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Critical Care > Critical Care > Flashcards

Critical Care Flashcards

1
Q

MAP

A

CO x SVR

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2
Q

Cardiac index

A

cardiac output / BSA

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3
Q

cardiac output

A

kidney gets 25%
brain gets 15%
heart gets 5%

CO increases with HR up to 120-150 beats/min then starts to go down because of diastolic filling time

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4
Q

Preload

A

end diastolic length, linearly related to end-diastolic volume (EDV) and filling pressure

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5
Q

Afterload

A

resistance against the ventricle contracting (SVR)

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6
Q

Strove volume

A

determined by LVEDV, contractility, and afterload
= LVEDV - LVESV
*atrial kick accounts for 15-30% of LVEDV

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7
Q

Ejection fraction

A

stroke volume (LVEDV - LVESV) / EDV

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8
Q

End diastolic volume (EDV)

A

determined by preload and distensibility of the ventricle

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9
Q

End systolic volume (ESV)

A

determined by contractility and afterload

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10
Q

Anrep effect

A

automatic increase in contractility secondary to increase afterload

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11
Q

Bowditch effect

A

automatic increase in contractility secondary to increase heart rate

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12
Q

O2 delivery

A

CO x arterial O2 content (CaO2) = CO x (Hgb x 1.34 x O2 saturation + 1 [PO2 x 0.003])

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13
Q

O2 consumption (VO2)

A

CO x (CaO2 - CvO2); CvO2 = venous O2 content

  • normal O2 delivery-to-consumption ratio is 5:1; CO increases to keep this ratio constant
  • O2 consumption is usually supply independent (consumption does not change until low levels of delivery are reached)
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14
Q

Right shift on oxygen-Hgb dissociation curve (O2 unloading)

A

increase CO2, increase temperature, increase ATP production, increase 2,3-dpg production, or decrease pH

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15
Q

Increase SvO2 (saturation of venous blood, normally 75% +/- 5%)

A

occurs with increase shunting of blood or decrease O2 extraction (sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation)

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16
Q

Decrease SvO2

A

occurs with increase O2 extraction or decrease O2 delivery (decrease O2 saturation, decrease cardiac output)

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17
Q

Wedge

A

may be thrown off by pulmonary HTN, aortic regurgitation, mitral stenosis, mitral regurg, high PEEP, poor LV compliance

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18
Q

Swan-Ganz catheter

A

should be placed in zone III (lower lung)

  • hemoptysis after flushing Swan-Ganz catheter - increase PEEP, which will tamponade the pulmonary artery bleed, mainstem intubate nonaffected side; can try to place fogarty balloon down the affected side; may need thoracotomy and lobectomy
  • relative contraindications - previous pneumonectomy, left bundle branch block
  • approx catheter distances to wedge - R SCV 45cm, R IJ 50cm, L SCV 55cm, L IJ 60cm
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19
Q

primary determinants of myocardial O2 consumption

A

increase ventricular wall tension and HR; can lead to myocardial ischemia

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20
Q

Unsaturated bronchial blood

A

empties into pulmonary veins; thus LV blood is 5 mm Hg (P02) lower than pulmonary capillaries

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21
Q

Alveolar - arterial gradient

A

10 - 15 mm Hg normal in nonvent pt

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22
Q

blood with lowest venous saturation

A

coronary venous blood (30%)

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23
Q

Acute adrenal insufficiency

A

cardiovascular collapse, characteristically unresponsive to fluids and pressors

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24
Q

Chronic adrenal insufficiency

A

hyperpigmentation, weakness, weight loss, GI symptoms, increase K, decrease Na, fever, hypotension

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25
Q

Steroid potency

A

1X - cortisone, hydrocortisone
5X - prednisone, prednisolone, methylprednisolone
30X - dexamethasone

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26
Q

Neurogenic shock

A

loss of sympathetic tone

  • usually have decrease heart rate, decrease blood pressure, warm skin
  • tx: give volume 1st, then phenylephrine after resuscitation; give steroids for blunt spinal trauma with deficit
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27
Q

