Cram The Pance - S1E24 50 High Yield Cardiology Questions

Episode Date: May 28, 2021

50 high yield cardiology questions to help you prepare for your Pance, Panre and Eor’s. ►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so this week's podcast is going to be a little bit different than the normal format. What this podcast is going to be dedicated to, it's going to be 50. What I feel is high yield questions for the cardiology section for the pants. And I picked two or three questions from each blueprint topic, from the NCCA blueprint for the cardiology section for the pants. So I feel like this will be pretty useful. It's going to be, again, different than the normal format that I do. But I feel like this will help as well, especially as a quick cram before an exam, if you have a cardiology exam coming up or even before the pants. Let's get into it 50 quick questions on cardiology for the pants.

So let's start with number one. Describe the ECG findings on a patient with multifocal atrial tachycardia. Describe the ECG findings on a patient with multifocal atrial tachycardia. It's going to be a heart rate above 100 and P waves with at least three different morphologies. You can compare that to wandering atrial pacemaker where the only difference is the heart rate is less than 100. You can remember that by thinking wandering atrial pacemaker. I just think of always somebody just wandering atrial pacemaker. around slowly like an old person wandering around slow it's a slower heart rate that's the only

difference so multifocal each will attack cardia over 100 and peeves of at least three different morphologies number two what is the most common type of cardiomyopathy that's dilated cardiomyopathy over 90% of the cases question three what are the most what are the four known classes or medications known to reduce mortality risk in patients with heart failure four classes to reduce mortality risk in heart failure Remember bash. It's going to be beta blockers, ACE inhibitors, spiroinolactone, and hydrolyzine with nitrates. Remember, of course, your ACE inhibitors, anything within that, those subclasses, the ARBs, the angiotensor receptor, enduotensor 2 receptor blockers, or even your ARNI, which is in Tresto. Number four, what is the first line treatment for acute paracarditis? First line treatment for acute paracarditis is going to be ns. So ibuprofen, aspirin, endomethcin. Question 5, describe the three classic findings on ECG in a patient with Wolf Parkinson White. Three classic findings on ECG and a patient with Wolf Parkinson White is going to be Delta Wave.

And this is due to the slow muscle fiber to fiber muscle contraction and it leads to this upstroke of the QRS and it's a slurred upstroke. So delta wave is number one, which is that slurred QRS. Number two is going to be short PR interval less than 0.12 seconds. And this is due to the rapid AV conduction through that accessory pathway that bypasses the AV node and then finally a Y QRS complex So three classic findings will parkinson white delta wave short PR interval Y QRS complex Question six what is Kusmal sign? What is Kus small sign? It's a paradoxical rise in jugular venous pressure with inspiration Which is opposite of what normally happens normally JVP falls with inspiration to the reduced pressure and the expanding thoracic cavity

But due to some forms of right ventricular dysfunction, impaired filling, the opposite occurs, and it can be seen in restrictive cardiomyopathy, constrictive paracchariditis, and right ventricular infarction. So number seven, what is the first line pharmacologic agent for treatment of hypertrophic cardiomyopathy? First line med for hypertrophic cardiomyopathy. It's going to be beta blockers. It reduces the heart rate at rest and exercise permits improve left ventricular filling,

which reduces that left ventricular outflow obstruction. It can also alleviate left. It can also reduce the myocardial oxygen consumption, which improves the chest pain in these patients. So beta blockers first line met for hypertrophicardiomyopathy. Number eight, what is the most common type of congenital heart disease? Most common type of congenital heart disease. That's ventricular septal defect.

Number nine, what is the first line treatment for torsades to points, which is that variant of polymorphic VTAC. So first line treatment for Toursaz de point, I don't know if it's DePontes or DePoints. It's going to be IV mag. IV magnesium sulfate. The magnesium works because it decreases the influx of calcium, which suppresses that abnormal early depolarization. So Torsaz de points, remember IV magnesium sulfate.

Number 10, describe the murmur in patent ductis arteriosis. Remember PDA. continuous machine-like murmur. It's best heard in the left upper sternal border, the pulmonic area. So remember, PDA is like a little palm pilot, little machine. So you have that continuous machine like murmur. Number 11, in patients with orthostatic or postural hypotension, in which symptoms are not adequately controlled with non-pharmacologic measures, like increased salt intake, fluid intake, what's going to be your first-line medication that you're going to use in these patients? So first-line medication in patients with orthostatic hypotension, it's going to be fluia-cortizone, which is a synthetic mineral corticoid, and the main effect of this med is to increase blood volume.

