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Cardio Exam 1 > 8 - Circulatory Shock > Flashcards

8 - Circulatory Shock Flashcards

1
Q

What is shock?

A

Shock can be thought of as a generalized state of tissue hypoperfusion with relatively or absolutely inadequate cardiac output

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2
Q

What is cardiogenic shock?

A

When the etiology of the shock is related to severely depressed cardiac function

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3
Q

What is hypovolemic shock?

A

When the etiology of the shock is related to reduced circulating blood volume

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4
Q

What is distributive, vasogenic or low-resistance shock?

A

When the etiology of the shock is related to severely reduced resistance

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5
Q

What is ostructive shock?

A

When the etiology of the shock is related to obstructive pathologies

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6
Q

What is another name for hypovolemic shock?

A

“Cold shock”

This is because blood pressure is low causing cold, pale, clammy skin

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7
Q

How does heart rate and respiratory rate respond to hypovolemic shock?

A

With the low blood volume, the reflex mechanism is to increase heart rate and increase respirations

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8
Q

What causes hypovolemic shock?

A

Hemorrhage

Lack of blood decreases both venous return and cardiac output

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9
Q

What accounts for the cyanosis seen in hypovolemic shock from hemorrhage?

A

Underperfusion of the skin

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10
Q

What is the result of this underperfusion?

A

Anaerobic glycolisis with large amounts of lactic acid as a by-product

If there is severe lactic acidosis, cardiac function depresses myocardial function, decreases the responsiveness of peripheral vasculature to catecholamines and the patient may lose consciousness

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11
Q

With the decreased blood pressure, baroreceptors will be activated - what is the result?

A

The baroreflex causes tachycardia, activation of the chemoreflex and therefore tachypnea

So pretty much…

  • The patient will have a racing heart rate due to low BP
  • The patient will have a rapid respiratory rate due to low oxygen and high CO2 in the blood
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12
Q

What will result from a severe sustained hemorrhage?

A

Phasic changes in heart rate

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13
Q

Describe the phasic changes in heart rate resulting from a severe sustained hemorrhage

A

The once fast heart rate slows down due to vagal activation

Tachycardia will then return

The cycle will continue like this

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14
Q

What happens to the vasculature in severe sustained hemorrhage?

A

Widespread vasoconstriction in both arteries and veins

- This helps sustain cardiac filling pressure

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15
Q

What happens to renal function in severe sustained hemorrhage?

A
  • Renal function is depressed
  • Metabolic products are retained and can further damage renal function, and combined with hypotension, can lead to acute renal failure
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16
Q

Describe the recovery period from moderate hemorrhage

A

Recovery can occur in 12-72 hours

  • Hepatic protein synthesis restores plasma proteins within several days
  • Epo (erythropoietin) restores red cell concentration within one week
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17
Q

How do you treat shock?

A

Treatment of shock must be targeted to the cause and helping the physiological mechanisms activated as a result of the shock

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18
Q

How do you treat shock from hemorrhage?

A

For hemorrhage, rapid restoration of volume by transfusion of whole blood is indicated

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19
Q

How do you treat shock from a burn?

A

For shock associated with burn, primarily plasma volume is lost, so the treatment includes replacement with plasma

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20
Q

What is important to keep in mind when treating patients with shock?

A

Tissue dehydration can ensue if a patient is treated with hypertonic solutions, as fluid is drawn from the tissues to equilibrate with the capillary (Starling forces)

So pretty much, don’t treat them with fluid too rich in sodium or other ions because it will dehydrate the tissue in order to balance it out

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21
Q

What are the three main cardiovascular crises that lead to shock?

A

1 - Severely depressed myocardial functional ability
2 - Grossly inadequate cardiac filling (due to low mean circulatory filling pressure)
3 - Profound systemic vasodilation either due to abnormal presence of vasodilators or an absence of neurogenic tone from sympathetics

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22
Q

Describe some situations in which cardiogenic shock would occur

A

Cardiogenic shock occurs whenever cardiac pumping ability is compromised

  • Result of severe arrhythmias
  • Abrupt valve malfunction
  • Coronary occlusions
  • Myocardial infarction
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23
Q

What is the direct consequence of cardiogenic shock?

A

Significantly decreased cardiac output

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24
Q

Describe some situations in which hypovolemic shock would occur

A
  • Significant hemorrhage (usually greater than 20% of blood)
  • Fluid loss from severe burn
  • Chronic diarrhea
  • Prolonged vomiting
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25
Q

How do these situations induce shock?

A

By depleting body fluids and thus circulating blood volume

26
Q

What is the direct consequence of hypovolemic shock?

A

Inadequate cardiac filling and reduced stroke volume

27
Q

What are some situations that would reduce cardiac filling but are not related to hypovolemia?

A
  • Cardiac tamponade (fluid accumulation in pericardial sac)
  • Pulmonary embolus (a clot from a vein which lodges in the pulmonary vessel)

Both of these prevent adequate diastolic filling

28
Q

Describe a situation in which anaphylactic shock would occur

A

Severe allergic reaction to an antigen to which the patient has developed a sensitivity to

  • Insect bite
  • Antibiotic
  • Foods
29
Q

What else do we call this immunological event?

A

Immediate hypersensitivity reaction

30
Q

What mediates an immediate hypersensitivity reaction?

A

Several substances

  • Histmine
  • Prostaglandins
  • Leukotrienes
  • Bradykinin
31
Q

What is the result of an anaphylactic shock?

A
  • Substantial arteriolar vasodilation
  • Increases in microvascular permeability
  • Loss of peripheral venous tone
32
Q

What do these conditions in anaphylactic shock lead to overall?

