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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
Starlings Law
an increase in ventricular volume increases muscle fiber length and tension, thereby enhancing contraction and improving stroke volumeTO A POINT
26
afterload
resistance- experienced by ventricles during systole- must be adequate to aid in circulation and CO
27
vasoconstriction and CO
- increases blood flow velocity- increases CO to a POINT, may decrease
28
vasodilation and CO
- decreases blood flow velocity- decreases CO
29
pulmonary vascular resistance + equation
right ventricular afterload[(MPAP - PCWP) / CO] x 80typical: 150 to 250 mm HgMPAP: mean pulmonary artery pressure
30
systemic vascular resistance + equation
left ventricular afterload[(MAP - CVP) / CO] x 80typical: 80 to 1200 mm Hg
31
contractility
force of contraction- shortening of myocardial fibers generating sufficient pressure to propel blood forward- inotropic
32
inotropic
affecting force of muscle contraction
33
chronotropic
affecting heart rate
34
increase force of contraction (effect on CO)
increase CO
35
decrease force of contraction (effect on CO)
decrease CO
36
ejection fraction + typical
The percentage of blood ejected from the heart during systole.55 to 75%
37
blood pressure + equation
measured force of the volume of blood against vessel wall- hydrostatic pressure x resistance- CO x SVRSVR = systemic vascular resistance
38
systolic blood pressure
amount of pressure/force generated by the LV to distribute blood into the aorta with each heart contraction
39
diastolic blood pressure
amount of pressure/force against the arterial walls during the relaxation phase of the heart
40
pulse pressure equation
SBP - DBP
41
mean arterial pressure equation
(SBP + 2DBP)/3
42
hypovolemic shock
volume losstreatment: restore intravascular volume
43
cardiogenic shock
pump failure (acute decompensated heart failure, dysrhythmia, MI)treatment: increase pump effectiveness
44
distributive shock
loss of vascular resistance (neurogenic, sepsis, anaphylaxis)treatment: volume expansion, vasoconstriction
45
obstructive shock
mechanical impairment of filling or contracting (pericarditis, cardiac tamponade, outflow obstruction, massive PE)treatment: correct the cause, maximize preload, decrease afterload
46
stages of shock: initial
compensatory- increased sympathetic stimulation, HR- mild vasoconstriction
47
stages of shock: non-progressive
compensatory- continued sympathetic stimulation- chemical compensation- anaerobic metabolism in non-vital organs
48
stages of shock: progressive
uncompensated- anoxia of non-vital organs- hypoxia of vital organs- overall anaerobic metabolism (hyperkalemia, metabolic acidosis)
49
stages of shock: refractory
irreversible- severe tissue hypoxia- toxic metabolites- multiple organ dysfunction syndrome (MODS)- death
50
systolic failure (cardiogenic)
EF < 40%think: squeeze
51
diastolic failure (cardiogenic)
EF often > 40%think: fill
52
cardiac tamponade
fluid accumulates rapidly in the pericardium and cause a sudden decrease in cardiac output EMERGENCY!
53
compensatory mechanisms
- augment CO & MAP (baroreceptors)- vasomotor cortex: pons & medulla (cerebral cortex, chemoreceptors)- SNS- ANS
54
shock nota bene
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
compensatory mechanisms: SNS
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
adverse effects of compensatory mechanisms
- 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
compensatory mechanisms lead to (adverse)
- increased afterload- increased workload- increased O2 demandfill up heart too much - too much fluid - heart can't beat anymore
58
shunting
diversion of blood by vasoconstriction of microcirculation
59
shock s/s mnemonic
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
nursing care goals for shock
- 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
nursing interventions mnemonic
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
crystalloids to give
isotonic!!- normal saline (0.9%)- lactated ringer's
63
colloids to give
- albumin (synthetic for religious reasons)- blood products- hetastarch
64
why avoid IM injections for shock nursing intervention?
body prioritization of muscles down, injection not going anywhere

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