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Critical Care > Shock > Flashcards

Shock Flashcards

1
Q

Oxygen Delivery and Shock

A
  • when shock is occurring o there is any problem with cardiac output, oxygen delivery is compromised
  • there should be sufficient hemoglobin along with cardiac output and oxygen hemoglobin saturation
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2
Q

Baroreceptors

A
  • how the body maintains homeostasis
  • located in carotid and aortic sinuses
  • sensitive to changes in pressure (as in decreased BP)
  • receptors tell the medulla there is low pressure > medulla tells the body to vasoconstrict to try to maintain BP
  • if high BP is sensed > medulla tells body to vasodilate and slow down the HR
  • if pt is in rapid rate like SVT, physician may massage carotids to create or initiate this reflex and hopefully HR will slow
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3
Q

Shock: Definition

A

syndrome characterized by decreased tissue perfusion and impaired cellular metabolism

which results in an imbalance between supply of and demand for O2 and nutrients

impacts all body systems:

  • influenced by compensatory mechanisms
  • influenced by successful interventions
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4
Q

Normal Physiology: Regulation of BP

A
  • BP is product of CO and SVR
  • BP decreases when CO or SVR is low

Decrease in BP > decrease in diameter of vessels > decreased flow through the vessel resulting in the inability to keep the vessel open

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5
Q

Renin-Angiotensin System

A

when low volume shock (hypovolemic or cardiogenic shock) occurs, this compensatory mechanism is to vasoconstrict

Angiotensin 1 converts to angiotensin 2 which causes 3 things to be released:

  1. Aldosterone = vasoconstriction
  2. Renin = helps us absorb sodium and water
  3. ADH = kicks in so we don’t urinate.

Together they increase CO and maintain BP and pull blood to core of body to perfuse heart/lungs/brain

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6
Q

Shock: Pathophysiology

A

Shock begins with cardiovascular system failure

Alteration in at least one of four components:

  • blood volume (low)
  • myocardial contractility (impaired)
  • blood flow (decreased)
  • vascular resistance (decrease)
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7
Q

Stress Hormones

A

adrenaline

cortisol (glucose secretions)

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8
Q

Classifications of Shock

A

Low blood flow:
cardiogenic shock
hypovolemic shock
-absolute hypovolemia: external loss of whole blood or loss of other body fluids
-relative hypovolemia: pooling of blood or fluids, fluid shifts (third spacing, volume is not gone from pt, it’s not in vasculature where it belongs), internal bleeding, massive vasodilation

Maldistribution (distributive) Shock:

  • Neurogenic Shock
  • Anaphylactic Shock
  • Septic Shock
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9
Q

Stages of Shock

A

Pre-shock:

  • “warm shock” or compensated shock
  • some changes in VS, slowed cap refill
  • subtle presentation so much have an index of suspicion

Shock:

  • compensatory mechanisms overwhelmed
  • s/sx appear

End-organ dysfunction:

  • progressive dysfunction
  • leads to irreversible organ damage and pt death
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10
Q

Clinical Features of Shock

A
  • oliguria: shunting to vital organs, volume depletion
  • cool, clammy skin: vasoconstriction to shunt blood to vital organs
  • hypotension: absolute <90 mmHg systolic or relative
  • mental status changes: agitation, confusion, delirium, obtunded (not have any reaction to any noxious or tactile stimuli)
  • metabolic acidosis: decreased clearance of lactic acid b/c of decreased perfusion to cells, they’ve moved from aerobic metabolism to anaerobic metabolism
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11
Q

Hypovolemic Shock

A

inadequate circulating volume (shock starts and sx are seen with 15% or more fluid volume loss occurs)

acute blood volume loss of 35% or more = life threatening

many causes

compensation = vasoconstriction

assessment: vessels, pressure, labs (fluids, electrolytes, blood, acid/base balance)
tx: give fluids/blood

