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ABSITE > 16 Critical Care > Flashcards

16 Critical Care Flashcards

1
Q

Mean arterial pressure

A

MAP = CO x SVR

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2
Q

Cardiac index

A

CI = CO/BSA

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3
Q

Define preload

A

Left ventricular end-diastolic length

Lineraly related to LV end diastolic volume and filling pressure

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4
Q

What percentage of CO does kidney get? Brain? Heart?

A

Kidney 25%
Brain 15%
Heart 5%

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5
Q

Define afterload

A

Resistance against the ventricle contracting

SVR

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6
Q

Define stroke volume

A

Determined by LVEDV, contractility and afterload

SV = LVEDV - LVESV

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7
Q

Define ejection fraction

A

EF = SV/LVEDV

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8
Q

Determinants of end-diastolic volume

A

Preload

Distensibility of the ventricle

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9
Q

Determinants of end-systolic volume

A

Contractility

Afterload

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10
Q

Define Anrep effect

A

Automatic increase in contractility secondary to increased afterload

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11
Q

Define Bowditch effect

A

Automatic increase in contractility secondary to increase heart rate

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12
Q

How do you determine the arterial O2 content?

A

CaO2 = Hgb x 1.34 x O2sat + (Po2 x 0.003)

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13
Q

How do you determine O2 delivery?

A

O2 delivery = CO x CaO2 x 10

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14
Q

How do you determine O2 consumption?

A

Vo2 = CO x (CaO2 - CvO2)

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15
Q

Normal O2 delivery-to-consumption ratio?

A

5:1
CO increase to keep this ratio constant
O2 consumption is supply independent (until very low levels of delievery are reached)

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16
Q

Causes of right shift of Oxyhemoglobin curve?

A 
O2 unloading
Increased CO2
Increased 2,3-DPG
Increased temp
Increased ATP
Increased H+ ions (decreased pH)
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17
Q

Increased SvO2 occurs when:

A

Increased shunting of blood
Decreased oxygen extraction (i.e. sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hyptohermia, paralysis, coma, sedation)

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18
Q

Decreased SvO2 occurs when:

A

Increased O2 extraction

Decreased O2 delivery

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19
Q

Things that can effect pulmonary wedge pressure?

A 
Pulmonary hypertension
Aortic regurgitation
Mitral stenosis
Mitral regurg
High PEEP
Poor LV compliance
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20
Q

Hemoptysis after flushing Swan-Ganz catheter?

A 
Increase PEEP (tamponade the pulmonary artery bleed)
Mainstem intubate non-affected side
Fogarty balloon down mainstem on affected side
Possible thoracotomy and lobectomy
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21
Q

Relative CI to swan-ganz catheter?

A

Previous pnumonectomy

Left bundle branch block

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22
Q

Approximate Swan-Ganz catheter distance to wedge?

A

RSCV 45cm
RIJ 50cm
LSCV 55cm
LI 60cm

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23
Q

What is the only way to measure pulmonary vascular resistance?

A

Swan-Ganz catheter (NOT ECHO)

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24
Q

When should you take wedge pressure?

A

End-expiration

Ventilatory method does not matter

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25
Q

Primary determinants of myocardial O2 consumption?

A

Increased ventricular wall tension

Heart rate

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26
Q

Normal A-a gradient in a non-ventilated patient?

A

10-15mmHg

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27
Q

Blood with lowest venous saturation?

A

Coronary sinus blood (30%)

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28
Q

Adrenal insufficiency

A

MCC - withdrawal of exogenous steroids
Acute: cardiovascular collapse, unresponsive to fluids or pressors, nasuea/vomiting, abdominal pain, fever, lethargy, decreased glucose, hyperkalemia
Tx: Dexamethasone

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29
Q

Steroid potency?

A

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

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30
Q

Neurogenic shock

A

Loss of sympathetic tone
Associated with spine or head injury
Decreased HR, decreased BP, warm skin
Tx: give volume 1st, phenylephrine after resuscitation

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31
Q

Initial alteration in hemorrhagic shock?

