Right ventricular infarction

Important yet a neglected topic

1. RIGHT VENTRICULAR INFARCTION DR. VIJAY YADAV DM RESIDENT 1 ST YEAR MCVTC, IOM

2. Introduction Acute myocardial infarction (MI) involving only the right ventricle is an uncommon event. In 1930, Sanders first described the syndrome of RVMI with the triad of hypotension, increased JVP, and clear lung fields. RV involvement in myocardial infarction was first described in 1974. In 1979, Cohn published a classic report in which RVMI was described as distinct entity. Occurs in 30-50% of Inferior wall STEMI. Isolated RVMI occurs in 3-5% of cases. RVMI is associated with higher in-hospital morbidity and mortality due to profound hemodynamic and electrical complications which occur in approximately 50 percent of affected individuals. Mortality from RV shock = Mortality from LV shock RV recovery >>>> LV recovery

3. ANATOMY AT A GLANCE Right Ventricle Trabeculated endocardial surface Thin walled (< 5mm) Three papillary muscles Moderator band Triangular shaped cavity Tricuspid atrioventricular valve with relatively apical insertion Crista supraventricularis separates the tricuspid and pulmonary valves Left Ventricle Smooth endocardial surface Thick walled Two papillary muscles False tendon Elliptical shaped cavity Mitral atrioventricular valve with relatively basal insertion The mitral and aortic valves share fibrous continuity

4. RV PHYSIOLOGY AT A GLANCE The RV wall is thinner (< 5mm) and more complaint than the LV wall. Composed of circumferential fibers in the subepicardium and longtudional fibers in the subendocardium . There is inward, longitudinal, and circumferential traction in RV due to LV contraction. Longitudinal shortening is the major contributor to the overall RV performance. Normal RV contraction occurs as a peristaltic wave directed from inflow to infundibulum. RV pumps the same stroke volume as the LV but uses only 25% of the stroke work because of low resistance of pulmonary vasculature. RV is closely connected to LV: Share a wall (IVS) RV free wall is attached to the anterior and inferior IVS Have mutually encircling epicardial fibers Share the same intrapericardial space Ventricular Interdependence

5. ARTERIAL SEGMENT ARTERIAL BRANCH PERFUSED REGION ECG EFFECTS OF ISCHEMIA Proximal segment Conus branch Outflow tract of RV SA nodal branch SA node Sinus bradycardia Right atrial branch Atrial free wall Atrial fibrillation Atrial infarct pattern Middle segment Lateral RV branch Lateral RV free wall STE and Q waves in leads V3R – V6R Acute Marginal Inferior(Posterior) RV free wall Distal segment AV nodal branch AV node AV block Posterior descending segment Posterior lateral LV branch Posterior descending artery Posterior LV Inferior septum Inferior LV free wall STE and Q waves in II, III, aVF

6. Factors that make the right ventricle less susceptible to infarction:

7. 1) Coronary perfusion in the right ventricle occurs in both systole and diastole LC blood flow is impeded by extravascular compressive forces generated by systolic LV contraction. These forces are so high that LC blood flow is briefly reversed. LC blood flow increases to a maximum early in diastole and then falls gradually following the decline in aortic pressure during the remainder of diastole . Because of a lower developed pressure in the RV, there is no systolic inhibition of RC blood flow. RC blood flow follows the shape of the aortic pressure curve and remains appreciable throughout the entire cardiac cycle.

8. 2) Reduced myocardial oxygen demand because of smaller muscle mass and low afteralod . 3) Reduced myocardial oxygen uptake and blood flow 4) Oxygen extraction reserve 5) More extensive collateral flow from left to right coronary arteries  6) Greater degree of ischemic preconditioning 7) Ability to downregulate the metabolic demand during coronary hypoperfusion .

9. Pathophysiology RVI results in reduced RV systolic contraction (RVSP and PP are decreased) RVI results in RV diastolic dysfunction (elevated r ight sided filling pressures like CVP, RA, and RVEDP). Reduction in RV output & blood supply to the lungs. Reduced pulmonary flow decreases pulmonary venous return to LA and LV. (decreases LV preload and LV filling). Reduced LV output and systolic BP. RVI leads to RV dilatation which alters the motion of IVS; i.e. leftward shift of septum during diastole which further impedes LV filling and eventually reduces CO. LV dyssynchrony due to abnormal septal motion and loss of AV synchrony when there is AV block also leads to decreased CO. Dilatation of RV enlarges tricuspid annulus which results in functional TR that further reduces RV output. When RCA occlusion is proximal to right atrial branch, RA ischemia occurs that diminishes its contraction and increases RA pressure and further increases the probability of atrial arrhythmia.

