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STEP 2 > Shock > Flashcards

Shock Flashcards

1
Q

What belongs to distributive shock?

A

SEPTIC
ANAPHYLAXIC
NEUROGENIC

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2
Q

Neurogenic shock. Primary disturbance?

A

Nerve injury –> no SNS response

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2
Q

Sepsis. Primary disturbance?

A

peripheral vasodilation

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3
Q

Sepsis. Result of venous dilation?

A

decr preload –> decr. CVP and PCWP

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4
Q

Sepsis. Result of arterial dilation?

A

decr. afterload (decr. SVR) –> decr. BP.

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5
Q

Sepsis. Mechanism that leads to decr. CVP and PCWP? 2

A
  1. peripheral venous dilation (due to proinflammatory mediators) –> pooling of blood in dilated veins
  2. increased vascular (capilary) permeability (third-spacing).
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6
Q

Sepsis early stage features?

A

EARLY STAGE (hyperdynamic stage):
decr. SVR, decr. BP, incr. CO and HR. (warm)

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7
Q

Sepsis early stage mechanism that incr. CO?

A

Hypotension + inflammation from sepsis –>

A compensatory increase in sympathetic drive increases
I. cardiac contractility and II. HR
resulting in increased cardiac output (CO)/cardiac index (CO per body surface area) despite reduced left ventricular preload).

ALSO:
1. the large decrease in SVR and 2. a baroreceptor reflex–mediated increase in heart rate (ie, tachycardia) –> incr. CO.

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8
Q

sepsis. whats the point of incr. CO?

A

CO increased to maintain tissue perfusion.

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9
Q

sepsis. what venous oxygen?

A

Incr. MvO2
The high rate of blood flow through the systemic capillaries prevents complete extraction of oxygen by the tissues=incomplete extraction of oxygen, resulting in high mixed venous oxygen saturation –> May develop lactic acidosis from tissue hypoperfusion.

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10
Q

sepsis. late stage features?

A

LATE STAGE (hypodynamic):
incr. SVR, decr. CO –> grave deterioration (cold)

!!!As shock progresses, tissue ischemia and accumulation of cytotoxic mediators eventually cause a reduction in CO –> with end-organ dysfunction./In shock end-organ damage = due to inadequate oxygen delivery to the organs and tissues of the body.

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11
Q

septic shock temperature?

A

SEPTIC SHOCK – hyper and hypothermia. Septic shock can present with either hyper- or hypothermia; hypothermic presentation may be due to cytokine-induced dysregulation of temperature control in the hypothalamus and is associated with poorer outcomes.

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12
Q

neurogenic shock. mechanism?

A

No SNS response –> NO SNS mediated incr. in HR and cardiac contractility –> decr. CO.

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13
Q

neurogenic shock. features?

A

decr. SVR, bradycardia, low cardiac index (output), low PCWP

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14
Q

neurogenic shock. what oxygen (MvO2)?

A

decr. MvO2 = improved peripheral oxygen extraction due to lower flow

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15
Q

CVP distributive - septic?

A

decreased

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16
Q

PCWP distributive - septic?

A

decreased

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17
Q

Cardiac index (LV output), distributive - septic?

A

increased (early phase)
decreased in late stage when deterioration happens

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18
Q

SVR distributive - septic?

A

decreased

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19
Q

SvO2 distributive - septic?

A

increased (fast flow –> incomplete extraction of O2 in tissues)

20
Q

CVP distributive - neurogenic?

A

decreased

21
Q

PCWP distributive - neurogenic?

A

decreased

22
Q

Cardiac index (LV output), distributive - neurogenic?

A

decreased (no SNS response, reflex)

23
Q

SVR, distributive - neurogenic?

A

decreased (no SNS response, reflex)

24
Q

SvO2, distributive - neurogenic?

A

decreased (slow flow –> maintained extraction of O2 in tissues)

25
Q

Cardiogenic shock. primary disturbance?

A

Left ventricle failure

26
Q

PCWP cardiogenic shock?

A

increased

26
Q

CVP cardiogenic shock?

A

increased
Also incr. pressure in right atrium

27
Q

Cardiac index (LV output) cardiogenic shock?

A

DECREASED (main feature)

28
Q

SVR cardiogenic shock?

A

increased (compensatory increase due to low CO)

29
Q

SvO2 cardiogenic shock?

A

decreased

30
Q

Hypovolemic shock main disturbance

A

decreased blood volume

31
Q

CVP Hypovolemic shock?

A

decreased

32
Q

PCWP Hypovolemic shock?

A

decreased

33
Q

CO Hypovolemic shock?

A

decreased

34
Q

SVR Hypovolemic shock?

A

Increased (compensatory incr.)

35
Q

SvO2 Hypovolemic shock?

A

decreased

36
Q

in hypovolemic what is activated as compensation?

A

SNS and RAAS

37
Q

hypovolemic. How CO is maintained?

A

Stimulation of the heart (SNS) results in increased contractility and heart rate, helping to maintain cardiac output.

38
Q

hypovolemic. kidney role?

A

Increased renal sodium and water retention help to prevent further volume loss.

Per raas sistema

39
Q

hypovolemic resuscitation with i/v fluids. what is result? 2

A

Intravenous fluids increase the intravascular and left ventricular end-diastolic volumes. The increase in preload stretches the myocardium and increases the end-diastolic sarcomere length, leading to an increase in SV and CO by the Frank-Starling mechanism.

40
Q

if hypovolemia due to diarrhea. what electrolyte disturbance?

A

loss of bicarbonate in the stool, further contributing to metabolic acidosis and a compensatory increase in ventilation.

41
Q

obstructive shock primary disturbance?

A

impeded cardiopulmonary blood flow (PE, PTX, tamponade)

42
Q

CVP in obstructive shock?

A

increased

43
Q

PCWP in obstructive shock?

A

decreased

44
Q

CO in obstructive shock?

A

decreased

45
Q

SVR in obstructive shock?

A

increased (compensation)

46
Q

SvO2 in obstructive shock?

A

decreased

47
Q

PCWP specifically in tamponade (obstructive shock)?

A

preload of left heart is decreased, BUT duo to external compression PCWP is paradoxically increased

STEP 2 (9 decks)

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