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Principles IV > Shock > Flashcards

Shock Flashcards

1
Q

What is shock?

A

Inadequate oxygen delivery to meet metabolic demands resulting in global tissue hypo perfusion and metabolic acidosis.

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2
Q

Can shock occur with normal blood pressure?

A

YEP!

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3
Q

What happens to oxygen delivery during shock?

A

inadequate systemic O2 delivery activates autonomic responses to maintain systemic oxygen delivery.

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4
Q

Where does blood flow go during shock?

A

redirects tot he heart, kidneys and brain. Other beds are restricted.

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5
Q

explain the pathway from pain to shock

A

pain-> hemorrhage ->cortical perception of traumatic injury -> hormone and inflammatory mediators are released -> sympathetic nervous system releases catecholamines (NE, epi, dopamine, cortisol) -> vasoconstriction, increases in HR and increase CO -> RAAS ->decreased O2 delivery

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6
Q

What are 5 cellular responses to decreased systemic O2 delivery?

A

ATP depletion- ion pump dysfunction

  • hydrolysis of cell membranes and cell death
  • individual cells take up fluid
  • depletion of intravascular fluid
  • cell edema occludes adjacent capillaries
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7
Q

What is no reflow phenomenon?

A

prevents reversal of ischemia even with restoration of adequate macro-circulation

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8
Q

What is the bodies intrinsic goal during shock?

A

To maintain cerebral and cardiac perfusion.

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9
Q

What mediators do ischemic cells produce?

A
  • lactate
  • free radicals
  • inflammatory factors (prostacyclin, thromboxane, prostaglandins, leukotrienes, endothelin, etc.)
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10
Q

What happens when the these mediators are released?

A

systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms.

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11
Q

What is global tissue hypoxia?

A

endothelial inflammation and disruption. Inability of O2 delivery to meet demands.

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12
Q

When global tissue hypoxia (GTH) ensues, what is the result?

A

lactic acidosis, cardiovascular insufficiency, increased metabolic demands.

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13
Q

What happens to the central nervous system during GTH?

A

triggers a neuroendocrine response. Regional glucose uptake in the brain changes, reflexes and cortical activity are depressed (referable with mild hypo perfusion).
Failure to recover neurological function is a sign of poor prognosis.

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14
Q

What happens to the kidneys and adrenal glands during GTH?

A

Maintain GFR by selective vasoconstriction and concentration of blood flow in medulla and deep cortical area.
Prolonged hypotension -> decreased cellular energy -> inability to concentrate urine -> patchy cell death -> tubular necrosis -> renal failure

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15
Q

What happened to the heart during GTH?

A

cardiac function is well preserved in the late stages. Lactate, free radicals, and other humoral factors act as negative inotropes and, in a bleeding patient, may produce cardiac dysfunction as the terminal event in the shock spiral.

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16
Q

Trauma patient with cardiac disease….

A

Fixed stroke volume inhibits the body’s inability to increase blood flow in response to hypovolemia and anemia.
Tachycardia is the only option.
Shock in the elderly may therefor be rapidly progressive and not respond predictably to fluid administration.

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17
Q

What happens to the lung in GTH?

A

filter for the inflammatory by-products of the ischemic body. Immune complex and cellular factors accumulate in pulmonary capillaries.

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18
Q

Explain at the cellular level whats happening with the lungs?

A

Neutrophil and platelet aggregation, increased capillary permeability, destruction of lung architecture, ARDS, (the lung is the sentinel organ for the development of multi organ system failure in a traumatic patient)

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19
Q

Does pure hemorrhage, in the absence of hypoperfusion, produce pulmonary dysfunction?

A

NO

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20
Q

Is traumatic shock more than just a hemodynamic disorder?

A

yes

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21
Q

What happens to the gut during GTH?

A

One of the earliest organs affected by hypoperfusion. May be the prime trigger for MOSF. Intense vasoconstriction occurs early and frequently leads to “no reflow” phenomenon. Intestinal cell death -> breakdown in the barrier function in the gut -> increased translocation of bacteria to the liver and lung -> potentiation of ARDS.

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22
Q

What happens to the liver during GTH?

A

complex microcirculation; potential for repercussion injury during recovery from shock. Hepatic cells are metabolically active and contribute to the ischemic inflammatory response and to irregularities in blood glucose. Absence of liver after shock is almost always lethal.

