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x 6113 > final cram > Flashcards

final cram Flashcards

1
Q

significant levels of troponin

A

I - 0.35

T - 0.2

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2
Q

cardiac tamponade

A

muffled heart sounds
↑ CVP
paradoxical pulse (gt 10mm)
- abnormally large decrease in SBP during inspiration

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3
Q

CURB-65

A

PNEUMONIA!

Confusion
B*U*N gt 7
Respiratory rate g/e 30
BP - SBP gt/eq 90 or DBP lt/eq 60)
65

Scoring:
0-1: outpatient treatment
2: hospital admission
3-5: ICU consideration

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4
Q

SIRS Criteria

A

2+ of…

HR gt 90
RR lt 20 - 32 gt
T lt 36 - 38 gt
- 96.8 - 100.4F
WBC lt 4k - 12k gt
- immature neuts gt 10
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5
Q

sepsis

A

SIRS likely s/t infection; positive cultures add to validity but not required

PROBABLE OR CONFIRMED INFECTION!!!

clinical s/s: tachycardic, tachypnic, hypotensive, hypoxic, confused/lethargic/agitated, hyperthermic → Hypothermic

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6
Q

severe sepsis

A

sepsis + at least 1 sign of hypoperfusion or organ dysfunction (new, not explained by other etiology)

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7
Q

septic shock

A

severe sepsis associated with

  • refractory hypotension (BP lt 90/60) despite adequate fluid resus
  • and/or serum lactate gt 4.0

occurs with evidence of perfusion abnormalities: lactic acidosis, oliguria, AMS
- not perfusing brain, kidneys, lungs can’t compensate, other organ dysfunctions

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8
Q

shock: management & hemodynamics goals

A

supportive therapy while finding/managing/tx shock source

  • MAP gt 60
  • CVP 8-12
  • CI gt 2.1
  • UOP gt 0.5 mg/kg/hr
  • SaO2 gt 92%
  • SVO2 gt 70

remember: septic has its own criteria

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9
Q

ARDS: definition

A

acute lung injury manifested by non-cardiogenic pulmonary edema

result of inflammatory lung injury

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10
Q

2 things present in all shock

A
  • inadequate tissue perfusion

- cellular hypoxia (leads to dysfunction

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11
Q

s/s hypovolemic shock apparent when

A

gt 15% volume lost

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12
Q

vasopressors + hypovolemic shock

A

CAUTION. fill before you squeeze!

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13
Q

main causes of obstructive shock x3

A

THINK FILLING & EMPTYING

decreased ventricular fill:

  • cardiac tamponade
  • tension pneumothorax

decreased ventricular emptying
- main PA or saddle PE

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14
Q

volume/vasopressor + obstructive shock

A

gentle - it’s temporizing

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15
Q

shock + vasopressin

A

adjunct if not getting a good response from patient

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16
Q

1 cause of cardiogenic shock

A

MI

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17
Q

neurogenic shock classic triad

A

bradycardia
massive vasodilation
hypothermia

d/t parasympathetic overstimulation

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18
Q

neurogenic shock: avoid what drug and why?

A

phenylephrine - unopposed A1 activity could potentially worsen the shock

bradycardia d/t reflex vagus nerve - it’s a CNS effect esp at high doses

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19
Q

anaphylactic shock meds list

A

EPINEPHRINE !!! - CV collapse without
- vasopressor & mast cell stabilizer (prevent histamine release)
IM 1:1,000 → Dose 0.1-0.5mg q10-15 min
IV 1: 10,000 → Dose 0.1 – 0.25mg q 5-15min

H1 blocker: Benadryl (only block receptor)
H2 blocker: Famotidine (Pepcid)
Respiratory: Albuterol
Corticosteroid: methylprednisolone

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20
Q

epinephrine + anaphylactic shock

A
  • CV collapse without
  • vasopressor & mast cell stabilizer (prevent histamine release)

IM 1:1,000 → Dose 0.1-0.5mg q10-15 min
IV 1: 10,000 → Dose 0.1 – 0.25mg q 5-15min

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21
Q

late phase anaphylactic reactions

A
  • 6-12 hrs after initial rxn
  • typically follow favorable response to treatment
  • treated the same way

implications:
- airway mgmt: keep pts intubated 14-16 hours
- line maintenance: leave big IVs in
- ICU care: code cart & epi nearby