Hemorrhagic shock

A

initial alteration is increase diastolic pressure

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28
Q

Cardiac tamponade

A
  • causes decreased diastolic ventricular filling and hypotension
  • Beck’s triad - hypotension, JVD, muffled heart sounds
  • Echo - shows impaired diastolic filling of right atrium initially (1st sign of cardiac tamponade)
  • pericardiocentesis blood does not form clot
  • tx: fluid resuscitation initially; need pericardial window or pericardiocentesis
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29
Q

hemorrhagic shock

A

decrease CVP, PCWP, CO; increase SVRI

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30
Q

septic shock

A

decrease CVP, increase CO, decrease SVRI

*severe septic shock that leads to cardiac dysfunction can cause decrease CO and increase SVRI

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31
Q

Cardiogenic shock

A

increase CVP and PCWP, decrease CO, increase SVRI

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32
Q

Neurogenic shock

A

decrease CVP and PCWP, decrease CO, decrease SVRI

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33
Q

Hypoadrenal shock

A

decrease CVP and possibly increase PCWP, decrease CO, decrease SVRI

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34
Q

Early sepsis triad

A

hyperventilation, confusion, respiratory alkalosis

  • early gram negative sepsis - decrease insulin, increase glucose (impaired utilization)
  • late gram-negative sepsis - increase insulin, increase glucose (secondary to insulin resistance)
  • hyperglycemia - often occurs just before patient becomes clinically septic
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35
Q

Fat emboli

A

signs include petechia, hypoxia, and confusion; sudan red stain may show fat in sputum and urine; most common with lower extremity (hip, femur) fractures

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36
Q

Pulmonary emboli

A

echo will show RV strain
*suspect PE and PA systolic pressures > 40, decrease PO2 and PCO2, respiratory alkalosis, chest pain, cough, dyspnea, increase heart rate

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37
Q

Air emboli

A

place patient head down and roll to left (keeps air in RV and RA), then aspirate air with central line or PA catheter to RA/RV

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38
Q

Intra-aortic balloon pump (IABP)

A
  • inflates on T wave (diastole); deflates on P wave or start of Q wave (systole)
  • aortic regurgitation contraindication
  • place tip of catheter just distal to left subclavian (1-2 cm below the top of the arch)
  • used for cardiogenic shock (after CABG, MI) or in patients with refractory angina
  • decreases afterload (deflation during ventricular systole)
  • improves SBP (inflation during ventricular diastole), which improves coronary perfusion
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39
Q

Alpha 1 receptor

A

vascular smooth muscle constriction; gluconeogenesis, glycogenolysis

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40
Q

Alpha 2 receptor

A

venous smooth constriction

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41
Q

Beta 1 receptor

A

myocardial contraction and rate

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42
Q

Beta 2 receptor

A

relaxes bronchial smooth muscle, relaxes vascular smooth muscle; increases insulin, glucagon, renin

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43
Q

dopamine receptors

A

relax renal and splanchnic smooth muscle

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44
Q

dopamine

A
  • 0-5 ug/kg/min - dopamine receptors (renal)
  • 6-10 ug/kg/min - beta-adrenergic (heart contractility)
  • > 10 ug/kg/min - alpha-adrenergic (vasoconstriction and increase BP)
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45
Q

dobutamine

A
  • 5-15 ug/kg/min - beta-1 (increase contractility mostly)

* >15ug/kg/min - beta-2 (vasodilation, increase HR)

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46
Q

Milrinone

A
  • phosphodiesterase inhibitor (increase cAMP)
  • results in increase calcium flux and increase myocardial contractility
  • also causes vascular smooth muscle relaxation and vasodilation
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47
Q

Phenylephrine

A

*alpha-1, vasoconstriction

48
Q

Norepinephrine

A
  • low dose - beta-1 (contractility)
  • high dose - alpha-1 and alpha-2
  • potent splnachnic vasoconstrictor
49
Q

Epinephrine

A
  • low dose - beta-1 and beta-2 (increase contractility and vasodilation); can decrease BP at low doses
  • High dose - alpha-1 and alpha-2 (vasoconstriction); increase cardiac ectopic pacer activity and myocardial O2 demand
50
Q