10. Elevated right sided filling pressure in the presence of normal pulmonary artery and left sided filling pressure is the hallmark of RVI RA pressure: 10 mm Hg PCWP: 1-5 mm Hg Sensitivity: 73% Specificity: 100%

11. Diagnosis

12. Symptoms Signs Clinical Features Chest pain Diaphoresis Nausea and Vomiting Syncope (if AV block) Palpitation Dizziness Anxiety Triad of hypotension, raised JVP, and clear chest Jugular venous pressure: Prominent a wave & x descent if RA ischemia is absent Diminished a wave, x & y descents if RA ischemia is present If TR present: Prominent a wave, c-v wave ( Lancisi’s sign), & y descent and absent x descent Kussmaul’s sign: Highly predictive of RVMI in the setting of IWMI Pulsus paradoxus Right sided S3

13. INFERIOR WALL MI RIGHT CORONARY ARTERY LEFT CIRCUMFLEX ARTERY STE III > II ST depression aVL > I S/R ratio in aVL > 3 V3/III sign (ST↓ V3/ STE III ratio) <0.5: Prox RCA 0.5-1.2: Distal RCA >1.2: LCx RAD of ST vector (lead III) STE II > III No ST ↓ in aVL S/R ratio in aVL < 3 V3/III sign > 1.2 LAD of ST vector (lead II)

14. RVMI FROM 12 LEAD ECG ST elevation in III > II (Pathognomonic of RVMI ) ST elevation in V1 > V2 ST elevation in V1 + ST depression in V2 (Highly specific for RVMI) ST elevation in aVF > ST depression in V2 Isoelectric ST segment in V1 with marked ST depression in V2 ST depression in I + aVL > 2 mm ST depression in V2 ≤ 50% of STE in aVF ST depression in V3 < ½ STE in III Isolated RVMI from non-dominant RCA: ST elevation in V1-V4 (mimics AWMI; ST segment maximal in V1 in RVMI whereas it is minimal in AWMI) ST elevation in the right sided leads is a transient phenomenon, lasting less than 10 hours in 50% of patients with RV infarction

15. RVMI FROM A RIGHT SIDED ECG The precordial leads are placed over the right side of the chest in a mirror image pattern to normal. Right sided leads V4R, V5R, & V6R should be obtained in any patient with inferior wall infarction. ST elevation in V4R > 1mm: Sensitivity: 100% Specificity: 87% Positive predictive value: 92% Correlates with occlusion of proximal RCA.

16. Diagnosing RVMI is a rule in IWMI STE in V1 and III>II in IWMI

17. Echocardiography Sensitivity: 82% & Specificity: 93% for detection of RVI. The specificity may be decreased by pre-existent pulmonary diseases (COPD, PE) Most specific: RV free wall hypokinesia RV dilatation with paradoxical septal motion RA dilatation and increased RAP RV systolic dysfunction Functional tricuspid regurgitation : Hallmark Persistent bowing of IAS from right to left (RAP > LAP) Patent PFO on saline contrast echo leading to profound hypoxemia Dilated IVC with poor respirophasic variation

18. Qualitative Quantitative RV dilatation In A4CH view Mildly enlarged: RV is enlarged but < LV Moderately enlarged: RV = LV Severely enlarged: RV > LV Apex of heart comprised of RV In RV focused A4CH at end-diastole RV basal diameter > 4.2 cm RV midcavity diameter > 3.5 cm RV longitudional diameter > 8.6 cm RVOT PLAX proximal diameter > 3.5 cm RVOT PSAX distal diameter > 2.7 cm

19. Measured at end-diastole Major dimension: > 53mm Distance from the superior wall to the TA Minor dimension: > 44mm Distance from interatrial septum to the anterolateral wall RA area: > 18 cm2 IVC diameter (cm) Response to sniff RA pressure (mm Hg) ≤ 2.1 > 50% collapsible 3 ≤ 2.1 < 50% collapsible 8 > 2.1 < 50% collapsible 15 RA dilatation Estimation of RAP

