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Undeleted > Shock > Flashcards

Shock Flashcards

1
Q

cardiac output

A

volume of blood being pumped by the heart per minute

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2
Q

typical cardiac output (adult)

A

4-6 L/min

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3
Q

shock

A

systemic abnormal cellular metabolism occurring when tissue oxygenation does not meet the needs to maintain cellular functionSUPPLY != DEMAND

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4
Q

what is systole?

A

atrial fillingventricular emptying

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5
Q

what is diastole?

A

atrial emptyingventricular filling

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6
Q

ischemia

A

insufficient flow of oxygenated blood

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7
Q

hypoxia

A

reduction of O2 supply to tissues

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8
Q

cyanosis

A

visual sign of ischemia, which can be due to hypoxia

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9
Q

results of decreased CO

A
  • anaerobic metabolism- necrosis
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10
Q

anaerobic metabolism involves…

A
  • altered ATP production - lactic acid production- pH alterations- Na/K pump failure (cellular edema, electrolyte imbalance)i
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11
Q

cardiac output equation

A

heart rate x stroke volume

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12
Q

typical heart rate

A

60 - 100 bpm

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13
Q

effect of tachycardia on CO

A

increases TO A POINT- CAN make the heart beat more often, CAN’T make it contract faster

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14
Q

effect of bradycardia on CO

A

decreases

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15
Q

stroke volume

A

amount of blood ejected by LV in each contraction- affected by HR, preload, afterload, contractility

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16
Q

typical amount of blood ejected by LV each contraction

A

55 - 100 ml range70 ml typical finding

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17
Q

typical cardiac output

A

4 to 8 liters per minute

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18
Q

cardiac index + typical

A

cardiac output requirements accounting for body size; determined by dividing the cardiac output by the body surface area2.7 - 3.2 L/m^2

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19
Q

preload

A

volume- degree of muscle fiber stretch within ventricles prior to systole (recoil)- caused by volume of blood within the ventricle

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20
Q

right ventricle preload

A

central venous pressure (CVP) 2-8 mm Hg

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21
Q

how to determine preload? right ventricle

A

direct: central line (NOT PICC)indirect: echo

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22
Q

left ventricle preload

A

left ventricle end diastolic pressure (LVEDP)/pulmonary capillary wedge pressure (PCWP) 8-12 mm Hg

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23
Q

how to determine preload? left ventricle

A

direct: left atrial lineindirect: pulmonary artery catheter (Swan Ganz catheter), echo

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24
Q

Swan Ganz catheter

A

pulmonary artery catheter

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25
Q

Starlings Law

A

an increase in ventricular volume increases muscle fiber length and tension, thereby enhancing contraction and improving stroke volumeTO A POINT

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26
Q

afterload

A

resistance- experienced by ventricles during systole- must be adequate to aid in circulation and CO

27
Q

vasoconstriction and CO

A
  • increases blood flow velocity- increases CO to a POINT, may decrease
28
Q

vasodilation and CO

A
  • decreases blood flow velocity- decreases CO
29
Q

pulmonary vascular resistance + equation

A

right ventricular afterload[(MPAP - PCWP) / CO] x 80typical: 150 to 250 mm HgMPAP: mean pulmonary artery pressure

30
Q

systemic vascular resistance + equation

A

left ventricular afterload[(MAP - CVP) / CO] x 80typical: 80 to 1200 mm Hg

31
Q

contractility

A

force of contraction- shortening of myocardial fibers generating sufficient pressure to propel blood forward- inotropic

32
Q

inotropic

A

affecting force of muscle contraction

33
Q

chronotropic

A

affecting heart rate

34
Q

increase force of contraction (effect on CO)

A

increase CO

35
Q

decrease force of contraction (effect on CO)

A

decrease CO

36
Q

ejection fraction + typical

A

The percentage of blood ejected from the heart during systole.55 to 75%

37
Q

blood pressure + equation

A

measured force of the volume of blood against vessel wall- hydrostatic pressure x resistance- CO x SVRSVR = systemic vascular resistance

38
Q

systolic blood pressure

A

amount of pressure/force generated by the LV to distribute blood into the aorta with each heart contraction

39
Q

diastolic blood pressure

A

amount of pressure/force against the arterial walls during the relaxation phase of the heart