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12
Q

Hypovolemic Shock and Beta Blockers

A

if pt is taking beta blockers, they won’t have compensatory tachycardia associated w/ this shock

won’t know if they are in hypovolemic shock until it’s too late b/c we won’t see reflex tachycardia

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13
Q

Hypovolemic Shock and Renal Failure

A

renal failure will mask the deterioration of the client b/c we won’t see oliguria

pt’s chronic renal failure may be anuric for a considerable amount of time

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14
Q

Hypovolemic Shock and the Cardiac System

A
  • response in seconds
  • baroreceptors signal body to excrete hormones needed to compensate
  • HR and contractility increase > bounding pulses and vasoconstriction occurs
  • as shock progresses, these compensatory mechanisms lessen and CO lowers d/t failure of the pump (pulses become weaker)
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15
Q

Shock and the Vasculature System

A

low volume shock:

  • SVR increases, vessels vasoconstrict
  • pulse pressure narrows

maldistribution shock:

  • SVR decreases, vessels vasodilate
  • pulse pressure widens
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16
Q

Hypovolemic Shock and the GI System

A
  • blood is shunted from the GI organs to more needed areas
  • O2 supply to gastro mucosa suffer (n/v) > infections occur d/t development of bacterial growth > sepsis and GI bleeding
  • damage to liver occurs w/ alteration in clotting factors and inability to filter and spleen become unable to filter
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17
Q

Hypovolemic Shock and Renal System

A

Renin: holds on to water and sodium to restore tissue perfusion

Angiotensin II is produced and vasoconstriction occurs b/c of aldosterone being released.

Adrenal cortex is stimulated to produce glucocorticoids > increase in glucose for energy for the body to keep compensatory mechanisms going)

ADH: pt urine output is going to decrease (either oliguric or anuric)

End stages of shock = renal ischemia occurs b/c renal arteries have been constricted for so long, so kidneys aren’t getting any perfusion > AKI > decreased UOP.

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18
Q

Hypovolemic Shock and the Respiratory System

A

early shock: pt RR can be 2x normal amount
-tachypneic in order to keep up with cardiac O2 demand (tachycardia is occurring) and compensatory mechanisms

as shock progresses: the ventilatory effort will decline, and respirations will be shallow as pt is getting fatigued from tachypnea

  • mechanical ventilation may be necessary before they stop breathing
  • pulmonary edema possible by the capillaries becoming permeable through hydrostatic pressure changes (3rd spacing happens and capillaries are becoming more permeable and fluid is building in alveoli)
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19
Q

Hypovolemic Shock and the Neurological System

A

body shunts blood to the brain w/in seconds when compensating during shock

MAP > 60 for cerebral blood flow to remain at a normal level

mental function is decreased when acid-base abnormalities and low BP lead to hypoxia

decreased LOC and mental status changes are early signs that something bad is going on w/ pt

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20
Q

Hypovolemic Shock and Metabolic System

A

O2 deficit increases > cells switching to anaerobic glycolysis > lactic acid production > depression of the myocardium
-tachycardia is occurring and now lactic acid is depressing hearts ability to squeeze at this high rate

lactate levels greater than 4mmol/L means severe acidosis

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21
Q

Types of Shock

A

Directly related to the 3 major structures of the cardiovascular system:

  • Heart: cardiogenic shock
  • Blood/fluid: hypovolemic shock
  • Vessels: distributive/maldistribution shock
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22
Q

SIRS

A

systemic inflammatory response syndrome

widespread systemic inflammatory response (WBC increase)

Associated w/:

  • infection
  • trauma
  • shock
  • pancreatitis
  • ischemia

most frequently associated w/ sepsis

release of mediators into systemic system > increased permeability of endothelial walls > fluid shifts into intravascular spaces > depletion of intravascular volume > relative hypovolemia
-3rd spacing, edema

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23
Q

Third Spacing Edema

A

caused by increased capillary permeability
-leaky capillaries are leaking fluid out of cells into tissues

tx: infusion of colloids (aka volume expanders)
- albumin
- hespan
- dextran

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24
Q

Volume Expanders (Colloids)

