Shock/Mods Flashcards
(65 cards)
1
Q
Adequate blood flow to tissues and cells requires: (3)
A
- effective cardiac pump
- adequate vasculature/circulatory system
- sufficient blood volume
2
Q
shock is essentially…….
A
decreased tissue perfusion
3
Q
4 types of shock
A
- hypovolemic
- cardiogenic
- obstructive
- distributive
4
Q
examples of causes of hypovolemic shock. (3)
A
bleeding, dehydration, diarrhea
5
Q
examples of causes of cardiogenic shock.(2)
A
MI,HF
6
Q
examples of causes of distributive shock.(3)
A
-septic, neurogenic, anaphylactic
7
Q
examples of causes of obstructive shock. (3)
A
- PE
- tension pneumothorax
- cardiac tamponade
8
Q
What are the three stages of shock?
A
- compensatory
- progressive
- irreversible
9
Q
Acid Base Balance for each stage of shock
A
- Compensatory –> respiratory alkalosis
- progressive –> metabolic acidosis
- irreversible –> profound acidosis
10
Q
Compensatory stage clinical manifestations (6)
A
- normal BP
- increased lactic acid (metabolic acidosis)
- increased RR, deep respirations (compensatory respiratory alkalosis)
- anxious/confused
- skin is cool/clammy
- decreased UO
11
Q
Progressive stage Clinical Manifestations: respiratory decompensation (4)
A
- rapid, shallow breaths, crackles
- pulmonary hypoperfusion and hypoxemia
- pulmonary capillaries leak: pulmonary edema and diffusion abnormalities, alveolar collapse
- can progress to ARDS
12
Q
Progressive stage Clinical Manifestations: cardiovascular decompensation IMPAIRED PUMP!!! (3)
A
- tachycardia
- low co
- MI
13
Q
Progressive stage Clinical Manifestations: Neurological decompensation (3)
A
- decreased cerebral perfusion, hypoxia
- mental status changes
- lethargy –> loss of consciousness
14
Q
Progressive stage Clinical Manifestations: renal decompensation (3)
A
- MAP < 65; decreased GFR
- AKI
- oliguira
15
Q
Progressive stage Clinical Manifestations: hepatic decompensation (3)
A
- decreased blood flow to liver: impaired liver metabolism
- increased lactic acid and ammonia
- increased billirubin: jaundice
16
Q
Progressive stage Clinical Manifestations: GI decompensation and ischemia (3)
A
- stress ulcer; risk for GI bleed
- GI necrosis: bloody diarrhea
- bacteria toxins enter blood stream: sepsis
17
Q
Progressive stage Clinical Manifestations: hematologic decompensation (2)
A
- cytokines activate clotting cascade
- DIC
18
Q
Irreversible or Refractory stage clinical manifestations (6)
A
- severe organ damage: no response to treatment
- acute metabolic acidosis
- reserves of ATP depleted –> no cell metabolism causing cell damage
- respiratory system damage: no adequate oxygenation/ventilation despite vent support
- CV system damage: no adequate MAP despite vasopressors
- multiple organ dysfunction progressing to complete organ failure
19
Q
Shock Assessment: CNS early and late stages
A
- Early –> anxiety/restlessness
- Late –> coma
20
Q
Shock assessment: CV system early and late (BP, HR)
A
Early BP and HR–> BP is normal or slightly elevated and HR is > 100
Late BP and HR –> BP is < 90 and HR < 60
21
Q
BP and SHOCK (3)
A
hypotension: SBP less than 90 mmHg
if hypertensive: decrease of more than 40 mmHg from baseline
Map < 65
22
Q
Shock assessment: respiratory early and late
A
early –> rapid, deep respirations, hyperventilation (RR > 20), respiratory alkalosis (compensating for metabolic acidosis)
Late –> shallow respirations, poor gas exchange
23
Q
Shock assessment: renal system (early and late)
A
Early –> sodium retention, water reabsorption, Oliguria < 0.5 ml/kg/hr, increased BUN, creatinine WNL
Late –> AKI with decreased GFR
24
Q
Shock Assessment: GI system (early and late)
A
early –> decreased bowel sounds, distention, Nausea, constipation
late –> damage to microvilli causing bacteria translocation increasing risk of infection
25
Shock assessment: Hepatic (4)
- altered liver enzymes
- clotting disorders
- inability to metabolize meds
- increased susceptibility to infection
26
Shock assessment: hematological
DIC
27
Shock assessment: integumentary.
