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Critical Care > 🌡️Shock > Flashcards

🌡️Shock Flashcards

1
Q

Shock

A

the body can no longer meet cellular oxygen demands (anaerobic)
inadequate blood flow resulting in decreased perfusion

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2
Q

Shock Diagnosis

A

MAP <60 or evidence of organ hypoperfusion

Lactate = higher
ABD = higher
Bicarb = lower

Blood becomes acidotic

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3
Q

Shock - Initial Stage

A

Baroreceptors detect changes in volume –>
Decreased cardiac output
Decreased tissue perfusion

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4
Q

Shock - Compensatory Stage

A

body tries to self correct by SNS responses (neural, hormonal, chemical)

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5
Q

Neural compensation (4)

A

increase HR/contractility
arterial/venous vasoconstriction (clamping down peripheral)
shunting of blood to vital organs
catecholamines released

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6
Q

Hormonal compensation (3)

A

activate renin
stim anterior pituitary (1) and adrenal medula (2)

2(release ADH resulting in decreased sodium and water excretion)
2(catecholamines)
1(release glucocorticoids to increase blood sugar)

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7
Q

Chemical compensation

A

increase rate and depth of respirations to correct acidosis

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8
Q

Shock - Progressive stage

A

compensatory fails resulting in SIRS
now anaerobic metabolism produces large lactic acid

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9
Q

Progressive stage vascular effects (4)

A

increased vascular permeability
intravascular hypovolemia
tissue edema
decline in tissue perfusion

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10
Q

Progressive stage cellular effects (4)

A

apoptosis
Na+/K+ fails causes cells to swell/die
Mitochondria swells and ruptures
Cells cannot use o2

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11
Q

Progressive stage cardiac effects (4)

A

ventricular failure from release of myocardial depressant cytokines
microvascular thrombosis
lactic acidosis –> MASSIVE vasodilation

NEGATIVE inotropic effects –> weakened pump

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12
Q

Progressive stage pulmonary effects (4)

A

acute respiratory failure, respir distress, lung injury
increase cap membrane permeability

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13
Q

Acute respiratory distress syndrome

A

refractory hypoxemia leaving alveoli to drown in fluid/protein

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14
Q

Progressive stage neurologic effects (3)

A

microvascular thrombosis
↓
cerebral hypo perfusion (changes in orientation)
↓
SNS dysfunction (b1 +b2 depression, temp failiure, coma)

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15
Q

Progressive stage GI effects (4)

A

necrotic bowl/ liver/ pancreas
GI/hepatic/pancreatic failure

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16
Q

Progressive stage renal/hematologic effects (2)

A

quickest to be effected

Acute tubular necrosis –> DNR nephrons :(
DIC

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17
Q

Disseminated Intravascular Coagulation (DIC)

A

consumptive coagulopathy (blood is going from liquid to solid)
AEB: septic shock, trauma, OB emergency

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18
Q

DIC clinical manifestations (4)

A

decreased perfusion to tissues –> dusky/mottled
Occult (GI) and Overt (errrrwhere) bleeding
Petechiae and ecchymosis

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19
Q

Common lab findings for DIC:

A

Elevated PT, PTT
Decrease fibrinogen/platelets
Metabolic acidosis (decreased perfusion to tissue)
Elevated Fibrin degration product ( MOREEE BLEEEDING) 😝
+ D-dimer

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20
Q

What med is used to treat DIC?

A

HEPPARRRRIIINNNNNNNNNN🥰😎😎😎😎🤩

🤚🏼STOP body process to form clots

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21
Q

Shock - Refractory stage (3)

A

correction is difficult
cell hypoxia and death impending
multi-organ dysfunction syndrome

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22
Q

Hypovolemic shock causes

A

Decreased intravascular volume
Internal fluid shift
(GI bleed, ruptured spleen, hemothorax, third spacing, hemorrhagic pancreatitis)

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23
Q

Hypovolemic shock loss of (3)

A

WHOLE BLOOD –> hemorrhage
PLASMA –> burns/decubitus
BODY FLUID –> suctin v/d diuretic, DKA

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24
Q

Pathophys hypovolemic shock

A

Decreased intravascular volume
↓
decrease venous return (POOL IS ASSOCIATED WITH PRELOAD SO DECREASE DAWG)
↓
decrease ventricular filling ( how we gonna fill if we dont have volume)
↓
Decrease SV and cardiac output
IF WE CANT OUTPUT WHAT GONNA HAPPEN TO ORGANS💀💀☠️☠️☠️☠️💀☠️☠️☠️💀☠️☠️👽

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25
Q

Hypovolemic shock clinical manifestations (7)

A

No volume? DW we will just increase HR and RR 🤭😏🤪
Postural vitals >20 systolic >10 diastolic with position changes
Oliguria (kidneys be like 🖕🏼🖕🏼🖕🏼😡😡🤬🤬🤬🤬🤬🤯)
cool, pale, clammy skin
weak pulse
flat vein
decreased LOC

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26
Q

Hypovolemic shock diagnostic tests (5)

A

increased sodium (hypernatriemia
decreased HBG
ABG/Lactate/imagining relating to exam

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27
Q

Hypovolemic shock hemodynamic profile

A

DECREASED preload, CVP, PCWP, CO and BP

INCREASED AFTERLOADDDDD SVR HIGH ( we tryin to compensate)
🐭🐱(catecolamine (epi/norepi) and raas (fluid retention)= cats and rats)

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28
Q

Primary therapy for hypovolemic shock

A

🥄🧊🧊🧊🌊🌊🌊🌊💦💦💦💦💧💨💨💨💨💨💧💧💧💧💧
IV FLUIDS BBY!!!