A

expand volume of cell itself

colloids go into cells and make cells bigger within vessel walls therefore it makes it harder for that cell to get out of vascular bed and leak into tissues

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25
Q

Things Needed to Maintain Homeostasis:

A
  • strong pump (cardiac)
  • intact pipes (vessels)
  • sufficient fluid volume (blood/fluid)
  • adequate acid/base balance
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26
Q

Shock Triad of Death

A

the things that occur in shock and cause death:

  • coagulopathy (halt in coagulation cascade)
  • hypothermia (decreased cardia performance)
  • metabolic acidosis (lactic acidosis)
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27
Q

Causes of Hemorrhagic Hypovolemic Shock

A

loss of whole blood

  • trauma
  • childbirth
  • GI bleeding
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28
Q

Causes of Hypovolemic Shock (decrease of intravascular fluid)

A
  • fever
  • diaphoresis
  • GI distress from n/v/d or NG suctioning
  • renal dysfunction
  • 3rd spacing w/ buns or peritonitis
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29
Q

Hypovolemic Shock: Assessment

A
  • RR increases until fatigued and then stops
  • increase in resting HR by 10bpm in elderly, 20bpm in normal adults (significant sign)
  • starts as hypertension d/t compensatory mechanisms causing vasoconstriction, then BP decreases and pulse pressures narrow b/c decrease in stroke volume
  • low systolic = late sign of shock

-assess all peripheral pulses (bounding initially then weaker in later stages of shock)

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30
Q

Hypovolemic Shock: Orders

A
  • fluid challenge
  • fluid replacement (NS or LR)
  • vasopressors if fluid replacement isn’t enough
  • transfusion (if d/t hemorrhage, may need TCXM)
  • Colloids
  • Epinephrine, Norepinephrine
  • Dopamine
  • Labs (CBC, CMP, Troponin)
  • Foley w/ hourly volume
  • VS

*troponin gathered b/c heart has been beating fast for a long time and if there is lactic acid troponin levels will be effected and pt can have MI as result of hypovolemic shock

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31
Q

Lactated Ringers for Hypovolemic Shock

A

-electrolytes lost w/ fluids so LR can replace these better than NS

  • LR helps w/ acidosis: if pt is acidotic d/t high levels of lactic acid, we will give LR b/c it stimulates liver to convert it to bicarb
  • avoid in pt’s w/ hx of liver failure
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32
Q

Priorities for Hypovolemic Shock

A
  • ABC’s
  • 2 large bore IVs
  • fluid replacement (including blood)
  • elevate legs to level of heart
  • monitor electrolytes d/t high volume of fluid (and blood) being administered
  • high levels of calcium in blood products for preservation
33
Q

Cardiogenic Shock

A

pump problem/decreased contractility

causes:

  • ventricular ischemia, structural problems, dysrhythmias
  • 40% or more of myocardium damaged > cardiogenic shock (reasons for this include: septal/papillary muscle rupture, ventricular aneurysm)

ventricle unable to pump > decreased SV/CO/BP and tissue perfusion

ventricles can’t empty w/ every beat so blood backs up > overload pulmonary circulation (crackles in lungs) > pulmonary congestion/hypoxia d/t lack of diffusion > ARDS

34
Q

Cardiogenic Shock: Assessment

A
  • hypotension (usually palpated BP)
  • weak, fast HR
  • decreased CO
  • increased PAWP (increased volume of left side of heart, preload is going up)
  • decreased mentation
  • diminished heart sounds
  • dysrhythmias
  • cool, pale skin, diaphoretic
  • UOP < 30ml/hr, if any
  • lung sounds: crackles, wheezing
  • pink frothy sputum
  • ABG: initially respiratory acidosis d/t increase in RR and CO2, then metabolic acidosis d/t increase in lactic acid
35
Q