A

Increased diastolic pressure

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32
Q

Cardiac tamponade

A

Causes cardiogenic shock
Decreased ventricular filling
ECHO shows impaired diastolic filling of right atrium first (weakest wall)
Tx: Rescucitation, pericardial window/pericardiocentesis

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33
Q

Beck’s triad

A

Hypotension
Jugular venous distention
Muffled heart sounds

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34
Q

Decreased CVP/PCWP
Decreased CO
Increased SVR

A

Hemorrhagic shock

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35
Q

Decreased CVP/PCWP
Increased CO
Decreased SVR

A

Septic shock (hyperdynamic)

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36
Q

Increased CVP/PCWP
Decreased CO
Increased SVR

A

Cardiogenic (i.e. MI, cardiac tamponade)

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37
Q

Decreased CVP/PCWP
Decreased CO
Decreased SVR

A

Neurogenic (i.e. head or spinal cord injury)

Adrenal insufficiency

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38
Q

Early sepsis triad

A

Hyperventilation
Confusion
Hypotension

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39
Q

Early gram-negative sepsis

A 
Decreased insulin
Increased glucose (impaired utilization)
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40
Q

Late gram-negative sepsis

A 
Increased insulin
Increased glucose (insulin resistance)
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41
Q

Neurohormonal response to hypovolemia - Rapid

A

Epinephrine and norepinephrine release
Adrenergic release
Results in vasoconstriction and increased cardiac activity

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42
Q

Neurohormonal response to hypovolemia - Sustained

A

Renin (from kidney - vasconstriction and water resorption)
ADH (from pituitary - reabsorption of water)
ACTH (from pituitary - increases cortisol)

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43
Q

Fat emboli

A

Petechia, hypoxia, confusion
Sudan red stain may show fat in sputum and urine
Most common from LE fractures, orthopedic procedures

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44
Q

Pulmonary emboli

A 
Chest pain and dyspnea
Decreased PO2 and PCO2
Respiratory alkalosis
Increased HR and RR
Hypotension and shock if massive

Tx: HEparin, coumadine; consider open or percutaneous emboliectomy if in shock despite massive pressors and inotropes

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45
Q

Most common source of PEs?

A

Iliofemoral region

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46
Q

Treatment of air emboli?

A

Patient head down and roll to left (keeps air in RV/RA)

Aspirate air out with central line to RA/VA

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47
Q

When does an intra-aortic balloon pump inflate? Deflate?

A

Inflates on T wave (diastole)

Deflates on P wave (systole)

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48
Q

CI to intra-aortic balloon pump?

A

Aortic regurgitation

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49
Q

Uses/effect of intra-aortic balloon pump?

A

Used for cardiogenic shock (after CABG or MI)
Refractory angina awaiting revascularization

Decreases afterload (deflation during ventricular systole)
Improves diastolic BP (inflation during ventricular diastole)
Which improves diastolic coronary perfusion

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50
Q

Alpha-1 receptors

A

Vascular smooth muscle constriction
Gluconeogenesis
Glycogenolysis

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51
Q

Alpha-2 receptors

A

Venous smooth muscle contriction

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52
Q

Beta-1 receptors

A

Myocardial contraction and rate (ionotrope and chronotrope)

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53
Q

Beta-2 receptors

A

Relaxes bronchial smooth muscle
Relaxes vascular smooth muscle
Increases insulin, glucagon, renin

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54
Q

Dopamine receptors

A

Relaxes renal and splanchnic smooth muscle

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55
Q

Dopamine (2-5ug/kg/min initially)

A

2-5ug/kg/min - dopamine receptors (renal)
6-10ug/kg/min - beta-adrenergic (heart contractility)
>10ug/kg/min - alpha-adrenergic (vasoconstriction and increased BP)

56
Q

Dobutamine (3ug/kg/min initially)

A

Beta-1 receptors

Increased contractility, tacycardia with higher doses

57
Q

Milrinone

A

Phosphodiesterase inhibitor - increases cAMP
Results in increased Ca flux and increased myocardial contractility
Vascular smooth muscle relaxation and pulmonary vasodilation

