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The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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Patient Summary

A man in his early 70s with ASCVD risk factors and known CAD (PCI to proximal LAD 4 years prior) presented with typical angina refractory to maximal medical therapy. A nuclear stress test showed a reversible perfusion defect in the RCA territory, and he was referred for PCI. Coronary angiogram showed severe stenosis of the proximal RCA and a DES was successfully deployed with TIMI 3 flow, though several large acute marginal branches were jailed.  

The night following PCI, the patient developed bradycardia, hypotension, and tachypnea. Physical exam showed newly elevated JVP, lower extremity edema, and bibasilar crackles without a new cardiac murmur. ECG showed ST elevation in V1-V4, and bedside echocardiogram showed a severely dilated RV with decreased systolic function. With concern for acute RV failure, the patient was fluid resuscitated, started on dopamine for chronotropy, and was admitted to the CCU. A Swan-Ganz catheter was placed, showing a CVP 12, RV 41/15, PA 36/20 (25), PCWP 18, CI 1.6 (by Fick method). The calculated PAPi was 0.84.  

The patient was transitioned to dobutamine to improve RV inotropy, epinephrine in the setting of hypotension, and inhaled nitric oxide in an attempt to decrease RV afterload. Despite these interventions, the patient had worsening shock, anuric renal failure requiring CVVH, and respiratory failure requiring intubation. A centrifugal RA to PA pump was placed (Protek Duo) for right-sided mechanical circulatory support, with improvement in RV hemodynamics and cardiogenic shock. Notably, a repeat angiogram was done, which showed a patent left coronary circulation as well as a right coronary artery without flow in the acute marginal branches. After 6 days of mechanical circulatory support, the patient was ultimately able to be weaned from vasoactive agents, and the Protek Duo was removed. He continued to have junctional bradycardia, and a permanent pacemaker was placed. After a nearly month-long admission, the patient was discharged to rehab; at 4 months follow-up, the patient’s RV function had improved on TTE, and he was not limited from heart failure symptoms.  

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Case Media

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Episode Schematics & Teaching

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The CardioNerds 5! – 5 major takeaways from the #CNCR case

1) Don’t forget about the RV, because it sure won’t forget about you! Cardionerds, how do you break down the pathophysiology of acute RV failure? 

• Understanding the pathophysiology of RV failure requires a basic understanding of RV physiology. Normal RV function depends on systemic venous return, RV afterload, pericardial compliance/constraint, and native RV contractility. Remember, the thin-walled RV requires much less energy to generate output compared to the LV as the RV is pumping into the highly compliant, low-resistance pulmonary circulation. Overall, the RV is highly sensitive to changes in RV afterload. 
• Thus, when we think of acute RV failure, our primary considerations are factors that rapidly increase RV afterload (e.g., pulmonary embolus), as well as conditions with decreased RV contractility (e.g., RV ischemia). The RV is more adept to tolerating changes in volume rather than pressure (since it is coupled to the low-resistance, high compliance pulmonary circulation). Contrast this with the LV, which tolerates changes in pressure more than volume. An acute increase in RV afterload can abruptly precipitate a fall in RV cardiac output! 
• With an acute decreased in RV contractility (e.g., RV infarct), the RV can dilate leading to functional TR; this can further exacerbate RV dilation, leading to impaired LV filling due to ventricular interdependence. As the septum shifts leftward, this can impair LV filling by increasing LVEDP and lead to hypotension. Direct RV injury can promote more RV injury/ischemia, as elevated right heart pressures can cause coronary sinus congestion reducing coronary blood flow and leading to more RV ischemia. 
• For more detailed explanation of Right-Sided Heart Failure, see this fantastic Scientific Statement from the AHA! 

2) Lets focus on ischemic RV disease: what is the coronary supply to the RV, and how does coronary blood flow to the RV differ than that of the LV? 

