Shock Flashcards

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1
Q

what is shock?

A

Definition: cellular and tissue hypoxia -Impaired O2 delivery/utilization -Increased O2 consumption Why do we care? When it becomes irreversible > multi-organ failure and death Critical to identify and treat quickly before tissue death Usually see low BP (not always)

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2
Q

what decreases O2 supply? what increases O2 demand?

A

Decrease supply: -Pump failure -Decreased total blood volume -Poor vascular tone What can increase demand -Exercise -Infection -Meds/toxins -Hypermetabolic states

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3
Q

blood pressure =

A

blood pressure = CO x SVR CO = SV x HR

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4
Q

early signs of shock

A

-MAP decreased by 10mmHg from baseline -effective compensation -O2 is shunted to vital organs -tachycardia

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5
Q

compensatory signs of shock

A

-MAP decreased by 10-15mmHg from baseline -increased renin, increased ADH -vasoconstriction -decreased pulse pressure -increased heart rate -decreased pH -resless -apprehensive

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6
Q

progressive signs of shock

A

-MAP decreased 20mmHg from baseline -tissue/organ hypoxia -decreased urine (oliguria) -weak rapid pulse -decreased pH -sensory neural changes

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7
Q

refractory signs of shock

A

-excessive cell/organ damage -multi system organ failure -decreased pH

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8
Q

Hypovolemic shock

A

-inadequate myocardial contractility -sympathetic over activity leads to vasoconstriction in order to maintain BP -Despite normal BP, organs are poorly perfused due to a reduction in blood flow -your cardiac circuit is fine, blood vessels are working, but blood volume is depleted -dehydration is hypovolemic shock

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9
Q

Causes of hypovolemic shock

A

Hemorrhagic -trauma -GI bleed -AAA rupture -ruptured ectopic pregnancy -post-partum hemorrhage Non-Hemorrhagic -GI loss (vomiting/diarrhea) -inadequate intake -environmental/neglect -burns

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10
Q

Treatment of hypovolemic shock

A

-ABCs -good IV access -VOLUME - start with crystaloid -blood if bleeding (massive transfusion protocol) -pressors - norepinephrine -definitive management (stope bleeding, OR/endoscopy if needed, treat underlying condition) -If they have no pulse (including carotid and femoral pulses) – DO CPR!!!

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11
Q

Cardiogenic shock

A

-Poor myocardial contractility -sympathetic over activity leads to vasoconstriction in order to maintain BP -despite normal or high BP, organs are poorly perfused due to a reduction in blood flow -High venous pressure leads to fluid extravasation and oedema

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12
Q

cardiogenic shock causes

A

-myocardial ischemia or infarction -valvular disease -cardiomyopathy -myocarditis -toxins

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13
Q

treatment of cardiogenic shock

A

-ABCs (C also call cardiology) -oxygenation/intubation -IV access -careful fluid resuscitation -inotropes/vasopressors (dobutamine/norepinephrine) -definitive management (cath lab for stent/balloon pump vs. OR for CABG/valve replacement) (coronary artery bypass graft)

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14
Q

distributive shock

A

-with adequate fluid therapy, the heart usually compensates by inncrease rate and contractility, although this might not be enough -capillary leak worsens hypovolemia and causes edema (including pulmonary) -changes above lead to a reduction in BP and organ perfusion -vessels dilate causing relative hypovolemia and reduction in SVR

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15
Q

distributive shock causes

A

-septic shock (overwhelming systemic infection) -anaphylactic shock (food, medication, contrast, insects) -neurogenic shock

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16
Q

regulation of vascular tone

A

-systemic: neural and hormonal -local: myogenic and humoral -humoral = chemical substances (hormones, etc.) in blood or other body fluids

17
Q

treatment of distributive shock

A

-ABCs -IV access -Fluids -Vasopressors (norepinephrine) -sepsis (look for source, antibiotics (broad), source control (surgery if needed)) -anaphylaxis (epinephrine (0.3mg IM), steroids, H1/H2 blockers, decontamination) -Neurogenic (C collar/stabilize spine, atropine/pressors, steroids controversial, NSG intervention)

18
Q

Obstructive shock

A

-myocardium contracts against high afterload -sympathetic over activity leads to vasoconstriction in order to maintain BP -despite normal BP, organs are poorly perfused due to a reduction in blood flow -back pressure leads to venous congestion

19
Q

Causes of obstructive shock

A

-cardiac tamponade - cant fill the heart; obstruction = pericardial effusion -tension pneumo - cant fill the heart; obstruction = air in chest -PE - cant fill the heart; obstruction = large clot in PA -severe aortic stenosis - cant pump out into aorta; obstruction = stenotic aortic valve

20
Q

treatment of obstructive shock

A

-ABCs -IV access -Fluids carefully -tamponade - pericardiocentesis -tension pneumo - chest tube -aortic stenosis - valve replacement -PE - thrombolytics/anticoagulation

21
Q

is this person in shock

A

-ill appearing -abnormal vitals (hypotension, tachycardia) -weak pulses -mental status changes -cool/clammy extremities

22
Q

how do you know what type of shock?

A

-history -exam -Ultrasound!

23
Q

basic principles of management of shock

A

-recognize quickly -move to a code room/get help -ABCs -IV access -nook and cranny -diagnostic/therapeutic interventions at the same time -frequent reassessments: BP (art line/central line for CVP), lactate clearance, hemoglobein (>10), urine output (>0.5 ml/kg/hr)

24
Q

alpha and beta receptor effects on cardiovascular system

A

-B1 and a little B2: both increase heart rate, contractility and speed conduction -B2: stimulation leads to VASODILATION -A1: stimulation causes VASOCONSTRICTION -sympathetic neurotransmitters are noradrenaline and adrenaline

25
Q

Drugs and how they affect the a, b, D, and V receptors

A