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CCN > Shock > Flashcards

Shock Flashcards

1
Q

What is shock?

A

Clinical syndrome characterized by deceased tissue perfusion leading to impaired cellular metabolism. Begins as an adaptive response to injury / insult then progresses to multi-system organ failure

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2
Q

What are the three major classifications of shock?

A

1) Hypovolemic (Loss of volume)
2) Cardiogenic (Decreased contractility)
3) Distributive (Vasodilatory) –> Neurogenic, anaphylactic, septic

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3
Q

What are the 4 stages of shock?

A

1) Initial
2) Compensatory
3) Progressive
4) Refractory

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4
Q

What happens in the initial stage?

A

Nonspecific cellular changes but no clinical manifestations

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5
Q

What happens in the compensatory stage?

A

Compensatory mechanisms shunt blood to vital organs.

1) Nervous system compensation
2) Hormonal compensation
3) Chemical compensation

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6
Q

What is nervous system compensation?

A

SNS compensation:

Heart: Baroreceptors in aortic arch and carotid sinus increase HR, FOC, SV to increase CO and BP

Lungs: Increase RR, bronchodilation

Blood vessels: Constrict in skin, GIT, kidneys. Dilate in coronary arteries, skeletal muscles

Pupils: Dilate
Sweat glands: Increase activity

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7
Q

What is hormonal compensation?

A

Kidneys –> Decrease blood flow stimulates RAAS, Angiotensin II causes peripheral vasoconstriction. Adrenal cortex stimulated to release aldosterone increasing Na and H2O reabsorption

Adrenal medulla –> Release epinephrine, norepinephrine

Adrenal cortex –> Release aldosterone and glucocorticoids

Liver –> Secrete ACTH, leads to production of glucocorticoids (increases BG from glycogenolysis)

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8
Q

What is chemical compensation?

A

Lungs –> Decreased blood flow causes deadspace units, triggers chemoreceptors to increase RR. Causes resp alkalosis and eventually combined acidosis

Neuro –> Hyperventilation decreases CO2 causes cerebral vessels to constrict, decrease O2 to brain

Capillary –> Decreased CO causes cells to extract more O2

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9
Q

What happens in the progressive stage?

A

Ongoing compensatory mechanisms work against the pt, vasoconstriction causes adverse effects

1) Cellular function
2) Capillary dynamics
3) Systemic circulation
4) Specific organ systems

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10
Q

How is cellular function affected in the progressive stage?

A

Arteriolar vasoconstriction –> Decreased BF, decreased O2 and decreased ATP production. Cells switch to anaerobic metabolism, lactic acid produced which decreases FOC.

  • -> Pt goes into metabolic acidosis.
  • -> Impaired cellular function releases toxic substances accumulating in tissues and altering local environment
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11
Q

How are capillary dynamics affected in the progressive stage?

A

Acidic tissue environments from impaired cellular function causes pre-capillary sphincters to relax but post-capillary sphincters constrict. Histamine release further increases capillary permeability.

  • -> Increased hydrostatic pressure, histamine, pt becomes edematous as fluid leads out of intra-vascular space, decrease CO, decrease CA perfusion, ischemia
  • -> Blood becomes more viscous, increasing afterload, capillary sludging causes coagulopathy
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12
Q

What happens when blood becomes more viscous?

A

As fluid is lost, increased viscosity leads to:

Increased afterload 
Capillary sludging (aggregation of RBCs, platelets, large proteins) causing coagulopathy, DIC
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13
Q

How is the systemic circulation affected by the progressive stage?

A

Decreased perfusion to periphery causes distal ischemia of tissues. Pulses weaker, then absent, local ischemia progresses to necrosis and becomes infection risk

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14
Q

How are specific body organs affected by the progressive stage?

A

Damage due to acidosis and prolonged vasoconstriction:

Heart –> Increased O2 consumption with decreased perfusion, arrythmias

Brain –> Initially vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation

Kidneys –> Nephron hypoxia, acute kidney injury

GI –> Ischemia to interstitial lumen cells leads to hemorrhage and bacterial translocation

Liver –> Decrease in phagocytosis (Kuppfer cells) thus blood from GI tract cant get filtered. Impaired metabolism, detoxification, liver ischemia

Pancreas –> Release proteolytic enzymes and MYOCARDIAL DEPRESSANT FACTOR (increases splanchnic vasoconstriction, interferes with role of calcium?)

Lungs –> Pulmonary vasoconstriction increases CO2, acidosis leads to interstitial and alveolar pulm. edema, decreased surfactant production causes atelectasis and decreased compliance

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15
Q

What are the cycles of the refractory stage?

A

1) Cycle of cardiac failure
2) Cycle of acidosis
3) Cycle of cerebral ischemia
4) Cycle of blood clotting

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16
Q

What is the cycle of cardiac failure?

A

Decreased CO –> Decreased CA perfusion –> Ischemia –> Decreased FOC (worsened by acidosis and MDF) –> Arrythmias

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17
Q

What is the cycle of acidosis?

