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1

cardiac output

volume of blood being pumped by the heart per minute

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typical cardiac output (adult)

4-6 L/min

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shock

systemic abnormal cellular metabolism occurring when tissue oxygenation does not meet the needs to maintain cellular function

SUPPLY != DEMAND

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what is systole?

atrial filling
ventricular emptying

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what is diastole?

atrial emptying
ventricular filling

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ischemia

decreased supply of oxygenated blood

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hypoxia

reduction of O2 supply to tissues

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cyanosis

visual sign of ischemia, which can be due to hypoxia

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results of decreased CO

- anaerobic metabolism
- necrosis

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anaerobic metabolism involves...

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

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cardiac output equation

heart rate x stroke volume

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typical heart rate

60 - 100 bpm

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effect of tachycardia on CO

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

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effect of bradycardia on CO

decreases

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stroke volume

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

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typical amount of blood ejected by LV each contraction

55 - 100 ml range
70 ml typical finding

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typical cardiac output

4 to 8 liters per minute

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cardiac index + typical

cardiac output requirements accounting for body size; determined by dividing the cardiac output by the body surface area

2.7 - 3.2 L/m^2

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preload

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

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right ventricle preload

central venous pressure (CVP) 2-8 mm Hg

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how to determine preload? right ventricle

direct: central line (NOT PICC)
indirect: echo

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left ventricle preload

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

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how to determine preload? left ventricle

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

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Swan Ganz catheter

pulmonary artery catheter

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Starlings Law

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

TO A POINT

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afterload

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

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vasoconstriction and CO

- increases blood flow velocity
- increases CO to a POINT, may decrease

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vasodilation and CO

- decreases blood flow velocity
- decreases CO

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pulmonary vascular resistance + equation

right ventricular afterload

[(MPAP - PCWP) / CO] x 80

typical: 150 to 250 mm Hg

MPAP: mean pulmonary artery pressure

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systemic vascular resistance + equation

left ventricular afterload

[(MAP - CVP) / CO] x 80

typical: 80 to 1200 mm Hg

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contractility

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

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inotropic

affecting force of muscle contraction

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chronotropic

affecting heart rate

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increase force of contraction (effect on CO)

increase CO

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decrease force of contraction (effect on CO)

decrease CO

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ejection fraction + typical

The percentage of blood ejected from the heart during systole.

55 to 75%

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blood pressure + equation

measured force of the volume of blood against vessel wall
- hydrostatic pressure x resistance
- CO x SVR

SVR = systemic vascular resistance

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systolic blood pressure

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

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diastolic blood pressure

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

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pulse pressure equation

SBP - DBP

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mean arterial pressure equation

(SBP + 2DBP)/3

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hypovolemic shock

volume loss

treatment: restore intravascular volume

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cardiogenic shock

pump failure (acute decompensated heart failure, dysrhythmia, MI)

treatment: increase pump effectiveness

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distributive shock

loss of vascular resistance (neurogenic, sepsis, anaphylaxis)

treatment: volume expansion, vasoconstriction

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obstructive shock

mechanical impairment of filling or contracting (pericarditis, cardiac tamponade, outflow obstruction, massive PE)

treatment: correct the cause, maximize preload, decrease afterload

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stages of shock: initial

compensatory
- increased sympathetic stimulation, HR
- mild vasoconstriction

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stages of shock: non-progressive

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

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stages of shock: progressive

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

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stages of shock: refractory

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

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systolic failure (cardiogenic)

EF < 40%
think: squeeze

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diastolic failure (cardiogenic)

EF often > 40%
think: fill

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cardiac tamponade

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

EMERGENCY!

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compensatory mechanisms

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

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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

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compensatory mechanisms: SNS

immediate
- vagus nerve reflex (PS control of heart, GI)
- vessels: increase constriction/resistance, venous return
- heart: increase HR, FOC

slower/long term
- posterior pituitary: ADH
- adrenal cortex: aldosterone

- hypothalamus: thirst regulation center
- adrenal medula: epinephrine (adrenaline), norepi
- decreased renal perfusion
- kidney: RAA

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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

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compensatory mechanisms lead to (adverse)

- increased afterload
- increased workload
- increased O2 demand

fill up heart too much - too much fluid - heart can't beat anymore

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shunting

diversion of blood by vasoconstriction of microcirculation

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shock s/s mnemonic

S: kin - cool, decreased pulses, prolonged cap refill, clammy, cyanotic, pallor
H: eart - increased HR, dysrhythmia
O: xygen - tachypnea
C: onsciousness, level of: anxiety, irritability, restlessness, confusion, coma
K: idney - oliguria (<30cc) + concentrated

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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

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nursing interventions mnemonic

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

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crystalloids to give

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

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colloids to give

- albumin (synthetic for religious reasons)
- blood products
- hetastarch

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why avoid IM injections for shock nursing intervention?

body prioritization of muscles down, injection not going anywhere

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