Integrated Cardiovascular Physiology

hypovolemia is a decrease in intravascular volume due to

hemorrhage

GI loss (diarrhea, vomiting)

loss from capillaries to interstitium (burns, anaphylaxis)

renal loss

excessive sweating

immediate circulatory changes due to hypovolemia

decrease in central and peripheral venous pressure

decrease in venous return

decrease in cardiac filling, EDV, SV, CO

aterial hypotension

reduced blood flow to cutaneous, splanchnic and renal circulations

fast acting compensatory responses to hypovolemia to preserve MAP

baroreceptor reflex increases SNS activity to heart and peripheral resistance muscles

cardiopulmonary reflex increases SNS activity, and increases vasopressin (ADH) while decreasing ANP

chemoreceptor reflex increases SNS, increased ventilation, and increases HR

CNS ischemic response increases SNS to peripheral resistance vessels

fast acting cardiopulmonary reflex on hypovolemia to preserve MAP

increases SNS activity, increase ADH while decreasing ANP to increase fluid retention and increase blood volume

fast acting baroreceptor cardiopulmonary reflex on hypovolemia to preserve MAP

decrease stretch = increase SNS to heart and vessels

increase HR, increase constriction, increase venous pressure and return which increases TPR

increase EDV to increase SV

MAP = CO x TPR so MAP increases

intermediate compensatory responses of hypovolemia to preserve MAP

epinephrine increases SNS activity to adrenal medulla, stimulate heart and peripheral resistance vessels

renin-angiotensin-aldosterone increases SNS activity to JG cells to increase peripheral vasoconstriction and vascular volume

vasopressin (>30%) increases to increase peripheral vasoconstriction and vascular volume in response to decrease stretch

capillary fluid shift (500ml): reduced hydrostatic pressure favors absorption to increase vascular volume

hepatic glycogenolysis: increased osmolality (20 mOsm) moves water to extracellular to increase plasma volume

long term response to hypovolemia to compensate MAP

renal fluid system: enhanced renal absorption of Na and water which increases extracellular fluid volume

hepatic albumin synthesis: increased albumin increases absorption and vascular volume

enhanced thirst: angiotensin II, vasopressin, hypotension to increase water absorption

the state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, then if prolonged, irreversible cellular injury

hypovolemic shock

what is the cause of poor perfusion

prolonged hypotension

stages of hypovolemic shock

nonprogressive (compensated shock)

progressive shock

irreversible shock

nonprogressive/compensated shock

occurs with <25% of blood loss

compensatory mechanisms return MAP towards normal without outside therapy

progressive shock

severe hypovolemia >30% blood loss for 3-4 hours

without therapy shock becomes worse until death, therapy can return to normal

circulatory system deteriorates, reduced SNS vasoconstriction, deleterious positive feedback cycles

irreversible shock

30-40% blood loss

compensatory mechanisms exhausted

no therapy is beneficial

CV responses to upright posture

venous return decreased (venous pooling)

decrease in CO and BP with decreased venous return

rapid compensatory responses to upright posture

decrease in BP activates baroreceptor to sense decreased stretch

• increase HR by withdrawing vagal tone and increasing SNS

• increase TPR by increasing SNS to visceral organs, skeletal muscle and skin arterioles

increase in HR and TPR increases vasopressin secretion

if compensatory mechanisms are insufficient

cerebral perfusion decrease and person may faint (orthostatic hypotension)

CV response to prolonged standing

use muscle pump to break up column of blood

• increases venous return

• reduces capillary filtration in ankles/feet so less fluid buildup

CV response to dynamic exercise

increased metabolic work = increase blood flow

needs increase in oxygen delivery to active muscles

• increase ventilation, CO, muscle blood flow (vasodilation in skeletal muscles) and vasoconstriction in splanchnic and visceral organs to redirect to muscles

• increase in CO due to increased HR via decreased vagal and increased SNS, frank starling in effect = venous return increased

whole body oxygen formula

VO2 = CO x (CaO2 - CvO2)

why does TPR decrease during exercise

MAP increases and vasodilation in active skeletal muscle decreases TPR to allow for blood flow to skeletal muscles

exercise effect on a-v O2 difference

it increases the difference between arterial and venous O2 levels

decreased PO2 in tissue = greater use of O2 = decreased Hb affinity for O2 to allow skeletal muscle to use O2

cardiovascular responses to exercise

increased contractility, increased LVEDV due to increased preload = increased stretch = increased contraction = increased force

increase in MAP, large increase in SBP, little change in DBP = increase PP

decrease in TPR to allow blood flow

what receptor increases stroke volume

B adrenergic to increase contractility and therefore increase stroke volume

what directly increases ventricular filling (LVEDV)

increased venous return through muscle pump and splanchnic circulation venoconstriction

increase in skin blood flow due during exercise

skin blood flow can increase when exercising in heat

skin and muscle compete for blood flow during exercise

• distribution determines performance of the heart

as skin BF increases ventricular filling decreases

what is compensation for enhanced cutaneous flow during exercise

enhanced splanchnic and renal vasoconstriction

brain and CNS require cooling and cannot sacrifice skin BF to increase LVEDV

cardiovascular drift

phenomenon where HR increases as SV decreases during prolonged exercise in hot or neutral environment