A

Decreased renal function –> Decreased resp function (increase CO2), decreased cellular function (Increase lactic acid) –> Mixed acidosis –> Decrease CO + Pre-capillary sphincters relax decrease circulating fluid

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18
Q

What is the cycle of blood clotting?

A

Decreased blood volume –> Clot formation –> Decreased blood flow + Sluggish capillary flow, DIC –> Cellular hypoxia –> Acidosis

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19
Q

What is the cycle of cerebral ischemia?

A

Decreased CO –> Cerebral ischemia –> Initially causes vasoconstriction due to SNS response, then SNS response is LOST leading to decreased HR and vasodilation –> BRAIN DEATH –> Cardiac arrest, resp arrest

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20
Q

How much volume needs to be lost for hypovolemic shock?

A

15-30%, 750 - 1500mls

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21
Q

What is the etiology of hypovolemic shock?

A

1) Internal losses (Third spacing, internal hemorrhage)

2) External losses (Whole blood loss, coagulation disorders, plasma, fluid loss)

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22
Q

What is pathophys of hypovolemic shock?

A 
Decrease intravascular volume
Decrease venous return 
Decrease filling pressures
Decrease SV
Decreased CO 
Decreased tissue perfusion
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23
Q

What is pulsus parodoxus associated with?

A

Hypovolemia (decreased preload and left side, decreased BP on inspiration)

24
Q

Treatment of hypovolemic shock?

A

Fluid replacement –> Crystalloid / colloid / blood, should be warmed if large amount.

Inotropes / vasopressors

25
Q

What are crystalloids?

A

NS, RL
Use isotonic solutions first, increase extracellular volume without altering electrolyte concentration of plasma. RL most compatible.

26
Q

What are colloids?

A

Plasma proteins (FFP clotting factors, abumin). FFP MUST BE GIVEN COLD

27
Q

What are blood products?

A

RBCs (improve O2 carrying capacity of blood), Cryoprecipitate (contains fibrinogens and other clotting factors)

28
Q

What is the etiology of cardiogenic shock?

A

1) Coronary cardiogenic shock –> After acute MI decrease FOC
2) CA are fine but myocardium is sick decreasing FOC. Can be caused by viral infections, myocarditis, cardiomyopathies

29
Q

What is 3 main pathophys of cardiogenic shock?

A

Systolic dysfunction, impaired LV contracility
Decrease tissue perfusion –> RAAS INCREASES AFTERLOAD
***Further decrease CO

Inadequate systolic emptying of LV
***Pulm. edema intra alveolar edema

Diastolic dysfunction, impaired LV compliance
Decreased preload, decreased CO

30
Q

How does systolic dysfunction result in cardiogenic shock?

A 
Impaired LV contracility 
Decrease SV, CO, BP 
Decrease tissue perfusion --> RAAS INCREASES AFTERLOAD 
Decrease CA perfusion 
Ischemia 
Decrease FOC 
***Further decrease CO
Inadequate systolic emptying of LV
Increase LV filling pressures, increase LAP
Increase pulm. venous pressure 
Increase pulm. capillary pressure 
***Pulm. edema intra alveolar edema
31
Q

What is RV failure and what does it result in?

A

Caused with RV infarct, PE, pulm HTN, ARDS, sepsis. High RAP > 15 can result in:

RV ischemia
RV failure resulting in decreased LV filling
RV overload, tricuspid regurg and septal shift into LV
Decreased CO due to decreased LV filling pressures

32
Q

What are clinical findings specific to RV failure?

A

Portal HTN, distended neck veins, chest may be clear as backflow is systemic

33
Q

What are the key hemodynamic differences between RV and LV failure?

A

RVF: Increased RAP, decreased PADP, PCWP
LVF: Increased PADP, PCWP

34
Q

What is treatment for LVF?

A

LVF causes fluid backup into lungs, pulmonary hydrostatic pressure pulm edema.

Treat: IDENTIFY CAUSE, INCREASE TISSUE PERFUSION
Dobutamine / Milrinone (FOC, decrease adterload)
Levophed
Diuretic (preload reduction)
Vasodilating agents once BP restored to decreased heart workload
Antiarrythmics
IABP (Can decrease afterload without decreasing MAP)

35
Q

What is treatment for RVF?

A

RVF causes blood to backflow into systemic venous circulation causing portal HTN, peripheral and cerebral edema.

Treat: OPTIMIZE PRELOAD
Pulmonary vasodilators to decrease pulm htn
Inotropic agents (FOC)
Treat cause

36
Q

How does the intra-aortic balloon pump work?

A

Sits in the aorta below left subclavian artery and above the renal vessels. Inflated with helium, works by COUNTERPULSATION.

IAB is inflated at the beginning of DIASTOLE and deflated in SYSTOLE. With inflation it displaces blood into the coronary and carotid arteries and distal systemic circulation, increases renal blood flow reducing RAAS. When deflated it creates potential space (Vacuum) in aorta which makes LV ejection easier.

***Improves CA perfusion and decreases LV workload

37
Q

What is the overall theme of distributive shock?

