If you’ve made it this far in your cardiology journey, congratulations! This is Part 2 of high yield cardiology to help guide you on your journey through Step 1 and beyond. (If you haven’t checked out Part 1 yet, now is the time.)
I want to reiterate here the importance of this system and how your understanding of it can help you grasp physiological concepts throughout the rest of your studies. That being said, let’s dive in!
High-Yield Cardiology Topics for Step 1
Congenital Heart Disease
Congenital heart disease is usually split into two categories: “Early cyanotic (Right-to-left shunting)” and “Late cyanotic (Left-to-right shunting).”
The 5 cyanotic pathologies usually require surgical intervention or maintenance of the patent ductus arteriosus quickly after birth. These five defects are remembered because they all begin with “T” and can be remembered in a numerical order:
1. Truncus Arteriosus
This is a defect in which the truncus arteriosus fails to divide into the pulmonary trunk and the aorta resulting in 1 vessel (hence it is number 1 on the list). The aorticopulmonary septum is the structure which normally divides the aorta and pulmonary trunk, but it has failed to form here. Many of these patients will also have a ventricular septal defect.
2. Transposition of the great arteries
Normally the aorta leaves the left ventricle with oxygenated blood and deoxygenated blood returns to the right atrium to then leave the right ventricle via the pulmonary artery to be reoxygenated. In this condition the aorta leaves via the right ventricle, before blood is oxygenated and takes blood to the rest of the body only for it to return to the right atria to be recirculated again.
The pulmonary artery leaves the left ventricle to be oxygenated by the lungs which then returns to the left atria to be sent to the lungs again rather than systemically. This means that there are two—which why this is second on the list—distinct loops that are separate from each other. This defect is due to the aorticopulmonary trunk forming, but not spiraling as it should. The classic chest XR appearance is “egg on a string.” This defect is unfortunately incompatible with life without a way to mix the blood from these two systems such as a VSD, PFO, or PDA).
3. Tricuspid atresia
“Tri,” meaning three, is third on the list. This is simply the absence of the tricuspid valve. This makes blood from the right atria unable to cross to the right atrium for circulation. You can imagine that for blood to get to the right ventricle, it would have to cross to the left atrium via an ASD and then from the left ventricle to the right ventricle via a VSD, which are both required for life.
4. Tetralogy of Fallot
The most famous of the congenital heart defects actually has four components and is fourth on the list for that reason. This condition is due to the infundibular septum shifting anterosuperiorally.
Pulmonary stenosis is the most important prognosticator for these patients. Given the pulmonary stenosis, the right ventricle must pump through a higher resistance circuit causing hypertrophy and a “boot shaped heart” on chest XR.
The third component is the overriding aorta in essence taking up the space that the pulmonary artery usually occupies.
Finally, the fourth component is a VSD. This condition has what are known as “tet spells” which occur when the baby cries exercises or anything that increases Right ventricle outflow obstruction. The solution is to squat which increases systemic resistance which decreases the right-to-left shunt and allows for increased oxygenation.
5. Total Anomalous Pulmonary Venous Return
TAPVR (5 letters) is when pulmonary veins drain into the right atria rather than the left. Often these patients have ASD or PDA to allow for right-to-left shunting.
Non-cyanotic lesions, left-to-right shunts include ventricular septal defect, atrial septal defect, and patent ductus arteriosus. These conditions increased the amount of blood volume in the right heart which increases pulmonary blood flow. This constantly increased volume causes remodeling of the vascular system which eventually causes pulmonary arterial hypertension which increases work for the right ventricle. When the right ventricle must work harder, hypertrophy occurs which will eventually overcome the forces of the left side of the heart, switching the left-to-right shunt to a right-to-left shunt.
Ischemia
Ischemia, at its core, is the lack of adequate oxygen delivery tissues when that be from hypoxia or from decreased blood volume/delivery. Oxygen is the currency and oxygen demand is the price that every tissue carries to be healthy. This price varies depending on how much work is being asked of the tissue, not unlike the electrical grid. When there is too much electrical demand in a city and no mechanism to increase the supply, brown outs (or full blackouts) occur, which are akin to ischemia in the human body.