A

Reduction in total peripheral resistance and reduction in cardiac output

33
Q

What causes septic shock?

A

Septic shock is also caused by profound vasodilation but specifically from substances released into the circulating blood by infective agents

34
Q

What is the most common toxin that causes septic shock?

A

Endotoxin

- A lipopolysaccharide released from bacteria

35
Q

What is the mechanism of action of endotoxin?

A

Endotoxin induces the formation of nitric oxide synthase in endothelial cells, vascular smooth muscle and macrophages

This causes these sources to then produce a large amount of nitric oxide, which is a potent VASODILATOR

36
Q

What term do we sometimes use to describe both anaphylactic and septic shock states?

A

Distributive shock

Remember this is because we see widespread vasodilation with each of these

37
Q

Describe a situation in which neurogenic shock would occur

A
  • Deep general anesthesia

- A reflex response to deep pain associated with traumatic injuries

38
Q

Describe what produces neurogenic shock

A
  • Neurogenic shock is produced by a loss of vascular tone via inhibition
  • It may also be accompanied by an increase in vagal activity (significantly slows the heart rate)
39
Q

What is another term used for neurogenic shock?

A

Vasovagal syncope

40
Q

What is an example of a mild form of neurogenic shock?

A

When someone hears really bad news and passes out

The transient syncope evoked by strong emotions is a mild form of neurogenic shock and is quickly reversibel

41
Q

What are the type of compensatory responses that are elicited from the various forms of shock?

A
  • Autonomic responses that you would expect from any ordinary low BP
  • More intense cardiac and peripheral vascular compensation
42
Q

What happens to the respiratory rate in compensated shock? Why?

A

Rapid and shallow breathing occurs, which promotes venous return to the heart by action of the respiratory pump.

43
Q

What happens to renin release in compensated shock? Why?

A

Increased renin release from the kidney as a result of sympathetic stimulation promotes the formation of the hormone, angiotensin II, which is a potent vasoconstrictor and participates in the increase in total peripheral resistance even in mild shock states

44
Q

What happens to circulating levels of vasopressin (ADH) in compensated shock? Why?

A

Increased circulating levels of vasopressin (also known as antidiuretic hormone) from the posterior pituitary gland contribute to the increase in total peripheral resistance

45
Q

What induces the release of vasopressin in compensated shock?

A

This hormone is released in response to decreased firing of the cardiopulmonary and arterial baroreceptors

46
Q

What happens to circulating levels of epinephrine in compensated shock? Why?

A

Increased circulating levels of epinephrine from the adrenal medulla in response to sympathetic stimulation contribute to systemic vasoconstriction

47
Q

What happens to capillary hydrostatic pressure in compensated shock? What is the effect of this?

A

Reduced capillary hydrostatic pressure resulting from intense arteriolar constriction reduces capillary hydrostatic pressure and promotes fluid movement from the interstitial space into the vascular space.

48
Q

What is increased in the liver due epinephrine and norepinephrine?

A

Glycogenolysis

This results in a release of glucose and a rise in blood (and interstitial) glucose levels and, more importantly, a rise in extracellular osmolarity

49
Q

What does an increased extracellular osmolarity result in?

A

This will induce a shift of fluid from the intracellular space into the extracellular (including intravascular) space

50
Q

What is autotransfusion?

A

A process that can move as much as a liter of fluid into the vascular space in the first hour after the onset of shock

51
Q

What compensatory measures account for this?

A

Increased glucose in the blood and reduced capillary hydrostatic pressure

52
Q

What long-term compensatory measures exist in the hypovolemic state?

A

Production and release of antidiuretic hormone (vasopressin) from the posterior pituitary
- This promotes fluid retention in the kidneys

Activation of the renin-angiotensin-aldosterone pathway
- This promotes rental sodium retention (via aldosterone) and the thirst sensation (via angiotensin II)

53
Q

How long do the long-term compensatory measures take to work?

A

These processes contribute to the replenishment of extracellular fluid volume within a few days of the shock episode.

54
Q

Describe the situation in which overwhelming vasoconstriction due to sympathetic activation is harmful

A

Perfusion of tissues other than the heart and brain may become inadequate even if normal arterial pressure is maintained from the vasoconstriction

Blood flow through liver, GI and kidneys may be reduced enough to cause ischemia and permanent damage

Patients who seem fine or had seemingly mild shock may die several days later from renal failure or sepsis from bacteria penetrating GI tract, etc.

55
Q

Describe the progression of shock

A

Shock may enter a progressive stage where the general cardiovascular situation degenerates

It may continue to the irreversible stage where no intervention can halt the cardiovascular system collapse and death

56
Q

How much do we know about this progression?

A

Not that much

57
Q

What do we know about this progression?

A

Bodily homeostasis can progressively deteriorate with prolonged reductions in organ blood flow

58
Q

What is the consequence of homeostatic disturbance?

A

An adverse affect on various components of the cardiovascular system so that arterial pressure and organ blood supply are further reduced

59
Q

How can we describe this as “positive feedback process”?

A

Reduced arterial pressure leads to alterations that further reduce arterial pressure rather than correct it (i.e., a positive feedback process).

We call this “decompensation” or “decompensatory mechanisms”

60
Q

What decompensation events will occur?

A
  • Lower blood pressure
  • Reduced sympathetic drive
  • Vasodilation
  • Further lowering of BP
61
Q

Why is there a reduced sympathetic drive?

A

Not completely understood

It happens when the shock is severe enough or has persisted for long enough and the condition becomes progressive and decompensatory mechanisms come into play

Cardio Exam 1 (15 decks)

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