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CVS Physiology > Hemorrhage & Sock > Flashcards

Hemorrhage & Sock Flashcards

1
Q

What is the result if chronic hemorrhage?

A

Leading to anemia and may be hypotension, but it may reflect a serious disease.

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2
Q

Describe the body responsed to loss of different blood percentages.

A

Less than 10%, no significant effect on COP or ABP, as blood donation.
10-20%, variable degrees of compenated hemorrahgic shock occurs
>20%, the shock becomes uncompensated
>30%, the shock becomes irreversible

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3
Q

What is the aim of body compensatory mechanisms in shock?

A

Correct drop in ABP and blood volume.

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4
Q

Mention Immediate compensatory reactions that correct ABP

A
  1. Diminished rate of discharge of impulses from arterial & atrial baroreceptors
  2. Chemoreceptors stimulation
  3. CNS ischemic response
  4. Increased production of Ang II & ADH
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5
Q

Mention effect of Diminished rate of discharge of impulses from arterial & atrial baroreceptors

A
  1. VC of arterioles ex brain & heart, leading to pale and cold skin, dec GFR & diminished urine volume.
  2. Venoconstriction to inc VR & COP
  3. INC symp discharge to heart inc rate & contractility, a rapid weak pulse.
  4. Inc symp discharge to adrenal medulla & inc CA which stimulate reticular formation causing restlessness & inc VR due to inc muscle tone.
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6
Q

Describe mechanisms if stimulation of chemoreceptors

A
  1. Diminished blood flow to aortic & carotid bodies (less than 80 mmHg)
  2. Hypoxia produces lactic acid & H+
  3. PO2 less than 60 mmHg
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7
Q

Describe results of chemoreceptor stimulation

A

Inc sympathetic discharge to heart & vessels & dec vagal tone
Stimulation of rapid breathing & rapid shallow breathing

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8
Q

GR: CNS ischemic reflex is active below ABP 60 mmHg

A

Because that us the lower limit if the range of cerebral autoregulation

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9
Q

Describe effect of Ang II

A

Arteriolo p4 & venoconstriction, thirst sensation, inc aldosterone (thus inc Na+ reabsorption)

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10
Q

Describe effect if ADH in shock

A

VC & inc blood volume by dec urine output

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11
Q

Mention mechanisms to correct blood volume in shock (short-term)

A

Capilary fluid shift phenomenon
Plasma protiens are restored by movement of labile tissue and liver proteins to plasma
RBCs are restored by contraction of splenic capsule

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12
Q

Mention mechanisms to correct blood volume in shock (long-term)

A
  1. Plasma volume is restired within 12-72 hrs by thirst & hormonal conservation
  2. Plasma proteins are replaced by hepatic synthesis 3-4 days
  3. RBCs are 4-8 weeks due to inc release of erythropoietin hormone leading to inc in erythropoiesis
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13
Q

Define circulatory shock

A

It is acute decrease in tissue perfusion so that the amount of O2 & nutients reaching the the cells is not sufficient to maintain life processes particularly in vital organs like brain & heart.

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14
Q

GR: ABP is not a good measure for progression of shock

A

Because ABP is strongly defended by several regulatory mechanisms, as decrease in ABP would be compensated by more VC which dec tissue oerfusion and priduce more shock.

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15
Q

Write a short note on hypovolemic shock

A

It is due to dec in volume of circulating blood, due to blood loss as in hemorrhage, plasma loss in burns, nody fluid loss in vomiting & diarrhea.
The heart is normal but VR and thus COP is reduced, compensation is through VC of splanchnic & skeletal muscle BVs.

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16
Q

Write a short note on cardiogenic shock

A

There is severe reduction in the pump function of the heart as in massive MI, the VR and heart filling are normal but CO is dec because of HF, compensation is mainly by VC leading to cold pale skin.

17
Q

Define low resistance shock

A

The CO and blood volume are normal but they are relatively inadequate due to sudden inc in vascukar capacitance as a result of marked VD. Hypotension is due to reduced MCP & peripheral resistance. The type of shock is also “warm shock” because skin is not cold as hypovolumic or cardiac shock.

18
Q

What are causes of low resistance shock?

A 
Neurogenic shock:
Deep general anaesthesia 
Spinal shock
Brain damage
Generalized VD in severe pain & strong emotions
……….
Anaphylactic shock
19
Q

In anaphylactic shock, …..cells release…..

An example is ……

A

Mast, histamine

Incomoatible blood transfusion

20
Q

Mention elements of septic shock

A

Low resistance, cardiogenic & hypovolemic shock

21
Q

Mention cause of septic shock

A
  1. Generalized VD, inc blood flow to infected areas further deprives healthy tissues from blood flow.
  2. Increase capillary permeability with resultant loss of plasma in tissues
  3. Cardiac depression
22
Q

Mention elements of traumatic/surgical shock

A 
Neurogenic shock (low resistance due to severe pain)
Extenal hemorrhage as well as bleeding into tissues (hypovolemic shock)
23
Q

Define compensated shock

A

In which normal compensatory circulatory mechaisms can cause full recovery without help from outside. These compensatory mechanisms are immediate acting on ABP & CO and delayed, restoring blood volume.

24
Q

Define decompensated shock

A

In which without therapy, the shock becomes steadily worse until death

25
Q

Define refractory shock

A

In which shock has progressed to such an extent that all forms of known therapy are inadequate to save the oerson’s life, although for the moment they are alive.

26
Q

GR: Compensatory mechanisms fail to prevent deterioration, in decomensated shock

A

They are replaced by decompensatory mechanisms (+ve feedback) mechanisms, giving rise to viscous cycle which leads to rapid death to the patient.

27
Q

Explian the decompensatory mechanisms

A
  1. Severe cerebral ischemia with VMC failure.
  2. Metabolic acidosis (cardiac depresssion & arteriolar VD, inc capillary filtration & further dec in blood volume)
  3. HF due to myocardial ischemia, lactic acid, myocardial toxic factor from pancreas & release of toxins from dead gram -ve barcteria in intestine
  4. Hypercoagulability of blood
28
Q

GR: Coronary blood vessels are blocked in decomp shock

A

Due to blood hypercoagulability

29
Q

GR: Release of MTF

A

From pancreas due to anoxia

30
Q

GR: Hypercoagulability of blood in decompensated shock

A

Due to sluggish blood flow and toxins from ischemic tissues which may block blood flow.

31
Q

Describe sequence of events in refractory shock

A
  1. Strong VC of precapillary sphincters causes hypoxic tissue damage with release of deleterious substances.
  2. After sometime precapillary sphincter opens while postcapillary resistance remains high
  3. This leads to stagnantion of blood in capillaries, escape of plasma, more hypovolemia
  4. Blood cells start forming rouleux formation and small clot fragments.
  5. After some time venules relax and allow abnormal contents to reach circulation leading to PE & lung comp
32
Q

First organ damaged by refractory shock is ….., leading to …..

A

Liver

Decreased metabolism & detoxification + coagulopathy

33
Q

GR: Shock lung occurrence

A
  1. Decreased blood flow, damaging endothelium & epithelium
  2. PE by products of capillary imbalance between pre and post capillary resistances
  3. Failure of synthesis of pulmonary surfactant leading ti edema and collapse.
34
Q

Describe effect if refractory edema on:

  1. Intestine
  2. RES
A
  1. Breakdown intestinal mucosa with easy access of intestinak bacteria and endotoxins to circukation
  2. Lack of opsonization and dec phagocytosis & Ab formation.

CVS Physiology (15 decks)

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