Right Ventricular Infarction - Morning report 040411
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This document provides a summary of a cardiology division morning report discussing a 56-year-old woman who presented with chest pressure and shortness of breath. She had a history of obesity, diabetes, hypertension, and low ejection fraction. Tests showed significant coronary artery disease involving the left anterior descending, left circumflex, and right coronary arteries, as well as reduced right ventricular function. She developed complete heart block and required inotropic support. Her condition initially stabilized but she remained in heart block. Plans were made for pacemaker placement, but her rhythm improved with theophylline. The discussion focused on management strategies for right ventricular ischemia including restoration of rhythm, optimization of preload and oxygen delivery, inotropes, re
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Right Ventricular Infarction - Morning report 040411
- 1. Cardiology Division MorningCardiology Division Morning ReportReport Michael G. Katz, MD Fellow in Cardiovascular Disease University of Rochester April 4, 2011
- 2. HPI 56 year old morbidly obese, diabetic WF with cardiac RF of HTN, and HL. Nurse by training, but on medical disability due to chronic low back pain. Non-smoker. Lives with husband, son, and daughter. In her usual state of sedentary health until day of presentation. 2
- 3. Other cardiac history April 2010, symptoms of SOB EKG: LBBB TTE: • LVEF 40-45% • Septal, anterior, and inferior mild HK Regadenoson nuclear SPECT: • LVEF 44% • Mild global hypokinesis • Normal rest/rest perfusion 3
- 4. Presentation January 2011 Awoke from sleep at 12am with L-sided, moderate intensity, chest pressure. Radiation to L shoulder and neck. Associated with SOB. Spontaneously remitted, but recurred at 3am. Took NTG x2, but when discomfort unrelieved, called EMS. Brought to Mary Imogene Bassett Hospital, Cooperstown, NY. 4
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- 7. LHC pLAD 50%, mLAD 80%, D1 50% Normal LCx Ostial RCA 100% LV-gram: 45-50% 7
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- 10. RHC RA 18 RV 29/21/23 PA 29/22/27 PCWP 21 10
- 11. Transferred to SMH for further management (eg. Medicine of the Highest Order). Arrived intubated, sedated, on IABP, with temporary RV pacing wire, on norepinephrine 2.5 mcg/min. HR 84 BP 115/46 Repeat Swan: • RA 18 • PA 43/24 • CO/CI 2.6/1.35 11
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- 14. Clinical Summary Medical management? Further assistive support? Electrophysiologic prognosis, timeline, device requirement?
- 15. Dobutamine added Paceport PA Catheter placed for sequential AV pacing WBC in mid-20s (work-up over first 24 hours without evidence of systemic infection) 15
- 16. TTE on Admission
- 17. Right Ventricular Function and Ischemia
- 18. “Thus the right ventricle may be said to be made for the sake of transmitting blood through the lungs, not for nourishing them.” - William Harvey, 1616
- 19. • Most anteriorly situated chamber • Behind sternum • Shape of RV is complex: • RV appears triangular when viewed from • the side and crescent shaped when viewed in cross section • influenced by the position of the interventricular septum • Under normal loading and electrical conditions, the septum is concave toward the LV in both systole and diastole
- 20. RV delimited by the annulus of the tricuspid valve and by the pulmonary valve. RV Can be described in terms of 3 components: 1. the inlet, which consists of the tricuspid valve, chordae tendineae, and papillary muscles; 2. the trabeculated apical myocardium; 3. the infundibulum, or conus, which corresponds to the smooth myocardial outflow region
- 21. RV contrtraction is sequential: • contraction of the inlet and trabeculated myocardium and ending with the contraction of the infundibulum (approximately 25 to 50 ms apart) • Contraction of the infundibulum is of longer duration than contraction of the inflow region
- 22. The RV contracts by 3 separate mechanisms: 1. Inward movement of the free wall, which produces a bellows effect 2. Contraction of the longitudinal fibers, which shortens the long axis and draws the tricuspid annulus toward the apex; and 3. Traction on the free wall at the points of attachment secondary to LV contraction. Shortening of the RV is greater longitudinally than radially.
- 23. • RV afterload represents the load that the RV has to overcome during ejection • Heightened sensitivity to afterload change in comparison to LV • In clinical practice, pulmonary vascular resistance (PVR) is the most commonly used index of afterload
- 24. • Blood supply of RV varies by dominance • pRCA flow occurs in both diastole and systole • 80% of pop R dominant, RCA supplies RV • Lateral wall of the RV is supplied by the marginal branches of the RV • posterior wall and the inferoseptal region are supplied by the PDA • Anterior wall of the RV and the anteroseptal region are supplied by branches of the LAD • The infundibulum derives its supply from the conal artery, • separate ostial origin in 30% of cases. • separate ostium explains the preservation of infundibular contraction in the presence of pRCA occlusion Coronary Perfusion of RV
- 25. RV seems particularly resistant to ischemia More favorable oxygen supply-demand ratio • Lower O2 requirement due to smaller muscle mass in comparison to LV • Improved O2 delivery due to biphasic nature of coronary blood flow Left to right collateral blood flow ? – Direction perfusion of myocardium from RV via thesbian veins 25
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- 31. 48 hours after admission to CCU Remains in 3rd degree AVB RHC similar to admission High FiO2 and PEEP requirements Pressors weaned to dobutamine alone Ihaled epoprostenol added 31
- 32. Thereafter… FiO2 and PEEP requirements improved. Hemodynamics stabilized and IABP was weaned off. Pressors were quickly weaned. Although there was now intermittant sinus rhythm, patient remained in 3rd degree AVB for the majoriy of time. It was thought that atrial rhythm would be slow to return. Plans for PPM pacer were made, but before this a trial of theophyline was attemped. 32
- 33. Treatment 1) restoration of physiologic rhythm 2) optimization of ventricular preload 3) optimization of oxygen supply and demand 4) parenteral inotropic support for persistent hemodynamic compromise; 5) reperfusion, and 6) mechanical support with intra-aortic balloon counterpulsation and RV assist devices. 33
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- 35. Prognosis? 35
- 36. Many patients show spontaneous improvement in hemodynamic status in 3 to 10 days regardless of revascularization.1,2 RV performance may normalize in over 3 to 12 months.3,4,5 36 1. J Am Coll Cardiol 1984;4:931–9 2. Circulation 1987;75:996–1003 3. Br Heart J 1977;39:1319–23 4. Circulation 1987;75:996–1003 5. Am Heart J 1990;119:816–22 Pre-”modern” era of PCI
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- 39. Results Successful Unsuccessful N 40 12 Persistent hypotension 5 10 VT/VF 10 6 Death 0 7 39 These are the only 5 that lived!