• Compared to the LV, the RV is more resistant to irreversible ischemia. Coronary blood flow to the RV occurs both in systole and diastole, RV myocardial oxygen demand at rest is lower than that of the LV with smaller muscle mass, and there is often extensive collateral circulation from the left coronary system. However, RV coronary perfusion pressure can decrease rapidly in the setting of systemic hypotension and increased RV intracavitary pressure.  
• In most patients, the RV is supplied by the RCA via RV acute marginal branches largely supplying the anterior RV free wall. Significant RV involvement in an RCA culprit acute myocardial infarction tends to only occur if the occlusion is proximal to the acute marginal branch. Furthermore, the extent of RV involvement may be attenuated by the amount of left to right collateralization.  
• Note, the LAD supplies the RV apex, as well as a portion of the RV anterior wall that is contiguous with the anterior septum. Notably, in patients with a left dominant coronary system or in patients with a chronically occluded RCA with extensive left to right collateral flow, more than half of the RV free wall may be supplied by the left system. 

3) Now that we know what causes acute RV failure, what can we do to assess for acute RV failure, both at the bedside and with advanced diagnostics? 

Physical exam: In acute RV failure, we will likely see elevated neck veins +/- Kussmaul’s sign, hypotension, possibly clear lungs depending on etiology, and tricuspid regurgitation murmur. Enjoy Ep #58 – Constrictive Pericarditis CN5 for more details on right-sided exam findings! 

ECG: Unfortunately, the standard 12-lead ECG provides limited definitive information on RV failure. However, we should evaluate for acute occlusive myocardial infarction (MI) involving the RV, including ST elevation in the inferior leads (classically with III > II), V1 > V2, and/or V1 +/- ST depression in V2. Right-sided leads can further confirm acute occlusive MI, with STE > 1mm in lead V4R sensitive and specific for RV infarct. With a large RV infarct, we may see brady-arrhythmias. Other signs of acute RV failure may include RV strain pattern (e.g., ST depression and T wave inversions in V1-V3). Enjoy Ep #60 – Massive PE for more on ECG changes in acute PE and RV failure! 

CT: While usually not obtained in the setting of acute RV failure unless evaluating for acute PE or parenchymal lung disease, RV:LV ratio >1.0, pulmonary trunk enlargement, and contrast reflux into the inferior vena cava and hepatic veins suggest right heart failure. A gated cardiac contrast-enhanced CT can provide more information about chamber size/function and valvular pathology. 

TTE: Echo is crucial in the diagnosis of RV failure! One of the first things to pay attention to is RV size, with RV dilation being a poor prognostic sign; RV:LV ratio > 1 is associated with increased in-hospital mortality in some studies of acute PE patients. Evaluate the position of the interventricular septum, which may be flattened in systole suggestive of RV pressure overload and/or in diastole suggestive of volume overload. RV systolic function can be assessed by tricuspid annular plane systolic excursion (TAPSE) which is a marker of longitudinal myocardial shortening with abnormal being less than 1.6 cm. There are limitations to use of TAPSE, but it remains a relatively specific test for RV dysfunction. An estimation of pulmonary artery systolic pressure (PASP) should be done utilizing the TR jet; however, in the setting of severe TR, the doppler envelope is often low velocity and early peaking because of high RA pressure making PASP difficult to estimate. The IVC should be evaluated for size, response to respiration and hepatic vein reversal. There are many more aspects to review regarding acute RV failure and RV systolic function like fractional area change, tissue doppler velocity, and RV strain (see the references below!), but also remember to evaluate for specific pathology, including signs of acute PE such as McConnell’s sign. 

RHC: In the setting of acute right heart failure, a right heart catheterization may be necessary to guide therapy. An elevated right atrial pressure, and specifically an elevated right atrial pressure to pulmonary capillary wedge pressure ratio can be indicative of right heart failure; the specific ratio depends on disease state, but generally >0.6 to 0.8 suggestive of RV failure. PA pulsatility index (PAPi) has become a useful tool in evaluating for RV failure specifically in the setting of acute myocardial infarction. An abnormal value depends on disease state as RV pulsatility is not only a function of RV function, but also pulmonary vascular resistance and capacitance. 

4) So, what’s the big deal? How does acute RV failure cause shock? 

• Decreased RV cardiac output, combined with a dilated RV, leads to interventricular septal shift towards the left, compromising LV filling (preload) as discussed above. Decreased LV preload eventually leads to decreased LV cardiac output and hypotension, causing end-organ damage and decreased coronary perfusion. Elevated right-sided filling pressures with systemic venous congestion can lead to hepatic and renal congestion, exacerbating fluid retention. Decreased coronary perfusion can leads to decreased oxygen delivery to a failing RV that already has a higher oxygen demand (due to increased RV afterload and wall tension). This, ultimately can cause further RV ischemia and collapse in RV function. This physiologic phenomenon is referred to as the RV Spiral of Death.  

