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Critical Care > 🌡️Shock > Flashcards

🌡️Shock Flashcards

(85 cards)

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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
Hypovolemic shock clinical manifestations (7)
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
26
Hypovolemic shock diagnostic tests (5)
increased sodium (hypernatriemia decreased HBG ABG/Lactate/imagining relating to exam
27
Hypovolemic shock hemodynamic profile
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)
28
Primary therapy for hypovolemic shock
🥄🧊🧊🧊🌊🌊🌊🌊💦💦💦💦💧💨💨💨💨💨💧💧💧💧💧 IV FLUIDS BBY!!!
29
Cardiogenic shock - cardiac etiology (4)
ischemia causing 40% or greater damage (usually caused by MI) ventricular wall/pap muscle/septal rupture cardiomyopathy aortic stenosis
30
Cardiogenic shock - non-coronary etiology
usually can reverse cardiac tamponade restrictive pericarditis PE Pulmonary Hypertension Tension pneumo
31
Cardiogenic shock clinical manifestations (noninvasive) (8)
rapid/thready pulse narrow pulse pressure (120/105) JVD arrhythmia angina cool, pale, moist skin oliguria altered AxO
32
Cardiogenic shock clinical manifestations (pulmonary findings) (4)
dyspnea, tachypnea, crackles ABG --> decreased Pa/Sa 02 decreased PaC02
33
Cardiogenic shock diagnostic tests (4)
cardiac enzymes(troponin/CKNB) BNP Echo (ejection fraction) coronary angio
34
Cardiogenic shock hemodynamic profile
REMEMBER CARDIO = PUMP ISSUE CO/CI and BP is LOW PRELOAD is INCREASED (CVP/PCWP) AFTERLOAD is INCREASED!!!!!!!!!!!!!!!!! SVR is high
35
Cardiogenic shock pharmacologic therapy (4)
POSITIVE inotropes (digoxin, dopamine, dobutamine) Nitrates, diuretics, opioids --> BP IS LOW already so use with CAUTION Vasopressors
36
Cardiogenic shock invasive treatment
early revascularization IABP LVAD surg/transplant
37
Intra-aortic Balloon Pump
Goal: decrease myocardial workload to improve perfusion to corn air ie, reduce afterload ALSO improves miss kidney's R Ter IE
38
what is out of intra-aortic balloon pump's scope of practice?
she cannot measure hemodynamic pressures (ASIDE FROM BP) not a pacemaker
39
Nursing interventions for IABP (3)
HOB < 30 degrees (d/t hip flexion) can do reverse trendelenburg monitor pedal pulses, LOC, U/O, bleeding flush artery q1 hour (patency)
40
What treatment is appropriate for cardiogenic shock
POSITIVE INOTROPIC AGENT nitroprusside, dobutamine WE GOTTA PUMP IT UP!! GET YO PUMP ON! PUMP CITY BABY!
41
Distributive shcok
MASSIVE VASODILATION 🌫️🌫️🌫️🌫️ increase of vascular space for same volume of fluid which decreases venous return, SV, CO either neurogenic, anaphylactic or septic
42
Neurogenic shock
DISTRIBUTIVE loss of sympathetic tone by injury to spinal cord, spinal anesthesia, stress, severe pain, OD
43
Neurogenic shock clinical manifestations (3)
Hypotension Bradycardia (nervous system cannot compensate) Hypothermia
44
Neurogenic shock treatment (3)
remove cause volume replacement vasopressors
45
Anaphylactic shock
DISTRIBUTIVE antigen/antibody
46
Anaphylaxis chemical response (2)
Histamine --> vasodilation, decreased SVR, decreased BP Serotonin --> increased cap permeability, decreased volume, decreased BP
47
Anaphylactic shock causes (5)
drug, contrast, blood, bites/sting, food
48
Anaphylactic shock clinical manifestations (6)
pruritis erythema urticaria --> hives angioedema laryngeal edema hypotension
49
Anaphylactic shock treatment(6)
PREVENTION, remove antigen EPINEPHRINE airway corticosteroid fluids Positive inotropic agents
50
Sepsis
life threatening organ dysfunction
51
Septic shock
hypotension not responsive to fluid resuscitation --> perf abnormal
52
Sepsis clinical manifestations
Altered mental status (<15 GCS) Tachypnea (>22) Hypotension (<100 SBP) QSOFA + IF ALL THREE Tachycardia, fever, fatigue, nausea, increase WBC with left shift
53
Early recognition of sepsis