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22
Q

anaphylactic shock + airway management important implication

A

keep intubated 14-16 hours after event - concern for late anaphylactic reaction

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23
Q

sepsis: hemodynamic goals

A

within 6 hours of presentation/symptoms

CVP g/e 8-12mmHg 
MAP g/e 65mmHg
UOP g/e 0.5ml/kg/hr
SVO2 g/e 70%
Lactate lt 2mmol
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24
Q

surviving sepsis: goal directed treatment within 3 hours

A

Within 3 hours presentation of SIRS + strong indication organ failing

  • Measure lactate level
  • Obtain cultures before abx:
    – 2 blood cultures
    – +/- Urine culture
  • broad spectrum antibiotics
  • 30ml/kg crystalloid “fluid challenge” for:
    –hypotension
    OR
    – lactate g/e 4mmol/L
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25
Q

surviving sepsis: goal directed treatment within 6 hours

A

Within 6 hours presentation of SIRS + strong indication organ failing

  • vasopressors (for hypotension that doesn’t respond to initial fluid resuscitation)
    • GOAL: MAP g/e 65mmHg
    • NE first, then dopamine, then vasopressin
  • if persistent hypotension after initial fluid administration (MAP lt 65mmHg)
    OR
    initial lactate was g/e 4mmol/L, re-assess volume status + tissue perfusion

-re-measure lactate if initial elevated

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26
Q

septic shock treatment considerations

A
  • Fluids (crystalloids; albumin if needed)
  • Vasopressors (NE, epi, vasopressin)
  • Inotropes if cardiac dysfxn (Dobutamine, esp. w/ HF)
  • Corticosteroids (only if unable to meet hemodynamic goal)
  • Blood product administration (Goal Hgb 7-9g/dL)
  • Sedation if intubated (Propofol, not benzos: ICU delirium risk)
  • BG monitoring q2h/insulin use (goal BG 110-180 mg/dL)
  • Renal replacement therapy in ARF
  • Early but slow enteral feeding (GI perf/peritonitis – be cautious)
  • DVT/GI prophylaxis (Lovenox, heparin, PPI/H2 antagonist)
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27
Q

septic shock

A
  • Fluids (crystalloids; albumin if needed)
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28
Q

septic shock - Vasopressors

A

NE, epi, vasopressin

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29
Q

septic shock inotropes

A
  • if cardiac dysfxn (Dobutamine, esp. w/ HF)
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30
Q

septic shock - corticosteroids

A

only if unable to meet hemodynamic goal

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31
Q

septic shock - goal hgb

A

Goal Hgb 7-9g/dL

with blood product admin

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32
Q

septic shock - Sedation if intubated

A

Propofol, not benzos: ICU delirium risk

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33
Q

septic shock - BG monitoring

A

q2h/insulin use (goal BG 110-180 mg/dL)

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34
Q

septic shock + ARF?

A

renal replacement therapy

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35
Q

septic shock - early but slow enteral feeding

A

GI perf/peritonitis – be cautious

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36
Q

septic shock - DVT/GI prophylaxis

A

Lovenox, heparin, PPI/H2

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37
Q

documentation/evaluation of volume resuscitation in septic shock x2

A

EITHER repeat focused exam (after initial fluid resuscitation) – VS, CV, cap refill, pulse, skin findings

OR 2+ → 
CVP
ScvO2 
Bedside CV US
dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
38
Q

how do we know a shock patient is better?

A
  • stable VS with ↓ pharm/non-pharm support: HR 60-90, MAP gt 65, CVP 8-12
  • adequate UOP: 0.5 - 1.0 ml/kg/hr
  • evidence of adequate O2 delivery/utilization: SVO2 65 - 75
  • lactate levels normalized
  • improvements in PE
39
Q

SIRS: hypotension refractory to fluid replacement consideration

A

(a) hang 1000mL NS/LR, 200mL stays in vascular bed
- - LR requires functional liver to create buffer

(b) hang 1000mL D5W bag, 800mL stays in vascular bed
guidelines: LR or NS

40
Q

ARDS: first major change

A

Inability to oxygenate

Further destruction of alveoli
- shunting (blood passing by non-vent alveoli & bypassing ventilated)

refractory to O2 increase: junk in alveoli = UP THE PEEP

41
Q

ARDS: second major change

A

Narrowing of small airways

Damage to lung microvasculature
- V/Q imbalance d/t alveolar dead space (alveoli full of junk) = no gas exchange

42
Q

ARDS: third major change

A

Elevated pulmonary artery pressure (vasoconstriction d/t hypoxia)

Increased PVR

Not an increase in wedge!