40
Q

pulse pressure equation

A

SBP - DBP

41
Q

mean arterial pressure equation

A

(SBP + 2DBP)/3

42
Q

hypovolemic shock

A

volume losstreatment: restore intravascular volume

43
Q

cardiogenic shock

A

pump failure (acute decompensated heart failure, dysrhythmia, MI)treatment: increase pump effectiveness

44
Q

distributive shock

A

loss of vascular resistance (neurogenic, sepsis, anaphylaxis)treatment: volume expansion, vasoconstriction

45
Q

obstructive shock

A

mechanical impairment of filling or contracting (pericarditis, cardiac tamponade, outflow obstruction, massive PE)treatment: correct the cause, maximize preload, decrease afterload

46
Q

stages of shock: initial

A

compensatory- increased sympathetic stimulation, HR- mild vasoconstriction

47
Q

stages of shock: non-progressive

A

compensatory- continued sympathetic stimulation- chemical compensation- anaerobic metabolism in non-vital organs

48
Q

stages of shock: progressive

A

uncompensated- anoxia of non-vital organs- hypoxia of vital organs- overall anaerobic metabolism (hyperkalemia, metabolic acidosis)

49
Q

stages of shock: refractory

A

irreversible- severe tissue hypoxia- toxic metabolites- multiple organ dysfunction syndrome (MODS)- death

50
Q

systolic failure (cardiogenic)

A

EF < 40%think: squeeze

51
Q

diastolic failure (cardiogenic)

A

EF often > 40%think: fill

52
Q

cardiac tamponade

A

fluid accumulates rapidly in the pericardium and cause a sudden decrease in cardiac output EMERGENCY!

53
Q

compensatory mechanisms

A
  • augment CO & MAP (baroreceptors)- vasomotor cortex: pons & medulla (cerebral cortex, chemoreceptors)- SNS- ANS
54
Q

shock nota bene

A

always go through all four stages, time in each varies- body prioritizes organs VERY WELL & very QUICKLY- if patient needs to poop or puke, heart attack imminent

55
Q

compensatory mechanisms: SNS

A

immediate- vagus nerve reflex (PS control of heart, GI)- vessels: increase constriction/resistance, venous return- heart: increase HR, FOCslower/long term- posterior pituitary: ADH- adrenal cortex: aldosterone- hypothalamus: thirst regulation center- adrenal medula: epinephrine (adrenaline), norepi- decreased renal perfusion- kidney: RAA

56
Q

adverse effects of compensatory mechanisms

A
  • increasing HR, FOC, workload (increased O2 demand, inadequate supply)- decompensation (heart failure, dysrhythmia, MI)- fluid volume overload (systemic & pulmonary edema, CHF)- shunting - decreased cap blood flow to cells/tissues/organs
57
Q

compensatory mechanisms lead to (adverse)

A
  • increased afterload- increased workload- increased O2 demandfill up heart too much - too much fluid - heart can’t beat anymore
58
Q

shunting

A

diversion of blood by vasoconstriction of microcirculation

59
Q

shock s/s mnemonic

A

S: kin - cool, decreased pulses, prolonged cap refill, clammy, cyanotic, pallorH: eart - increased HR, dysrhythmiaO: xygen - tachypneaC: onsciousness, level of: anxiety, irritability, restlessness, confusion, comaK: idney - oliguria (<30cc) + concentrated

60
Q

nursing care goals for shock

A
  • optimize tissue perfusion: blood flow, CO, BP, prevent ischemia- rest (keep ‘em warm, NO SHIVERS)- pain: don’t want increased metabolic demands- ventilation: decrease O2 demand
61
Q

nursing interventions mnemonic

A

V: entilation - airway, semi-fowlers, gradual activity increaseI: nfusion - I&O, IV (crystalloids, colloids), GI tract assessment, flat or elevated legs, dietary mods/restrictionsP: harmacology - O2, chrono/inotropic meds, vasoactive meds, AVOID IM

62
Q

crystalloids to give

A

isotonic!!- normal saline (0.9%)- lactated ringer’s

63
Q

colloids to give

A
  • albumin (synthetic for religious reasons)- blood products- hetastarch
64
Q

why avoid IM injections for shock nursing intervention?

A

body prioritization of muscles down, injection not going anywhere

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