acute rv failure physiology to management

ACUTE RV FAILUREPHYSIOLOGY TO MANAGEMENT

Dr. DEV PAHLAJANI MD,FACC,FSCAIHOD INTERVENTIONAL CARDIOLOGY BREACH CANDY HOSPITAL MUMBAI

Venous Return Physiology

• “Most People have a Cardiocentric view of the World.” – Michael O’Conner

• The Heart can only pump out, what comes in. Therefore the main job of the RV is to maintain a low right atrial pressure so that Venous Return is optimized.

Anatomy The RV is triangular in shape

Divided into three regions –Inlet–Apex–Infundibulum or Conus

Both Ventricles are composed of a 3D network of muscle fibers

Circulation 2008;117:1436-1448

In idiopathic PAH, the RV is characterized by increased end-diastolic volume, change of the

normal ventricular conformation tetrahedron to a crescentic trapezoid, and varying degrees of

right ventricle hypertrophy

Voelkel NF et al Circulation, Volume 114(17) 2006

The RV in severe idiopathic PAH assumes a spherical shape with a greater cross-sectional area than the LV, which is normally larger

Right ventricle in pulmonary hypertension /RVI

Mechanisms of RV Dysfunction in Critically Ill Patients

Lahm et al JACC Vol. 56, No. 18, 2010.

Effect of Ventricular Afterload• As a result of the lower pulmonary circuit pressures the period of

Iso volumic contraction is less compared to the LV (or Pressure loaded RV). This results in decreased Myocardial oxygen demand.

• Additionally the point of semi lunar valve closure is delayed leading to a prolonged ejection phase.

Normal pressures and vascular resistance in the pulmonary and systemic

circulationsSystolic Diastolic

Right ventricle 15- 25 1- 7 Pulmonary artery 8- 12 Left ventricle 90-140 5- 15 Aorta 60- 90 Pulmonary vascular resistance

150 – 250

Systemic vascular resistance

900-1400

Leo G. K and Barnard M CEACCP , Vol 7 (3) 2007

Aortic Pressure and Coronary Blood Flow

Frank-Starling Law of the Heart

• States that strength of ventricular contraction varies directly with EDV– Is an intrinsic property

of myocardium– As EDV increases,

myocardium is stretched more, causing greater contraction & SV

Hemodynamic effects of fluid loading in acute massive pulmonary embolism

Anatomy

In ≤10% of patients, the left circumflex CA supplies perfusion to a larger extent of the RV than usual, through posterior diagonal branches off the posterior descending CA and from acute marginal branches of an ongoing circumflex

after the crux.

Right ventricular infarction- Elsevier Health, 2006

RCA Distal

RVI Haemody

• Increased RV compliance

• Increased RVEDP and RA pressure

• Shift of IVS to left --LV interdependence

• Increased LVEDP

• Reduced stroke volume

Anatomical changes in RV infarction

Normal atrial size andanatomy

Enlargement of the right side of the heart as a consequence of RVinfarction.


RV infarction (RVI)

• RVI rarely isolated Associated with 30-50 % acute INF STEMI

• The syndrome of RVI is that of low output and hypotension.

• Responsible for some cardiogenic shock cases and a larger proportion of hypotensive inferior infarction cases.


Relationship to different infarcts

Infarct Location RV Dysfunction RV FACAnterior 16.7% 42.5 ± 10%

Inferior only 22.9% 40.1 ± 10%Anterior and inferior 26.9% 38.7 ± 11%

Any inferior 24.2% 39.5 ± 11%Other 11.8% 41.2 ± 8.5%


Clinical presentation • Hypotensive inferior infarction

• Inferior infarction, cardiogenic shock

• Inferior infarction with venous distention, Kussmaul sign

• Inferior infarction, BP intolerant of GTN

• Larger biomarker rise than anticipated from inferior infarction

• Greater amount of hypotension than expected from a first

infarct with a small or moderate creatine kinase rise


• TOP, ECG shows complete heart block with an irregular wide complex ventricular rhythm. There is no pacemaker capture due to RV infarction.

• MIDDLE, CXR shows normal-sized cardio pericardial silhouette, no pulmonary edema.

• BOTTOM, ECG on arrival shows asystole with ventricular escape beats.

CASE STUDY

• 49 yrs. male

• Chest pain few hours

• Persistent hypotension BP 80/60,hr 60

• Pale

• Lungs clear

• Raised troponins

CASE STUDY

• Post PPCI - pain free

• Persistent hypotension despite fluid load

• Adequate urine output

• Dopamin, nor ad.