Number 12, describe the potential findings on chest x-ray and a patient with coartation of the aorta. It's going to be posterior rib-notching and a figure-3 sign. Remember that figure-3 sign is due to that pre-and-post co-citation dilatation, so you have that little indentation. there looks like a three on the x-ray so posterior rib notching figure three on the corotation of the aorta and a chest x-ray 13 what is the most common type of atrial septal defect most common type of atrial septal defect is going to be osteum secundum its most common type of ASD counts for around 75 to 80% of all cases of ASD describe the findings in bex triad which is seen in cardiac tamponade the three

findings in cardiac tampon on bex triad is going to be muffled heart sense or distant heart sounds, increased JVP, and then hypotension. Question 15. Describe the ECG findings in a patient with paracardial effusion. The ECG findings in a patient with paracardial effusion, there's two things you're looking for. The first one is electrical alternance. That's the cycling of the QRS axis. You're going to have a tall QRS, followed by a short QRS, tall, short, tall, short,

and then so on. It's because of the mechanical swinging of the heart back and forth. And then the second thing you're looking for on ECG with a patient with paracardial fusion is going to be a low voltage of the QRS complex. So you see these little tiny QRS complexes. 16. What is the most common valve involved in a patient with infective endocarditis who is an IV drug user? Most common valve patient with endocarditis is an IV drug user.

Remember, want to try drugs. That's your tricuspid valve. Want to try drugs, DRI. 17. What is the most common organism seen in subacute endocarditis, which infects damage or vulnerable valves. Most common organism in sub-acute endocarditis, that's going to be streptococcus viradans. Remember, viridans, the V stands for vulnerable valves. So you remember that sub-acute endocarditis. 18, what are Roth spots? What are Roth spots? Roth spots are retinal hemorrhages or lesions,

xenophondoscopy in patients with endocarditis. Remember that from Jane. That's Roth spots and endocarditis. What is the empiric treatment regimen for a patient with prosthetic valve endocarditis? So what is the empiric treatment regimen? Patient with prosthetic valve endocarditis? It's going to be vancomycin, gentomicin, and refampin. What is the most common clinical manifestation seen in a patient with endocarditis? Most common clinical manifestation, that's going to be fever. Persistent fever, the most common clinical manifestation.

And remember the F is fever. F stands for fever and the mnemonic from. Jane. So remember that's fever off spots, Osler nodes, murmur, Janeway lesions, anemia, nail bed hemorrhages, and emboli. 21, in an uncomplicated non-African-American patient, which four drug classes will you choose from for initial monotherapy to treat hypertension? Those four classes are going to be aces, arbs, calcium channel blockers, and thyside type diuretics. 22, what is the most common cause of secondary hypertension? Most of the most

common cause of secondary hypertension is going to be a renal vascular cause like renal artery stenosis. Remember, you're less common causes or Cushing syndrome, Fiochromocytoma, corretation of the aorta but if you're talking about the most common cause of secondary hypertension, it's going to be a renal vascular cause, normally renal artery stenosis. 23, what blood pressure reading is stage one hypertension defined as. So stage one hypertension is going to be 130 to 139 systolic and or it can be either one 80 to 89 diastolic. So if they're anywhere from 130 to 139 and 80 to 89 diastolic, that's going to be stage one hypertension.

And then, of course, remember, stage two is anything 140 or higher and or 90 or higher diastolic. Question 24. What are the two medication classes that should be used in a patient with a history of diabetes or chronic kidney disease? So what are the two medication classes that should be used in a patient with a history of diabetes or chronic kidney disease. These are the two hypertension medications, of course. That's going to be your ACEs or your ARBs. And remember the reason behind this is ACEs and ARBs have this

vaso dilatory effect on the efferrant arterial, and that decreases glomerator capillary pressure, and that's why you use ACEs and ARBs. They decrease the progression of diabetic kidney disease. So those are the hypertensive medications you want to use in those patients. 25 and a patient, we're halfway there, and a patient with hypertensive emergency, describe the rate of reduction for blood pressure over 24 hours. Of course, a patient with no history of ischemic stroke, aortic dissection, you're going to decrease your mean arterial pressure by 10 to 20% in the first hour, and then an additional 5 to 15% over the next 23 hours.

And really quickly, this is just because if we decrease the blood pressure too quickly, and these patients who have chronic hypertension, their organs and vascular beds have been accustomed to this high-pressure state, and if you pull down that blood pressure too fast, It can actually lead to ischemia in the vascular of these organs. So question 26, what hypertension or which hypertension medication class should be used cautiously in diabetic patients. So which hypertensive medication class should be used cautiously in diabetic patients? It's going to be beta blockers due to the fact that they can mask the symptoms of hypoglycemia.

