CV Function in Pathology Flashcards

1
Q

What are the 5 main pathological situations that interfere with the homeostatic fuction of the CV system?

A
circulatory shock
coronary artery disease
acute coronary occlusion
chronic heart failure
hypertension
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2
Q

What is circulatory shock in general terms?

A

severe reduction in blood supply to the body tissues - metabolis needs ot tissues aren’t met

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3
Q

Is arterial pressure low or high in circulatory shock?

A

low - even with compensatory mechanisms

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4
Q

Circulatory shock occurs in what 3 primary disturbances?

A
  1. severely depressed myocardial functional ability
  2. grossly inadequate filling due to low mean circulatory filling pressure
  3. Profound systemic vasodilation
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5
Q

What are the two general cuases a profound systemic vasodilation?

A

abnormal presence of powerful basodilators

abscence of neurogenic tone

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6
Q

What are the five potential consequences of those primary distrubances? i.e. what re the 5 different forms of shock?

A
cardiogenic shock
hypovolemic shock
anaphylactic shock
septic shock
neurogenic shock
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7
Q

What happens in cardiogenic shock?

A

the cardiac pumping is compromised, leading to decreased CO

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8
Q

What are some of the causes of cardiogenic shock>

A

severe arrhythmia, abrupt valve malfunctions, MI, coronary occlusiosn

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9
Q

What happens in hypovolemic shock?

A

depletion of body fluids leading to decreased blood volume, reduced cardiac filling and reduced SV

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10
Q

What are some of the causes of hypovolemic shock?

A

significant hemorrhage (over 20% blood volume), fluid loss from severe burns, chronic diarrhea, prolonged vomiting

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11
Q

What happens in anaphylactic shock?

A

severe allergic reaction to antigen sensitivity leads to release of histamine, prostaglandins, leukotrienes, bradykinin

this leads to decreased arteriolar vasodilation leading to increased microvascular permeability, loss of venous tone and decreased TPR and CO

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12
Q

WHat happens in septic shock?

A

severe vasodilation due to release of substances into the blood stream by infective agnets - especially endotoxin released from bacteria

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13
Q

How does endotoxin lead to vasodilation

A

it induces the formation of ntiric oxide synthase in endothelial cells which leads t oincreased NO, increased cGMP and increased dephosphorylation and vasodilation

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14
Q

What happens in neurogenic shock?

A

loss of vascular tone due to inhibition of normal tonic activity of sympathetic vasoconstrictor nerves

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15
Q

What are some causes of neurogenic shock?

A

deep general anesthesia
reflex response to deep pain
vasovagal falls under this cateogy, but it’s transient

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16
Q

What is the autonomic nervous system response to shock?

A

grately increased sympathetic nerve activity

17
Q

What symptoms will be seen because of the increased sympathetic nerve activity?

A

pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction

18
Q

If the compensatory response isn’t working, what symptoms will you see in shock?

A

abnormally low arterial pressure, reduced cerebral perfusion

results in dizziness, confusion and LOC

19
Q

What are the renal compensations in shock?

A
  1. increased ADH to increased fluid retention
  2. Increased aldosterone to increase Na and fluid retention
  3. Angiotension increase to cause vasoconstriction
20
Q

The increased sympathetic activity occurs because the body wants to increase CO and MAP. But what’s the downside of this?

A

you shunt blood to the important heart and brain, but this decreases blood flow to the other organs, so they’ll gradually fail

21
Q

What occurs with breathing in shock?

A

you go to rapid, shallow breathing, which promotes venous return via action of the respiratory pump

22
Q

Do you get increased or reduced capillary hydrostatis pressure during shock? Why?

A

You get intense arteriolar constriction, leading to reduced capillary hydrostatic pressure, encouraging fluid retention

23
Q

What does the liver do in shock and why?

A

it increases glycogenolysis (induced by epi and NE) to release lots of glucose

this glucose causes an increase in extracellular osmolarity, which serves to shift fluid form the itnracellualr space to the extracellular space - essentially taking tissue fluid back into the CV system

24
Q

This increased glycogenolysis and reduced capillary hydrostatic pressure response are collectively referred to as what?

A

autotransfusion - can move as much as 1 L of fluid into the vascular space in the first hour after onset of shock!

25
What comprises the decompensation in shock?
as the organs continue to lack perusion, they will fail and bodily homeostasis will deteriorate, adversely affecting the CV system further
26
If the ischemia from gradually worsening CAD is not too severe, what is the local response and is it successful?
local metabolic vasodilator mechanisms compensate to reduce arteriolar resistance in order to improve coronary flow can be effective is not too severe
27
What is the response to an acute coronary occlusion?
very similar to cardiogenic shock
28
What are the two general types of dysfunction in heart failure?
systolic and diastolic dysfunction
29
What 5 alterations in the myocytes occur in systolic dysfunction?
1. reduced Ca2+ sequestration in SR 2. increased Na/Ca exchanger, so lower Ca2+ concentrations in the cell 3. low affinity of troponin for Ca2_ 4. altered substrate metaoblism from fatty acids to glucose oxidation 5. Impaired respiratory chain activity with impaired energy production
30
In heart failure, do you have reflexive increase in sympathetic or parasympathetic activity?
sympathetic - you have decreased CO and thus decreased arterial pressure
31
What is the good aspect of long-term compensation with sympathetic activity in systolic dysfunction?
the higher than normal sympathetic activity causes a rise in blood volume (sympathetic induced renin release) which increases mean circulatory filling pressure and raises CO closer ot normal and allows reduction of sympathetic activity back to near normal (the "compensated state of heart failure")
32
What is the bad aspect of long-term compensation with sympathetic activity in systolic dusfunction on the heart?
the fluid retenion will cause both peripheral and central venous pressures to be much higher than normal this causes chronically high EDV and the excessive cardiac dilation further impairs cardiac function because of increased total wall tension and stress - ultimately increased myocardial oxygen demand
33
What is the bad aspect of long-term compensation on overall organ function?
the fluid retention will cause both peripheral and central venous pressure to be high which adversely affects organ function because you get high venous pressure with transcapillary fluid filtration, edema and congestion
34
What are some potential causes of diastolic dysfunction?
1. decreased caridac tissue compliance 2. increased myofibrillar passive stiffness 3. delayed myocyte relaxation in early diastole 4. inadequate ATP levels 5. Residual low-grade cross-bridge cycling during diastole
35
Pulmonary hypertension is above what?
20 mmHg
36
What happens with chronic pulmonary hypertension?
cor pulmonale - you get systemic edema, chest pain and fatigue
37
What is cor pulmonale linked to?
chronic hypoxia as in COPD or cystic fibrosis
38
What percentage of HTN cases are primary or essential HTN?
about 90% - you just treat the symptom and not the cause because you can't find the case