Cardiogenic Shock: Tx

A
  1. fluids
  2. inotropic agents (digoxin, dobutamine, dopamine)
  3. vasoconstrictors
  4. vasodilators
  5. vasopressors
  6. Intraaortic Balloon Pump (IABP)
36
Q

Principles of Cardiogenic Shock Management

A

Optimize CO by:

  • inotropes
  • HD monitoring (PA Catheter)
  • Tx dysrythmias
  • electrolyte management
  • vasopressors are used thoughtfully (will increase SVR > increased workload of the heart)
  • IABP asap

decrease LV workload by:

  • vasodilators
  • narcotics (sedative to decrease myocardial O2 demand)
  • IABP or VAD
  • Impella and ECMO
  • supplemental O2 w/ mechanical ventilation if needed
37
Q

IABP

A

provides counter-pulsation

inflates during diastole > increase perfusion to coronary arteries

deflates during systole > decreases workload the LV and gives heart a chance to rest

requires 1:1 nursing care

risks:
- bleeding
- clotting
- infection
- PADIS
- limb ischemia b//c of vessel it’s entered in

-used in cardiogenic shock, after surgery/MI/acute HF

38
Q

Cardiogenic Shock: Priorities

A
  • ABC’s
  • VS, breath sounds, mental status
  • suction as needed
  • BP
39
Q

Cardiogenic Shock: Meds

A
  • lasix
  • potassium
  • milrinone
  • dobutamine
  • dopamine
  • digoxin
  • morphine
  • nitroglycerine (if BP can handle it, decreases afterload)
  • nipride: for poor perfusion or HTN crisis (lower pressure)
  • ASA
  • epinephrine IV
  • levophed (norepinephrine)
40
Q

Dobutamine

A
  • inotrope that doesn’t increase HR
  • does not vasoconstrict (mild dilation)
  • can give w/ dopamine
  • monitor for chest pain and dysrhythmias
  • must be tapered off
41
Q

Epinephrine

A

used if cardiogenic shock is life threatening b/c it has side effect of increasing heart workload and pulse
-alpha/beta stimulate (inotrope and peripheral vasoconstriction, dilates core)

42
Q

Levophed (norepinephrine)

A

causes profound vasoconstriction, tissue necrosis if IV infiltrates

client will lose digits/limbs if prolonged administration

43
Q

Obstructive Shock

A

obstruction of blood flow through cardiopulmonary system d/t right ventricular failure from PE or severe pulmonary HTN

need to find cause of MI

5 H's:
hypovolemia
hypoxia
hypothermia
hydrogen ion (acidosis)
hyper/hypokalemia
4 T's:
toxins
tamponade
tension pneumothorax
thrombosis
44
Q

Sx of PE

A

anxious
impending sense of doom
JVD
pulseless paradoxus

45
Q

Distributive Shock

A

Anaphylactic shock: vasodilation b/c histamine release

Neurogenic shock: vasodilation d/t injury to brain or spinal cord or both > compensatory mechanisms. of SNS (fight or flight) have been inhibited > body relying on PSNS which is vasodilation

Septic shock: mass release of toxins from bacteria cause vasodilation

46
Q

Septic Shock

A

systemic inflammatory response to infection

leading cause of death in ICU

most common causes:
-invasive procedure, tubes, lines

deadliest form of shock

golden tx period is first 6 hours

47
Q

Septic Shock: Pathophysiology

A
  • massive vasodilation of myocardial depression d/t histamine and pathogenic toxin reaction that occur > decreased venous return/preload/afterload/BP and increased cardiac workload to try to compensate
  • microemboli (clotting activated b/c WBCs trying to deal w/ bacteria) > MODS when clots block vessels and no perfusion past those clots (hypoxia and cell death with lactic acid build up) > fluid/protein shift to interstitial space (third spacing) > DIC when clotting factors are used up
48
Q

