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Module 10 > Cardiovascular Related Physiological Adaptation to Disease > Flashcards

Cardiovascular Related Physiological Adaptation to Disease Flashcards

1
Q

what pressures are reduced during hemorrhage

A
  1. arterial
  2. systolic
  3. pulse pressure
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2
Q

what are the clinical signs of hemorrhage

A
  1. pulse is rapid and feeble
  2. mucous membranes are pale
  3. respiration is rapid
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3
Q

why does cardiac output drop in hemorrhage

A
  1. decreased CVP
  2. decreased preload
  3. decreased SV
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4
Q

what does a drop in cardiac output lead to

A

drop in blood pressure

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5
Q

what occurs if there is a 40-50% drop in BP

A

see a partial recovery

some will go on to recover BP over few hours, others begin to decline and BP drops until death

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6
Q

how does the baroreceptor reflex work to recover BP drop in a hemorrhage (3)

A
  1. reduction in BP leads to decreased baroreceptor stimulation
  2. increased sympathetic activity –> leads to tachycardia, increased contractility, increased vasoconstriction
  3. decreased parasympathetic activity
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7
Q

what does vasoconstriction lead to

A

increased CVP

contraction of spleen leading to an increased blood volume –> pumps more RBC into circulation

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8
Q

what does arteriole vasoconstriction lead to

A

increased TPR

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9
Q

where is vasoconstriction absent and where is it most severe during hemorrhage

A

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)

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10
Q

how does the chemoreceptor reflex lead to recovery of hemorrhage

A

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

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11
Q

how does cerebral ischemia assist in recovery from hemorrhage

A

will occur if BP drops too far

sets off sympathetic discharges as a reflex response

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12
Q

what is atrial volume receptor reflex

A

adds to increased sympathetic activity during hemorrhage (same as baroreflex but responding to volume in atrium)

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13
Q

how does reabsorption of tissue fluids lead to recovery from hemorrhage

A

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

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14
Q

what is the RAAS system

A

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

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15
Q

what other changes to the baroreceptor reflexes bring about

A
  1. acts through the hypothalamus to induce sensation of thirst and increase water intake
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16
Q

what is the recovery timeline from hemorrhage (3)

A
  1. takes 1-2 days to replace volume
  2. replacement of plasma protein by liver takes several days
  3. replacement of RBC takes several weeks (take awhile to regenerate)
17
Q

what are decompensatory mechanisms to hemorrhage

A

there are positive feedback mechanisms making situation worse

they induce vicious cycles leading to death

18
Q

what are the decompensatory mechanisms in hemorrhage (5)

A
  1. cardiac failure
  2. acidosis
  3. CNS depression
  4. change in clotting
  5. inhibition of immune system
19
Q

how does cardiac failure occur during hemorrhage

A
  1. hypotension reduces coronary blood flow
  2. depresses ventricular function
  3. reduces CO
  4. reduces pressure
  5. reduces Q
20
Q

how does acidosis occur during hemorrhage

A
  1. reduced Q leads to anoxia
  2. increased lactic acid production
  3. reduced H+ secretion by kidney
  4. acidosis reduces CV response to catecholamines

*blood becomes acidic, all organs are less responsive, sympathetic activation which won’t allow increase in BP

21
Q

how does CNS depression occur in hemorrhage (4)

A
  1. reduced Q to CNS leading to increased sympathetic output
  2. if Q falls further however the cardiac and vasomotor centres become depressed
  3. leads to loss of sympathetic tone
  4. reduces CO –> further decreases cerebral Q
22
Q

how do changes in clotting occur in hemorrhage

A
  1. initially there is an increase in clotting
  2. eventually clotting time is prolonged
  3. aggravates hemorrhage
23
Q

how does inhibition of immune system occur during hemorrhage

A
  1. leads to invasion of endotoxins into systemic circulation
  2. 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

24
Q

what determines whether or not an animal will recover from hemorrhage

A
  1. the degree of hemorrhage and
  2. individual variation

more severe the blood loss the greater chance of going into decompensation

25
Q

draw a flow diagram to explain compensatory and decompensatory mechanisms for hemorrhage

A
26
Q

what is the definition of heart failure

A

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

27
Q

what are possible causes of heart failure

A
  1. coronary artery disease
  2. hypoxia
  3. myocarditis
  4. valve disease
28
Q

what are the two responses to heart failure and what is their overall mechanism

A

depressed contractility will reduce SV and CO –> depressing BP

  1. 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
  2. drop in BP induces baroreceptor reflex: increase in sympathetic activity. This increases HR and contractility

overall –> maintain BP near normal at rest (exercise intolerance)

29
Q

draw a flow diagram indicating the responses to heart failure

A
30
Q

what are the complications of heart failure

A
  1. edema
  2. exercise intolerance
  3. inadequate perfusion of “non-critical” organs
  4. cardiac decompensation
  5. 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
  6. 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
31
Q

how does heart failure lead to edema

A

accumulation of blood in veins increases hydrostatic pressure

(starling forces pushes fluid out to tissues)

32
Q

what type of edema does LV failure lead to

A

pulmonary edema: pushing of blood and fluid into the parenchyma of lungs (cough)

33
Q

what type of edema does RV failure lead to

A

systemic edema

brisket edema in cattle

34
Q

how does heart failure lead to exercise intolerance

A

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

35
Q

how does heart failure cause inadequate perfusion of “non-critical” organs

A

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
36
Q

what does indaquate perfusion to the gut cause in heart failure

A

damage can occur via ischemia to intestinal mucosa

lead to bacteria and toxins getting from gut into blood stream leading to septic shock

37
Q

how does cardiac decompensation occur in heart failure (kidney, pulmonary edema, explain these)

A

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

Module 10 (27 decks)

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