-skin color, temp, texture, and turgor --> central/peripheral cyanosis (late/unreliable sign)
28
General management (4)
- identify and treat underlying cause
- restore optimum circulation (fluid replacement to restore intravascular volume, vasoactive meds: restore vasomotor tone and improve cardiac function)
- minimize O2 consumption and enhance oxygen delivery to tissues
- supplemental O2, mechanical vent
- nutritional support for increased metabolic requirements during shock
29
Fluid resuscitation: (4)
- rapid infusion of crystalloid and colloid solutions (NS or LR) --> 30ml/kg NS
- blood products
- insufficient fluid causes an increased incidence of morbidity and mortality from lack of tissue perfusion
- excessive fluid: systemic and pulmonary edema, ARDS, abdominal compartment syndrome, MODS
30
Pharmacological Support (5)
- vasoactive meds: improve hemodynamics
- given when fluid therapy cannot maintain MAP
- Regulate CO, HR, preload, afterload, and contractility
- vasoactive meds require frequent VS monitoring
- use central line to prevent infiltration
31
Medications that improve contractility. (4)
-dopamine, dobutamine, epinephrine, milrinone
32
Vasodilators (2)
- nitroglycerin
| - nitroprusside.
33
vasopressor agents (5)
- norepinephirine (levophed)
- dopamine (intropin)
- phenylephrine. (neosynephrine)
- vasopressin
- epinephrine
34
Other pharmacological agents besides vasoactive (7)
- sedatives: propofol, Verced, precedex
- analgesics: fentanyl, morphine
- insulin: increased glucose metabolism
- corticosteroids: hydrocortisone, methylprednisone
- Antibiotics
- low-molecular weight heparin to prevent DVT
- h2-receptor antogonist (famotidine) or PPI. (pantoprazole) to prevent gastric stress ulcer
35
body temp regulation (4)
- rapid administration of IV fluids may reduce temp
- hypothermia (decreased cardiac contractility, impairs CO, impairs oxygenation)
- fluid warmer
- warm blankets
36
nutritional support (3)
- increased metabolic rate, increased energy requirements
- enteral nutrition (within 24-48 hours of admission, preferred route, not for paralytic ileus)
- parenteral nutrition (given if enteral nutrition not tolerated)
37
most common cause of hypovolemic shock
decreased intravascular volume
38
Clinical manifestations of hypovolemic shock (5)
- increased HR
- increased RR
- decreased BP
- Decreased SV
- decreased CO. (skin pale)
39
treatment for hypovolemic shock (9)
- restore volume: MAP> 65, UO > 0.5ml/kg/hr, CVP WNL, HR WNL
- restore gas exchange: O2 sat, RR, PaO2 and PaCO2 WNL
40
Causes of cardiogenic shock (common (2) and noncoronary (5) )
- most common: MI, HR
| - non-coronary: hypoxemia, acidosis, hypoglycemia, hypocalcemia, K imbalances
41
Cardiogenic shock clinical manifestations (7)
- dysrhythmias
- angina
- tachycardia, decreased BP
- increased preload: increased CVP
- pulmonary congestion: dyspnea, SOB, coughing up pink-tinged, foamy sputum
- decreased CO: oliguria (impaired organ perfusion)
- anxiety
42
Cardiogenic shock management (4)
- correct underlying cause
- promote contractility: dopamine, dobutamine
- decrease myocardial oxygen demand: bed rest, ventricular assist device, reduce preload and afterload
- increase oxygen supply to tissues
43
Cardiogenic shock management: procedures
- thrombolytics
- PCI
- CABG
- intra-aortic balloon pump
- VAD
44
Cardiogenic Shock management: pharmacology (4)
- fluids: monitor for overload
- decrease preload: diuretics, venous vasodilators
- increase CO: dopamine, dobutamine
- decrease afterload: hydralazine
45
obstructive shock clinical manifestations (4)
- chest pain
- dyspnea, hypoxia
- JVD
- cause-dependent findings
46
Management of obstructive shock: treat cause
- cardiac tamponade (pericardiocentesis)
- tension pneumothorax (thoraacentesis and chest tube)
- pulmonary embolism (fibrinolytic and anticoagulant)
- aortic stenosis, dissection: emergency surgery
47
Distributive Shock: what happens in the body (4)
- loss of sympathetic tone or release of biochemical mediators