43
Q

ARDS: first phase

definition + s/s

A

exudative - first 72 hours

  • angry neuts increase lung injury & cap permeability
    • increased alveolar edema
    • macrophages + mediators = pulmonary bed vasoconstriction = V/Q mismatch (blood bypass ventilated alveoli) = pulm htn
clinical s/s: may only see tachypnea & dyspnea
•	Coarse crackles
•	Cyanosis
•	Tachycardia
•	Lungs less compliant
•	Dec ventilation of alveoli
•	Hypercapnia
44
Q

ARDS: second phase

definition + s/s

A

proliferative - 4 to 21 days

  • resolution of pulmonary edema
  • type II pneumocytes hyperplasia
  • proliferation fibroblasts
  • hemorrhagic exudate → granulation tissue (hyaline membrane)

s/s: PROGRESSIVE HYPOXEMIA

45
Q

ARDS: third phase

definition + s/s

A

remodeling & fibrosis - 14 to 21 days

  • alveoli + bronchioles obliterated
  • decreased FRC
  • more V/Q mismatch/shunting

clinical s/s
initial: restlessness, respiratory alkalosis s/t hyperventilation (↑ pH, ↓ paCO2, HCO2 normal) + non-specific complaints

rapid progression to: respiratory distress, non-compliant lungs (more P to get same TV), crackles everywhere, elevated pulmonary airway pressure (PIIP), REFRACTORY HYPOXEMIA
P/F lt 200

46
Q

P/F definition for ARDS

A

lt 200

47
Q

normal PF

A

gt 286

lt 200 represents significant shunt gt 20% - ARDS

48
Q

a/A + PaO2/PAO2

A

a/A - what’s available in blood vs what’s available in alveoli

P/P - % O2 diffusing across alveoli into blood

normal: gt 45% or 0.75

49
Q

diagnostic criteria for ARDS

A
  • Bilateral pulmonary infiltrates (whiting out on CXR)
  • PCWP lt 18mmHg (no LVHF - normal 5-12)
  • Severe hypoxemia
  • PaO2/FiO2 lt 200
50
Q

Berlin Criteria Definition of ARDS

A

mild: P/F 201-300
moderate: P/F 101 - 200
severe: P/F lt 100

51
Q

ARDS management goals

A

maximize pulmonary gas exchange

optimize O2 delivery to tissues

prevent further organ injury

52
Q

septic shock: evidence of perfusion abnormalities

A

occurs with evidence of perfusion abnormalities (lactic acidosis, oliguria, mental status changes, other organ dysfunctions)

53
Q

EF + sepsis

A

low d/t myocardial depressant factor

54
Q

sepsis causes

A

bacteria 85% of time

  • gram neg (like e coli) release endotoxins - inflammatory cascade
  • gram pos
55
Q

surviving sepsis: fluid resuscitation

A

crystalloids - begin in ED

  • 1st 30 min bolus 500-1000cc (cryst)
  • 30 ml/kg/hr for hypotension or lactate gt 4

GOAL: CVP g/e 8 or CVP on vent g/e 12

goals not met? consider PBRC (goal hct g/e 30%)

56
Q

surviving sepsis: blood products considerations

A

consider PRBC if hgb lt 7
- goal hct g/e 30%

platelets

  • plt lt 5000
  • plt 5-30k + high risk for bleeding
57
Q

surviving sepsis: mechanical ventilation considertions

A
  • target TV 6ml/kg (low)
  • PEEP (beware tension pneumo)
  • permissive hypercapnia
  • sedation: intermittent bolus OR continuous with daily interruption/lighting to produce awakening
58
Q

MODS

A

begins with SIRS = subtle changes = dysfunction/ progressive failure 2+ organ systems d/t circulating mediators + clinical conditions

59
Q

SIRS to MODS transition

A

a) Failure to control source of inflammation/infection
b) Persistent perfusion deficit
c) Flow-dependent O2 consumption (abnormal DO2 & VO2)
d) Necrotic tissue

60
Q

SIRS/MODS patho summary

A

a) Maldistribution of vol → vasodilated + third spacing
b) Imbalance O2 supply/ demand (abnormal DO2 and VO2)
c) Hypermetabolic

if A + C can’t be fixed MODS OCCURS

the problem: inflammatory/immune response is over-activated, the body
can’t clear the mediators and toxic metabolites fast enough and a self-perpetuating cycle exists

61
Q

when does MODS occur?

A

after SIRS when vasodilation, third spacing, and hypermetabolic state can’t be fixed

62
Q

MODS: hyperdynamic CV response

A

INITIAL RESPONSE

↑ CO, HR, DO2, VO2
↓ PAWP, CVP, SVR

63
Q

MODS: hypodynamic CV response

A

many mediators = myocardial depressants; their continued influence = ↓ myocardial contractility/function

↓ CO, DO2, VO2
↑ CVP
Tachycardia, dysrhythmias, weak pulses

64
Q

why does MODS hypodynamic CV response happen?

