Pulmonary Hypertension Flashcards
Define: Pulmonary Hypertension
Abnormally increased pressure within pulmonary vasculature
Causes of Pulmonary Hypertension
- Increased pulmonary blood flow
- Increased pulonary vascular resistence
- Increased pulonary venous pressure
What is Precapillary pulmonary hypertension?
Increase of pulonary vascular resistence without increase in pulmonary venous pressure.
Typically due to:
- vasoconstriction
- pulmonary arterial changes due to vascular disease
What is postcapillary pulmonary hypertension?
Pulmonary hypertension associated with increase in pulmonary venous pressure.
AKA: PULMONARY VENOUS HYPERTENSION
Occurs with
- left sided heart disease
- increase left atrial pressure
Increase left atrial pressure + increase venous pressure = increase right atrial load
What is “passive” pulmonary hypertension?
What does it indicate?
Post-capillary pulmonary hypertension can occur on its own, secondary to severe left heart failure that leads to pulmonary arterial vasoconstriction and pulonary vascular disease; increasing pulmonary vascular resistence.
This is also known as CHRONIC postcapillary pulmonary hypertension.
What is reactive pulonary hypertension?
What is it a result of?
Passive pulmonary hypertension + increase pulmonary vascular resistance
It is a result of chronic and severe left sided heart disease.
What are causes for increase in pulmonary vascular resistance?
- sustained increase in pulmonary arterial pressure secondary to vasoconstriction or pulmonary arterial remodeling/vascular disease or both.
~~~
e.g.: Wall stiffening
endothelial dysfunction
vascular inflammation
thrombosis
fibrosis
~~~ - increase pulmonar blood flow (left to right cardiac shunt)
- chronic pulmonary venous pressure (left-sided heart disease).
What can result from increase in pulmonary vascular resistance?
Increase in right ventricular afterload
Which can trigger right ventricular hypertrophy mixed between wall thickening and chamber dilation.
If sustained, can cause and manifest as right-sided heart failure: increase systemic venous pressure subsequent pleural +/- abdominal effusion.
Which structural or functional changes can be seen on echocardiography in patients with pulmonary hypertension?
- Changes to ventricles (e.g. RV hypertrophy, systolic dysfunction left ventricular underfilling, flattening of the interventricular septum)
- Changes to pulmonary artery e.g. dilation, altered blood flow
- Changes to right atrium
- Changes to caudal vena cava
How do you estimate systolic pulmonary arterial pressure? (in absence of right ventricular obstruction)
- Quantity peak tricuspid velocity
- convert to pressure gradient between right atrium and right ventricle in systole
Pressure gradient = 4 x velocity [m/s]^2
Scaling the degree of pulmonary hypertension
Pressure gradient
mild: 30-50mmHg
moderate: 50-75 mmHg
severe: >75 mmHg
Must also consider
severity of clinical signs
degree of structural and functional changes
tricuspid regurgitation velocity
6 groups of classification of pulmonary hypertension
- Pulmonary Arterial Hypertension (PAH)
- Left-sided Heart Disease (LHD)
- Respiratory Disease/Hypoxia
- Pulmonary thrombic (PE) or thromboemolitic disease (PTE)
- Parastic Disease (heartworm or angiostrongylus)
- Multi-factorial or unclear mechanism
Pathophysiology of Group 1
Pulmonary hypertension:
Pulmonary arterial hypertension
cause: many cases unknown, but can be enetic, drug/toxin induced or secondary to underlying disease.
Pathologic changes:
- increased activity of vasoconstrictors
- decreasd vasodilation
- vascular wall remodeling: endothelial proliferation, smooth muscle proliferation, chronic inflammation
- injured endothelium (from increase in pressure)–> activating blood clots and producting blood clots taht further o struct blood flow
Pathophysiology of Group 2
Pulmonary hypertension:
Left-sidd heart disease
Left sided heart disease affecting its ability to pump effectively or fill properly
Bood backs into lungs causing:
- congestion and increase pulmonary pressure
- fluid leak from vessels to lung tissue = pulmonary edema
- fluid filled alveoli; impede gas exchange = respiratory symptoms
2 criteria for pulmonary hypertension secondary to left-sided heart disease
- Documentation of left-sided heart disease
- Documentation of unequivocal left-atrial enlargement (indicates ncrease in left atrial pressure) - post capillary pulmonary hypertension.
It is unlikely for PH to be secondary to MMVD/LHP unless unequivocal left atrial enlargement is identified.
Pathophysiology of Group 3 Pulmonary Hypertension
respiratory disease/hypoxia
When O2 is low, pulmonary vessels constrict in attempt to shunt blood to better-ventilated regions of the lungs.
Risk factors:
- chronic obstructive pulmonary fibrosis
- long-term exposure to high altitudes
- pulmonary fibrosis
- obstructive sleep apnea
Pathophysiology of Group 4 pulmonary hypertension
pulmonary artery obstruction
Chronic clot formations may travel to the lungs and block pulmonary arteries. If clots do not resolve, vessels can become narrower and stiffer.
What are the pharmakodynamics of Phosphodiesterase 5-inhibitors (PDE5i)?
PDE5i causes accumulation of cyclic guanosine monophosphate (cGMP) in pulmonary smooth muscle by inhibiting cGMP catabolism
accumulation of cGMP = relaction of vascular smooth muscle
also inhibits pulmonary arterial smooth muscle cell hypertrophy
effective at lowering pulmonary vascular resistance and delaying adverse remodeling of pulmonary arteries
Also thought to improve mycardial function and limit cardiac hypertrophy
Why should the decision to start PDE5i be based on echo?
Administered PDE5i will increase left atrial pressure, pulmonary venous and pulmonary capillary pressure potentially culminating in iatrogenic pulmonary edema.
What are treatment options for managing pulmonary hypertension?
- Initial management: address triggering factors, reduce right ventricular afterload by administering PDE5i
- Respiratory / hemodynamic resuscitation: O2 therapy, fluid volume to optimize preloa, diuretic sometimes indicated to optimize blood volume and right ventricular preload
- In cases of severe decompensation due to impared cardiac output from right systolic dysfunction; positive inotropy can be conisidered (caution because of vasodilatory effects may result in hypotension). May need to start on norepinephrine