Isoproterenol

A
  • beta-1 and beta-2, increase heart rate and contractility, vasodilates
  • side effects: extremely arrhythmogenic; increase heart metabolic demand (rarely used); may actually decrease BP
51
Q

Vasopressin

A
  • V-1 receptors - vasoconstriction of vascular smooth muscle
  • V-2 receptors (intrarenal) - water reabsorption at collecting ducts
  • V-2 receptors (extrarenal) - mediate release of factor VIII and von Willebrand factor
52
Q

Nipride

A

arterial and venous dilator

  • cyanide toxicity at doses > 3 ug/kg/min for 72 hours; can check thiocyanate levels and signs of metabolic acidosis
  • tx: amyl nitrite, then sodium nitrite
53
Q

Nitroglycerin

A

predominately venodilation, modest effect on coronaries; decrease myocardial wall tension by decrease preload

54
Q

Hydralazine

A

alpha blocker

55
Q

Lung compliance

A

change in volume / change in pressure

  • high compliance means lungs easy to ventilate
  • pulmonary compliance decrease in patients with ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema
56
Q

Aging (re: lungs)

A

decrease FEV1 and vital capacity, increase functional residual capacity (FRC)

57
Q

V/Q ratio

A

highest in upper lobes, lowest in lower lobes

58
Q

Ventilator

A
  • increase PEEP to improve oxygenation (alveoli recruitment) –> improves FRC
  • increase rate or volume to decrease CO2
59
Q

Normal weaning parameters

A
  • negative inspiratory force (NIF) > 20
  • FiO2 < 35%
  • PEEP 5 (physiologic)
  • pressure support 5
  • RR < 24 / min
  • HR < 120
  • PO2 > 60 mm Hg
  • PCO2 < 50 mm Hg
  • pH 7.35 - 7.45
  • saturations > 93%
  • off pressors
  • follows commands
  • can protect airway
60
Q

FiO2 < = 60%

A

prevents O2 radical toxicity

61
Q

Barotrauma

A
  • high risk if plateaus > 30 and peaks > 50

* consider prophylactic chest tubes

62
Q

PEEP

A

*improves FRC and compliance by keeping alveoli open –> best way to improve oxygenation

63
Q

Excessive PEEP complications

A

decrease RA filling, decrease CO, decrease renal blood flow, decrease urine output, and increase pulmonary vascular resistance

64
Q

High frequency ventilation

A

used a lot in kids; tracheoesophageal fistula, bronchopleural fistula

65
Q

Inverse ratio ventilation

A

helps reduce barotruama

  • normal 1:2 I:E phase
  • go to 2:1
66
Q

Total lung capacity

A

lung volume after maximal inspiration

TLC = FVC + RV

67
Q

Forced vital capacity

A

maximal exhalation after maximal inhalation

68
Q

Residual volume

A

lung volume after maximal expiration (20% TLC)

69
Q

Tidal volume

A

volume of air with normal inspiration and expiration

70
Q

Functional residual capacity

A

lung volume after normal exhalation

  • FRC = ERV + RV
  • surgery (atelectasis ), sepsis (ARDS), and trauma (contusion, atelectasis, ARDS) all decrease FRC
71
Q

Expiratory reserve volume

A

volume of air that can be forcefully expired after normal expiration

72
Q

Inspiratory capacity

A

maximum air breathed in from FRC

73
Q

FEV1

A

forced expiratory volume in 1 second (after maximal inhalation)

74
Q

Minute ventilation

A

TV x RR

75
Q

Restrictive lung disease

A 
decrease TLC (Total lung capacity), decrease residual volume (RV), decrease FVC (Forced vital capacity) 
*FEV1 can be normal or increase
76
Q

Obstructive lung disease

A

increase TLC, increase RV, decrease FEV1

*FVC can be normal or decreased

77
Q

Dead space

A

normally to the level of the bronchiole (150mL); increase with drop in cardiac output, PE, pulmonary HTN, ARDS, excessive PEEP; can lead to high CO2 buildup
*area of lung that is ventilated but not perfused