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23
Q

What happens to skeletal muscle during GTH?

A

Not metabolically active during shock; tolerates ischemia well. Skeletal muscle mass -> of lactic acid and free radicals.
sustained ischemia ->increased intracellular Na and free water -> further depletion of intravascular and interstitial fluid.

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24
Q

What is Multiorgan dysfunction syndrome

A

progression of physiologic effects as shock ensues. cardiac depression, reap distress, renal failure, and DIC.
Result is end organ failure.

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25
Q

Symptoms of shock

A

pallor, diaphoresis, hypotension, tachycardia, prolonged cap refill, diminished urine output, narrowed pulse pressure

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26
Q

diagnosis of shock

A

physical exam (VS, mental status, skin color, temp, pulses)
infectious source
labs (cbc, chemistries, lactate, coags, cultures, ABG)

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27
Q

further studies that should be performed

A

CT of head, lumbar puncture, wound cultures, acute and series, and/pelvis CT or US, cortisol level, fibrinogen, FDPs, d-dimer

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28
Q

what historical questions do you ask for the pt in shock

A

recent illness, fever, chest pain, SOB, and pain, commodities, medications, toxins/ingestions, recent hospitalizations or surgeries, baseline mental status.

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29
Q

physical exam for a pt in shock

A

vitals, CNS (mental status), skin (color, temp, rashes, sores), CV (JVD, heart sounds), reap (lung sounds, RR, o2 sats, ABG), GI (and pain, rigidity, guarding, rebound), renal (urine output)

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30
Q 
Is this pt in shock?
Patient looks ill
Altered mental status
Skin cool and mottled or hot and flushed
Weak or absent peripheral pulses 
SBP <110
Tachycardia
A

yepperz!

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31
Q

If you can palpate a pulse at the neck, radial, femoral or tibial you know the BP is at least…..

A

neck-60
radial- 70
Femoral- 80
Tibial- 90

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32
Q

Types of shock

A

hypovolemic, septic, cardiogenic, anaphylactic, neurogenic, obstructive

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33
Q

What type of shock is this? 68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin

A

hypovolemic

34
Q

types of hypovolemic shock

A

non-hemorrhagic and hemorrhagic

35
Q

causes of non-hemorrhagic shock

A 
Vomiting
Diarrhea
Bowel obstruction, pancreatitis
Burns 
Neglect, environmental (dehydration)
36
Q

causes of hemorrhagic shock

A 
GI bleed
Trauma
Massive hemoptysis
AAA rupture
Ectopic pregnancy, post-partum bleeding
37
Q

How do you care for hypovolemic shock?

A

ABC’s, 2 large bore IV’s or a central line, crystalloids (NS or LR),
PRBC’s (O neg or cross matched, 1:1:1), Control any bleeding, definitive treatment

38
Q

tests to be done pre-op on shock patients

A 
ABG/lactate
CBC
Electrolytes
BUN, Creatinine
Coagulation studies
Type and cross-match 
AND
As indicated
CXR
Pelvic x-ray
Abd/pelvis CT
Chest CT
GI endoscopy
Bronchoscopy
Vascular radiology
39
Q

What type of shock is this?
An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.4, hypotensive with a widened pulse pressure, tachycardic, with warm extremities

A

septic shock

40
Q

what is important to know about hypotension for septic shock?

A

Hypotension secondary to Sepsis that is resistant to adequate fluid administration and associated with hypoperfusion

41
Q

what is the criteria for SIRS

A 
Temp > 38 or < 36
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12 or < 4 
Plus the presumed existence of infection
Blood pressure can be normal
42
Q

refractory hypotension in septic shock

A

after bolus of 20-40ml/Kg patient still has the following
SBP <65mmHg
decrease of 40mmHg from baseline

43
Q

clinical signs of septic shock

A

hyperthermia or hypothermia, tacycardia, wide pulse pressure, low blood pressure (SBP <90), mental status change

BEWARE OF COMPENSATED SHOCK

44
Q

ancillary studies for shock

A

cardiac monitor, pulse ox, CBC, chem 7, coags, LFTs, lipase, UA, ABG with lactate, blood cultures, urine culture, CXR, foley cath

45
Q

treatment for septic shock

A

2 large bore IV’s, NS IV bolus 1-2L wide open (if not contraindicated), supplemental O2, empiric antibiotics

46
Q

refractory hypotension in septic shock

A

after bolus of 20-40ml/Kg patient still has the following
SBP <65mmHg
decrease of 40mmHg from baseline

47
Q

So what do you do if you have persistent hypotension in these people?

