Lecture 24 & 25: Pulmonary Hypertension
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26 terms
Terms | Definitions |
|---|---|
 Pulmonary Artery (Swan-Ganz) Catheter: -Function -Normal Pressures (RAP, RVP, PAP, PCWP, LVP, AoP) | Catheter inserted into a peripheral vein and advances to RA •Balloon inserts into pulmonary artery to measure pulmonary artery wedge pressure - must be deflated in 5-15 secs in order to prevent pulmonary infarction Normal Pressures •RAP = 5 •RVP = 25/5 •PAP = 25/10 •PCWP = LAP = 10 •LVP = 120/10 •AoP= 120/80 •Normal: LV diastolic = LAP = PCWP = PA diastolic |
| Complications from SG Catheter Use | •Infection - whenever placing s/t foreign inside •Hemorrhage - chance of puncturing vein/heart •Pneumothorax - chance of puncturing lung through subclavian vein •Arrhythmias - catheters can kick off arrhythmias •Pulm infarct - if balloon is left blown up for to long, can lead to pulmonary infarct •Pulm artery rupture - if balloon blown up too clickly •Knotting •Misleading values: bubbles, clots, kinking, imbalance, zero point error •Mechanical vent effects •Misinterpretation - tachycardia, pulmonary HTN |
| Cardiac index (CI) | is a vasodynamic parameter that relates the cardiac output (CO) to body surface area (BSA) CI=CO/Body Surface Area = [SV+HR]/BSA |
| Risk Stratification & analysis of pathophysiology post MI in CCU: Normal CI & normal LV filling pressures | Normal CI & normal LV filling pressures - mortality low & greater danger is extension of infarction |
| Risk Stratification & Analysis of Pathophysiology post MI in CCU: Pulmonary congestion | Pulmonary congestion - normal CI but high LVP above 18 leading to congestion •Seen on CXR and rales heard in chest •Variety of diastolic dysfunction |
| Risk Stratification & Analysis of Pathophysiology post MI in CCU: Hypovolemia | Hypovolemia - CI low and LVP pressures low (normal) •CO improves w/ fluid restoration tho severely depressed LV function may not |
| Risk Stratification & Analysis of Pathophysiology post MI in CCU: Pump failure | Pump failure - CI low & LV Pressure high - poor tissue perfusion, cardiogenic shock •High rate of mortality |
| Determination of the cause of hypotention in CCU: Cardiogenic shock | Cardiogenic shock - elevated LV filling pressure - low CI and poor tissue perfusion ➢Lower LV filling pressures & needs tissue expansion |
| Differentiation of Heart Failure from pulmonary infection or ARDS as cause of Infiltrates & Rales | Congestion caused by elevated PCWP & LV failure - acute pulmonary edema - need diuretics & inotropes ➢ARDS - PCWP normal but needs ventilator support & antibiotics |
| Determination w/o catheter but by apply principles: -LV Pressure -Hypovolemic Hypotension -Low CO | LV filling pressures estimated by presence of rales, pulmonary congestion on Xray & initial response to diuretics Hypovolemic hypotension recognized by improvement in BP after fluid challenge Low CO seen w/ low BP, low urine output, cook skin & decreased mentation |
| Unique Aspects of the Pulmonary Vascular System | Pulmonary Vascular System's Uniqueness: Low pressure system - normal pressure of 25/10 w/ a mean of 15 •High blood flow - only single bed receiving entire CO •Low resistance •PVR = PA - LA / CO x 80 = 80-160 dynes High pulmonary vascular reserve - flow can increase 2-3x w/ no increase in PAP due to drop in PVR •w/ exercise and flow increase of 3-4x, PAP may rise Respond to oxygen & acidosis - pulmonary arterioles constrict in response to hypoxia or acidosis •Prevents shunting of blood through regions that are not well ventilated & assures anatomical match of ventilation & flow |
