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ABSITE > Fiser Chapter 16 CRITICAL CARE > Flashcards

Fiser Chapter 16 CRITICAL CARE Flashcards

1
Q

Normal CO

A

4-8 L/min

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2
Q

Normal CI

A

2.5-4 L/min/m^2

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3
Q

Normal SVR

A

800-1400

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4
Q

Normal PCWP

A

11 +/- 4 (7-15)

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5
Q

Normal CVP

A

7 +/- 2

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6
Q

Normal PAP

A

25/10

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7
Q

Normal SvO2 (mixed venous O2 sat)

A

75

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8
Q

MAP equation

A

MAP = CO x SVR

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9
Q

CI equation

A

CI = CO/BSA

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10
Q

Blood flow to organs

A

25% kidney
15% brain
5% heart

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11
Q

EF equation

A

SV/LVEDV

(LVEDV-LVESV)/LVEDV

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12
Q

Anrep effect

A

automatic increase in contractility 2/2 increased afterload

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13
Q

Bowditch effect

A

automatic increase in contractility 2/2 increased HR

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14
Q

CaO2 (arterial O2 content) equation

A

CaO2 = Hgb x 1.34 x O2 sat + (pO2 x 0.003)

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15
Q

O2 delivery equation

A

CO x CaO2 x 10

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16
Q

VO2 (O2 consumption) equation

A

VO2 = CO x (CaO2 - CvO2)

Normal O2 delivery-to-consumption ration 5:1
CO increases to keep this constant

O2 consumption is usually supply independent

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17
Q

Right shift O2-Hgb dissociation curve causes (increased O2 unloading)

A

CADET

Increased CO2, ATP production, acidosis, 2,3-DPG production, elevation, temperature

Normal p50 (O2 at which 50% of O2 receptors saturated) = 27 mm Hg

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18
Q

Causes of increased SvO2 (saturation of venous blood)

A

Normally 75%
Increased in shunt or decreased O2 extraction (sepsis, cirrhosis, CN tox, hyperbaric O2, hypothermia, paralysis, coma, sedation)

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19
Q

Causes of decreased SvO2 (saturation of venous blood)

A

Normally 75%

Decreased in increased O2 extraction or decreased O2 delivery (decreased O2 sat, decreasedCO, malignant hyperthermia)

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20
Q

Wedge may be thrown off by

A 
Pulm HTN
Aortic regurgitation
Mitral stenosis
Mitral regurgitation
High PEEP
Poor LV compliance
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21
Q

Swan-Ganz cath placement

A

Zone III (lower lung)
R SCV 45 cm L SCV 55 cm
R IJ 50 cm L IJ 60 cm

PVR can be measured only with Swan-Ganz (not Echo)

Wedge pressure should be measured at end-expiration

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22
Q

What do you do if there is hemoptysis after flushing Swan-Ganz cath?

A

Increase PEEP to tamponade pulmonary artery bleed
Mainstem intubate non-affected side
Fogarty balloon down mainstem on affected side
May need thoracotomy and lobectomy

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23
Q

What are the relative contraindications to Swan-Ganz cath?

A

Previous pneumonectomy

Left bundle branch block

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24
Q

Primary determinants of myocardial O2 consumption

A

Ventricular wall tension and HR

Increase can lead to MI

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25
Q

Normal alveolar-arterial gradient

A

10-15 mm Hg in normal nonventilated patient

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26
Q

What blood has the lowest venous saturation?

A

Coronary sinus blood (30%)

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27
Q

Shock definition

A

Inadequate tissue oxygenation

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28
Q

Adrenal insufficiency MCC

A

Withdrawal of exogenous steroids

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29
Q

Adrenal insufficiency manifestations

A

CV collapse, unresponsive to fluids and pressors
nausea, emesis, abdominal pain, fever, lethargy, decreased glucose, hyperkalemia