78
Q

COPD

A

increase work of breathing due to prolonged expiratory phase

*work of breathing normally 2% of total body VO2

79
Q

ARDS

A

mediated by cellular inflammatory processes, increase proteinaceous material, increase gradient, increase shunt
*most common cause is sepsis

80
Q

Acute lung injury

A

acute onset
bilateral pulmonary infiltrates
PaO2/FiO2 < = 300
PAOP < 18 mm Hg or no clinical evidence of LAH (left arterial hypertension

81
Q

Acute respiratory distress syndrome

A

acute onset
bilateral pulmonary infiltrates
PaO2/FiO2 < 200
PAOP < 18 mm Hg or no clinical evidence of LAH (left arterial hypertension

82
Q

SIRS

A

*mediated by TNF-alpha and IL-1; temperature > 38 or < 36, RR > 20, PC02 < 32, WBC > 12,000 or < 4,000, HR > 90

83
Q

Endotoxin (lipopolysaccharide - LipidA)

A

most potent stimulus of SIRS

84
Q

SIRS
Sepsis
Septic Shock
MOD

A 
SIRS:
*temp > 38 or < 36 
*HR > 90
*WBC > 12000 or < 4000
*RR > 20 or PaCO2 < 32
SEPSIS:
*sirs with infection
SEVERE SEPSIS
*sepsis with organ dysfunction
SEPTIC SHOCK
*septic and arterial hypotension despite fluid
MOD
*progressive but reversible dysfunction of 2 or more organs
85
Q

Pulmonary organ dysfunction

A

need for mechanical ventilation; PaO2:FiO2 ratio < 300 for 24 hours

86
Q

Cardiovascular organ dysfunction

A

need for inotropic drugs to maintain adequate tissue perfusion or CI < 2.5 L/min/m^2

87
Q

Kidney organ dysfunction

A

creatinine > 2 times baseline on 2 consecutive days or need for renal replacement therapy

88
Q

Liver organ dysfunction

A

bilirubin > 3 mg / dL on 2 consecutive days or PT > 1.5 control

89
Q

Nutrition organ dysfunction

A

10% reduction in lean body mass; albumin < 2.0 g/dL or total lymphocyte count < 1,000

90
Q

CNS organ dysfunction

A

GCS < 10 without sedation

91
Q

Coagulation organ dysfunction

A

platelet count < 50,000 / uL; fibrinogen < 100 mg/dL or need for factor replacement

92
Q

Aspiration

A

pH < 2.5 and volume > 0.4 cc/kg associated with increase degree of damage
*most frequent site is posterior portion of RUL and superior portion of RLL

93
Q

Mendelson’s syndrome

A

chemical pneumonitis from aspiration of gastric secretions

94
Q

Atelectasis

A

bronchial obstruction and respiratory failure are main causes

  • most common cause of fever in first 48 hours after operation
  • fever, tachycardia
  • increased in patients with COPD, upper abdominal surgery, obesity
  • tx: incentive spirometry
95
Q

Things that throw off a pulse ox

A

nail polish, dark skin, low flow states, ambient light, anemia, vital dyes

96
Q

Pulmonary vasodilation

A

bradykinin, PGE1, prostacyclin (PGI2), nitric oxide

*alkalosis

97
Q

Pulmonary vasconstriction

A

histamine, serotonin, TXA2, epinephrine, norephinephrine, hypoxia, acidosis

98
Q

Pulmonary shunting

A

occurs with nitroprusside (Nipride), nitroglycerin, and nifedipine

99
Q

Most common cause of postop renal failure

A

hypotension

*70% nephrons need to be damaged before renal dysfunction occurs

100
Q

FeNa

A

(urine Na / Cr) / (plasma Na / Cr) –> best test for azotemia

101
Q

Prerenal cause of acute renal failure

A

FeNa < 1%, urine Na < 20, BUN / Cr ratio > 20, urine osmolality > 500 mOsm; otherwise consider renal cause of azotemia

102
Q

Oliguria

A

1st - make sure patient is volume loaded (CVP 11-15 mm Hg)
2nd - try diuretic trial –> furosemide (lasix) / butanamide
3rd - dialysis if needed

