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monster management > 6113 final all > Flashcards

6113 final all Flashcards

1
Q

significant levels of troponin

A

I - 0.35T - 0.2

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2
Q

cardiac tamponade

A

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

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3
Q

CURB-65

A

PNEUMONIA! ConfusionBUN gt 7Respiratory rate g/e 30BP - SBP gt/eq 90 or DBP lt/eq 60)65Scoring:0-1: outpatient treatment2: hospital admission3-5: ICU consideration

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4
Q

SIRS Criteria

A

2+ of…HR gt 90RR lt 20 - 32 gtT lt 36 - 38 gt- 96.8 - 100.4FWBC 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 requiredPROBABLE 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 4.0occurs 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 70remember: septic has its own criteria

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9
Q

ARDS: definition

A

acute lung injury manifested by non-cardiogenic pulmonary edemaresult 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 & EMPTYINGdecreased ventricular fill:- cardiac tamponade- tension pneumothoraxdecreased 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

bradycardiamassive vasodilationhypothermiad/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 shockbradycardia 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 minIV 1: 10,000 → Dose 0.1 – 0.25mg q 5-15min H1 blocker: Benadryl (only block receptor)H2 blocker: Famotidine (Pepcid)Respiratory: AlbuterolCorticosteroid: 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 minIV 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 wayimplications: - 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/symptomsCVP g/e 8-12mmHg MAP g/e 65mmHgUOP g/e 0.5ml/kg/hrSVO2 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) ORinitial 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/dLwith 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 findingsOR 2+ → CVPScvO2 Bedside CV USdynamic 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 oxygenateFurther 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 PVRNot an increase in wedge!

43
Q

ARDS: first phasedefinition + 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 htnclinical s/s: may only see tachypnea & dyspnea• Coarse crackles• Cyanosis• Tachycardia• Lungs less compliant• Dec ventilation of alveoli• Hypercapnia

44
Q

ARDS: second phasedefinition + 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 phasedefinition + s/s

A

remodeling & fibrosis - 14 to 21 days- alveoli + bronchioles obliterated- decreased FRC- more V/Q mismatch/shuntingclinical s/sinitial: restlessness, respiratory alkalosis s/t hyperventilation (↑ pH, ↓ paCO2, HCO2 normal) + non-specific complaintsrapid progression to: respiratory distress, non-compliant lungs (more P to get same TV), crackles everywhere, elevated pulmonary airway pressure (PIIP), REFRACTORY HYPOXEMIAP/F lt 200

46
Q

P/F definition for ARDS

A

lt 200

47
Q

normal PF

A

gt 286lt 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 alveoliP/P - % O2 diffusing across alveoli into bloodnormal: 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 201-300moderate: P/F 101 - 200severe: P/F lt 100

51
Q

ARDS management goals

A

maximize pulmonary gas exchangeoptimize O2 delivery to tissuesprevent 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 4GOAL: 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/infectionb) Persistent perfusion deficitc) 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) Hypermetabolicif A + C can’t be fixed MODS OCCURSthe 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↑ CVPTachycardia, 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 PERRLACN III, IV, VI is EOM intact - each is responsible for 2 movements

66
Q

stage 1 hypertension + drugs

A

140-159/90-99Thiazide 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 LVearly diastolic, bell, mitral area Left lateral position may increase the soundAssociate 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 CONTRACTIONlate diastolic, bell, mitral areaLeft lateral position may increase the soundAssociated 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 ALDOSTERONEfluid retention ADHvasoconstriction 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 releaseserves 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 catecholaminesreduce 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 bowelPERIPHERAL vasoconstriction, ↓ UOP, cool skin, gas exchange, bowel sounds

85
Q

beta nerve fibers release

A

Epi - ↑ BG, heart & lung vasodilation, blood flow=O2 deliveryNE - ↑ 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 neededActivity level • 3= Sedentary • 5= Moderate • 10= Strenuous

monster management (29 decks)

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