Cardiovascular System: The Integrated System for Blood Pressure Regulation Prepared by iqra ayub

Kidney Facts ~50 gallons of blood pass through the 2 kidneys every day ~1.3 quarts of urine produced from the 50 gallons Kidneys about the size of a computer mouse Several important functions including role in maintaining BP

Objectives Compare and contrast the integrated system of both short-term and long-term (including kidney involvement) regulation of arterial blood pressure Compare and contrast the effects of various physiologic stressors on the integrated regulation of the cardiovascular system

Objectives (cont.) Describe components in measuring cardiac output Describe factors that contribute to the homeostatic disruption of normal circulatory function

What We Already Know Rapidly Acting Arterial Pressure Control Mechanisms SNS: effect on total peripheral vascular resistance and capacitance and cardiac pump Shift of fluid through the capillary walls

What We Are Missing Long-term control mechanisms for arterial blood pressure

Long-term mechanisms for BP Regulation Related to maintaining homeostasis of body fluid volume Based on maintaining a balance between intake and output of body fluid Overall regulation of kidney excretion of H2O and Na+ Variables account for variation in blood volume

Simple Concept Increase in extracellular fluid results in increased blood volume and arterial pressure Normal body response: kidneys excrete excess extracellular fluid and returns the pressure to normal Mechanism reverses if reduced blood volume

Terminology/General Concepts Pressure diuresis Pressure natriuresis blood volume blood pressure Excess salt intake: increase H2O retention – increase MAP

Volume X Pressure {Guyton & Hall, 2006} 8 Urinary Volume Output (x normal) 1 20 200 Arterial Pressure mmHg

Renal Output Curve and Net Water/Salt Intake Over long-term, water and salt intake must equal output Demonstrated at equilibrium point of curve Two determinants of long-term arterial pressure Location of renal output curve (shift?) Level of intake line

TPR, Arterial Pressure and Kidney Function Arterial Pressure = CO X TPR If increase TPR: Get acute rise in arterial pressure However, normal kidney function will respond by returning arterial pressure to the pressure level of the equilibrium point – Why?

Effect of Fluid Volume on Arterial Pressure Increased extracellular fluid volume Increases blood volume Increased mean circulatory filling pressure Increased venous return Increased CO Increased arterial pressure

CO: Two Mechanisms to Increase Arterial Pressure Direct effect Increased CO increases pressure Indirect effect Autoregulation

Salt Intake Effect of Na+ greater than effect of H2O Why? Amount of salt accumulation in body is main determinant of extracellular fluid volume

Chronic Hypertension MAP > 110 mmHg Results of pathology With dialysis, what happens if patient’s body fluid level is not kept at a normal level?

Renal Mechanisms for Control of BP Review: 1st mechanism of kidney control of arterial pressure 2nd system: Renin-Angiotensin

Renin-Angiotensin System Renin – hormone that acts as an enzyme; released when arterial pressure drops – i.e., when renal perfusion is inadequate Helps raise arterial pressure Can be life-saving system in circulatory shock

Renin-Angiotensin Pathway Renin (kidney) Decreased Arterial Pressure Angiotensin I Renin substrate (angiotensinogen) Angiotensin II Vasoconstriction Inactivation Retention (salt/H2O) Increased Arterial Pressure

Angiotensin and Salt/Water Retention Direct effect: on kidneys to retain salt and water Indirect effect: causes adrenal glands to secrete aldosterone which increases salt/water reabsorption by kidneys

Renin-Angiotensin and Salt Regulation Allows body to deal with widely varying Na+ intake and maintain normal BP salt intake extracellular volume arterial pressure renin and angiotensin renal retention of Na+ and H2O Return of extracellular volume almost to normal Return of arterial pressure almost to normal

Primary Hypertension = “Silent Killer” Unknown Cause – i.e., not secondary to a known cause Influence of weight gain and sedentary lifestyle PT role?

Weight Gain and Obesity Role in HTN Cardiac output increased SNS activity increased Angiotensin II/Aldosterone levels increased

Treatment Options in HTN Lifestyle modifications Pharmacological Vasodilator drugs Natriuretic or diuretic drugs

Summary of Mechanisms to Control Arterial Pressure Rapid (seconds) Semi-rapid (minutes/hours) Long-term (hours/days/months/years)

Additional Circulatory Factors Cardiac Output Venous Return

Cardiac Output and Venous Return Cardiac output controlled by venous return under most normal unstressful conditions Factors in the peripheral circulation affecting venous return to the heart (not heart itself) Sum of local blood flows contribute to venous return CO inversely related to TPR

Heart Influence on CO Frank-Starling Law Receptors Heart is limiting factor if receives more venous return than it can handle

Cardiac Output Normal: ~5L/min Normal CO plateaus at ~13 L/min without any special stimulation Hypereffective heart Hypoeffective heart

How Can We Measure CO? Fick Principle CO (L/min) = O2 absorbed per minute by the lungs (ml/min)/A-VO2 difference (ml/L of blood)