Pulmonary Circulation Distribution PDF

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