58
Q

Phenylephrine (10ug/kg/min initially)

A

Alpha-1

Vasoconstriction

59
Q

Norepinephrine (5ug/min initially)

A

Low doses - Beta-1 (increased contractility)

High dose - Alpha-1 and Alpha-2 (veno and vaso constriction)

60
Q

Epinephrine (1-2ug/min initially)

A

Low dose - Beta-1 and B-2 (increased contractility and vasodilation; can decrease BP at low dose)
High dose - Alpha-1 and Alpha-2 (veno and vaso constriction; can increase cardiac ectopic pacer activity and myocardial O2 demand)

61
Q

Isoproterenol (1-2ug/min initially)

A

B-2 and B-2 (increased contractility, vasodilates)

AE: extremely arrhythmogenic, increased heart metabolic demand, may actually decrease BP

62
Q

Vasopressin

A 
V1 receptors - vasocontriction of vascular smooth muscle
V2 receptors (intrarenal) - water reabsoprtion at collecting ducts
V2 receptors (extrarenal) - mediate release of factor VII and vWF
63
Q

Nipride

A

Arterial vasodilator
Cyanide toxicity at dose >3ug/kg/min for 72hrs
Check thiocyanate levels and signs of metabolic acidosis

64
Q

Treatment for cyanide toxicity

A

Amyl nitrate

Then sodium nitrite

65
Q

Nitroglycerin

A

Predominately venodilation with decreased myocardial wall tension from decreased preload
Moderate coronary vasodilator

66
Q

Hyrdalazine

A

a-blocker

Lower BP

67
Q

Compliance

A

Change in volume / change in pressure
High compliance means lungs are EASY to ventilate
Decreased: ARDS, fibrotic lung disease, reperfusion injury, pulmonary edema, atelactasis

68
Q

Effect of aging on the lungs?

A

Decreased FEV1
Decreased vital capacity
Increased functional residual capacity

69
Q

V/Q ratio

A

Ventilation/perfusion ratio
Highest in upper lobes
Lowest in lower lobes

70
Q

Why does increasing PEEP improve oxygenation?

A

Increased alveoli recruitment

Improves FRC

71
Q

How to you decrease CO2?

A

Increase respiratory rate

Increase tidal volume

72
Q

Normal weaning parameters?

A 
NIF > 20
FiO2 < 40%
PEEP 5
Pressure support 5
RR < 24
HR <120
PO2 > 60mmHg
PCO2 < 50mmHg
pH 7.35-7.45
Saturation >93%
Off pressors
Follows commands
Can protect airway
73
Q

Puts you at risk for barotrauma? How do you decrease the risk?

A

Plateau > 30
Peak > 50

Need to decrease TV
Consider pressure control ventilation

74
Q

Complications of excessive PEEP?

A 
Decreased RA filling
Decreased CO
Decrease renal blood flow
Decease urine output
Increase pulmonary vascular resistance
75
Q

Total lung capacity

A

Lung volume after maximal inspiration

TLC = FRC + RV

76
Q

Forced vital capacity

A

Maximal exhalation after maximal inhalation

77
Q

Residual volume

A

Lung volume after maximal expiration (20% TLC)

78
Q

Tidal volume

A

Volume of air with normal inspiration and expiration

79
Q

Functional residual capacity

A

Lung volume after normal exhalation

FRC = ERV + RV

80
Q

What can decrease functional residual capacity?