Tx: dexamethasone

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30
Q

Steroid potency

A

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

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31
Q

Neurogenic shock symptoms and treatment

A

Loss of sympathetic tone
Spine or head injury
Decreased HR, BP, warm skin

Tx: Give volume first, then phenylephrine

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32
Q

Hemorrhagic shock initial alteration

A

Increased diastolic pressure

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33
Q

Cardiac tamponade mechanism of hypotension

A

Decreased ventricular filling

Echo: impaired diastolic filling of RA

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34
Q

Beck’s triad

A

Hypotension, JVD, muffled heart sounds

Cardiac tamponade

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35
Q

Cardiac tamponade tx

A

Fluid resuscitation

Pericardial window or pericardiocentesis

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36
Q

Early sepsis triad

A

Hyperventilation
Confusion
Hypotension

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37
Q

Blood glucose in sepsis

A

Hyperglycemia often occurs just before clinically septic

Early GN sepsis: increased glucose, decreased insulin (impaired utilization)

Late GN sepsis: increased glucose and insulin (insulin resistence)

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38
Q

Hypovolemia neurohormonal response

A

Rapid: adrenergic release -> vasoconstriction and increased cardiac activity

Sustained: RAS -> renin from kidney -> vasoconstriction and water resorption; ADH from pituitary -> water reabroprtion; ACTH from pituitary -> cortisol

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39
Q

Sudan red stain

A

May show fat in sputum and urine in fat embolism

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40
Q

Where do most PEs arise from?

A

Iliofemoral region

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41
Q

If PE patient is in shock despite massive pressors and inotropes?

A

After heparin and Coumadin, consider open or percutaneous (suction catheter) embolectomy

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42
Q

Air emboli tx

A

Trendelenburg, role to left (keeps air in RV and RA), then aspirate air out with central line or PA catheter to RA/RV

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43
Q

IABP mechanism

A
  • Inflates on T wave (diastole): improves diastolic BP, improves diastolic coronary perfusion
  • Deflates on P wave (systole): decreases afterload
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44
Q

IABP contraindication

A

Aortic regurgitation

45
Q

IABP catheter location

A

Just distal to L subclavian (1-2 cm below top of arch)

46
Q

IABP uses

A

Cardiogenic shock after CABG or MI

Refractory angina awaiting revasc

47
Q

Alpha-1 receptor

A

Vascular smooth muscle constriction

Gluconeogenesis and glycogenolysis

48
Q

Alpha-2 receptor

A

Venous smooth muscle constriction

49
Q

Beta-1 receptor

A

Myocardial contraction and rate

50
Q

Beta-2 receptor

A
  • Relaxes bronchial smooth muscle
  • Relaxes vascular smooth muscle
  • Increases insulin, glucagon, and renin
51
Q

Dopamine receptors

A

Relax renal and splanchnic smooth muscle

52
Q

Dobutamine MoA

A

Beta-1: increases contractility mostly; tachycardia with higher doses

53
Q

Milrinone MoA

A

Phosphodiesterase inhibitor: increases cAMP -> increased Ca flux and myocardial contractility; also vascular smooth muscle relaxation and pulmonary vasodilation

54
Q

Phenylephrine MoA

A

Alpha-1 vasoconstriction

55
Q

Norepinephrine MoA

A

Low dose: beta-1 increased contractility

High dose alpha-1 and alpha-2

Potent splanchnic vasoconstrictor

56
Q

Epinephrine MoA

A

Low dose beta-1 and beta-2 increased contractility and vasodilation, but can decrease BP

High dose alpha-1 and alpha-2 vasoconstriction; increased cardiac ectopic pacer activity and myocardial O2 demand

57
Q

Isoproterenol MoA

A

Beta-1 and beta-2 increased HR and contractility, vasodilation

SE: Very arrhythmogenic; increases heart metabolic demand, may actually decrease BP

58
Q

Vasopressin MoA

A

V1- receptor vasoconstriction of vascular smooth muscle

V-2 receptor intrarenal water reabsorption at collecting ducts; extrarenal mediates factor VIII and vWF release

59
Q

Nipride MoA

A

arterial vasodilator

CN toxicity; can check thiocyanate levels and metabolic acidosis

60
Q

CN toxicity treatment

A

Amyl nitrite, then sodium nitrite

61
Q

Nitroglycerin MoA

A

Venodilation with decreased myocardial wall tension by decreasing preload; moderate coronary vasodilator