Sepsis 1 Hour Bundle

A
  • obtain lactate level
  • obtain blood cultures prior to antibiotic therapy
  • administer broad spectrum antibiotics
  • rapidly administer 30ml/kg crystalloids for hypotension or lactate level greater than or equal to 4mmol/L
  • administer vasopressors if hypotensive during or after fluid resuscitation
49
Q

Septic Shock: Phases

A 
Early Phase (hyperdynamic state)
Hemodynamic Phase
50
Q

Septic Shock: Early Phase

A
  • increased CO (increase HR in response to low BP)
  • decreased SVR (massive vasodilation)
  • decreased right atrial pressure (decreased preload and afterload)
  • tachycardia (compensation for hypotension)
  • tachypnea
  • decreased BP

-if pt does not respond to fluid bolus, we will give vasopressors

51
Q

Septic Shock: S/Sx

A
  • wide pulse pressure (from vasodilation)
  • skin warm/flushed (fever)
  • decreased LOC (from vasodilation)
  • decreased UOP (fluid shifts to interstitial spaces)
  • fever (fever = 98.9 in geriatric population)
52
Q

Septic Shock: Hemodynamic Phase

A
  • decreased CO (ventricular failure)
  • increased peripheral resistance (compensate for low BP)
  • increased right atrial pressure (increased afterload d/t acidosis from myocardial hypoxemia)
  • blood pools
  • increase HR
  • increase RR (pulmonary edema, pulmonary HTN from permeable capillaries - will hear crackles)
53
Q

Septic Shock: Priorities

A
  • ABC’s
  • look for altered mental status (early cue of decreased cerebral perfusion)
  • fluid volume replacement up to 6L
  • medications to maintain adequate tissue perfusion
  • antibiotic therapy
  • care of source of infection (if wound or catheter related)
54
Q

Septic Shock: Meds

A
  • Levophed (norepinephrine) for vasoconstriction: make sure they have adequate volume first or it’s going to be harder to give fluids if we vasoconstrict first
  • O2
  • Antibiotics (first broad spectrum then switched to specific once cultures results come back)
  • Epinephrine (if needed)
  • antipyretics (for fever)
55
Q

Sepsis 3 Hour Bundle

A
  • lactate level
  • blood cultures before administration of antibiotics
  • broad-spectrum antibiotics
  • administer 30 mL/kg crystalloids for hypotension or lactate greater than or equal to 4 mmol/L
  • can start vasopressors if fluids aren’t increasing BP enough
56
Q

Sepsis 6 Hour Bundle

A
  • vasopressors to maintain a MAP > 65 for hypotension unresponsive to initial fluid resuscitation
  • reassess volume status and tissue perfusion if MAP < 65 or initial lactate is greater than or equal to 4 mmol/L
  • remeasure lactate level if initial level was elevated
57
Q

Neurogenic Shock: Pathophysiology

A
  • loss of SNS tone > PSNS taking over
  • massive vasodilation > decrease in venous return > decrease CO > decrease BP and HR
  • HR decreases (only shock where you see bradycardia-baroreceptors are inhibit so no compensatory tachycardia)
  • temp decreases and they take on ambient environment temp
  • loss of sweat response below injury
  • loss of bowl/bladder function
  • lasts 1-6 wks
58
Q

Neurogenic Shock: Cause

A
  • any event that interrupts SNS
  • most common is spinal cord injury above level of T6
  • TBI
  • spinal anesthesia
  • insulin shock
  • heat stroke
  • CNS depressants

*occurs w/in 30 min of spinal cord injury

59
Q

Neurogenic Shock: Tx

A
  1. Fluids
  2. Positive inotropes
  3. Vasoconstrictors (dopamine)
  4. Vasodilators
  5. Solu Medrol: controversia b/c high doses of steroid in spinal cord injury pts do help reduce edema around spinal cord > quicker recovery and less musculoskeletal deficits, but immunosuppressive

asymptomatic bradycardia? give nothing
symptomatic bradycardia? atropine and pacemaker