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29
Q

Cardiogenic shock - cardiac etiology (4)

A

ischemia causing 40% or greater damage (usually caused by MI)
ventricular wall/pap muscle/septal rupture
cardiomyopathy
aortic stenosis

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30
Q

Cardiogenic shock - non-coronary etiology

A

usually can reverse
cardiac tamponade
restrictive pericarditis
PE
Pulmonary Hypertension
Tension pneumo

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31
Q

Cardiogenic shock clinical manifestations (noninvasive) (8)

A

rapid/thready pulse
narrow pulse pressure (120/105)
JVD
arrhythmia
angina
cool, pale, moist skin
oliguria
altered AxO

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32
Q

Cardiogenic shock clinical manifestations (pulmonary findings) (4)

A

dyspnea, tachypnea, crackles

ABG –> decreased Pa/Sa 02 decreased PaC02

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33
Q

Cardiogenic shock diagnostic tests (4)

A

cardiac enzymes(troponin/CKNB)
BNP
Echo (ejection fraction)
coronary angio

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34
Q

Cardiogenic shock hemodynamic profile

A

REMEMBER CARDIO = PUMP ISSUE

CO/CI and BP is LOW

PRELOAD is INCREASED (CVP/PCWP)
AFTERLOAD is INCREASED!!!!!!!!!!!!!!!!! SVR is high

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35
Q

Cardiogenic shock pharmacologic therapy (4)

A

POSITIVE inotropes (digoxin, dopamine, dobutamine)
Nitrates, diuretics, opioids –> BP IS LOW already so use with CAUTION
Vasopressors

36
Q

Cardiogenic shock invasive treatment

A

early revascularization
IABP
LVAD
surg/transplant

37
Q

Intra-aortic Balloon Pump

A

Goal: decrease myocardial workload to improve perfusion to corn air ie, reduce afterload

ALSO improves miss kidney’s R Ter IE

38
Q

what is out of intra-aortic balloon pump’s scope of practice?

A

she cannot measure hemodynamic pressures (ASIDE FROM BP)
not a pacemaker

39
Q

Nursing interventions for IABP (3)

A

HOB < 30 degrees (d/t hip flexion) can do reverse trendelenburg
monitor pedal pulses, LOC, U/O, bleeding
flush artery q1 hour (patency)

40
Q

What treatment is appropriate for cardiogenic shock

A

POSITIVE INOTROPIC AGENT
nitroprusside, dobutamine

WE GOTTA PUMP IT UP!! GET YO PUMP ON! PUMP CITY BABY!

41
Q

Distributive shcok

A

MASSIVE VASODILATION 🌫️🌫️🌫️🌫️
increase of vascular space for same volume of fluid which decreases venous return, SV, CO
either neurogenic, anaphylactic or septic

42
Q

Neurogenic shock

A

DISTRIBUTIVE
loss of sympathetic tone by injury to spinal cord, spinal anesthesia, stress, severe pain, OD

43
Q

Neurogenic shock clinical manifestations (3)

A

Hypotension
Bradycardia (nervous system cannot compensate)
Hypothermia

44
Q

Neurogenic shock treatment (3)

A

remove cause
volume replacement
vasopressors

45
Q

Anaphylactic shock

A

DISTRIBUTIVE
antigen/antibody

46
Q

Anaphylaxis chemical response (2)

A

Histamine –> vasodilation, decreased SVR, decreased BP
Serotonin –> increased cap permeability, decreased volume, decreased BP

47
Q

Anaphylactic shock causes (5)

A

drug, contrast, blood, bites/sting, food

48
Q

Anaphylactic shock clinical manifestations (6)

A

pruritis
erythema
urticaria –> hives
angioedema
laryngeal edema
hypotension

49
Q

Anaphylactic shock treatment(6)

A

PREVENTION, remove antigen
EPINEPHRINE
airway
corticosteroid
fluids
Positive inotropic agents

50
Q

Sepsis

A

life threatening organ dysfunction

51
Q

Septic shock

A

hypotension not responsive to fluid resuscitation –> perf abnormal

52
Q

Sepsis clinical manifestations

A

Altered mental status (<15 GCS)
Tachypnea (>22)
Hypotension (<100 SBP)
QSOFA + IF ALL THREE
Tachycardia, fever, fatigue, nausea, increase WBC with left shift

53
Q

Early recognition of sepsis

A

SIRS/qSOFA
Labs –> increased lactate, coags, liver/renal function, procalcitonin!!!!!!!!!!!