They suppress that adrenergically mediated symptoms like tachycardia, tremors and things like that. patients don't feel how they normally do with low blood sugar so we can kind of mask those symptoms so beta blockers avoidin diabetics if possible which medication class would be best to use in a patient with both hypertension and benign prosthetic hyperplasia so they have BPH and they have hypertension you could use alpha-1 blockers like terazosin all your zocin meds they work on both so that's a good class to use for them 28 describe the main differences between dihydropyridine and non-dihydroperidine calcium channel blockers. So the main differences between the two, dihydropyroidine only vasodilate, or your non-dihydropyrodin, vasodilate as well as influence

cardiac conduction and contractility. That's the important thing. Remember, your non-dihydropyrodines are going to be deltisem and verapamil, DNV. So you think of DNV, you think of decrease velocity of the heart. So you see those meds. You think DNV, remember, decreased velocity of the heart. They affect the contractility and the conduction of the heart, their non-deadropyridines. 29, what are the five main adverse drug reactions from ACE inhibitors? Five main adverse drug reactions from ACE inhibitors, like lysinepril, all your prills. That's going to be Chad, if you remember Chad. It's going to be cough, hypercalemia, and hyperurisemia, angioedema, and dose one hypotension.

So you remember Chad, and that's cough, hypercalemia, hyperurisemia, angioedema, and dose one hypotension. Question 30, bisoprolol, Esmalol, Atenolol, and Metoprololol are all what subclass of beta blockers? So, Besoprolol, Esmalol, Atenol, and Metoprolol are all cardioselective. They only block beta-1 receptors, and if you remember, that name spells B-E-A-M. You can think of a beam of light, and it's focused and only affects one area, only affects the beta-1 receptors. That's how I always remembered those ones. Question 31, name all of the diastolic murmurs.

All of the diastolic murmurs, if you know these, you know all your systolic, because just by method of exclusion. If it's not in this list, you know, it's systolic. So diastolic murmurs are going to be mitral stenosis, pulmonary regurgitation, aortic regurgitation, and tricuspid stenosis. If you didn't watch my murmur podcast or my murmur video, this spells Miss Prarts. So if you remember Miss Prarts died, you remember Miss Pratt. D.E.D. Diasolic. And then the MSP-R-A-R-T-S, all stand for all of those murmurs. I just went over. So it's not on that list. They're systolic. So it's easy way to remember which is which. 32 described the murmurs of, describe the murmur of aortic stenosis. The murmur of aortic stenosis is going to be systolic.

Crescendo de crescendo, meaning it goes up, peaks, and then comes back down. And it also radiates to the carotid. So that's aortic stenosis. What is the most common cause of mitral regurgis? in the USA. Most common cause of mitral regurgitation in the USA is going to be mitral valve prolapse. 34 describe Quinky's pulse. So Quinky's pulse is going to be a capillary pulsation in the fingertips or nail beds and this is seen in aortic regurgitation. So it's seen in the fingertips. I always remembered Quinky is seen in the pinky because Quinky is seen in the fingers. So you remember Quinky is seen in the pinky. You'll help you remember that. 35, what is the most common cause of mitralstinosis? Mitrostenosis, most common cause is going to be rheumatic heart disease. It's almost always the cause of mitral stenosis. That's rheumatic heart disease.

36, which population will commonly have an atypical presentation during an acute MI? Atypical presentation during an acute MI. It's going to be women, elderly, and diabetics. Women elderly and diabetics will usually have an atypical presentation during acute MI. 37, what is the treatment of choice? in a patient with cocaine induced MI. So you remember with cocaine induced MI, you have a vasospasm in those coronary arteries. You want to stop the spasm. You're going to use calcium channel blockers. That's going to be your first line. Nitrates are a close second line. So calcium channel blockers generally for cocaine induced in my 38.

An inferior wall, MI will be seen in which leads on EKG. Inferior wall MI, you're going to see leads to three and AVF, 2, 3 and AVF, 2, 3 and AVF on inferior wall am i 39 which cardiac biomarker peaks the fastest so remember the biomarker troponins you have ckmb you have myoglobin if you remember myomai you're fast you can remember myoglobin it's your fastest peaking biomarker cardiac biomarker myoglobin 40 post m i pericarditis is known as post m i post myocardial infarction pericarditis is known as dressler syndrome What is the most common clinical manifestation of left-sided heart failure? Most common clinical manifestation of left-sided heart failure.

Remember when this happens, all of the blood is backing up into the lungs. You have all this back-up fluid in the lungs. It's going to be dyspnea. That's going to be the most common clinical manifestation, left-sided heart failure. 42. For a patient with recurrent deep vein thrombosis, despite adequate anticoagulation therapy, or in a patient where anticoagulation therapy is contrary, indicated, what will be the next appropriate treatment option. So you have a patient with DVT,

you've given them anticoagulation, it's not working, they're still getting DVTs, or anticoagulation therapy is not contraindicated, and these patients are going to use an IVC filter. So that's a filter in the inferior vina cava, stops the clots from getting any further than the IVC there. 43, we're almost done. What is the first line treatment for patients with sinus bradycardia who are symptomatic or patients who have evidence of? of hemodynamic instability. So first line treatment for patients with sinus bradycardia who are symptomatic or they have evidence

of hemodynamic instability, you're gonna give these patients atropine. So normally a 0.5 milligram IV push. You can repeat it every three to five minutes. Max dose is three milligrams, so atropine. Overall, what is the most common cause of heart failure? Most common cause of heart failure, it's gonna be coronary artery disease.