NEURO ASSESSMENT Q1HR

60
Q

Anaphylactic Shock

A
  • severe allergic reaction
  • person has been exposed to antigen previously and body developed antibodies against it
  • can begin w/in 20 min after exposure to substance
  • death can be w/in minutes
61
Q

Antigen/Antibody Reponse

A
  • massive vasodilation > decrease in BP > increase in HR > widened pulse pressure
  • vascular permeability > third spacing, swelling, edema > hypovolemia from fluid shift
  • bronchospasm > wheezing
62
Q

Anaphylactic Shock: Assessment

A
  • first sign = anxiety, uneasiness
  • flushing
  • sneezing
  • urticaria/itching
  • weakness/nausea/dizziness
  • diaphoresis
  • edema
  • wheezing
63
Q

Anaphylactic Shock: Tx

A
  • Remove causative agent (food, med, insect stinger, latex, blood transfusion)
  • ABCs (monitor airway, give O2, establish IV)
  • Meds: Epi, Benadryl (Zantac if allergic to Benadryl), steroids, dopamine, albuterol
64
Q

Contraindications to Epinephrine Infusion (IV)

A
  • over 50YO
  • cardiac Hx
  • SBP > 160
  • DBP > 140
  • tachycardia > 140
  • ectopy
  • pregnancy

*can still give epi SQ

65
Q

Meds w/ Postive Inotropic Effect

A

dopamine
dobutamine
low doses of epinephrine

*increase contractility (SV and CO)

66
Q

Meds that Increase Afterload

A

epinephrine
norepinephrine
dopamine

67
Q

Meds that Decrease Afterload

A

nitroglycerine
nitroprusside

*vasodilation

68
Q

DIC

A

disseminated intravascular coagulation

imbalance between coagulation and anticoagulation

first clotting > hemorrhage once all clotting factors are used up

usually fatal

caused by other diseases or conditions

associated w/ septic shock

will have decreased LOC, tachycardia, oliguria/hematuria

69
Q

DIC: Causes

A 
infection/sepsis
trauma/burns
surgery
malignancy
OB complications
immune disorders
snake bites
70
Q

DIC: S/Sx

A
  • large, multiple ecchymosis
  • oozing from current and old IV sites
  • GI bleeding
  • bleeding from every orifice
71
Q

DIC: Dx

A
  • blood smear showing fragmented RBCs
  • decreased platelets
  • decreased fibrinogen
  • prolonged PT and aPTT
72
Q

DIC: Tx

A
  • heparin: prevents clots, releases clotting factors
  • cryoprecipitate: fresh frozen plasma and platelets
  • treat underlying cause (sepsis, etc)
73
Q

MODS

A

multiple organ dysfunction syndrome

progressive dysfunction of two or more organ systems

can occur after any severe injury or illness

74
Q

MODS: Causes

A

most common = sepsis and septic shock (b/c of microemboli that occur and block perfusion)

75
Q

MODS: Organs Severely Affected

A
  • lungs
  • splanchnic bed
  • liver
  • kidneys
76
Q

MODS: Clinical Manifestation

A
  • tachypnea, hypoxemia
  • petechiae, bleeding (DIC)
  • jaundice
  • abdominal distention
  • oliguria/anuria
  • tachycardia
  • hypotension
  • change in LOC
77
Q

MODS: Management

A
  • control infection if sepsis is cause
  • provide adequate tissue oxygenation
  • hemoglobin about 7-9
  • restore intravascular volume (fluid resuscitation or blood, crystalloids)
  • support organ function
78
Q

Blood Transfusions

A

recommended when hemoglobin decreases to less than 7-7.5 in the absence of extenuating circumstance in adults such as myocardial ischemia, severe hypoxemia or acute hemorrhage

79
Q

GI Prophylaxis

A

only for those w/ risk for GI bleeding (those in sepsis or septic shock)

PPI or H2 blocker

Critical Care (14 decks)

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