• Weaned off after 3 days

Why all patients do not respond to fluids?

• LV dysfunctio due to leftward shift of IVS

• Increased LVEDP

• Reduced LV compliance and cavity

• RV dilat. leads to increased int pericardial pressure

• Geometric deformity

In idiopathic PAH, the RV is characterized by increased end-diastolic volume, change of the

normal ventricular conformation tetrahedron to a crescentic trapezoid, and varying degrees of

right ventricle hypertrophy

Voelkel NF et al Circulation, Volume 114(17) 2006

The RV in severe idiopathic PAH assumes a spherical shape with a greater cross-sectional area than the LV, which is normally larger

Right ventricle in pulmonary hypertension /RVI

Venous return caves

PrognosisOutcome No RV Dysfunction RV Dysfunction

OR for RV Dysfunction (95%

CI)Death 14.5% 38.0% 3.6 (2.1–6.2)CVD 12.2% 32.9% 3.5 (2.0–6.3)HF 17.2% 30.4% 2.1 (1.2–3.7)

Death or HF 26.7% 50.6% 2.8 (1.7–4.7)Recurrent MI 13.3% 10.1% 0.7 (0.3–1.6)

Leonardo A.M. Zornoff, et al JACC,2002;39(9):1450-1455.

In Hospital Outcomes

• In hospital outcomes in patients with predominant RV and LV shock.

Jacobs KA et al , JACC, 2003;41(8):1273-1279.

1 month post infarction survival

• At 1 month after infarction, almost all survivors have normal RV systolic function, but few have normalized LV systolic function.


Treatment in RVI and LVI

LV INF.CLASS 3

• Modest diuresis

• IV NTG/nitropruss

• ACE inhibitors

• Volume restriction

• IABP+ PCI

RV INF.FAILURE

• Restrict diuretics

• No vasodilators

• No ACE inhibitors

• Volume++

• PPCI and IABP if LV failure

Therapy of different cases • Asymptomatic case Avoid diuretics and vasodilators that may precipitate low

output and hypotension• Symptomatic low-output state and normotensive with RA

pressure or pulmonary capillary wedge pressure <15 mm Hg– Add fluid to increase the PCWP to 15-18 mm Hg. – If cardiac output does not increase adequately, add a

vasodilator.– If the cardiac output still does not– increase adequately, add dobutamine or amrinone.– Reperfusion therapy should be considered.


• Symptomatic low-output state and normotensive with RA pressure or PCWP >15 mm Hg– Add intravenous dobutamine or amrinone.– Additional vasodilator with fluid therapy support may be

added.– Primary PCI with stent treatment of choice

• Cardiogenic shock– Sustain BP with dopamine; additional dobutamine may

increase cardiac output.– Consider RV assist or pulmonary artery counter pulsation for

select cases.– Primary PCI therapy is strongly recommended

Therapy of different cases


RV INFARCION PPCI-JACC 1995

RV INFARCTION PPCI-JACC 1995

In Hospital Survival

• Survival curves for patients with predominant RV and LV shock.

• In-hospital survival rates were 46.9% for patients with

predominant RV shock 39.2% for patients with

LV shock.


Right Ventricle Recovery

The RV recovers more and faster than does the inferior wall of the LV


Transesophagealechocardiography

• Marked RA and RV dilation. The left-sided heart chambers are small• because of underloading. Interatrial septal bulging to the left side suggests that RA

pressure is greater than LA pressure. The right ventricular free wall is severely hypokinetic or akinetic, despite

• inotropic support. There is no pericardial effusion.

Differential diagnosis

• Under filling of the LV– Hypovolemia, may be from medications– RVinfarction

• • Vasodepression– Excessive effect of medications– Medication-induced anaphylaxis– Vagal vasodepressant state

• Tamponade• Ventricular septal rupture


Mortality

Mortality for patients with predominant RV and LV shock undergoing CABG and PTCA


Auto-Aggravation: The Vicious Cycle


Pressure–volume loops for the RV and LV.


THANK YOU!!

acute rv failure physiology to management

Education

rv dysfunction rv dysfunction

consequence of rv infarction

rv infarction rvi rvi

inferior infarction

mechanisms of rv dysfunction

larger right ventricle

cavity rv dilat

acute rv failure physiology