Cardiovascular Related Physiological Adaptation to Disease Flashcards
what pressures are reduced during hemorrhage
- arterial
- systolic
- pulse pressure
what are the clinical signs of hemorrhage
- pulse is rapid and feeble
- mucous membranes are pale
- respiration is rapid
why does cardiac output drop in hemorrhage
- decreased CVP
- decreased preload
- decreased SV
what does a drop in cardiac output lead to
drop in blood pressure
what occurs if there is a 40-50% drop in BP
see a partial recovery
some will go on to recover BP over few hours, others begin to decline and BP drops until death
how does the baroreceptor reflex work to recover BP drop in a hemorrhage (3)
- reduction in BP leads to decreased baroreceptor stimulation
- increased sympathetic activity –> leads to tachycardia, increased contractility, increased vasoconstriction
- decreased parasympathetic activity
what does vasoconstriction lead to
increased CVP
contraction of spleen leading to an increased blood volume –> pumps more RBC into circulation
what does arteriole vasoconstriction lead to
increased TPR
where is vasoconstriction absent and where is it most severe during hemorrhage
absent: in heart and brain
most severe in skeletal muscle, skin, splanchnic circulation
**renal vasoconstriction only occurs in severe hemorrhage –> sustained will lead to kidney damage and sloughing of mucosa in intestine (only takes few hours in dog)
how does the chemoreceptor reflex lead to recovery of hemorrhage
if BP does go very low the baroreceptor reflex is no longer sensitive and chemoreceptor will aid
responds to lack of oxygen, buildup of waste products
how does cerebral ischemia assist in recovery from hemorrhage
will occur if BP drops too far
sets off sympathetic discharges as a reflex response
what is atrial volume receptor reflex
adds to increased sympathetic activity during hemorrhage (same as baroreflex but responding to volume in atrium)
how does reabsorption of tissue fluids lead to recovery from hemorrhage
replacement of body fluids is a combination of capillary fluid shifts and hormone and behavioural changes
starlings forces which revolve around differences in oncotic pressure and filtration
loosing fluids so dropping BP –> accumulation of fluids in wrong places want retention of fluid within the blood vessels to maintain BP
what is the RAAS system
increased sympathetic activity increases renin secretion
through angiotensin II and aldosterone there is decreased Na+ excretion
reflexes to increase ADH which reduces water loss
conserves fluid
what other changes to the baroreceptor reflexes bring about
- acts through the hypothalamus to induce sensation of thirst and increase water intake
what is the recovery timeline from hemorrhage (3)
- takes 1-2 days to replace volume
- replacement of plasma protein by liver takes several days
- replacement of RBC takes several weeks (take awhile to regenerate)
what are decompensatory mechanisms to hemorrhage
there are positive feedback mechanisms making situation worse
they induce vicious cycles leading to death
what are the decompensatory mechanisms in hemorrhage (5)
- cardiac failure
- acidosis
- CNS depression
- change in clotting
- inhibition of immune system
how does cardiac failure occur during hemorrhage
- hypotension reduces coronary blood flow
- depresses ventricular function
- reduces CO
- reduces pressure
- reduces Q
how does acidosis occur during hemorrhage
- reduced Q leads to anoxia
- increased lactic acid production
- reduced H+ secretion by kidney
- acidosis reduces CV response to catecholamines
*blood becomes acidic, all organs are less responsive, sympathetic activation which won’t allow increase in BP
how does CNS depression occur in hemorrhage (4)
- reduced Q to CNS leading to increased sympathetic output
- if Q falls further however the cardiac and vasomotor centres become depressed
- leads to loss of sympathetic tone
- reduces CO –> further decreases cerebral Q
how do changes in clotting occur in hemorrhage
- initially there is an increase in clotting
- eventually clotting time is prolonged
- aggravates hemorrhage
how does inhibition of immune system occur during hemorrhage
- leads to invasion of endotoxins into systemic circulation
- induce a form of shock
if blood flow is reduced to the GI system –> anoxic –> ulcers –> bacteria can get into the bood –> endotoxins –> vasodilation –> drop BP further –> endotoxic shock
what determines whether or not an animal will recover from hemorrhage
- the degree of hemorrhage and
- individual variation
more severe the blood loss the greater chance of going into decompensation
draw a flow diagram to explain compensatory and decompensatory mechanisms for hemorrhage
what is the definition of heart failure
usually refers to a condition of depressed contractility and an inability of heart to provide the metabolic requirements of the body
can be restricted to one side or can be bilateral
what are possible causes of heart failure
- coronary artery disease
- hypoxia
- myocarditis
- valve disease
what are the two responses to heart failure and what is their overall mechanism
depressed contractility will reduce SV and CO –> depressing BP
- starling mechanism: if LV fails and SV goes down there is an accumulation of blood in the LA and pulmonary veins –> leads to increased preload and greater SV
- drop in BP induces baroreceptor reflex: increase in sympathetic activity. This increases HR and contractility
overall –> maintain BP near normal at rest (exercise intolerance)
draw a flow diagram indicating the responses to heart failure
what are the complications of heart failure
- edema
- exercise intolerance
- inadequate perfusion of “non-critical” organs
- cardiac decompensation
- vasoconstriction in kidney will increase TPR in HF and thus increase BP –> renal failure causes uremia, accumulation of waste products leads to depressed cardiac contractility, leads to further vasoconstriction
- pulmonary edema in LV failure –> accumulation of blood in LA is normally compensatory in that it increases SV but it also leads to pulmonary edeam
how does heart failure lead to edema
accumulation of blood in veins increases hydrostatic pressure
(starling forces pushes fluid out to tissues)
what type of edema does LV failure lead to
pulmonary edema: pushing of blood and fluid into the parenchyma of lungs (cough)
what type of edema does RV failure lead to
systemic edema
brisket edema in cattle
how does heart failure lead to exercise intolerance
normally during exercise you depend on sympathetic system to increase HR, SV and CO
in heart failure if sympathetic system is already active so individual is unable to cope with increased demand from skeletal muscle
get a big drop in BP and inadequate Q –> leads to rapid exhaustion
how does heart failure cause inadequate perfusion of “non-critical” organs
in severe HF the BRR responds to a falling arterial pressure to bring about vasoconstriction of kidney, splanchnic, resting skeletal muscle
- kidneys cannot form urine in a normal way leading to fluid accumulation
- waste products accumulate and lead to uremia
- get permanent damage to kidney –> often renal failure is the terminal event in chronic HF
what does indaquate perfusion to the gut cause in heart failure
damage can occur via ischemia to intestinal mucosa
lead to bacteria and toxins getting from gut into blood stream leading to septic shock
how does cardiac decompensation occur in heart failure (kidney, pulmonary edema, explain these)
once HF goes too far the body’s compensation mechanism starts to make matters worse leading to decompensation cycles
-vasoconstriction in kidney will increase TPR in HF and thus increase BP –> renal failure outlined causes uremia and accumulation of waste products leads to depressed cardiac contractility, this in turn leads to further vasoconstriction
in LV failure –> accumulation of blood due to reduced ejection in the LA is normally compensatory in that it increases SV. also leads to pulmonary edema –> affect blood oxygenation and the heart is critically dependent on oxygen –> hypoxia will reduce CO –> viscious cycle
