Pulmonary Hypertension Flashcards
How does Pulmonary Hypertension impairs Cardiac output and systemic perfusion?
With persistent elevations in pulmonary vascular resistance, the right ventricle (RV) dilates. RV dilation leads to increased ventricular wall tension during systole, increased oxygen consumption, and eventually decreased contractility.
With progressive RV dilation, the intraventricular septum displaces toward the left ventricle, which inhibits left ventricular filling and ultimately impairs cardiac output and systemic perfusion.
The most common symptom of Pulmonary HTN
Dyspnea
Physical Examination as the disorder worsens
Findings of RV failure emerge as the disorder worsens which include
PE:
JVE
(+) holosystolic murmur
increased intensity of P2 (pulmonary component of the second sound)
Ascites/Hepatomegaly
bipedal (lower extremity) edema
(5) ECG findings though neither sensitive nor specific
- Axis: Right axis deviation (most common)
- V1 - R/S is >1
- V5-6 - R/S <1
- S1Q3T3
- II, III, AVF: right atrial enlargement
Common chest radiographic abnormalities associated with pulmonary hypertension include
enlargement of the
1. right atrium
2. RV
3. hilar pulmonary arteries
The best initial diagnostic test to assess pulmonary hypertension in the ED.
Transthoracic echocardiography (TTE) is the best initial diagnostic test to assess pulmonary hypertension in the ED. Signs of disease severity include RV hypertrophy, decreased RV function, and tricuspid regurgitation
CARDIAC POCUS
PSAX right ventricle (RV) and left ventricle (LV).
1. Flattening of the interventricular septum occurring in systole, suggesting elevated right ventricular systolic pressures. This is also known as a D-shaped septum. Illustration of normal PSS view in top left corner.
Four Chamber view
- RV hypertrophy: an RV-to-left ventricle end-diastolic diameter >1
Initial management for hypovolemic patients
Volume overload can cause RV dilation, impaired left ventricular output, and compromise tissue perfusion. For hypovolemic patients, fluid challenges with 100- to 250 mL of isotonic crystal-loid is a good first step.
Preferred inotropic therapy for RV failure WITHOUT hypotension
DOBUTAMINE
if unable to tolerate MILRINONE
For RV failure without hypotension, inotropic therapy to augment contractility and RV afterload can improve cardiac output.
Dobutamine (a β1 agonist) is preferred, starting at 2 micrograms/kg/min and titrated to 10 micrograms/kg/min. Higher doses of dobutamine can cause tachydysrhythmias and hypotension.
For patients unable to tolerate dobutamine, MILRINONE, a phosphodiesterase-3 inhibitor, is an option. Initiate milrinone at 0.125 microgram/kg/min and titrate to a maximum of 0.75 microgram/kg/min. Higher doses of milrinone can cause hypotension and require cardiac output monitoring for titration.
Avoid this inotropes in Pulmonary HTN
Norepinephrine
-which may increase pulmonary vascular resistance and impair RV output
Adequate perfusion of the right coronary artery is necessary to main- tain RV function. To maintain right coronary artery blood flow, arterial pressure at the aortic root must be higher than the pulmonary artery pressure
Management for Chronic Pulmonary HTN in OPD
- Prostanoids - EpoPROSTenol, TrePROStinil, iloPROST
- Endothelial receptor antagonist
- boSENTAN, AmbriSENTAN - PDE5 inhibitors: Sildenafil, Tadalafil