Pulmonary Circulation Flashcards
Ohm’s Law to describe pulmonary flow
PPA - PLA = CO x PVR
PPA = mean pulmonary artery pressure PLA = LA (wedge) pressure PVR = pulmonary vascular resistance
Hypoxic pulmonary vasoconstriction
Alveolar hypoxia signals local arterioles to contract, directing blood flow away from hypoxic areas of the lung and optimizing V/Q matching
Zone 1
The physiologic region of the lung where PA > Pa > PV
Pulmonary microvasculature is compressed by the positive pressure within the alveoli; blood flow is minimal
Zone 1 is found in the apices of an upright person but is very minimal under healthy lung conditions
Zone 2
The physiological region of the lung where Pa > PA > PV
The driving pressure on the pulmonary circulation is the difference between arterial and alveolar pressure
Flow is greater than in Zone 1 but less than in Zone 3
Zone 3
The physiological region of the lung in which Pa > PV > PA
The driving pressure on pulmonary circulation is the difference between arterial and venous pressure; blood flow is greatest in this region
Equation to determine fluid movement across endothelium
Qf = Kf[(Pmv - Pi) - s(Pimv - Pii)
The difference between the hydrostatic pressure gradient and the oncotic pressure gradient
Edema safety factors
Decreased interstitial oncotic pressure (Pii) - fluid that enters the interstitial space in edema dilutes the interstitial oncotic pressure, pulling fluid back into the vessels
Increased interstitial hydrostatic pressure (Pi) - fluid that accumulates in the interstitium surrounding the microcirculation increases the interstitial pressure, opposing further fluid movement out of vessels
Increased plasma oncotic pressure - sudden loss of fluid from microvasculature increases vessel oncotic pressure via concentration of albumin, opposing further fluid movement out of the vessel
Lymphatic reserve system - edema accumulates only when the reserve capacity of the lymphatics is overwhelmed
2 types of pulmonary edema
Hydrostatic / Hemodynamic / Cardiogenic
Permeability
Hydrostatic (Hemodynamic, Cardiogenic) Pulmonary Edema
Requires microvascular pressures exceeding 25-30 mmHg (normal is 5-10mmHg)
Most commonly caused by left heart failure, mitral valve disease, and congenital heart disease; may also be caused by renal failure
Treated with diuretics
Permeability (non-cardiogenic) pulmonary edema
Caused by widespread injury to the pulmonary microvascular endothelium, altering the osmotic permeability coefficient from near 1 (total reflection) to near 0 (no reflection) of plasma protein; leads to edema formation even at normal microvascular hydrostatic pressures (Wedge pressure < 15 mmHg)
Caused by trauma, sepsis, inhalation of toxic gases, aspiration, amniotic fluid / fat embolism
Adult Respiratory Distress Syndrome
Alveolar flooding caused by diffuse damage to microvascular endothelium, resulting in widespread permeability pulmonary edema
Causes decreased compliance, impaired gas exchange with resultant hypoxemia; requires high pressures to inflate the lung
Treatment is supportive - mechanical ventilation with high FIO2 and pressures
Pulmonary Hypertension - Pressure Measurements
Defined as elevation of mean pulmonary arterial pressure above 25 mmHg
(Normal mean pulmonary arterial pressure is 15 mmHg)
Factors that increase PPA
PPA = CO x PVR + PLA; therefore PPA can be increased by
Increased PLA (left heart failure, mitral stenosis) Increased PVR Increased CO (in theory; PPA does not increase linearly with increased CO)
Classification of Pulmonary Hypertension - 5 main categories
- Pulmonary arterial hypertension
- Pulmonary hypertension due to left heart disease
- Pulmonary hypertension due to lung diseases and/or hypoxia
- Chronic thromboembolic pulmonary hypertension (CTEPH)
- Miscellaneous (unclear, multifactorial mechanism)
- Pulmonary arterial hypertension - causes
Idiopathic
Heritable
Drug/toxin induced
Associated with: connective tissue disease, HIV, portal hypertension, congenital heart disease, schistosomiasis
Idiopathic pulmonary arterial hypertension
Subset of Group 1 PH
Pre-capillary pulmonary hypertension due to unknown vascular causes
Characterized by sparing of the parenchyma; PFTs demonstrate normal lung physiology with selective decrease in DLCO
Primarily affects younger women; presents with RV hypertrophy and right sided heart failure
Treatment with vasodilators (CCBs, endothelin-1 blockers, phosphodiesterase inhibitors)
- Pulmonary hypertension due to lung disease / hypoxia
Caused by chronic hypoventilation, resulting in hypoxemic vasoconstriction; over time, chronic vasoconstriction leads to irreversible vessel wall remodeling with smooth muscle proliferation
Underlying causes of chronic hypoventilation: Emphysema, pulmonary fibrosis, sarcoid, asbestosis, silicosis
Pre-capillary pulmonary hypertension
Pre-capillary causes of pulmonary hypertension do not increase pressure in the microcirculation and do not cause pulmonary edema
Group 1 - Primary vascular disorders
Group 3 - Lung disease / hypoxia
Group 4 - CTEPH
Post-capillary pulmonary hypertension
Cardiac causes - left ventricular failure, mitral valve disease, atrial obstruction (i.e. Group 2 PH)
Pulmonary/venous causes - congenital stenosis of the pulmonary veins, pulmonary veno-occlusion
Increased resistance in the vessels distal to the capillaries causes microvascular hydrostatic pressure to increase, leading to pulmonary edema
Use of arterial vasodilators is contraindicated (increased pulmonary edema)
Treatment of PAH
Vasodilators - decrease right ventricular afterload and improve right heart function
Endothelin antagonists
NO pathway (Guanylyl cyclas activators, PDE5 inhibitors)
Prostacyclin enhancers
Calcium Channel blockers (special indication)
Indication for treatment of IPAH with CCBs
IPAH patients who have a significant pulmonary artery pressure decrease with administration of Ca2+ blockers are identified as having an “acute response” to administration of a pulmonary vasodilator (inhaled NO or IV prostacyclin) during right heart catheterization
To qualify as an “acute response”:
- Mean PA pressure must drop below 40 mmHg
- Mean PA pressure must drop by at least 10 mmHg
- CO cannot decrease
5% of patients respond and will be put on oral CCB
Visualization of PE on Chest X-Ray
Chest X-ray is most often normal; may observe a wedge-shaped infiltrate representing an area of infarct (Hampton’s Hump) or an area of decreased perfusion (Westermark Sign)
Lab tests for PE
Increased A-a gradient - suggests V/Q alterations
Elevated D-dimer - useful for negative predictive value
Visualization of clot in lung by CT angiography or VQ scan
Use of V/Q scan to diagnose PE
Patients are administered a radioactive tracer via IV which distributes to the perfused areas of the lung; they also inhale a radioactive gas, which distributes to ventilated regions of the lung
Areas with no perfusion but normal ventilation are suggestive of PE blocking circulation
Treatment of PE
Heparin + Warfarin x 6 months
Thrombolytic therapy for patients with hemodynamic compromise or evidence of right heart strain
Inferior vena cava filter for high risk patients
Acute surgical thrombectomy - last resort
Pulmonary Hypertension - Pathology
Muscular hypertrophy of pulmonary arteries
Muscularization of pulmonary arterioles
May involve plexiform lesions - replacement of central artery lumen by a proliferation of endothelial cells with multiple, “slit-like” lumens