- 41. Inhaled epoprostenol after heart transplant 41 n J Am Coll Cardiol 2001;38:923–31
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Editor's Notes
- presentation
- Post cath
- Temp wire, IABP, RHC
- the next day VF arrest, 2 rounds of CPR with with amiodarone drip started; bedside echo performed immediately after the code was reported to have inferior WMA with LVEF of 20%
- SMH presentation
- Underlying rhythm
- LV concentric LVH LVEF 45% LA 3.5 Trace TR PAS 36 mmHg TA 15 mmHg TR gradient 21 mmHg
- In contrast to the LV, twisting and rotational movements do not contribute significantly to RV contraction. Moreover, because of the higher surface-tovolume ratio of the RV, a smaller inward motion is required to eject the same stroke volume.
- Acute proximal RCA occlusion results in RV dysfunction in nearly 50% of cases with transmural infero-posterior infarction. Although the proximity of the culprit lesion and its relationship to RVFW perfusion correlates with the presence or absence of RVI in most patients, there are exceptions in which proximal occlusions do not result in RV ischemic dysfunction, attributable in most cases to restora- tion of RVFW perfusion through prominent collaterals or spontaneous antegrade reperfusion. In the rare cases in which RV ischemic dysfunction occurs in association with culprit lesions distal to the major RV branches, RV branch flow is impaired by adjacent thrombus or RV branch stenosis.
- In the past, however, the importance of RV function has been underesti- mated. This perception originated from studies on open- pericardium dog models and from the observation that pa- tients may survive without a functional subpulmonary RV (Fontan procedure). In the 1940s, studies using open- pericardium dog models showed that cauterization of the RV lateral wall did not result in a decrease in cardiac output or an increase in systemic venous pressure. 1–3 As was later dem- onstrated, the open-pericardium model did not take into account the complex nature of ventricular interaction. In 1982, Goldstein and colleagues2 showed that RV myocardial infarction (RVMI) in a closed-chest dog model led to signif- icant hemodynamic compromise. These findings were further supported by clinical studies demonstrating an increased risk of death, arrhythmia, and shock in patients with RVMI.
- When a closed pericardial model was developed RCA infarction in canines, it was shown that there was acute RV dilatation and consequent intrapericardial pressure elevation due to the pericardial constraint. There is also a reduction in RV systolic pressure, LV end diastolic size, CO, and aortic pressure. All of these findings normalized when the pericardium was incised. As filling progresses, the noncompliant right ventricle ascends a steep pressure-volume curve, lead- ing to a pattern of rapid diastolic pressure elevation. Right ventricular diastolic dysfunction adversely affects LV diastolic properties through diastolic interactions mediated by the reversed curved septum and exacerbated by elevated intrapericardial pressure (9,39–45). Acute RV dilation and elevated RV diastolic pressure shift the interventricular septum toward the volume-deprived left ventricle, thereby impairing LV compliance and further limiting LV filling. More than this, under normal conditions, it has been shown that early systolic bulging of the septum into RV, contributing to early generation of RV pressure and effective pulmonary blood flow. This observation may explain why decomposition more frequent with anterior or septal concomitant involvement. Hemodynamics in progressive pulmonary vascular disease. A decrease in pulmonary arterial pressure (PAP) in patients with PH may be a sign of low cardiac output (CO) and severe RV failure. PVR indicates pulmonary vascular resistance; PCWP, pulmonary artery capillary wedge pressure; and MPAP, mean PAP.
- With RVI: peak RV systolic pressure is depressed and RV relaxation is delayed. “a” wave is augmented as mean atrial pressure is increased. There is now a prominent x descent a relatively blunted y descent. The y descent is blunted because the RV is relatively dilated and stiffened by this point and this imparts resistance to early filling. Note that diastolic RV and LV pressures are elevated and equalized. With RAI: The mean RA pressure is elevated with now severe depression of the “a” wave and blunting of the x descent.
- High-grade atrioventricular (AV) block and bradycardia- hypotension without AV block commonly complicate infe- rior myocardial infarction (56–58) and have been attributed predominantly to the effects of AV nodal ischemia and cardioinhibitory (Bezold-Jarisch) reflexes arising from stim- ulation of vagal afferents in the ischemic LV inferoposterior wall (59–61). We and others have documented that in patients with acute RVI there is an increased incidence of high-grade AV block compared to those without right heart involvement (12,15,62–64). Recent observations from our laboratory now also document that bradycardia-hypotension without AV block is also more common in patients with RVI (65,66)