| Pulmonary HTN: -Definition -Early Stage Causes [4] | Def: PAP greater than 35/15 Causes: DECREASED CROSS SECTIONAL AREA of pulmonary vascular bed and thus increased PVR •Increase in back pressure (mitral stenosis, L CHF, Pulm Venous Obstruction) •Increase in pulm flow rate (shunts, high output states) •HYPOXIA - decreased alveolar pO2 -> spasm & medial hypertrophy in pulmonary arterioles adjacent to hypoxic alveoli, reversible •Pulmonary parenchymal disease - COPD due to smoking w/ cor pulmonale •Kyphoscoliosis; Muscular dystrophy & neuromuscular syndromes such as polio •Pickwickian syndrome - morbid obesity & hypoventilation •High altitude residence PULMONARY VASCULAR DISEASE - obliteration of vascular bed itself •Primary pulmonary HTN - idiopathic disorder, chiefly middle aged women w/ pulmonary arterioles that develop unexplained spasm, medial hypertrophy & intimal fibrosis •Pulmonary venous disease - anatomic obstruction of venous return |
| PVR = ? | PVR = PA - LA / CO x 80 = 80-160 dynes |
| Pulmonary HTN: Late Stage Causes [2] | INCREASED PULMONARY ARTERY BLOOD FLOW- states w/ chronic elevated pulmonary artery blood flow lead to increased PAPs - mostly benign and will stop when lower CO ➢Congenital heart disease w/ lesions causing L → R shunts: •ASD, VSD, patent ductus arteriorosus ➢Increased bronchial artery flow ➢High output states ➢Causes pulmonary HTN in 2 ways: •Normal resistance - amount of flow exceeds pulmonary vascular reserve •Secondary increase in pulmonary vascular resistance - increased flow leads to destruction of pulmonary arterioles, reducing cross sectional area of bed causing rise in PVR •Most dreaded complication of chronic L → R shunts •Can lead to Eisenmonger's syndrome - reversal of shunt to R → L and consequent oxygen desaturation of HB in systemic circulation INCREASED LEFT ATRIAL AND PULMONARY VENOUS BACK PRESSURE - most common ➢Mitral stenosis ➢Left sided CHF - systolic OR diastolic ➢Left atrial myoxoma ➢Pulmonary venous obstruction ➢All have elevated LAP and pulmonary venous pressures and may go back and cause RV thickening and RAP increase as well ➢2 reasons: •Back pressure from LA leads to passive increase in pulmonary capillary pressure & pulmonary arterial BP •At first PVR may still be normal although RV and PA have increased pressure so that pressure drop across lungs is still normal, RV must be generate higher systolic pressure •Secondary increase in PVR, pulmonary arterioles may hypertrophy & thus increase resistance - alveoli can thicken •w/ enough increased back pressure, may eventually develop increased PVR ➢Most common cause of pulmonary HTN & right sided HF is left sided HF w/ elevated LV diastolic pressure |
| Hemodynamic Consequences of Pulmonary HTN and RV Overload | Heart - RVH and dilation, and septal flattening Loud P2 and murmur of Pulm. Insufficient-diastolic blow. Tricuspid regurgitation - Lower left sternal border holosystolic murmur Right-sided CHF- JVD, edema, hepatomegaly, ascites. NOT pulmonary edema- unless 2/2 L.CHF |
| Primary Pulmonary Hypertension vs. Pulmonary Hypertension due to LV Failure | Primary pulm HTN - wedge pressure is normal Pulm HTN due to LV failure - wedge pressure is high |
| Causes of Increased PVR due to Decreased X-Sectional Area | Some pts. with increased back pressure e.g., MS Some pts. with increased forward flow e.g. ASD with late increased PVR (age 20-30) Congenital heart disease with early increased PVR- e. g., usual Eisenmenger's syndrome COPD with cor pulmonale Chronic hypoxia - high altitude residence, kyphoscoliosis, polio Pulmonary artery obstructive syndromes- * Pulmonary emboli, IVDU * Pulmonary arteritis - e.g., SLE, PSS * Primary pulmonary hypertension |