The heart, as opposed to other tissues, has a unique quality in that it extracts almost all of the oxygen that is supplied to it in the blood. This means that if the heart must work harder (increased oxygen demand) the only way to compensate is for increased blood delivery via increased hemoglobin, O2 saturation, or coronary flow. The ischemia that is caused when there is not an increase in oxygen delivery is termed angina.
Symptoms are typically substernal chest pain that radiate to the jaw not unlike a STEMI, the difference being that angina is typically relieved by rest and worsened by increase in activity (increased oxygen demand). Once this ischemia progresses to cardiac muscle damage, you do have and MI.
Cardiomyopathies
Cardiomyopathy means that there is a pathology of the cardiac muscle. There is ischemic cardiomyopathy which means that the muscle has weakened due to adequate oxygen delivery. There is also nonischemic cardiomyopathy which means cardiac muscle damage from congenital abnormalities, alcohol, use, stress (Takotsubo), viruses, or hypertrophic cardiomyopathy.
The highest yield of the nonischemic cardiomyopathies is hypertrophic cardiomyopathy. Inherited in an autosomal dominant pattern, think of this when the prompt gives you a patient who dies unexpectedly when playing a sport. The cause of this sudden death is from the septum growing too large and obstructing left ventricular outflow. As heart rate increases, the obstruction worsens. Therefore, lower heart rates and decreased contractility are important to avoid this death. What medications may also cause decreased heart rate? Beta blockers.
Heart Failure
Heart failure is the inability of the heart to push blood forward. This is an excellent topic to review the course of blood throughout the body. For example, if the left heart fails, blood builds up in the structure that is before it, AKA the lungs, which causes dyspnea. Right heart failure, most commonly due to left heart failure, causes backup in the venous system leading to peripheral edema, jugular venous distention, and hepatic congestion (Nutmeg liver).
When thinking of causes of heart failure, think of ways that may make it difficult to push blood forward. Things like hypertension which increases afterload for the left ventricle and ischemia which damages the pump itself. For the right side, pulmonary hypertension and COPD make it difficult to push blood through the pulmonary circuit. It is important to know the medications that decrease mortality in these patients versus only treating symptoms. ACE inhibitors, ARBS, angiotensin receptor-neprilysin inhibitors, beta-blockers and aldosterone all decrease mortality. Loop and thiazide diuretics help control symptoms but do not decrease mortality.
Shock
Shock is a massive, and extremely high yield topic and understanding shock will help you understand many aspects of cardiology and how the body works in general. Check out this post dedicated to the topic of shock to make it quick and easy to understand.
Tamponade
Surrounding your heart is a structure known as the pericardial sac. Between this sac and the heart itself is a potential space which can fill with blood under certain conditions, such as trauma. Blood in this space puts pressure on the heart which prevents it from functioning properly.
A high yield constellation that should make you think of tamponade is Beck’s Triad. This triad consists of muffled heart sounds due to poor transmission through the fluid, hypotension, and jugular venous distention because the vein cannot empty into the heart. Treatment for this is pericardial window or pericardiocentesis. While these are the treatments, always remember the ABCs of trauma and do not forget the steps that take place beforehand!
Antihypertensives
This genre of medications is probably the most commonly prescribed of them all. ACE inhibitors (lisinopril) help to stop pathological changes in the heart and prevent renal damage in those with diabetes. Thiazide diuretics increase your calcium. Then there are calcium channel blockers, loop diuretics, and beta blockers. It would behoove you to review each of these in detail by understanding the one or two specific characteristics that really set them apart but understand the goal is the same, decrease blood pressure.
Further Reading
We know—we barely scratched the surface. But that’s the challenge when aiming for the highest-yield coverage in limited space!
For even more high-yield Step 1 topics, check out these other posts on the blog:
- Now, That’s What I Call High-Yield: Pharmacology
- Now, That’s What I Call High-Yield: Musculoskeletal
- Now, That’s What I Call High-Yield: Neurology
Originally published January 2019, updated August 2025 by Landon Cluts