A

if no response ager 2-3L start a vasopressor (norepi, dopamine,etc) and titrate to effect. Goal is a MAP >60, consider adrenal insufficiency: hydrocortisone 100mg IV.

48
Q

What type of shock is this? A 55 yo M with hx of HTN, DM presents with “crushing” substernal CP, diaphoresis, hypotension, tachycardia and cool, clammy extremities

A

Cardiogenic

49
Q

defining features of cardiogenic shock

A

SBP < 90 mmHg
CI < 2.2 L/m/m2
PCWP > 18 mmHg

50
Q

What are the signs of cardiogenic shock?

A 
Cool, mottled skin
Tachypnea 
Hypotension
Altered mental status
Narrowed pulse pressure
Rales, murmur
51
Q

What can cause cardiogenic shock?

A 
AMI
 Sepsis
 Myocarditis
 Myocardial contusion
 Aortic or mitral stenosis
Hypertrophic cardiomyopathy
Acute aortic insufficiency
52
Q

Pathophys of cardiogenic shock

A
  • Often after ischemia, loss of LV function
  • Lose 40% of LV -> clinical shock ensues
  • CO reduction = lactic acidosis, hypoxia
  • Stroke volume is reduced
  • Tachycardia develops as compensation
  • Ischemia and infarction worsens
53
Q

treatment of cardiogenic shock for RV infarct

A

Fluids and Dobutamine (no NTG)

54
Q

treatment of cardiogenic shock for acute mitral regurg or VSD

A

Pressors (Dobutamine and Nitroprusside)

55
Q

Ancillary tests for cardiogenic shock

A

EKG
CXR
CBC, Chem 10, cardiac enzymes, coagulation studies
Echocardiogram

56
Q

How do you treat a patient with cardiogenic shock?

A
  • Goals- Airway stability and improving myocardial pump function
  • Cardiac monitor, pulse oximetry
  • Supplemental oxygen, IV access
  • Intubation will decrease preload and result in hypotension
  • Be prepared to give fluid bolus*
57
Q

treatment of cardiogenic shock for AMI

A
  • Aspirin, beta blocker, morphine, heparin
  • If no pulmonary edema, IV fluid challenge
  • If pulmonary edema
  • *Dopamine – will ↑ HR and thus cardiac work
  • *Dobutamine – May drop blood pressure
  • *Combination therapy may be more effective
  • PCI or thrombolytics
58
Q

What type of shock is this?
A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing.

A

Anaphylactic

59
Q

What is anaphylaxis?

A

a severe systemic hypersensitivity reaction characterized by multisystem involvement
***IgE mediated

60
Q

SO what does anaphylactoid mean?

A

clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure
***Not IgE mediated

61
Q

Symptoms of anaphylaxis

A

First- Pruritus, flushing, urticaria appear

Next- Throat fullness, anxiety, chest tightness (decreased compliance, increased peak airway pressures, shortness of breath and lightheadedness

Finally- Altered mental status, respiratory (wheezing) distress, hypotension, tachycardia, circulatory collapse

62
Q

Who is at the highest risk for death from anaphylaxis?

A

poorly controlled asthmatics

previous anaphylaxis

63
Q

What are the reoccurrence rates?

A

40-60% for insect stings
20-40% for radiocontrast agents
10-20% for penicillin

64
Q

Most common causes of anaphylaxis?

A 
Neuromuscular blocking agents (most common in anesthetized patients)
Antibiotics*
Heparin*
Protamine*
Insects
Food
65
Q

What does the “lump in my throat” or “hoarseness” signify for these patients?

A

heralds life threatening laryngeal edema

66
Q

what is a biphasic phenomenon?

A

occurs in up to 20% of patients- symptoms return 3-4 hours after initial reaction has cleared

67
Q

How long does it take for anaphylaxis to show symptoms?