103
Q

Indications for dialysis

A

fluid overload, increase K, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning

104
Q

Hemodialysis vs CVVH

A

HD - rapid, causes large volume shifts

CVVH - slower, good for ill pts who cannot tolerate the volume shifts (septic shock)

105
Q

Renin

A

released in response to decrease pressure sensed by juxtaglomerular apparatus in kidney

  • also released in response to increase Na concentrations sensed by macula densa
  • beta adrenergic stimulation and hyperkalemia also cause release
  • converts angiotensinogen (synthesized in liver) to angiotensin I
  • angiotensin-converting enzyme (lung) - converts angiotensin I to angiotensin II
  • adrenal cortex - releases aldosterone in response to angiotensin II
  • Distal Convoluted Tubule - aldosterone acts here to reabsorb more water by increase Na/K (ATPase on membrance, K secreted)
  • Angiotensin II - also vasoconstricts, increases HR, contractility, permeability, glycogenolysis, and gluconeogenesis; inhibits renin release
106
Q

Atrial natriuretic peptide or factor

A

released from atrial wall with atrial distention

  • inhibits Na and water resorption in collecting ducts
  • also a vasodilator
107
Q

Antidiuretic hormone

A
  • ADH, vasopressin
  • released by posterior pituitary gland when osmolality is high
  • acts on collecting ducts for water resorption
  • also a vasoconstrictor
108
Q

Renal toxic drugs

A
  • NSAIDs - cause renal damage by inhibiting prostaglandin synthesis, resulting in renal arteriole vasoconstriction
  • Aminoglycosides - direct tubular injury and laterrenal vasoconstriction
  • Myoglobin - direct tubular injury; tx: alkalinize urine
  • Contrast dyes - direct tubular injury; tx: premedicate with N-acetylcysteine and volume

*efferent limb of kidney controls GFR

109
Q

Brain death

A
  • precludes diagnosis - uremia, temperature < 30, BP < 70/40, desaturation with apnea test, drugs (phenobarbital, pentobarbital), metabolic derangements
  • must exist for 6-12h –> unresponsive to pain, absent caloric oculovestibular reflexes, absent oculocephalic reflex, positive apnea test, no corneal reflex, no gag, fixed and dilated pupils
  • EEG - electrical silence; MRA - can be used, will show no blood flow to brain
  • Apnea test - disconnected from ventilation; CO2 > 60 mm Hg or increase in CO2 by 20 is a positive test for apnea; if arterial pressure drops to < 60 or patient desaturates, the test is terminated
  • can still have deep tendon reflexes with brain death
110
Q

Carbon monoxide

A

can falsely increase O2 saturation reading on pulse ox

  • binds Hgb directly (creates carboxyhemoglobin)
  • can usually correct with 100% on vent (displaces carbon monoxide); may need hyperbaric O2 if really high
  • abnormal carboxyhemoglobin > 10%; in smokers > 20%
111
Q

Methemoglobinemia

A
  • from nitrites such as hurricaine spray; nitrites bind Hgb) - 02 sat reads 85%
    tx: methylene blue
112
Q

Critical illness polyneuropathy

A

motor > sensory neuropathy; occurs with sepsis; can lead to failure to wean from vent

113
Q

Xanthine oxidase

A

in endothelial cells, forms toxic oxygen radicals with reperfusion, involved in reperfusion injury
*also involved in metabolism of purines and breakdown to uric acid

114
Q

DKA

A
  • nausea and vomiting, thirst, polyuria, abdominal pain, increase glucose, increase ketones, decrease Na, increase K
  • tx: insulin and eventually glucose, so pt does not bottom out, isotonic solutions, K+ (although initial K will be high, it will be driven back into cells by insulin), HCO3- for pH < 7.25
115
Q

ETOH withdrawal

A

HTN, tachycardia, delirium, seizures after 48 hours

*tx: thiamine, folate, Mg, K, B12, PRN lorazepam (Ativan)

116
Q

ICU or hospital psychosis

A
  • generally occurs after third postoperative day and is frequently preceded by lucid interval
  • need to rule out metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes

Critical Care (1 decks)

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