Right Ventricle Flashcards
normal right ventricular structure
*long axis: shape of triangle
*short axis: half circle attached to the left ventricular septum
*right ventricle sits anterior, right behind the sternum (most at risk during a collision if sternum hits the wheel)
*ejects blood into the main pulmonary artery
comparing the right and left ventricle: EDV & EF
*R ventricle holds slightly more blood than the left ventricle (RV EDV > LV EDV)
*right ventricular ejection fraction is roughly 10% less than the left ventricle (stroke volume is the same)
comparing the right and left ventricle: walls
*the LV wall is much thicker than the RV wall
*this is b/c the LV is working against a pressure of 100-200 mmHg, but the RV is working against a pressure of < 30 mmHg
right ventricle - response to pressure overload
*RV responds in much the same way as the LV does to dealing with increased pressure → its WALL THICKENS
*causes of RV pressure overload:
1. pulmonary hypertension
2. pulmonic stenosis
right ventricle - response to volume overload
*RV responds in much the same wave as the LV does to dealing with increased volume → it DILATES
*causes of RV volume overload:
1. tricuspid regurgitation
2. pulmonic regurgitation
3. atrial septal defect
pulmonary vs. systemic resistance
*left: systemic arterioles → main driver of systemic vascular resistance (MAP = CO x SVR)
*right: pulmonary arterioles → main driver of pulmonary vascular resistance (MPAP = CO x PCWP)
-pulmonary vascular resistance is much lower than that in the systemic circuit
effect of oxygen on pulmonary arterioles
*unlike systemic arterioles, PULMONARY arterioles DILATE in the presence of oxygen [meaning they constrict in the absence of oxygen]
*this is b/c you want to get blood to where the oxygen is for gas exchange to take place in the lungs
*gas exchange minimized in locations where oxygen is reduced (pneumonia)
causes of pulmonary hypertension
*left-sided heart failure
*mitral stenosis
*primary pulmonary HTN
*COPD
*pulmonary embolism
*obstructive sleep apnea
*rheumatological processes (lupus/scleroderma)
how COPD → pulmonary HTN
*COPD destroys capillaries & creates large bullae
*COPD reduces oxygen level in lung → pulmonary arterial vasoconstriction
*inflammatory mediators → pulmonary arterial vasoconstriction
*reduced vascular space with same cardiac output → higher pressures within the pulmonary vascular space
how obstructive sleep apnea → pulmonary HTN
*airways blocked leads to decreased oxygen level - oxygen can’t get into the lungs
*low oxygen level → pulmonary arterial vasoconstriction, which causes pulmonary HTN
how pulmonary embolism → pulmonary HTN
*a PE blocks the pulmonary arteries, effectively reducing vascular space
*having the same cardiac output, the pressure inside the pulmonary arteries increases, which acutely makes the RV have to work harder
how pulmonary embolism → systemic HYPOtension & cardiovascular collapse
*a PE blocks the pulmonary arteries, effectively reducing vascular space & PREVENTS BLOOD FROM GETTING INTO THE LEFT VENTRICLE
*DECREASED LV FILLING → reduced cardiac output → reduced blood pressure
*life-threatening situation
pulmonary HTN leading to further pulmonary HTN
*as pulmonary arterioles hypertrophy from increased pressure, it can further exacerbate the problem
*hypertrophied arterioles are an effort to respond to increased pressure in the vessels, but increased hypertrophy can cause the pressure to get even higher
inferior STEMIs
ST elevations in II, III, and aVF (inferior MI) →
1. ST elevations in V1 → inferior MI with RIGHT VENTRICULAR INVOLVEMENT
OR
2. ST depressions in V1 → inferior MI with posterior involvement
clinical manifestation of right ventricular MI
*RV infarcts become HYPOTENSIVE when nitroglycerin is given
*how?:
-normal pulmonary vascular resistance is very low (<200 dynes), meaning that the afterload is already very low (there is not much we can do to decrease the afterload further)
-RV MI reduces contractility
-when nitroglycerin is given, stroke volume is reduced (SV was already compromised from decreased contractiltiy)