ICU (PGY3) Flashcards

1
Q

Definition of ARDS

A

Acute Respiratory Distress Syndrome: acute diffuse inflammatory lung injury resulting in increased pulmonary vascular permeability, increased lung weight, loss of aerated lung tissue with hypoxemia

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2
Q

Berlin Criteria for ARDS

A
  1. Acute - within 1 week of insult; 2. B/l GGO infiltrates; 3. Findings not explained by cardiogenic pulmonary edema; 4. PaO2/FiO2 of < 300
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3
Q

Normal PaO2

A

75- 100 mmHg

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4
Q

Categories of ARDS (based on PaO2/FiO2)

A

Mild: 200- 300
Moderate: 100-200
Severe: < 100

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5
Q

(3) phases of lung injury in ARDS

A
  1. exudative phase: immune cell mediated, proinflammatory
  2. proliferative phase: reabsorption of alveolar edema to restore normal alveolar architecture/function; 3. fibrotic phase: final phase
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6
Q

Causes of ARDS (2) categories

A
  1. Direct Lung Injury - infection, inhalational injury, toxins, drowning, high altitude sickness, burns, trauma, aspiration; 2. Indirect Lung Injury - sepsis, pancreatitis, drug OD, transfusion related (TRALI), DIC
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7
Q

MGMT of ARDS

A

supportive to LIMIT FURTHER INJURY - treat underlying cause (i.e., PNA). lung protective ventilation settings

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8
Q

Definition of lung protective ventilation settings (i.e., ARDS)

A
  1. Low Tidal volumes (VT 6 cc/kg) of IDEAL WEIGHT; 2. permissive hypercapnea (due to low tidal volumes) allow for pCo2 of 60-70 (normally 40); 3. Plateau pressures < 30 (to avoid VILI); 4. Recruitment to improve oxygenation (PEEP 30-40 heldd 30 seconds); 5. Consider proning in severe cases (PaO2/FiO2 < 150)
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9
Q

Definition of DIC

A

acquired coagulation syndrome resulting in excessive clotting and clotting factor consumption with subsequent bleeding in severely ill patients

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10
Q

Mechanism of DIC

A

coagulation cascade is activated and control mechanism are lost -
thrombin clots into capillaries and small vessels; as a result excessive clotting consumes the body’s store of clotthing factors and plts, clot deposition in microcirculation leads to hemolysis as RBC try to pass through, counter-regulatory system (the fibrinolytic system) gets activated and starts dissolving clots

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11
Q

Causes of DIC

A

bleeding/trauma, pregnancy (placental abruption, IUFD, amniotic fluid embolus, HELLP syndrome), ARDS, acute liver failure, pancreatitis, amlignancy, vasculitis, venom snake, transfusion reactions

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12
Q

Clinical Presentation of DIC

A

hypercoagulation, hyperfibrinolysis, mixed picture; end organ failure or gangrene in small vascular beds like fingers and toes - most common presentation in septic DIC patients; oozing from IV sites or sites of trauma

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13
Q

Lab values in DIC

A

low plts, high INR, low fibrinogen (used to make fibrin clots), high D-dimer, high PTT, high clotting time, low factor 2,5,7,10)

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14
Q

MGMT of DIC

A

treat underlying cause, fix lab abnormaliites - pRBC, plts, FFP, Vitamin K (INR > 1.5 or fibrinogen < 100)

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15
Q

FFP dosing

A

15 cc/kg

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16
Q

Dose of osmotic agents in ICP

A

3% NS 250 cc over 10-15 mins; Mannitol 1g/kg over 10 mins; NaBicarb 1-2 amps slow IV push over 10 mins

17
Q

EtCO2 target for high ICP (herniating)

A

PaCO2 of 35-39 mmHg; PaCO2 < 25 can cause profound cerebral vasoconstriction which can worsen hypoperfusion

18
Q

normal ICP range

A

5- 15 mmHg; mild intracranial HTN is 20 - 30 mmHg;

19
Q

TTP Mnemonic - “FAT RN”

A

fever, anemia (MAHA), thrombocytopenia (with purpura), renal sx, neuro sx

20
Q

HUS vs. TTP

A

TTP has more NEURO/CNS involvement vs. HUS has more renal involvement. HUS is usually incontext of diarrhea

21
Q

ITP vs. TTP

A

ITP pts are generally well appearing with normal RBC.

22
Q

DIC vs. TTP

A

DIC pts have multiple sites of bleeding, elevated INR/PTT and D-dimer vs. TTP pts do not bleed overtly, and have normal to mildly elevated INR/PTT, D-dimer

23
Q

TTP MGMT

A

plasma exchange if MAHA present (schistocytes, elevated LDH, elevated INDIRECT hyperbilirubinemia)