| Pulmonary Angiograms: Primary Pulmonary Hypertension | Normal: diffuse branching patter wiht smoothly tappering vessels and branches leading ot the periphery of the lung Primary pulmonary hyptertension: demonstrates marked "pruning" of small vessels with absent peripheral flow. No segmental or larger vascular abnormalities. |
| Potential Mediators involved in pathogenesis and maintenance of PPH | Constrictors and proliferators: Thomboxane A2 PAF Endothelin-1 Growth factos ?Estrogens Dilators and antiproliferators: PGI2 NO Growth inhibitors |
| Cor Pulmonale | Right ventricular dilation & hypertrophy secondary to pulmonary HTN Specifically due to disease in pulmonary parenchyma or pulmonary vessels Most common cause: COPD due to cigarette smoking |
| Cor Pulmonale: Pathophysiology | Alveolar hypoventilation •CNS disorders/bronchopulmonary disorders/thoracic cage disorders → •Alveolar hypoventilation → •Alveolar & arterial hypoxia (increase pCO2/acidosis) → •Pulmonary vasoconstriction → •Pulmonary HTN Reduction of pulmonary vascular bed •Obliterative vascular disease/ diffuse pulmonary fibrosis → •Reduced pulmonary vascular bed → pulmonary HTN |
| Factors causing & intensifying pulmonary HTN in cor pulmonale & COPD | Diffuse, irreversible anatomic changes in arterioles (intimal thickening, inflamm, media/muscular hypertrophy) Diffuse pulmonary arterial constriction secondary to hypoxia -> caused by: hypoxic acidosis and vasoactive substances Decreased number & area of pulmonary vessels - emphysema decreases total cross-sectional area of vascular bed & decreases recruitment of channels during periods of increased blood flow Erythrocytosis - w/ increased viscosity, hematocrits greater than 55%, can impede blood flow through lungs, increasing PVR Infections - & increased bronchial artery blood flow can increase CO and further exacerbate PA HTN |
| Cardiac Manifestations of COPD | Right ventricular dilation Arrhythmias - esp paroxysmal (short and frequent) atrial fibrillation, VTac, multifocal atrial tachycardia Left Ventricular failure - pulmonary infections leading to hypoxia |
| Cor Pulmonale: Treatment | Implications of Pathophysiology of cor pulmonale for treatment Chronic administration of oxygen as well as optimal pulmonary toilet can improve RV function Chronic low flow oxygen how to prevent progression of cor pulmonale High flow oxygen can be dangerous & may exacerbate systemic acidosis |
| WHO Classification of Pulmonary Arterial Hypertension | WHO Group I - Pulmonary arterial hypertension (PAH) -Idiopathic (IPAH) -Familial (FPAH) -Associated with other diseases (APAH): collagen vascular disease (e.g. scleroderma), congenital shunts between the systemic and pulmonary circulation, portal hypertension, HIV infection, drugs, toxins, or other diseases or disorders -Associated with venous or capillary disease WHO Group II - Pulmonary hypertension associated with left heart disease - Atrial or ventricular disease - Valvular disease (e.g. mitral stenosis) WHO Group III - Pulmonary hypertension associated with lung diseases and/or hypoxemia -Chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD) -Sleep-disordered breathing, alveolar hypoventilation - Chronic exposure to high altitude - Developmental lung abnormalities WHO Group IV - Pulmonary hypertension due to chronic thrombotic and/or embolic disease -Pulmonary embolism in the proximal or distal pulmonary arteries -Embolization of other matter, such as tumor cells or parasites WHO Group V - Miscellaneous |
| Clinical Recognition of Pulmonary HTN - physical exam | Loud P2 & murmur of pulmonary insufficiency Tricuspid regurgitation - lower left stern border holosystolic murmur Right sided CHF - JVD, edema, hepatomegaly, ascites NOT pulmonary edema - b/c due to high pressures in veins & capillaries not of arteries which is pulmonary HTN |
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