A

Surgery (atelectasis)
Sepsis (ARDS)
Trauma (contusion, atelectasis, ARDS)

81
Q

Expiratory reserve volume

A

Volume of air that can be forcefully expired after normal expiration

82
Q

Inspiratory capacity

A

Maximum air breathed in from FRC

83
Q

FEV1

A

Forced expiratory volume in 1 second after maximal inhalation

84
Q

Minute ventilation

A

MV = TV x RR

85
Q

Decreased TLC
Decreased RV
Decreased FVC

A

Restrictive lung disease

FEV1 can be normal or increased

86
Q

Increased TLC
Increased RV
Decreased FEV1

A

Obstructive lung disease

FVC can be normal or decreased

87
Q

Dead space

A 
Normally to the level of the bronchiole (150mL)
Area of lung that is ventilated but not perfused
Increases with:
- Drop in CO
- PE
- Pulmonary HTN
- ARDS
- Excssive PEEP
88
Q

COPD breathing changes

A

Increased work of breathing due to prolonged expiratory phase

89
Q

ARDS

A

Mediated by PMNs, increased proteinaceous material, increased A-a gradient, increased pulmonary shunt
Causes: Pnuemonia*, sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC

90
Q

Diagnostic criteria for ARDS

A

Acute onset
Bilateral pulmonary infiltrates
PaO2/FiO2 <300
Absence of heart failure (Wedge <18mmHg)

91
Q

Mendelson’s syndrome

A

Chemical pneumonitis from aspiration of gastric secretions

92
Q

Atelectasis

A

Collapse of alveoli resulting in reduced oxygenation
Sx: Fever, tachycardia, hypoxia
Tx: IS, pain control, ambulation

93
Q

What can make a pulse-ox inacurate?

A

Nail polish, dark skin, low-flow state, ambient light, anemia, vital dyes

94
Q

Causes pulmonary vasodilation?

A

PGE1
Prostacyclin (PGI2)
Nitric oxde
Bradykinin

95
Q

Causes pulmonary vasoconstriction?

A

HYpoxia
Acidosis
Histamine
Serotonin, TXA2

96
Q

Alkalosis - effect on pulmonary vasculature?

A

Pulmonary vasodilator

97
Q

Acidosis - effect on pulmonary vasculature?

A

Pulmonary vasoconstrictor

98
Q

Drugs that cause pulmonary shunting?

A

Nitroprusside
Nitroglycerin
Nifedipine

99
Q

Most common cause of postoperative renal failure?

A

Intra-op hypotension

100
Q

Amount of nephron that needs to be damaged before renal dysfunction?

A

70%

101
Q

FeNa

A

Fractional excretion of sodium
(Urine Na/Cr) / (plasma Na/Cr)
Best test for azotemia

102
Q 
Urine Osm >500
U/P osmolality >1.5
U/P creatinine >20
Urine sodium <20
FeNa < 1%
A

Prerenal azotemia

103
Q 
Urine Osm 250-350
U/P osmolality <1.1
U/P creatinine <10
Urine sodium >40
FeNa > 3%
A

Parenchymal azotemia

104
Q

Treatment of oliguria

A

Make sure patient is volume loaded (CVP 11-15mmHg)
Try diuretic trial (Lasix)
Dialysis if needed

105
Q

Indications for dialysis

A 
Fluid overload
Hyperkalemia
Metabolic acidosis
Uremic encephalopahty
Uremic coagulopathy
Poisoning
106
Q

Renin

A

Released in response to decreased pressure (JGA), increased Na (macula densa) concentration, beta-adrenergic stimulation and hyperkalemia

107
Q

Aldosterone

A

Acts at distal convoluted tubule to reabsorb water by up-regulating the Na/K ATPase (Na re-absorbed, K secreted)

108
Q

Effect of Angiotensin II

A 
Stimulates release of aldosterone
Vasoconstricts
Increases HR
Contractility
Glycogenolysis
Gluconeoenesis
Inhibits renin
109
Q

Atrial natriuretic peptide

A

Released from atrial wall with atrial distention
Inhibits Na and water resoprtion in the collecting ducts
Vasodilator

110
Q

Antidiuretic hormone (ADH, vasopressin)

A

Released by posterior pituitary gland when osmolality is high
Acts on collecting ducts for water resorption
Vasoconstrictor

111
Q

What controls GFR?

