Some students see cardiology and shudder. “That’s not one of my good subjects,” they’ll opine. I’ll say explicitly, that if you want to do well on Step 1 (or Step 2 or 3), you have to have some degree of mastery over the cardiology material on the exam. It is simply too important a system to maintain a second-rate knowledge of. If you bolster your knowledge in only one system throughout your study period, you will be best served by enhanced cardiac knowledge. The entirety of the body depends on perfusion – pumped blood that is saturated with oxygen. The heart is that pump. There’s so much interplay between the cardiovascular system and the nervous, pulmonary, renal, hepatic, and muscular system. Do what it takes to learn well, and you’ll have a strong footing in all of the other disciplines.
Take a peek at Part 1 for the other half of the high-yield material.
Congenital Heart Disease (8) – Massive peds overlap here! Plus, knowledge of congenital heart lesions will elevate your consciousness on how the heart works. The low-hanging fruit that will get you furthest? Know the 5 cyanotic lesions (they all begin with T) – truncus arteriosus, total anomalous pulmonary venous return, tricuspid atresia, transposition of the great vessels, and tetralogy of Fallot. It pays to know that cyanosis is driven by DEoxygenated blood from the right side of the heart shunting across to the left side and providing the systemic circulation (and therefore, the body and organs) with blue, deoxygenated blood. Tetralogy of Fallot is not only the most common cyanotic lesion, but also the one with the most testable material. Understand the 4 parts of the syndrome, and why afflicted youngsters squat to feel better (increased SVR = decreased shunting across the VSD).
As far as non-cyanotic lesions, patent ductus arteriosus, VSD, and coarctation are the most high-yield.
Ischemia (9) – Every tissue in the body has an oxygen demand, and an oxygen supply. Usually the supply is more than enough to meet demands, and the organs go on happily functioning. Anytime there is a demand that is not met by supply, the end result is dreaded ischemia. While ischemia is not specific to the heart, there is an important characteristic of the myocardium. It already extracts just about as much oxygen as can be extracted from the blood that supplies it. Therefore, if oxygen demand goes up, the only way to meet the demand is to increase oxygen(ated blood) delivery. This can be done by increasing hemoglobin, pO2, oxygen saturation, or coronary blood flow.
When demand exceed supply, the heart becomes ischemic. Ischemia leads to angina, which typically presents as substernal crushing pressure that can radiate into the arm or jaw. It is relieved by rest, and worsened by activity. New or worsening angina is deemed unstable, and often associated with EKG changes. Once we go off the deep end of ischemia and myocardium starts dying, we have a myocardial infarction.
Cardiomyopathies (7) – Put simply, a cardiomyopathy means a poorly functioning heart. You might hear the term ischemic cardiomyopathy, which means poor blood flow and lack of oxygen delivery to heart muscle has made it a weaker pump. Non-ischemic cardiomyopathy is a weak heart caused by another problem. Some etiologies of non-ischemic cardiomyopathy include alcohol use, congenital abnormalities like HoCM, and other disease states like Takotsubo (stress) or viral cardiomyopathy.
Hypertrophic obstructive cardiomyopathy (HoCM, above) is a very teachable and testable lesion. It is a hereditary autosomal dominant disease in which the septum of the heart grows out of proportion to the rest of the heart, shrinking the LV cavity and obstructing flow through the left ventricular outflow tract. The classic history is the athlete who passes out or dies on the basketball court. Sprinting up and down the court draining 3’s and grabbing rebounds is exactly counter to management of the condition. The goal is to aim for slow heart rates and decreased contractility, not the tachycardia and increased contractility that results from a full court drive. Drug of choice here is a beta-blocker.
Heart Failure (8.5) – Heart failure is unequivocally a huge public health burden. It occurs when forward flow of blood is impeded by a weakened or stiffened heart, leading to fluid backup. If the left heart is failing, this fluid can back up into the lungs, causing dyspnea. Right sided heart failure (often a sequela of left-sided heart failure), causes backup into the venous system, causing peripheral edema, jugular venous distention, and hepatic congestion. Main causes to consider for left-sided heart failure include chronic poorly controlled hypertension, as well as ischemia and myocardial infarctions. Right-sided failure can occur from failure on the left, or an intrinsic lung problem like COPD or pulmonary hypertension. Support with diuresis (furosemide) and inotropy (e.g. epinephrine, dobutamine) as needed.
Shock (10) – Again, a lecture and entire blog post in and of itself. Stay tuned for that one. In brief, know the 4 main categories of shock (hypovolemic, cardiogenic, obstructive, and distributive), and be able to give the etiologies for each.
Tamponade (8) – Your heart is gift-wrapped in fibrous pericardium. Normally that’s a great place to be. Unless said pericardium fills up with fluid, preventing the heart from filling and pumping appropriately. Your symptomatic constellation is named after Grammy-award winner Beck (just kidding; it was actually cardiac surgeon Claude Beck, who performed the first ever defibrillation in 1947). Beck’s triad consists of muffled heart sounds (poorly transmitted across that fluid-filled pericardium, hypotension secondary to inadequate filling/pumping by a very constrained heart, and jugular venous distention resulting from backup from the right side of the heart. Treat it by getting the fluid out, with pericardiocentesis or a pericardial window.
Antihypertensives (10) – Probably the most common drugs that you’ll encounter during your tenure at the hospital or clinic. Almost everybody seems to be on some blood pressure lowering agent. For a patient without comorbidities, your choices are numerous. Water pills (thiazides), ACE inhibitors, and calcium channel blockers are all fine choices. Patients that suffer from heart failure or have had MIs in the past do better with ACEi and beta-blockers. Diabetic hypertensives ward off further renal damage with the help of ACEi.
There’s the triple-distilled highest of high-yield material for Step 1 cardiology. This is only a skimming of the surface, so do what it takes to take it to deeper levels as time and brainpower permit. You will be glad you did.