A

60 minutes

68
Q

clinical diagnosis of anaphylaxis

A

airway compromise, hypotension, involvement of the cutaneous, GI, or reap systems.
look for drug, food, or insect exposure
***labs are worthless

69
Q

SO how do you treat this anaphylaxis?

A
  • **Stop triggering agent!
  • ABC’s
    • Angioedema and respiratory compromise require immediate intubation (if not already intubated)
  • IV, cardiac monitor, pulse oximetry
  • IVFs, oxygen
  • Epinephrine

Second line

  • Corticosteriods
  • H1 and H2 blockers
70
Q

Medications to treat anaphylactic shock

A

Epinephrine, 0.1 mg - 0.3 mg IM/IV of 1:1000
Repeat every 5-10 min as needed
Caution with patients taking beta blockers- can cause severe hypertension due to unopposed alpha stimulation
For CV collapse, 1 mg IV of 1:10,000

Vasopressin Adult, IV, 1-2 U initially for hypotension; 40 U IV for cardiac arrest

Phenylephrine Adult, bolus IV, 0.1-1 mg (maximum) repeated every 10-15 min; infusion IV, 40 mg diluted in 250 mL

Norepinephrine Adult, infusion IV, 0.05 μg/kg/min or 2-4 μg/min

Methylene blue Adult, bolus IV, 0.5-2 mg/kg; infusion IV, 0.5 mg/kg/h

71
Q

More medications

A

Corticosteroids

  • Methylprednisolone 125 mg IV
  • Prednisone 60 mg PO

Antihistamines

  • H1 blocker- Diphenhydramine 25-50 mg IV
  • H2 blocker- Ranitidine 50 mg IV

Bronchodilators

  • Albuterol nebulizer
  • Atrovent nebulizer
  • Magnesium sulfate 2 g IV over 20 minutes

Glucagon

  • For patients taking beta blockers and with refractory hypotension
  • 1 mg IV q5 minutes until hypotension resolves
72
Q

So what do you do with anaphylactic patients after you have treated them?

A
  • All patients who receive epinephrine should be observed for 4-6 hours
  • If symptom free, discharge home
  • If on beta blockers or h/o severe reaction in past, consider admission
73
Q

What type of shock is this?
A 41 yo M presents to the ER after an MVC complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities

A

neurogenic

74
Q

What is neurogenic shock?

A
  • Occurs after acute spinal cord injury
  • Sympathetic outflow is disrupted leaving unopposed vagal tone
  • Results in hypotension and bradycardia
  • Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)
75
Q

How long does neurogenic shock last?

A

1-3 weeks

76
Q

What if the injury is T1 or higher?

A

can disrupt the entire sympathetic system

higher injury= worse paralysis

77
Q

treatment of neurogenic shock

A

Remember c-spine precautions

Fluid resuscitation

  • Keep MAP at 85-90 mm Hg for first 7 days
  • Thought to minimize secondary cord injury
  • If crystalloid is insufficient use vasopressors

Search for other causes of hypotension

For bradycardia

  • Atropine
  • Pacemaker
78
Q

What type of shock is this?
A 24 yo M presents to the ED after an MVC c/o chest pain and difficulty breathing. On PE, you note the pt to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left

A

obstructive

79
Q

tension pneumothorax

A

-Air trapped in pleural space with 1 way valve, air/pressure builds up
-Mediastinum shifted impeding venous return
-Chest pain, SOB, decreased breath sounds
-No tests needed!
Tx: Needle decompression, chest tube

80
Q

Cardiac tamponade

A

-Blood in pericardial sac prevents venous return to and contraction of heart
-Related to trauma, pericarditis, MI
-Beck’s triad: hypotension, muffled heart sounds, JVD
-Diagnosis: large heart CXR, echo
Tx: Pericardiocentisis

81
Q

Pulmonary embolism

A

-Virscow triad: hypercoaguable, venous injury, venostasis
-Signs: Tachypnea, tachycardia, hypoxia
-Low risk: D-dimer
-Higher risk: CT chest or VQ scan
Tx: Heparin, consider thrombolytics

82
Q

Aortic stenosis

A
  • Resistance to systolic ejection causes decreased cardiac function
  • Chest pain with syncope
  • Systolic ejection murmur
  • Diagnosed with echo
  • Vasodilators (NTG) will drop pressure!
  • Tx: Valve surgery

Principles IV (18 decks)

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