54
Q

Diagnostic marker for septic shock

A

PROCALCITONIN

55
Q

Systemic Inflammatory Response Syndrome Criteria

A

Temp > 38 degrees C
Heart rate > 90 beats/min
RR > 20 or PaCO2 <32
WBC >12,000 or >10% bands
2+ = sirs

56
Q

Systemic Inflammatory Response Syndrome

A

inflammation, thrombosis and fibrinolysis
immune system is overwhelmed, feedback mech fails, process to protect is now harmful

57
Q

SIRS pathophysiology

A

micro-organism invades body resulting in inflammation
sheds protein/releases toxins to activate cascades (fibrinolytic/platelets) –> results in increased cap membrane permeability, clotting, maldistribution of BF, 02 supply/demand imbalance

58
Q

Sepsis vulnerable populations

A

young or old, immunosuppressant, trauma, addictive habits, invasive therapies

59
Q

Sepsis bundle

A

The best treatment option
group of therapies that have extensive EBP to back them

60
Q

Central line bundle

A

hang hygiene
barrier precautions
CHG
avoid femoral
review daily
record time/date of line placement

61
Q

Sepsis diagnostics

A

Appropriate cultures (urine, sputum, wound)
Blood cultures (FROM TWO SPOTS TO ID POTENTIAL CONTAMINATION)
one percutaneous and one from each vascular access

62
Q

Obtain cultures before:

A

antibiotics

63
Q

One hour resuscitation bundle for sepsis (3)

A

LACTATE –> if >4 REPEAT THEN rapid crystalloid therapy
blood cultures PRIOR TO (you know this cmon now)
vasopressors to maintain map >65

64
Q

Early septic shock clinical manifestations (5)

A

pink,warm, dry skin
CO normal/elevated (🐱🐱🐱🐱🐱)
decreased afterload
increase respirations
change mental status

65
Q

Early septic shock hemodynamics (4)

A

preload decreased (CVP/Wedge follows)
afterload decreased (low SVR/BP)
HR increased
contractility normal/increased

66
Q

Early septic shock therapy (3)

A

fluids, antimicrobial agents
cortiosteroids
supportive care –> DVT, hemodynamics, ventilation, electrolyte/glycemic control

67
Q

Progression of septic shock

A

SIRS –> MODS

increase cap wall permeability –> leaves vasculature –> interstitial/intra-cellular edema
decrease volume
increase viscosity

compensatory failing, decreased perfusion, mitrocondrial change

68
Q

Multi Organ Distress Syndrome

A

Failure 2+ separate organs
Hemostasis cannot be maintained without intervention

69
Q

Late septic shock

A

hypodynamic “cold phase”
increased mortality

70
Q

Late septic shock clinical manifestations (5)

A

cold, clammy skin, edema (anasarca), low CO, SEVERE HYPOTENSION

71
Q

Late septic shock hemodynamic profile

A

Increased preload (CVP, PCWP)
Afterload increased (SVR)
Contractility decreased (BP/CO very low)

72
Q

Late septic shock treatment (4)

A

supportive care
vasopressors
+ Inotropes
corticosteroids

73
Q

Supportive measures for ALL stages of shock (4)

A

maintain airway/ventilation, CO
restore intravascular volume (albumin/NS)
improve acidosis

74
Q

Therapy for low preload

A

POOLING ISSUE –> FILL IT UP WITH WATER
Position up if ventilation issue, position down if perfusion issue

75
Q

Crystalloid aministration

A

electrolyte, hypo/hypertonic
need large fluid volume, overload is a risk

76
Q

Colloid administration

A

usually albumin
keeps fluid in vascular compartment

77
Q

Hydrostatic vs oncotic pressure

A

Hydrostatic SBP
Oncotic ( albumin pulls into vasculature)

78
Q

Blood product administration

A

HGB <7.0
FFP for bleeding
Platelet if <5000 (30k for bleeding risk) (50k for surgery)

79
Q

Patient positioning: Preload

A

low = flat HOB, modified trendelenberg

80
Q

When preload is high you admin –>

A

diuretic, nitroglycerin, reduce fluid, patient positioning (elevate HOB)

specific to cardiogenic shock

81
Q

When preload is low you admin –>

A

FLUID
alpha one med (norepi, dopamin, epi, phenylephrine, vasopressin)

82
Q

AFTERLOAD IS LOW WITH which SHOCK

A

distributive

83
Q

When afterload is high you admin –>

A

nitroprusside, ACE-I, CCB,
IF BP IS OK

84
Q

WHEN CONTRACTILITY IMPAIRED YOU ADMIN

A

+ INOTROPIC AGENTS SUCH AS DOPAMINE, DOBUTAIN, MILRINONE, DIGOXIN

85
Q

corticosteroids for septic shock

A

When require vasopressin after fluid resus (IV hydrocortisone)
**pt make have relative adrenal insufficency

Critical Care (9 decks)

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