Low cardiac output can be because of Rt. Ventricular failure and pulmonary hypertension.
Preexisting conditions leading to this are-
- Rt.coronary artery disease,
- Rt.ventricular infarction,
- pulmonary hypertension.
Etiology
- Poor myocardial protection .
- Prolong ischaemic time or myocardial stunning.
- Coronary embolism of air.thrombi or particulate matter.
- Systolic hypotension which causes RV ischaemia.
- Acute pulmonary hypertension -1.vasoactive substances of blood product transfusions on CPB.
- LV dysfunction.
- Protamine reaction
- Hypoxia ,acidosis.
- ventricular pressure overload.
- RV dysfunction diagnosed by-high RA/PA PRESSURE,ratio of RV/LV -.>1
- RV dysfunction may contribute to progressive LV dysfunction.RV dilates ,its shifts IVS ro left side and impaire LV distensibility.
Pathophysiology
RV Dysfunction
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Interventricular septal shift to left
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Decreased left ventricular distensibility
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Progressive left ventricular dysfunction
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Decreased systemic perfusion pressure
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Causing right ventricular ischaemia
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Increased pulmonary artery pressure + increased right ventricular afterload
GOALS
- Optimize RV preload
- Maintain systemic perfusion
- Improve RV contractility
- Reduce RV afterload
- Reduce pulmonary vascular resistance
- Preloading with target of RA pressure 15-18 mmhg
- AV conduction is essential
- Correction of hypothermia,hypoxia & hyperventilation & decrease pulmonary vascular resistance
- Medications with positive inotropic effect while reducing PA pressure
☛ phosphodiasterase inhibitors-amrinine,milrinine
☛ isoprotenerol
Pulmonary vasodilators
- prostaglandins E1-potent pulmonary vasodilator <0.1 mcg/kg/min
- inhaled nitric oxide-endothelium derived releasing factor
☛ 20-40ppm administered in ventricular circulation
☛ Circulation should optimally make o2 & NO togenerate a low level of NO2 which is toxic to lung tissue
☛ Diastolic dysfunction impaired
☛ Systolic relaxation or decreased
☛ Diastolic compliance with inappropriate tachycardia