Next question, 45. What is the most effective medication? used to increase HDL levels in a patient. Most effective medication used to increase HDL levels in a patient. It's going to be nicotinic acid, also known as niacin. And just remember with niacin, they may not ask you many questions about niacin itself, but the common question that you'll get is actually about the adverse drug reactions with niacin. And the most common thing with niacin is to have flushing after you take the medication.

And that can be prevented by taking insides prior to taking the men. And you get this flushing because you get increased prostate glandids with niacin, so you give ensigns, which we know inhibit prostaglandins. So remember, niacin increases HDL levels, but it can give you flushing, so you take insets prior to use. 46, a 66-year-old male, the history of hypertension, presents to the ER. He complains of sharp pain in his upper back between his scapula. His blood pressure is unequal in both arms. What's the most likely diagnosis? So this is a classic presentation for aortic dissection.

He has history of hypertension, which is the most important risk factor for aortic dissection. He's a 66-year-old male, which fits the high-risk demographic. And he has a sharp or sometimes described as a tearing or knife-like upper back pain between the scapula. And the key is the unequal blood pressure between the two arms. Generally, there's a difference of over 20 millimeters of mercury between the arms. 47 describe the clinical manifestations in a patient with acute arterial occlusion. So clinical manifestations and a patient with acute arterial occlusion, you're going to remember your six P's, so that's going to be pain, pallor, so that you're going to have this pale

appearance of the leg, poikilothermia, which all that means is basically the legs no longer able to regulate the core body temp, the skin's going to be cold. That's what that complicated word means. pulselessness, so you're not going to feel a pulse, paristhias, and then paralysis, which is often a very late and severe findings. So remember your six P's for acute arterial occlusion, pain, pallor, poikilothermia, pulselessness, parestetias, and paralysis. 48, a patient that presents with intermittent clotication, atrophic skin changes like hair loss, thinning of the skin, and diminished pulse in the lower extremities should have what screening test,

performed to confirm the likely diagnosis. So again you have a patient that comes in. They're developing this intermittent clotication. They have atrophic skin changes like hair loss in the leg, thinning of the skin, and a diminished pulse in the lower extremities. What screening test should you do on these patients to confirm the likely diagnosis? It's going to be an ankle break ankle breakial index test. This patient described in this vignette with atrophic skin changes, intermittent clotication, diminished pulse. It's a classic description of peripheral artery, peripheral arterial disease and the test of choice for this is an acrobacheal index and normally less than

0.90 confirms p.A.D. 49. Describe the classic ECG findings and a patient with acute paracarditis. So you better know this one, you'll definitely be asked this at some point. So classic ECG findings in a patient with acute paracaraditis, it's going to be widespread or diffuse ST elevation in the precordial leads along with PR depression. It's generally seen this, this presentation on ECG generally seen in the first few hours or days after initial diagnosis. Later on you may see T-wave inversions and then it's followed by a normalization of the ECG. And just be aware that the way you differentiate this from a stemmy, you know, ST elevation, myocardial infarction is the lack of reciprocal ST segment changes.

So it's an important feature to differentiate acute paraccharides from acute myocardial infarction. So last question. During osculation, you hear a systolic. ejection murmur, best heard at the pulmonic area. It's crescendo de crescendo. And then you hear a wide fixed split S2. This is the key. The fixed split S2 wide. This patient likely has what condition. So again, systolic ejection murmur, best heard of the pulmonic area, crescendo de crescendo, and then a wide fixed split S2. That's going to be atrial septal defect. So even if you don't recognize the murmur, as soon as you see wide fixed split S2,

you should immediately be thinking ASD. And the way I always remember that, I went over this in the congenital heart disease podcast, but remember that A, it looks like somebody has their legs kind of like spread open doing a split, so that A is a split S2, and then A with your legs spread wide open,

it's wide, so wide split. And then I also remember the A stands for anchor, so it's like fixed. So fixed split wide S2. As soon as you see that, you should be thinking ASD. All right, so those are 50 quick, questions for cardiology.

Now, this is a little bit different than what I normally do. Let me know if this was helpful for you guys. I'm going to, of course, stick to the other podcasts I normally do, you know, going over topic by topic. But let me know if this is good to in between to help you, if it was beneficial or not. So thank you again, as always for listening to my podcast. Please leave me a review, subscribe. If you are liking the content, and please check out my YouTube channel.

It's under cram the pants. And as always, good luck on your pants, your panry, your EORs, and good luck in PA school. Thank you.