- intravascular volume pooling in peripheral blood vessels
- abnormal displacement of intravascular volume: relative hypovolemia
- Widespread vasodilation. and decreased SVR
48
Sepsis: response to microbial invasion (5)
- systemic inflammatory and immune response: organ injury
- gram (-) bacteria: most common microorganisms in sepsis
- increase in gram (+), viral, fungal infections causing sepsis
- increased capillary permeability results in fluid seeping from capillaries
- systemic injury leads to SIRS
49
Septic shock criteria (2016)
-post fluid resuscitation (bolus) hypoperfusion requiring vasopressors to maintain MAP > 65 or serum lactate > 2
50
septic shock general overview (5)
- impaired tissue perfusion
- metabolic acidosis
- failed compensatory mechanisms
- major vasodilation
- organ dysfunction
51
septic shock clinical manifestations (16)
- hypotensive, decreased CVP, decreased CO
- tachycardia --> bounding pulses
- increased RR
- hyperthermia: fever with warm, flushed skin
- decreased UO
- N/V/D, decreased GI motility
- hypermetabolism causing increased blood glucose and insulin resistance
- decreased platelets
- increased WBC, lactic acid, CRP, and procalcitonin (if bacterial origin)
52
septic shock 3 hour bundle
- blood cultures (if it doesn't interfere with starting abx)
- start ABX
- Bolus
53
Septic shock 6 hour bundle
-vasopressors to maintain MAP if bolus does not work
54
Neurogenic shock causes (3)
- spinal cord injury
- spinal anesthesia
- nervous system damage
55
neurogenic shock clinical manifestations (5)
- bradycardia
- hypotension
- warm, dry, flushed skin
- hypothermia
- increased risk of VTE
56
neurogenic shock management (5)
- stabilize spinal cord injury
- proper positioning spinal block patients
- HOB 30
- fluid resuscitation
- slow rewarming
57
Anaphylactic shock clinical manifestations- 3 defining characteristics
- acute onset of symptoms
- presence of 2 or more signs and symptoms
- CV compromise minutes to hours after exposure to antigen
58
anaphylactic shock clinical manifestations (10)
- headache, lightheadedness
- difficulty breathing (laryngeal edema)
- bronchospasm
- dysrthymias
- tachycardia and decreased BP
- angioedema
- diffuse erythema/generalized flushing
- N/V, abdominal pain
- pruritus
- feeling of impending doom
59
Anaphylactic shock management (4)
- remove causative agent
- protect and stabilize airway
- fluid resuscitation
- pharmacology (epinephrine, diphenhydramine, albuterol, corticosteroids)
60
Anaphylactic shock: epinephrine side effects
- tachycardia
- angina for at risk patients
- hypertension
- decreased UO
- bronchodilation
- administer albuterol
61
Most common cause of MODS
sepsis/septic shock
62
which organs are severely affected in MODS? (4)
- lungs
- splanchnic bed
- liver
- kidneys
63
MODS clinical manifestations (10)
- cardiac
- respiratory
- vascular
- neuro
- hematologic
- GI
- GU
- endocrine
- pH
- damage by inflammatory mediators, tissue hypoxia, and hypermetabolism
- cardiac: tachycardia, MI, HF
- Respiratory: tachypnea/hypoxemia, ARDS
- vascular: decreased BP greater than 40 mmHg from baseline, MAP < 65 mmHg
- neurological: change in LOC, severe --> coma with brain damage
- hematologic: coagulopathy, petechiae/bleeding, DIC
- GI: liver dysfunction, jaundice, abdominal distention --> necrosis
- GU: AKI, oliguria --> anuria
- endocrine: hyperglycemia
- metablic acidosis
64
Management of MODS patient (4)
- support patient and monitor organ perfusion until organ insults are halted
- control infection (abx)
- provide adequate ventilation, tissue oxygenation and perfusion (maintain 88-92% O2 sat, maintain hemoglobin above 7-9)
- restore intravascular volume (aggressive fluid resuscitation, isotonic crystalloids)
65
end of life communication (4)
- priority: family communication, inclusion on decision-making
- contract organ procurement organization
- follow hospital and organ procurement policies and procedures
- ***CARE NURSE WILL NOT INITIATE DISCUSSION ON ORGAN DONATION***