A

Alterations in blood vessels leading to decreased peripheral resistance (SVR) and increased vascular capacity (vasodilation)

38
Q

What is SIRS?

A

Systemic Inflammatory ResponseSyndrome

1) Temp > 38 or < 36
2) HR > 90
3) RR > 20 or PaCO2 <32
4) WBC > 12000 or < 4000

39
Q

What is sepsis?

A

Life threatening organ dysfunction due to dysregulated host response to infection.

SEPTIC SHOCK is syndrome in which there are profound circulatory, cellular, and metabolic abnormalities that increase mortality >40%

40
Q

What is SOFA?

A

Sepsis related organ failure assessment

1) PaO2 / FiO2 (Resp)
2) GCS (Neuro)
3) Platelets (Hem)
4) Creatinine (Renal)
5) Bilirubin (Liver)
6) HTN / Vasopressors (CV)

41
Q

What is quick SOFA?

A

2/3 criteria warrant closer investigation:

1) Resp rate > 22
2) Altered mentation
3) SBP < 100

42
Q

How to clinically identify septic shock?

A

Pt has been fluid resuscitated adequately and yet:

1) Require vasopressors to maintain MAP > 65
2) Serum lactate > 2

43
Q

How do bacteria cause septic shock?

A

Release of endotoxins located in cell wall of bacteria, released on death of bacteria and creates biochemical changes

44
Q

What is the pathophys of sepsis?

A

Excess of pro-inflammatory OR anti-inflammatory mediators cause harm to organs

1) Increased inflammatory response (Vasodilation, increased metabolic rate)
2) Increased coagulation (Decreased perfusion, DIC)
3) Decreased fibrinolytic activity (Traps platelets, further decrease in perfusion)

45
Q

What are other pathophys changes seen in sepsis?

A

1) Decreased activated protein C (balances inflammatory process, coagulation, fibrinolysis)
2) Hormonal imbalance (Vasopressin and cortisol NOT released, worsening shock)
3) Multi-organ dysfunction
4) Myocardial depression
5) Massive systemic vasodilation, increased metabolic rate, vessel permeability, pt warm and flushed

46
Q

What is the pathophys of cellular hypoxia and cell death in sepsis?

A

Pts have difficulty taking up or metabolizing available O2 despite normal delivery. Anaerobic metabolism occurs, lactic acid builds up, damage occurs to organs.

Lack of ATP redisposes NA/K pumps to fail, Na stays in the intracellular compartment drawing water in. Cellular organelles swell, energy production cannot be done, cells digestive organelles rupture and release digestive enzymes killing itself.

47
Q

What are hemodynamics seen in septic shock?

A

Decreased RAP, PCWP, PAP
VERY LOW SVR
Increased SVO2
Increased CO/CI due to vasodilation (severe decrease in afterload)

48
Q

Treatment for septic shock?

A

Measure lactate (goal to resus to normalize lactate)
Blood cultures
Broad spectrum antibiotic
Aggressive IV resus (30ml/kg IV crystalloid)
Vasopressors (Epi, Norepi, Vaso, Dobutamine) NO DOPAMINE

49
Q

What is neurogenic shock?

A

Resulting from loss or suppression of sympathetic tone resulting in high CO however short lived

50
Q

What is etiology of neurogenic shock?

A

Injury of spinal cord affecting sympathetic innervation to blood vessels, edema around spinal cord, high levels of spinal anaesthesia, vasomotor centre depression from drugs, hypoglycemia (lack of ATP to send out sympathetic outflow)

51
Q

What happens with loss of SNS tone?

A

1) Inhibition of baroreceptors –> Brady –> Decreased CO
2) Peripheral vasodilation –> Decreased afterload, preload, decreased BP, CO
3) Impaired thermoregulation –> Assume room temp –> Decrease CO

52
Q

What are the specific presentations of neurogenic shock?

A

CNS: Loss of reflexes below injury
Skin: Warm, pink, DRY (Vasodilated)
HR: Bradycardic
Temp: Inability to sweat

53
Q

Treatment of neurogenic shock?

A 
Treat cause 
Prevent CNS instability: Treat hypovolemia with fluid, treat arrythmias, hypotension 
Caution when suctioning, have atropine 
Maintain normothermia 
Monitor reflexes
54
Q

What is anaphylactic shock?

A

Result of immediate hypersensitivity reaction with immunologic (Antigen-antibody) or non-immunologic activation of mediator releasing biochemical markers.

**Decreased tissue perfusion and shock

55
Q

What is pathophys of anaphylactic shock?

A

Release of mediators
Peripheral vasodilation, increased cap permeability, smooth muscle constriction
Decreased BP, SVR, preload, coronary vasoconstriction
Decreased CO, tissue perfusion

56
Q

Why is C-reactive protein tested for anaphylactic shock?

A

Measures degree of inflammatory response, assess if treatments are working

57
Q

Treatment of anaphylactic shock?

A

Remove causative antigen

Epi, antihistamines (benadryl, ranitidine), steroids, IV fluids

CCN (27 decks)

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