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)
right ventricular MIs: treatment
*many people with RV MIs get nitroglycerin and do fine
*if someone becomes hypotensive, give IV fluids [they won’t get pulmonary edema b/c that is a left-sided problem]
Eisenmenger’s Syndrome (stage 1)
*the development of pulmonary hypertension due to a left-to-right cardiac shunt
*when SVR > PVR, blood shunts through defect left to right
*this means that oxygenated blood goes from arterial side to the deoxygenated side (from LV to RV in setting of VSD; from aorta to pulmonary artery in setting of PDA)
*pulmonary vasculature is exposed to systemic blood pressure → hypertrophy of pulmonary arteries & pulmonary arterioles
*as pulmonary arteries & arterioles hypertrophy, pulmonary vascular resistance increases, eventually impairing the lung’s ability to oxygenate
Eisenmenger’s syndrome (stage 2): effect on pulmonary vasculature
*pulmonary vasculature is exposed to systemic blood pressure → hypertrophy of pulmonary arteries & pulmonary arterioles
*as pulmonary arteries & arterioles hypertrophy, pulmonary vascular resistance increases, eventually impairing the lung’s ability to oxygenate
Eisenmenger’s syndrome (stage 3): right to left cardiac shunt
*when PVR > SVR, blood preferentially travels right to left through the shunt
*this means deoxygenated blood is going straight to systemic circulation (oxygen saturation goes down)
Eisenmenger’s syndrome - overview
- left-to-right cardiac shunt (SVR > PVR) → oxygenated blood moving from arterial side to deoxygenated side, exposing the pulmonary vasculature to systemic blood pressures
- hypertrophy of pulmonary arteries/arterioles in response to exposure to systemic blood pressure → pulmonary HTN
- pulmonary HTN → PVR > SVR → right-to-left cardiac shunt → deoxygenated blood moving straight into systemic circular (O2 sat decreases)
*note: once pulmonary HTN develops and blood starts shunting right-to-left, it is considered irreversible; only tx would be a heart/lung transplant
Eisenmenger’s syndrome - signs/symptoms
*clubbing
*polycythemia (secondary to decreased O2 sat)
*hemoptysis (secondary to pulmonary HTN)
*heart failure
*note: once pulmonary HTN develops and blood starts shunting right-to-left, it is considered irreversible; only tx would be a heart/lung transplant
the right ventricle as the systemic ventricle: L-TGA
*L-TGA: L-type transposition of the great vessels
*blood comes into RA → left ventricle → pulmonary artery → lungs → left atrium → RIGHT VENTRICLE → aorta
*right ventricle is not well-suited to handle the pressure that the left ventricle was designed to handle
*survival tends to be less than normal people (avg. life expectancy decreased; present with CHF in 30s-40s)
