo-decrescendo murmur in second right intercostal space with radiation to carotids what is the work-up?** this is indicative of aortic stenosis *transthoracic echocardiogram should be obtained in all patients with syncope (these symptoms he will have syncope due to pulsus parvus et tardus) he will likely need aortic valve replacement. right second intercostal space exercise stress testing is contraindicated in those with? suspected aortic stenosis. what is the treatment for digoxin overdose? fab antibody what drug has no mortality benefit in chf? digoxin: cardiac glycoside that helps increase the heart's contractility. It is therefore very useful for improving CHF symptoms like dyspnea and fatigue. Though it has no mortality benefit, digoxin has been shown to decrease hospitalization in patients with CHF. what is a first line drug in CHF? Captopril is an ACE inhibitor shown to improve mortality in CHF. It is a first line therapeutic agent what drug class provides symptomatic relief in CHF but no survival benefit? loop diuretics except for spironolactone. spironolactone was associated with a 30% reduction in overall mortality. ACE inhibitors, ARBs, beta blockers, and spironolactone all confer a survival benefit in? CHF while digoxin and furosemide (loop diuretics) can reduce CHF symptoms and hospitalizations, they do not improve survival. **- ST depression
- troponin elevation
- chest pain** NSTEMI *tx: cath lab for stent. initiate:
- duel antiplatelet therapy with aspirin and p2y12 receptor blockers (clopidogrel, prasugrel, ticagrelor)
- ACE inhibitor
- Beta blocker
- HMG-CoA reductase inhibitor
- aldosterone antagonist like spironolactone (if they have left ventricular ejection fraction below 40% dm type II) less than 1 ankle brachial index is suggestive of? peripheral artery disease PAD. <1 ankle brachial index predicts that the patient will have a heart attack within the next five years. especially if combined with intermittent claudication (pain on exertion of left leg which is why he got the test done in the first place). **- dry cough
- exertional dyspnea
- holosystolic murmur over the cardiac apex
- atrial fibrillation** left ventricular dysfunction presented as mitral regurgitation. this holosystolic murmur at the apex will radiate to the axilla. The most common symptoms of mitral regurgitation are exertional dyspnea and fatigue which are created by decreased cardiac output and increased pressure on the left atria. This increased pressure causes pulmonary congestion resulting in a dry cough and if bad enough, result in peripheral edema. what are some causes for mitral regurgitation? rhematic heart disease, infective endocarditis, or trauma. the other boring causes are: ischemic heart disease or hypertrophic cardiomyopathy. ascending aortic aneurysm can be associated with? aortic regurgitation, which would result in a diastolic murmur. **exertional dyspnea (as seen in mitral regurgitation) but also:
- elevated jugular venous pressure
- pulsatile hepatomegaly
- fluid overload** constrictive pericarditis diastolic murmur vs a systolic? systolic murmur of importance would be mitral. diastolic murmurs are:
- aortic regurgitation (maybe aortic aneurysm)
- tricuspid stenosis what is the most common cause of tricuspid stenosis? rheumatic heart disease *diastolic murmur. used to treat atrial fibrillation often?
beta blockers and aspirin. (reduce myocardial contractility and heart rate) stable angina is defined as chest discomfort occurring predictably with exertion and relieved with rest and it is a result of mismatch of myocardial oxygen supply and demand. beta blockers will reduce the myocardial oxygen demand. (often these patients are also given nitroglycerin PRN) used in the management of ventricular arrhythmias in patients with coronary artery disease and ischemic cardiomyopathy but has adverse effects which affect two different organ systems?
- pulmonary function
- thyroid. *chronic interstitial pneumonitis most commonly but also causes ARDS (occurs years to years after initiation of the drug). get a baseline chest radiograph and pulmonary function test and look for cough, fever, dyspnea). is a nonselective beta and alpha-adrenergic blocking agent often used in patients with congestive heart failure due to left ventricular systolic dysfunction? carvedilol Patient is having acute ST segment elevation MI but you note flash pulmonary edema (decompensated congestive heart failure with bradycardia) what do you not give before he goes to the cath lab? beta blockers should be avoided in this scenario. beta blockers are standard therapy in myocardial infarction but should be avoided in patients with decompensated congestive heart failure or bradycardia. give furosemide what do you give in stabilization of acute ST-elevation MI before they go to cath lab?
- supplemental o2 for dyspnea
- aspirin 325mg
- p2y12 clopidogrel
- nitrates (sublingual)
- beta blocker (unless hypotensive, bradycardia, chronic heart failure, heart block)
- high dose statin (atorvastatin 80mg)
- anticoagulation A potential late complication of radiation therapy? constrictive pericarditis which may present up to 10-20 years later. constrictive pericarditis often leads to right sided heart failure with cardiac cirrhosis from congestion, elevated JVP, and pericardial knock (mid diastolic sound). Tx: pericardectomy crescendo-decrescendo murmur heard at the lower left sternal border? hypertrophic obstructive cardiomyopathy. pulmonary capillary wedge pressure is increased when? cardiogenic shock due to MI. blood does not flow through the left ventricle so it backs up in the left antria where it then raises pulmonary capillary wedge pressure.
wondering P waves? third degree heart block which requires pacing. refer patient for a pacemaker. fibrinolytic therapy is not indicated unless there is? ST segment elevation imaging modality for suspected aortic dissection or pulmonary emboli? chest CT elevated erythrocyte sedimentation rate and chest pain suggests? rheumatic etiology such as pleuritis due to SLE *they will also have rash and joint pains chest pain which is reproducible with palpation? costochondritis suspected pericarditis testing modality? transthoracic echocardiogram to check for effusion. patient will feel worse when laying down or when breathing. when does post MI pericarditis occur and what is the tx? This is dressler syndrome. it occurs in the first several days after MI. patient will have pain with deep inspiration and will feel better when leaning forward. tx: is NSAIDs and avoid anticoagulation so as to avoid a hemorrhagic pericardial effusion.
**- hepatomegaly
- macroglossia
- waxy skin thickening
- nephrotic syndrome (protein in urine)** amyloidosis: deposition of insoluble fat protein fibrils in various organs and tissues throughout the body. causes restrictive cardiomyopathy. (restrictive cardiomyopathy usually causes right sided heart failure). you will know there is right sided heart failure if the lungs are not involved. If the lungs were involved it would be core pulmonale. Atrial fibrillation which is refractory to medical management should receive? radio catheter ablation targeting the pulmonary veins which is where the irregular synapse is occurring. reentrant circuit around the tricuspid annulus results in? atrial flutter while atrial fibrillation involves the pulmonary veins. what should be initiated in all patients within 24 hrs of an MI?