SIRS/qSOFA Labs --> increased lactate, coags, liver/renal function, procalcitonin!!!!!!!!!!!
54
Diagnostic marker for septic shock
PROCALCITONIN
55
Systemic Inflammatory Response Syndrome Criteria
Temp > 38 degrees C Heart rate > 90 beats/min RR > 20 or PaCO2 <32 WBC >12,000 or >10% bands 2+ = sirs
56
Systemic Inflammatory Response Syndrome
inflammation, thrombosis and fibrinolysis immune system is overwhelmed, feedback mech fails, process to protect is now harmful
57
SIRS pathophysiology
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
Sepsis vulnerable populations
young or old, immunosuppressant, trauma, addictive habits, invasive therapies
59
Sepsis bundle
The best treatment option group of therapies that have extensive EBP to back them
60
Central line bundle
hang hygiene barrier precautions CHG avoid femoral review daily record time/date of line placement
61
Sepsis diagnostics
Appropriate cultures (urine, sputum, wound) Blood cultures (FROM TWO SPOTS TO ID POTENTIAL CONTAMINATION) one percutaneous and one from each vascular access
62
Obtain cultures before:
antibiotics
63
One hour resuscitation bundle for sepsis (3)
LACTATE --> if >4 REPEAT THEN rapid crystalloid therapy blood cultures PRIOR TO (you know this cmon now) vasopressors to maintain map >65
64
Early septic shock clinical manifestations (5)
pink,warm, dry skin CO normal/elevated (🐱🐱🐱🐱🐱) decreased afterload increase respirations change mental status
65
Early septic shock hemodynamics (4)
preload decreased (CVP/Wedge follows) afterload decreased (low SVR/BP) HR increased contractility normal/increased
66
Early septic shock therapy (3)
fluids, antimicrobial agents cortiosteroids supportive care --> DVT, hemodynamics, ventilation, electrolyte/glycemic control
67
Progression of septic shock
SIRS --> MODS increase cap wall permeability --> leaves vasculature --> interstitial/intra-cellular edema decrease volume increase viscosity compensatory failing, decreased perfusion, mitrocondrial change
68
Multi Organ Distress Syndrome
Failure 2+ separate organs Hemostasis cannot be maintained without intervention
69
Late septic shock
hypodynamic "cold phase" increased mortality
70
Late septic shock clinical manifestations (5)
cold, clammy skin, edema (anasarca), low CO, SEVERE HYPOTENSION
71
Late septic shock hemodynamic profile
Increased preload (CVP, PCWP) Afterload increased (SVR) Contractility decreased (BP/CO very low)
72
Late septic shock treatment (4)
supportive care vasopressors + Inotropes corticosteroids
73
Supportive measures for ALL stages of shock (4)
maintain airway/ventilation, CO restore intravascular volume (albumin/NS) improve acidosis
74
Therapy for low preload
POOLING ISSUE --> FILL IT UP WITH WATER Position up if ventilation issue, position down if perfusion issue
75
Crystalloid aministration
electrolyte, hypo/hypertonic need large fluid volume, overload is a risk
76
Colloid administration
usually albumin keeps fluid in vascular compartment
77
Hydrostatic vs oncotic pressure
Hydrostatic SBP Oncotic ( albumin pulls into vasculature)
78
Blood product administration
HGB <7.0 FFP for bleeding Platelet if <5000 (30k for bleeding risk) (50k for surgery)
79
Patient positioning: Preload
low = flat HOB, modified trendelenberg
80
When preload is high you admin -->
diuretic, nitroglycerin, reduce fluid, patient positioning (elevate HOB) specific to cardiogenic shock
81
When preload is low you admin -->
FLUID alpha one med (norepi, dopamin, epi, phenylephrine, vasopressin)
82
AFTERLOAD IS LOW WITH which SHOCK
distributive
83
When afterload is high you admin -->
nitroprusside, ACE-I, CCB, IF BP IS OK
84
WHEN CONTRACTILITY IMPAIRED YOU ADMIN
+ INOTROPIC AGENTS SUCH AS DOPAMINE, DOBUTAIN, MILRINONE, DIGOXIN
85
corticosteroids for septic shock
When require vasopressin after fluid resus (IV hydrocortisone) **pt make have relative adrenal insufficency

Critical Care (9 decks)

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