Acute rv failure physiology to management

ACUTE RV FAILURE
PHYSIOLOGY TO MANAGEMENT
Dr. DEV PAHLAJANI MD,FACC,FSCAI
HOD 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
circulations
Systolic 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

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 and
anatomy
Enlargement of the right side of the heart
as a consequence of RV
infarction.

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 FAC
Anterior 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

Prognosis
Outcome 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

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

Transesophageal
echocardiography
• 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.

Acute rv failure physiology to management

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