Pulmonary HTN and Cor Pulmonale Flashcards
Pulmonary HTN def
elevated pressures in the pulmonary vasculature system
- arterial from right ventricle
- venous side coming back into the atrium
Cor Pulmonale def
elevated pressures in pulmonary vascular system leading to enlargement of the right side of the heart, usually the right ventricle
Right atrium pressure
5 mmHg
nickel
Left atrium pressure
10 mmHG
dime
Right ventricle pressure
25 mmHG quarter
left ventricle pressure
124 mmHG $1.25
what is normal pulmonary artery pressure
20/10
what is normal resting pulmonary artery pressure
around 15 mmHg
What pressure defines pulmonary hypertension
pulmonary artery pressure of =>25 mmHg
List of things that cause pulmonary hypertension
- Pulmonary arterial HTN (primary and secondary)
- Pulmonary venous HTN due to left sided heart disease
- Pulmonary hypertension associated with disorders of respiratory system
- Chronic thrombotic and/or embolic disease
- Disorders affecting pulmonary vasculature
Primary arterial PH
- sporatic
- familial
- pathophys is in small pulmonary arteries and arterioles
- increased contraction and decreased relaxation which elevates pressure
secondary arterial PH
- collagen vascular disease (RA, lupus, etc.)
- congenital: pulmonary left to right shunts, overload right side of heart
- portal HTN - back pressure to right side of heart
- HIV
- drugs/toxins
Pulmonary venous HTN
left sided heart disease
- ventricular heart disease
- valvular heart disease
- pulmonary veno-occlusive disease
what is pulmonary veno-occlusive disease?
veins returning to LA are clotted
PH associated with disorders of the respiratory system
- COPD
- Interstitial lung dz
- sleep disordered breathing
- alveolar hypoventilation disorders (central sleep disorder due to brain problem)
PH due to chronic thrombotic and embolic dz
- thromboembolic obstruction of proximal pulmonary arteries (chronic emboli)
- obstruction of distal pulmonary arteries (PE or sickle cell dz)
PH due to disorders affecting pulmonary vasculature
- sarcoidosis (fibrosis interferes with circulation, similar to COPD)
- scleroderma (collagen vascular dz)
Two classifications of pathophysiology
- pre-capillary - problem is in pulmonary artery or arteriole
- passive - pressure is on left side of the pulmonary capillary, pulmonary venous side or “back pressure” usually due to left sided heart disease
Mild clinical manifestations
fate and vague chest discomfort
severe clinical manifestations
wide range
- dyspnea (most common)
- SOB
- syncope
- atypical chest pain
true or false, PH is the most common cause of dyspnea when pt has PH
FALSE
- would never jump to PAH if pt has dyspnea, would suspect many other things first
PE findings with mild PH
no discernable physical findings
what are two major heart sounds heard on every healthy heart
S1 and S2
What is S1
closer of the AV valves
What is S2
A2 and P2 which are aortic and pulmonary valves
Which closes first, A2 or P2? Why?
A2
- pressure on the left side > right side so aortic pressure is higher which causes the aortic valve to close slightly faster than the pulmonic valve
Which heart sound is louder when listen at the base of the hearT? why?
S2, because you’re physically closer to the aortic and pulmonary valves
What happens on inspiration to heart sounds?
separation between A2 and P2
Why is there separation between A2 and P2 on inspiration
when inspire, pressure in chest drops, causes blood to flow faster and longer into the lungs
- Increase in blood volume across pulmonary valve causes it to close slower
what are two abnormal heart sounds
S3 and S4
What are S3 & S4
soccer analogy:
- sound of blood falling from atria to ventricles and “bouncing” bc ventricles are stiff and don’t give to cushion falling blood.
- S3 early diastole
- S4 late diastole
what are common high frequency sounds
S1
S2
murmurs
*listen with diaphragm
What are common low frequency sounds
gallops
*use bell
which type of valve insufficiency is common
tricuspid insufficiency
What are PE sx of PH
- increased intensity of P2
- murmurs of pulmonary and tricuspid insufficiency
- increased JVD
Why is S2 louder in PH
loudness is determined by amt of blood coursing back towards right ventricle after ventricular contraction and how sudden the motion is arrested when the valve closes.
why does PH have splitting of A2 and P2
- takes longer to get blood into pulmonary circulation, takes longer for pulmonary valve to close.
- “fixed splitting”
- split on inspiration AND expiration
where should S2 be loudest?
base
higher on chest
5 dx tests
Not useful: - Hx and PE - CXR - EKG More useful - echo-cardiogram Diagnostic - Right heart cath
Treatment of PH
pulmonologist or cardiologist :)
Except PE which is treated by generalist