5) Yikes! What can we do to break this spiral and medically manage RV failure? Is there a role for mechanical support? 

• Correct the initial insult to the RV! As we take measures to support the RV, we have to ensure we evaluate for the etiology of RV failure and treat the underlying cause. This includes PCI in the setting of RVMI, anticoagulation/thrombolysis/thrombectomy in the setting of PE, and medical management in the setting of sepsis! 
• Address preload! Remember, not all RV failure is created alike. An acute RV infarct may be highly pre-load dependent and may need fluid boluses. However, depending on the underlying pathology, excessive preload may be detrimental, leading to excess wall stress and RV dilation, which can potentially exacerbate left-ward septal shift and impede LV filling. Ventricular interdependence as a result of RV dilation and pericardial constraint may play a larger role in worsening acute RV failure than decreased RV ejection fraction, and thus decompression of the RV is necessary (e.g., diuretics, renal replacement therapy), as guided by exam +/-  RHC. 
• Reduce RV afterload! First, address reversible factors leading to pulmonary vasoconstriction including hypoxia and acidosis. In patients receiving positive pressure ventilation, PEEP should be optimized to avoid atelectasis, while also avoiding over distension of alveoli and worsened RV afterload. Non-selective systemic vasodilators (e.g., intravenous sodium nitroprusside > nitroglycerin) decrease systemic and pulmonary vascular resistance, and thus decrease LV and RV afterload. Selective pulmonary vasodilators, such as inhaled nitric oxide and epoprostenol can also be effective in specific patient populations.  
• Improve Contractility and Maintain Perfusion! Dobutamine and milrinone both improve RV inotropy at the cost of arrhythmogenicity. Both agents can also lead to vasodilation and thus whether hypotension worsens may depend on how effectively these agents assist in augmenting LV preload compared to systemic vasodilation. In the setting of hypotension, combined vasopressor and inotropic medications may be needed including norepinephrine and/or epinephrine. With escalating doses of vasoactive medications, vasopressin may be needed to maintain end-organ perfusion.  
• Assess chronotropy! RV infarcts increase the risk of bradycardia and AV block. Temporary pacing may be necessary in these patients.  
• In refractory acute RV failure, consider mechanical support! There are 3 main options for temporary RV mechanical support:  
  • VA-ECMO substantially reduces RV preload and afterload, though it can dramatically increase LV afterload VA ECMO is an indirect way to bypass the RV compared to MCS below.  
  • RA to PA extracorporeal pump (ex. Protek Duo and Tandem Heart RVAD) removes blood from the RA and delivers it into the PA using a centrifugal pump and an oxygenator can be added if needed. RV preload is reduced while increasing mean PA pressure and LV preload. 
  • Micro-axial flow device (e.g., Impella RP) with an inflow in the RA and an outflow in the PA. 

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References

1. Koo, B. K., Kang, H. J., Youn, T. J., et al. (2005). Physiologic assessment of jailed side branch lesions using fractional flow reserve. Journal of the American College of Cardiology, 46(4), 633–637. 
2. Fincke, R., Hochman, J. S., Lowe, A. M., et al. (2004). Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. Journal of the American College of Cardiology, 44(2), 340–348. 
3. Kapur, N. K., Esposito, M. L., Bader, Y., et al. (2017). Mechanical Circulatory Support Devices for Acute Right Ventricular Failure. Circulation, 136(3), 314–326.  
4. Konstam, M. A., Kiernan, M. S., Bernstein, D., et al. (2018). Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation, 137(20), e578–e622.  
5. Jeffers JL, Boyd KL, Parks LJ. Right Ventricular Myocardial Infarction. [Updated 2020 Aug 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431048/ 
6. Sanz, J., Sánchez-Quintana, D., Bossone, E., et al. (2019). Anatomy, Function, and Dysfunction of the Right Ventricle: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 73(12), 1463–1482.  
7. Korabathina, R., Heffernan, K. S., Paruchuri, V., et al. (2012). The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions, 80(4), 593–600.  

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CardioNerds Case Reports: Recruitment Edition Series Production Team

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