20. RV systolic dysdunction Tricuspid Annular Plane Systolic Excursion (TAPSE): < 16 mm Pulsed doppler peak velocity at the annulus: < 10 cm/sec RV Fractional Area Change (FAC): < 35% Normal: 32-60% Mildly reduced: 25-31% Moderately reduced: 18-24% Severely reduced: < 17% Reduced RV stroke volume: RVOT VTI < 12 cm = RV CO < 2.2 l Pulsed Doppler MPI > 0.40 Tissue Doppler MPI > 0.55

21. Pulsed wave doppler MPI Tricuspid valve inflow & Pulmonary valve outflow doppler tracings are acquired in RV modified A4CH and PSAX views. Time duration from the end of A wave to the onset of E wave is calculated. (TV closure to opening time) RVET from pulmonary doppler tracing is measured. Isovolumic time = (RVET – TV A to E duration) RVMPI = Isovolumic time/RVET In this case it is (386 – 271)/271 = 0.43

22. RV wall motion assessment Lateral & Inferior wall hypokinesia : Proximal RCA A nterior wall hypokinesia : LAD Inferior wall hypokinesia : PDA

23. Other Imaging studies for RVMI Radionuclide ventriculography & 99mTC-pyrophosphate myocardial scintigraphy are sometimes used. Standard imaging technique for detailed evaluation of RV structure & function. RV free wall myonecrosis is indicated by late gadolinium enhancement. Nuclear Imaging Cardiac MRI

24. Hemodynamic monitoring Done if a secure diagnosis of RVMI by echo is not possible. Done by placement of a pulmonary artery catheter. Done cautiously as ischemic RV is prone to catheter-induced ventricular arrhythmias. Characteristics of a hemodynamically significant RV infarct RA pressure ≥10 mm Hg Ratio of RAP to PCWP > 0.8 (Normal is < 0.6) Decreased cardiac index Equalization of diastolic filling pressures of RA, RV, PCWP & LV Square root sign

25. Differential diagnosis Acute pulmonary embolism Cardiac tamponade Constrictive pericarditis Restrictive cardiomyopathy Severe pulmonary hypertension Acute anteroseptal wall MI (STE in V1 and V2 seen with an RV injury pattern)

26. Management Optimization of RV preload: IV Fluid ( Isotonic saline) in patients with hypotension & low/N JVP 300-600ml preferably through central line over 10-15 minutes while serially assessing JVP and BP Invasive hemodynamic monitoring with a Swan Gang Catheter Target PCWP: not to exceed 20 mm Hg Avoidance of Nitrates, Diuretics, & Opoids : Cause venodilatation and further reduces RV preload Ionotropic agents: Hemodynamic instability (raised RAP & PCWP) despite adequate IVF Dopamine is the initial agent of choice (5 – 15 mcg/kg/min) Dobutamine @ 5 – 20 mcg/kg/min Milrinone Levosimenden

27. Coronary reperfusion: Either PPCI or thrombolysis can preserve both LV and RV function thereby improving clinical, hemodynamic, and survival parameters. Reduces chances of ventricular arrhythmias. RV function recovers completely within 24 hours.

28. Intra-Aortic Balloon Pump (IABP): Cardiogenic shock due to LV dysfunction Little benefits in shock due to RVMI Still can be used for temporary stabilization Increases RV perfusion pressure & improves septal contraction RV Mechanical assist devices: Medically refractory cases despite successful reperfusion Tandem-Heart Percutaneous Ventricular Assist Device

29. AV sequential pacing: The ischemic RV has a fixed stroke volume RV output depends upon heart rate & atrioventricular transport In patients requiring pacing, ventricular pacing alone may fail to increase cardiac output Atropine and Temporary pacemaker Inhaled Nitric Oxide: Decreases PVR without any effect on SVR Decreases RV afterload and increases BP Valve replacement or repair with annuloplasty rings PFO Occluder device for hypoxemia due to right to left shunt across IAS.

30. Standard MI treatment Aspirin P2Y12 receptor blocker Statin Anticoagulant Nitrate Opoids Beta blocker Diuretics GIVE DO NOT GIVE

31. Prognosis Higher incidence of cardiogenic shock, ventricular arrhythmia, advanced AV block, and death if PCI not done. In-hospital mortality: 23 and 53% with cardiogenic shock in 2 different studies. PPCI results in prompt & dramatic improvement in hemodynamics with excellent clinical outcomes. Determined by extent of LV involvement. Near complete RV recovery in 62-82% of patients within first few months Short term prognosis Long term prognosis

32. Anterior wall MI vs. Inferior wall MI

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