A

many mediators = myocardial depressants; their continued influence = ↓ myocardial contractility/function

65
Q

cranial nerve III vs IV, VI

A

CN III is PERRLA

CN III, IV, VI is EOM intact - each is responsible for 2 movements

66
Q

stage 1 hypertension + drugs

A

140-159/90-99

Thiazide OR consider ACEi, ARB, CCB, BB (no comorbs)

67
Q

stage 2 hypertension + drugs

A

≥ 160/100

2 drugs - Thiazide + ACEi, ARB, CCB, BB (no comorbs)

68
Q

Target Organ Damage (MI, HF, CVA, DM, CKD) + htn drugs

A
  • combo diuretic, ACEi, ARB, CCB, BB, Aldactone
  • lifestyle modification & pharm
  • if BP > 20/10 above goal → thiazide + other.
69
Q

use diaphragm

A

Diaphragm: medium-high sounds,S1, S2

70
Q

use bell

A

Bell: low pitched sounds

mitral stenosis, diastolic murmurs, S3, S4

71
Q

S3

A

indicates difficulty w/ passive filling LA to LV (mitral valve is open & blood is flowing in)

VENTRICULAR gallop – “Kentucky”
PASSIVE FILLING into noncompliant LV
early diastolic, bell, mitral area
 Left lateral position may increase the sound
Associate with HF (chronic or AMI)
72
Q

S4

A

“atrial kick” - difficulty with active filling, LA actively contracting (typically, compensate↑ CO by ~25% but if bad contraction—heart will lose atrial kick = s4) 

- ventricle can no longer take any more

ATRIAL gallop – “Tennessee”

Blood entering noncompliant ventricle during ATRIAL CONTRACTION

late diastolic, bell, mitral area

Left lateral position may increase the sound

Associated with CHF, MI, AoS, HTN, and CAD

 A-fib will NOT have an S4 (no atrial kick)

73
Q

you will not hear this heart sound with afib

A

S4 because a fib has no atrial kick

74
Q

summation gallop

A

S3 and S4

Implies significant HF

75
Q

S1

A

Best heard with the diaphragm

 Loudest at the apex

 Mitral and tricuspid valves close

76
Q

S2

A

Best heard with the diaphragm

 Loudest at the base

 Aortic and pulmonic valves close

77
Q

heart failure - decrease in CO leads to?

A

RAAS activation:
sodium retention secondary to ALDOSTERONE
fluid retention ADH
vasoconstriction increases afterload - ANGIOTENSIN II

78
Q

neurohormonal model

A

accounts for the effects of

  • prolonged sympathetic stimulation (first)
  • prolonged angiotensin release (kidneys need more volume)
  • prolonged aldosterone release

serves as the basis for the treatment of heart failure

79
Q

systolic heart failure: loop diuretics

A

do not impact neurohormonal model!

80
Q

heart failure: beta blockers positive benefits

A

reduce sympathetic nervous system response by decreasing circulating catecholamines

reduce overstimulation of renin angiotensin system

81
Q

most common reason for diastolic heart failure

A

chronic hypertension

82
Q

acetaminophen consideration

A

Interferes with warfarin to prolong PT/INR

Steven Johnson Syndrome

83
Q

Tetraology of Fallot

A

Pulmonary stenosis, VSD, and R to L Shunt (cyanotic)

84
Q

alpha nerve fibers release

A

NE - eye dilation, clammy, hypo bowel

PERIPHERAL vasoconstriction, ↓ UOP, cool skin, gas exchange, bowel sounds

85
Q

beta nerve fibers release

A

Epi - ↑ BG, heart & lung vasodilation, blood flow=O2 delivery

NE - ↑ free fatty, tissue perfusion, myocardial O2 needs

86
Q

prolonged stress response is what?

A

medulla secreting more catecholamines

87
Q

BP goal for young, healthy (less than 60)

A

lt 140/90

88
Q

BP goal for older adult (60+)

A

lt 150/90

89
Q

Max. Target HR

A

220 – Age

90
Q

ideal body weight

A

Women: 100 lb + 5 lb for every inch over 5 feet
Men: 106 lb + 6 lb for every inch over 5 feet

91
Q

caloric need

A

IBW x 10 = basal caloric needs

• Basal caloric needs + [IBW x activity level]= total cals needed

Activity level
• 3= Sedentary
• 5= Moderate
• 10= Strenuous

x 6113 (6 decks)

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