Right Ventricle Flashcards

1
Q

normal right ventricular structure

A

*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

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2
Q

comparing the right and left ventricle: EDV & EF

A

*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)

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3
Q

comparing the right and left ventricle: walls

A

*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

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4
Q

right ventricle - response to pressure overload

A

*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

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5
Q

right ventricle - response to volume overload

A

*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

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6
Q

pulmonary vs. systemic resistance

A

*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

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7
Q

effect of oxygen on pulmonary arterioles

A

*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)

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8
Q

causes of pulmonary hypertension

A

*left-sided heart failure
*mitral stenosis
*primary pulmonary HTN
*COPD
*pulmonary embolism
*obstructive sleep apnea
*rheumatological processes (lupus/scleroderma)

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9
Q

how COPD → pulmonary HTN

A

*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

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10
Q

how obstructive sleep apnea → pulmonary HTN

A

*airways blocked leads to decreased oxygen level - oxygen can’t get into the lungs
*low oxygen level → pulmonary arterial vasoconstriction, which causes pulmonary HTN

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11
Q

how pulmonary embolism → pulmonary HTN

A

*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

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12
Q

how pulmonary embolism → systemic HYPOtension & cardiovascular collapse

A

*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

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13
Q

pulmonary HTN leading to further pulmonary HTN

A

*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

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14
Q

inferior STEMIs

A

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

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15
Q

clinical manifestation of right ventricular MI

A

*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)

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16
Q

right ventricular MIs: treatment

A

*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]

17
Q

Eisenmenger’s Syndrome (stage 1)

A

*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

18
Q

Eisenmenger’s syndrome (stage 2): effect on pulmonary vasculature

A

*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

19
Q

Eisenmenger’s syndrome (stage 3): right to left cardiac shunt

A

*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)

20
Q

Eisenmenger’s syndrome - overview

A
  1. left-to-right cardiac shunt (SVR > PVR) → oxygenated blood moving from arterial side to deoxygenated side, exposing the pulmonary vasculature to systemic blood pressures
  2. hypertrophy of pulmonary arteries/arterioles in response to exposure to systemic blood pressure → pulmonary HTN
  3. 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

21
Q

Eisenmenger’s syndrome - signs/symptoms

A

*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

22
Q

the right ventricle as the systemic ventricle: L-TGA

A

*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)