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Flashcards in Shock Deck (70)
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1
Q

What are the two peices of data used to diagnose shock?

A

Hemodynamics andmixed venous O2

2
Q

A reflection of LAP, which, in the absence of mitral valve disease, is an indication of

A

LVEDP and LVEDV

3
Q

Left ventricular failure, aortic valve disease, mitral valve disease, and cardiogenic shock are conditions w/ increased

A

PCWP AND LAP

4
Q

When LAP is greater than 20 mmHG, we will likely see

A

Pulmonary Edema

5
Q

What is an example of a condition with increased PCWP but LOW left atrial pressure?

A

Pulmonary Artery Hypertension

6
Q

CO x the amount of oxygen in the arterial blood gives us the

A

Oxygen delivery to tissues

7
Q

CO x amount of oxygen in the venous blood gives us

A

Oxygen returne to the heart

8
Q

Mixed venous oxygen content is derived from the

A

Fick equation

9
Q

What is the Fick equation?

A

(CaO2 - CVO2)/CaO2

10
Q

If oxygen delivery declines than we see an increase in

A

Extraction ratio

11
Q

What are three factors that affect oxygen delivery?

A

CO, Hb, and PaO2

12
Q

Reflects the balance between oxygen delivery and oxygen demand

A

SvO2

13
Q

A physiological state characterized by insufficient oxygen delivery to the tissues

A

Shock

14
Q

We see no protein or RNA synthesis w/ low levels of

A

ATP

15
Q

Low ATP levels also causes failure of membrane ion pumps which leads to loss of

A

mb potential

16
Q

The cytosolic proton burden increases when we have low ATP levels. This causes

A

Acidosis

17
Q

Clinical shock is often accompanied by

A

Hypotension

18
Q

MAP less than 60 mm Hg in a previously normotensive person

A

Clinical Shock

19
Q

What are the two compensatory responses ot hypotension

A

Broreceptor response and renin-angiotensin system

20
Q

The baroreceptor respopnse autoregulates

A

Blood Pressure

21
Q

Decrease in arterial pressure leads to decreased baroreceptor firing in the

A

Carotid sinus and aortic arch

22
Q

Hypotension disinhibits the

A

Vasomotor center

23
Q

Decreased baroreceptor firing causes a decrease in inhibitory neurons which leads to increased sympathetic tone and increased

A

HR and contratility

24
Q

In response to low BP, the kidney releases

A

Renin

25
Q

Renin then causes activation of

A

AN-II

26
Q

AN-II then leads to which 3 things?

A
  1. ) Vasoconstriction
  2. ) Na+ resorption
  3. ) Net water resorption
27
Q

Metabolic rates of heart and brain are high with low nutrient stores. Therefore they are critically dependent on blood flow for

A

Oxygen delivery

28
Q

What are the visual features of low CO shock?

A

Cool, clammy skin, pale or gray color

29
Q

The cool, clammy skin and pale or gray color seen in low CO shock are the result of vasoconstriction which shunts blood from

A

Periphery to vital organs

30
Q

We can also see agitation/anxiety; “sense of impending doom” confusion; obtundation w/

A

Low CO shock

31
Q

Normal capillary refill time is less than

A

2 seconds

32
Q

What are some abnormal findings as far as vascularity to the hands?

A

Clubbing, splinter hemorrhage, and peripheral cyanosis

33
Q

A metabolic acidosis is a clasic feature of

A

Shock

34
Q

The metabolic acidosis in shock induces

A

Tachypnea

35
Q

This tachypnea results in a compensatory

A

Respiratory alkalosis

36
Q

Cardiogenic shock and myocardial infarction both decrease

A

Myocardial contractility

37
Q

A pulmonary embolism increases

A

Afterload

38
Q

Hypovolemic shock and obstructive shock are both causes of decreased

A

Preload

39
Q

Caused by a tension pneumothorax and pericardial tamponade

A

Obstructive shock

40
Q

Leading cause of death for patients with acute MI

A

Cardiogenic Shock

41
Q

Occurs in 5-7% of patients w/ acute MI

A

Cardiogenic shock

42
Q

More prominent in STEMI than NSTEMI and mortality approaches 80%

A

Cardiogenic shock

43
Q

Cardiogenic shock is the result of primary

A

Pump failure

i.e. MI in ventricle 40%

44
Q

Pathophysiology is: coronary occlusion/MI, profound depression of contractility, reduced CO, and low BP

A

Cardiogenic shock

45
Q

What are three clinical findings of cardiogenic shock?

A

Hypotension, hypoperfusion, and pulmonary congestion

46
Q

Tachycardia, faint pulses, soft heart sounds, and displaced apical impulse are the result of hypotension and low CO seen in

A

Cardiogenic shock

47
Q

Component of cardiogenic shock that causes agitation, disorientation, or lethargy w/ cool, clammy, or cyanotic extremities

A

Hypoperfusion

48
Q

Component of cardiogenic shock leading to pulmonary rales and elevated JVP

A

Pulmonary congestion

49
Q

Pulmonary congestion results in which murmur

A

S3

50
Q

Caused by intravascular volume depletion

A

Hypovolemic Shock

51
Q

Loss of blood cell mass and loss of plasma volume lead to

A

Hypovolemic shock

52
Q

The essential derangement of hypovolemic shock is

A

Decreased preload

53
Q

Class 2 hypovolemic shock can be recognized by

A

Narrow pulse pressure

54
Q

Characterized by cold, clammy skin, tachycardia, and a narrow pulse pressure

A

Hypovolemic shock

55
Q

The result of impaired venous return to the R or L ventricle

-caused by pericardial tamponade and tension pneumothorax

A

Obstructive shock

56
Q

Clinically presents w/ absent breath sounds, JVD, and tracheal deviation

A

Tension pneumothorax

57
Q

What are the three types of distributive shock?

A

Septic shock, neurogenic shock, and anaphylactic shock

58
Q

Decrease in peripheral vascular resistance despite increased vasopressors

A

Septic Shock

59
Q

Loss of sympathetic tonesecondary to spinal cord injury

A

Neurogenic shock

60
Q

Histamine, leukotriene C4, prostaglandin D2 release cause profound vasodilatation

A

Anaphylctic shock

61
Q

Third leading cause of death in US (from all causes)

-35-40% mortality

A

Septic Shock

62
Q

25-30% of cases of sepsis are caused by

A

Gram negative sepsis

63
Q

30-50% of cases of sepsis are caused by

A

Gram positive and mized sepsis

64
Q

Initiated by danger signals such as Pathogen-associated molecular patterns (LPS, flagellin, fimbria, DNA etc.)

A

Septic Shock

65
Q

We see distributive shock, diffuse endothelial injury, and altered microvascular flow w/

A

Sepsis

66
Q

Failure of vascular smooth muscle constriction

A

Distributive (vasoplegic) shock

67
Q

Inflammatory mediators can disrupt cell-cell contacts leading to

A

Edema

68
Q

We see a marked decrease in peripheral vascular resistance w/

A

Septic Shock

69
Q

CO and peripheral blood flow are increased w/

A

Setic shock

70
Q

Septic shock is characterized by diminished vasoconstrictor response to

A

Catecholamines