62
Q

Hydralazine MoA

A

alpha-blocker, lowers BP

63
Q

Dopamine MoA

A 
Dopamine receptors (renal)
Higher dose beta-adrenergic (heart contractility)
Higher dose alpha-adrenergice (vasoconstriction and increase BP)
64
Q

Lung compliance

A

Change in volume/
Change in pressure

decreased in ARDS, fibrosis, reperfusion injury, edema, atelectasis

65
Q

PEEP

A

Alveoli recruitment -> improves FRC and compliance -> best way to improves oxygenation

66
Q

Pressure support

A

Decreases work of breathing

67
Q

Prevent O2 radical toxicity by what

A

Keep FiO2 = 60%

68
Q

When do you get barotrauma?

A

Plateaus > 30, peaks >50

So decrease Tv and consider pressure control ventilation

69
Q

Excessive PEEP complications

A
  • Decreased RA filling
  • Decreased CO
  • Decreased renal blood flow
  • Decreased urine output
  • Increased pulmonary vascular resistance
70
Q

High frequency ventilation use

A

Kids
TE fistula
Bronchopleural fistula

71
Q

TLC

A

TLC = FVC + RV

72
Q

FRC

A

FRC = ERV + RV

Lung volume after normal exhalation

  • Decreased by atelectasis, ARDS, contusion/trauma
  • Improved with PEEP
73
Q

Dead space

A

Area of lung ventilated but not perfused; normally to level of bronchiole (150 mL)

Increases with: Drop in CO, PE, pulm HTN, ARDS, excessive PEEP; can lead to hypercapnia

74
Q

ARDS MoA

A

Neutrophils; increased proteinaceous material; increased A-a gradient; increased pulmonary shunt

MCC pneumonia
Other: sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC

75
Q

ARDS criteria

A

Acute onset
Bilateral pulmonary infiltrates
PaO2/FiO2 = 300
Absence of heart failure (wedge < 18 mm Hg)

76
Q

Aspiration, increased damage associated with what

A

pH < 2.5, volume > 0.4 cc/kg

77
Q

Mendelson’s syndrome

A

chemical pneumonitis from aspiration of gastric secretions

78
Q

Most frequent site of aspiration

A

superior segment of RLL

79
Q

Fever, tachycardia, hypoxia in first 48hr postop

A

Atelectasis: collapse of alveoli resulting in reduced oxygenation

Increased in patients with COPD, upper abdominal surgery, obesity

Tx: IS, pain control, ambulation

80
Q

What can throw off a pulse oximeter

A 
Nail polish
Dark skin
Low-flow states
Ambient light
Anemia
Vital dyes
81
Q

Causes of pulmonary vasodilation?

A 
PGE1
Prostacyclin (PGI2)
Nitric oxide
Bradykinin
Alkalosis
82
Q

Causes of pulmonary vasoconstriction?

A 
Hypoxia
Acidosis
Histamine
Serotonin
TXA2
83
Q

Causes of pulmonary shunting

A

Nitroprusside
Nitroglycerin
Nifedipine

84
Q

MCC of postop renal failure

A

Intra-op hypotension

70% nephrons need to be damaged

85
Q

FeNa

A

(urine Na/Cr) / (plasma Na/Cr)

Best test for azotemia

FeNa <1% in prerenal
FeNa >3% in parenchymal

86
Q

Urine measurements in prerenal failure

A 
Urine osmolarity >500
U/P osmolality >1.5
U/P creatinine >20
Urine sodium < 20
FeNa < 1%
87
Q

Urine measurements in parenchymal failure

A 
Urine osmolarity 250-350
U/P osmolality < 1.1
U/P creatinine < 10
Urine sodium > 40
FeNa > 3%
88
Q

Oliguria tx

A
  1. Volume load (CVP 11-15)
  2. Diuresis trial
  3. HD
89
Q

Dialysis indications

A 
AEIOU:
Acidosis
Electrolytes (hyperkalemia)
Ingestion (poisons)
Overload
Uremia (encephalopathy, coagulopathy)
90
Q

CVVH compared to HD

A

Slower
Good for ill patients who cannot tolerate large colume shifts (septic shock)
Hct increases by 5-8 for each liter taken off