A

Efferent limb of the kidney

112
Q

Renal toxic drugs

A

NSAIDs (inhibit PGE - renal arteriole vasoconstriction)
Aminoglycoside (direct tubular injury)
Myoglobin (DTI)
Contrast dye (DTI)

113
Q

Causes of SIRS

A 
Shock
Infection
Burn
Multi-trauma
Pancreatitis
Severe inflammatory responses
114
Q

What is the most potent stimulus for SIRS?

A

Endotoxin (lipopolysaccharide - Lipid A)

Stimulates TNF release

115
Q

Effect of TNF-a and IL-1 release?

A

SIRs

Capillary leakage, microvascular thormbi, hypotension, eventually end-organ dysfunction

116
Q

Criteria for SIRS

A

Temp >38 or < 36
HR >90
RR >20 or PaCO2 <32
WBC >12000 or < 4000

117
Q

Diagnostic criteria: end organ dysfunction.

Pulmonary

A

Need for mechanical ventilation

PaO2:FiO2 ratio <300 for 24hrs

118
Q

Diagnostic criteria: end organ dysfunction.

Cardiovascular

A

Need for ionotropic drugs

CI <2.5 L/min/m2

119
Q

Diagnostic criteria: end organ dysfunction.

Kidney

A

Creatinine >2x baseline on 2 consecutive days

Need for dialysis

120
Q

Diagnostic criteria: end organ dysfunction.

Liver

A

Bilirubin >3mg/dL for 2 days

PT > 1.5

121
Q

Diagnostic criteria: end organ dysfunction.

Nutrition

A

10% reduction in lean body mass
albumin 2.0
Total lymphocyte count <1

122
Q

Diagnostic criteria: end organ dysfunction.

CNS

A

GCS <10 without sedation

123
Q

Diagnostic criteria: end organ dysfunction.

Coagulation

A

Platelet count < 50
Fibrinogen <100
Need for factor replacement

124
Q

Diagnostic criteria: end organ dysfunction.

Host defenses

A

WBC < 1000

Invasive infection including bacteremia

125
Q

What precludes a diagnosis of brain death?

A

Temp <32
BP <90
Drugs (i.e. phenobarbital, pentobarbital, ETOH)
Metabolic derangemetns (hyperglycemia, uremia)
Desaturation with apnea test

126
Q

What must exist for 6-12 hours to diagnose brain death?

A 
Unresponsive to pain
Absent cold caloric oculovestibular reflexes
Absent oculocephalic reflex
No spontaneous respirations
No corneal reflex
No gag reflex
Fixed and dilated pupils
Positive apnea test

Still have deep tendon relfexes with brain death

127
Q

Apnea test

A

Patient is pre-oxygenated, catheter delivering O2 at 8L/min is placed at the carina through the ET-tube and CO2 should be normal before the start of the test

  • Disconnect from vent for 10 minutes
  • CO2 > 60mmHg or increase in CO2 by 20 is POSITIVE for apena
128
Q

What is a negative result for an apnea test?

A 
BP drops (<90mmHg)
Patient desaturates (<85%)
Spontaneous breathing
129
Q

Carbon monoxide

A

Can increase O2 sats on pulse-ox
Carboxyhemoglobin - HA, nausea, confusion, coma, death (<10% in normal, <20% in smokers)
Corrects with 100% O2

130
Q

Methemoglobinemia

A

From nitrates
O2 sat reads 85%
Tx: methylene blue

131
Q

Critical illness polyneuropathy

A

Motor > sensory neuropathy
Occurs with sepsis
Causes failure to wean from ventilation

132
Q

Xanthine oxidase

A

Is in endothelial cells
Forms toxic oxygen radicals with reperfusion
Also involved in metabolism of purines to uric acid

133
Q

DKA

A

Nausea/vomiting, thirst, polyruia, increased glucose, increased ketones, decreased sodium, increased potassium
TX: normal saline and insulin

134
Q

ETOH withdrawal

A

HTN, tachycardia, delirium, seizures (After 48hrs)

Tx: Thiamine, folate, B12, Mg, K, PRN lorazepam

135
Q

ICU psychosis

A 
Third POD day - preceded by lucid interval
Address metabolic (hypoglycemia, DKA< hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes

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