Now, That’s What I Call High Yield: Cardiology Vol. 1

  • /Reviewed by: Amy Rontal, MD
  • Surely you’ve heard that we are born with a finite number of heartbeats in the tank. When we run out, sayonara. So don’t waste them by getting anxious about cardiology on USMLE Step 1. As far as subjects go, the entire cardiovascular system is high-yield! It breaks my heart to have to winnow down all of the juicy details into what’s most important. But alas, I have no choice in the matter. What I can say for sure is that distilling all of this down into 1 post is not possible. Check out Part 2 here.

    Fetal circulation (6.5) – The transition from fetal to neonatal circulation is an amazing process, with extreme change happening in just a few breaths. Given its overlap with pediatrics, this material is certainly high yield. It all starts with mom, getting oxygen from her lungs, and delivering it via the spiral arteries to the placenta. From there, it travels through the umbilical vein through both the liver and the ductus venosus (a liver bypass route) to the IVC. Bear in mind, this is still oxygenated blood, unlike normal circulation, which carries deoxygenated blood to the right heart. Blood from the right heart shunts left via the foramen ovale (an “atrial septal defect”) and the ductus arteriosus. This highly oxygenated blood takes care of important organs like brain and heart, and eventually returns to mom via TWO umbilical arteries and finally the placenta.

    Now for the magic. Baby takes a breath, and that puff of oxygen dramatically reduces pulmonary vascular resistance, making the pulmonary arteries a more attractive lower resistance route for blood to travel. At the same time, prostaglandin production plummets which leads to a closure of the ductus arteriosus. To further stamp out that previous right → left shunt, the right sided pressure drop causes closure of the foramen ovale, and blood stops shunting across the atrial septum. Pure magic.

    Cardiac Output (9) – Cardiac Output is the name of the game. Every organ depends on cardiac output for the delivery of oxygenated blood to perfuse organs and keep them happy and functional. You will be well served to remember the simple equation P = Q * R; Pressure = Flow * Resistance. Physiologically, MABP = CO * SVR. Mean arterial blood pressure is cardiac output multiplied by systemic vascular resistance.

    And CO = SV * HR. Cardiac output is stroke volume times heart rate. NEVER forget that equation. It is at the very foundation of all things cardiac. For a more detailed discussion of these relationships, visit our hypotention how-to guide.

    Starling Curves (9) – The beauty of the Starling curve is its simplicity. It can be reduced down to this idea: An increase in preload leads to an increase in cardiac output, up to a point. Eventually, too much preload will distend the heart and its myocytes past that optimum point of stretch and output delivery. Healthy hearts can handle more preload and generate a stronger cardiac output. Patients in heart failure “fall off” the Starling curve and are prone to fluid overload. Put another way, there is a much smaller window for increased preload leading to increased cardiac output.

    Murmurs (7.5) – Murmur identification can get very confusing. The one thing that will never change is the phase of the heart cycle during which the murmur occurs. Aortic stenosis might be heard best in the “aortic” area, but in reality, it might be best identified in the “pulmonic” area. The murmur of aortic stenosis always occurs during systole. Commit to memory which murmurs are systolic (aortic stenosis, HoCM), which are holosystolic (VSD and mitral regurgitation), and which are diastolic (aortic regurgitation, mitral stenosis). Other high yield tidbits: aortic stenosis symptomatology makes you SAD, Syncope, Angina, and Dyspnea. Rheumatic heart disease most often presents as mitral stenosis.

    EKGs (10) – Reading EKGs can take years to master. We will defer discussion here so that we don’t end up with a 10,000 word dissertation. The long and short of it is: develop a systematic way to read EKGs. The same way, every time.

    Arrhythmias/Blocks (8) – As you deepen your knowledge of EKGs, you will come across some classic arrhythmias. Atrial fibrillation is hallmarked by a lack of P-waves and ventricular depolarization (QRS’s) occurring at seemingly random intervals. Don’t confuse this with ventricular fibrillation, a wavy jumble of nothing. If it’s VFib, shock it!

    See a sawtooth pattern? A-flutter. AV block comes in 4 flavors. First degree is nothing more than a long PR interval. Second degree is either a PR that goes longer, longer, longer dropped QRS (type I) or random dropping of QRS (type II). Type I is no big deal, type II necessitates a pacemaker. Third degree, or complete heart block involves a complete dissociation between atrial and ventricular depolarization. The atria pound away at a set rate, as do the ventricles, they are just not talking to each other and coordinating their efforts.

    Baroreceptors (8.5) – These regulatory receptors in the carotid body are clutch. They transmit signals via the glossopharyngeal nerve. If blood pressure goes down, these receptors sense a lower pressure, and decrease firing up the glossopharyngeal. The efferent limb strives to maintain balance, and will tip the autonomic nervous system’s balance to the sympathetic side and increase heart rate and blood pressure. It’s somewhat counterintuitive that “decreased baroreceptor firing” leads to a increased heart rate and blood pressure. Baroreceptors also work the opposite way when the carotid body gets slammed by higher pressures, and the body responds with parasympathetic output.