Pulmonary Circulation Distribution PDF

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Tamethia Perkins

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pulmonary circulation cardiovascular physiology anatomy biology

Summary

This document provides an overview of pulmonary circulation. It discusses factors influencing blood flow, zones of distribution (Zone 1, Zone 2, and Zone 3), and determinants of cardiac output (CO). The presentation also touches upon factors like blood gases, pharmacologic stimulation, pathologic conditions, and passive mechanisms affecting resistance.

Full Transcript

CIRCULATORY SYSTEM Tamethia Perkins MS, RRT-NPS, RRT-ACCS RT 3005/6005 DISTRIBUTION OF PULMONARY BLOOD FLOW Blood flow influenced by gravity, CO and PVR. GRAVITY – Blood is gravity dependent. – Distance from apex to base of 30 cm = P of 30 cmH2O or 22 mmHg. In...

CIRCULATORY SYSTEM Tamethia Perkins MS, RRT-NPS, RRT-ACCS RT 3005/6005 DISTRIBUTION OF PULMONARY BLOOD FLOW Blood flow influenced by gravity, CO and PVR. GRAVITY – Blood is gravity dependent. – Distance from apex to base of 30 cm = P of 30 cmH2O or 22 mmHg. Intraluminal P in the gravity-dependent areas is greater. gravity gravity Distribution in the 3 Zones  ZONE 1(apex) – Palveolar is sometimes greater than both the arterial and venous intraluminal P = blood is prevented from flowing through this region. (DEADSPACE) Positive P ventilation Dehydration Hemorrhage – In normal conditions the PAP is high enough to overcome the Palveolar. Zone 1 Distribution in the 3 Zones ZONE 2(mid portion) – P arterial > Palveolar = pulmonary capillaries are perfused. ZONE 3(bases) – Gravity-dependent area. – Both arterial and venous P > Palveolar = constant flow. 3 zones DETERMINANTS OF CO SV is determined by: – Ventricular preload End diastolic stretch amount before systole begins Amount filled determines vol ejected – Ventricular afterload Forces that impede blood flow (ie higher pressure in the vasculature) PVR/SVR – Myocardial contractility Ventricular Preload  Degree of myocardial fiber stretch before contraction (end-diastole).  Within limits, the more the myocardial fiber stretches, the greater the contractility.  Ventricular preload is reflected in the VEDV or VEDP. If VEDP increases = CO increases.  Frank-Starling law: relationship between VEDP and CO. – If ventricular compliance decreases = VEDP > VEDV. Frank-Starling curve Ventricular Afterload Force against which the ventricles must work to pump blood. Determined by: Total cross-sectional area of vascular space Vol and viscosity of blood ejected PVR = MPAP-MLAP (PWP) / CO X 80 Normal 20-120 dynes SVR = MAP – MRAP / CO X 80 Normal 800-1500 dynes The arterial systolic P better reflects the ventricular afterload. Myocardial Contractility Force generated by the myocardium. CO increases when contractility increases (positive inotropism). Clinically: – BP Increasing BP = increasing CO – Skin temperature More CO = warmer skin will be to touch, will appear pink VASCULAR RESISTANCE R= BP/CO If R increases = BP increases = increases afterload. Factors affecting pulmonary vascular R: – Active mechanisms – Passive mechanisms Active Mechanisms Abnormal blood gases Pharmacologic stimulation Pathologic conditions Blood Gases HYPOXIA  The PAO2 controls this response.  Direct blood away from the hypoxic lung to lung areas with higher PAO2.  Chronic hypoxia = pulmonary hypertension = COR PULMONALE. HYPERCAPNIA and ACIDOSIS  Pulmonary vascular resistance increases in response to hypercapnia.  More related to pH (H+)than CO2 itself. Pharmacologic Stimulation  Vasoconstriction in response to: – Epinephrine (alpha & beta) – Norepinephrin (alpha-arteries) – Dobutamine (beta-heart, lungs, skeletal muscles) – Dopamine (beta) – Phenylephrine (alpha) decongestant  Vasodilation in response to: – Oxygen – Isoproterenol – Aminophylline – Calcium-blocking agents Pathologic Conditions Vessel blockage or obstruction (thrombus) Vessel wall diseases (sclerosis) Vessel destruction (emphysema) Vessel compression (pneumothorax) Passive Mechanisms  In response to another mechanical change. – PAP changes – LA P changes – Lung volume changes Alveolar vessels Extra-alveolar vessels – Blood volume changes – Blood viscosity changes PAP changes  If PAP increases = pulmonary vascular resistance decreases. – High PAP = high distending intraluminal P = increases total cross-sectional area. – Induces Recruitment: opening of vessels that were previously closed. Distension: stretching or widening of vessels previously open. Both of this mechanisms have a limit. PAP changes Distension vs recruitment LA pressure changes If LA P increases = pulmonary vascular resistance decreases. Lung Volume Changes  Varies according to location of the vessel. – Alveolar vessels: thin = pleural P changes affect anatomy of the capillaries. As lungs are inflated, the R offered by the alveolar vessels progressively increases. During PPV, the transmural P can become negative, restricting blood flow. – Extraalveolar vessels: thicker. As lungs inflate, the transmural P increases, and the vessels distend. Extraalveolar vessels Extraalveolar vessels Lung Volume Changes Summary  At low lung volumes: – Extraalveolar vessels narrow and cause vascular R to increase. – Alveolar vessels widen and cause vascular R to decrease.  Combined effect: – PVR is lowest near FRC and increases in response to both high and low lung volumes. Combined effect Blood Volume and Viscosity Blood Volume As blood volume increases, distension and recruitment will ensue, and PVR decreases. Blood viscosity As viscosity increases, PVR increases. Summary of PVR

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