91
Q

RAAS

A
  1. hypotension, hypernatremia (sensed by macula densa), beta-adrenergic stiulation, or hyperkalemia -> JG apparatus releases renin
  2. Renin converts Angiotensinogen (synthesized in liver) to ATI
  3. ACE (from lung) converts ATI to ATII
  4. ATII vasoconstricts and increases HR, contractility, glycogenolysis, gluconeogenesis; inhibits renin release
  5. ATII also causes aldosterone release from adrenal cortex -> DCT -> upregulating NaK ATPase on membrane -> water reabsorbtion, Na re-absorbed, K secreted
92
Q

ANP

A

Atrial distention -> ANP release from atrial wall -> inhibits Na and water resorption in collecting ducts; also vasodilation

93
Q

ADH

A

High osmolality -> posterior pituitary releases ADH -> water resorption in collecting ducts; also vasoconstrictor

94
Q

Efferent limb of kidney

A

Controls GFR

95
Q

DCT

A

where ATII acts to upregulate NaK ATPase and cause Na, water reabsorbtion and K secretion

96
Q

Renal toxic drugs

A

NSAID: inhibits prostaglandin synthesis, causing renal arteriole vasoconstriction

Aminoglycosides: direct tubular injury

Myoglobin: direct tubular injury (Tx: alkalinize urine)

Contrast dyes: direct tubular injury (Tx: pre-hydration best; HCO3-, NAC)

97
Q

SIRS most potent stimulus

A

Endotoxin (lipopolysaccharide - lipid A)
Major components: TNF-alpha and IL-1
Results in capillary leakage, microvascular thrombi, hypotension, end-organ dysfunction

98
Q

SIRS definition

A

Temp > 38 or <36
HR > 90
RR > 20 or PaCO2 < 32
WBC >12 or <4

99
Q

Shock definition

A

Arterial hypotension despite adequate volume resuscitation

Inadequate tissue oxygenation

100
Q

Multi organ dysfunction definition

A

Progressive but reversible dysfunction of 2 or more organs arising from an acute disruption of normal homeostasis

101
Q

Brain death preclusions

A 
Temp <32
BP <90
Drugs (phenobarb, pentobarb, EtOH)
Metabolic derangements (hyperglycemia, uremia)
Desaturation with apnea test
102
Q

Brain death definition

A

6-12 hours of:

  • Unresponsive to pain
  • Absent cold caloric oculovestibular reflexes
  • Absent oculocephalic reflex (patient doesn’t track)
  • No spontaneous respirations
  • No corneal reflex
  • No gag reflex
  • Fixed and dilated pupils
  • Positive apnea test

*Can still have deep tendon reflexes with brain death

103
Q

Brain death on EEG or MRA

A

EEG: Electrical silence
MRA: No blood flow to brain

104
Q

Apnea test

A

Pre-oxygenation, and CO2 should be normal prior
Catheter delivering O2 at 8L/min is placed at carina through ETT-Disconnect from vent for 10 minutes

Positive test meets brain death criteria: CO2 >60 or increase in CO2 by 20

Negative test and cannot declare brain death, so put back on vent: If BP drops <90, desaturates <85%, or spontaneous breathing occurs

105
Q

Carbon monoxide poisoning

A
  • Falsely normal oxygen saturation on pulse ox
  • Binds Hgb directly, creates carboxyhemoglobin
  • HA, nausea, confusion, coma, death
  • Can usually correct with 100% oxygen on vent
  • Abnormal carboxyhemoglobin >10% (smokers >20%)
106
Q

Methemoglobinemia

A
  • From nitrites such as Hurricaine spray
  • Nitrites bind Hgb
  • O2 sat reads 85%
  • Tx: Methylene blue
107
Q

Critical illness polyneuropathy

A

Motor > sensory neuropathy
Occurs with sepsis
Can lead to failure to wean from vent

108
Q

Reperfusion injury

A

Xanthine oxidase: In endothelial cells, forms toxic oxygen radicals with reperfusion

XO also involved in the metabolism of purines and breakdown to uric acid

Most important mediator of reperfusion injury is PMNs

109
Q

EtOH withdrawal

A

HTN, tachy, delirium, seizures after 48hr

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

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