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Fiser ABSITE Review + Decker + TrueLearn > Chapter 16 - Critical Care > Flashcards

Chapter 16 - Critical Care Flashcards

1
Q

How do you calculate MAP?

A

MAP = (CO x SVR) + CVP

MAP = 2/3 DBP + 1/3 SBP

Target is often 65 as anything less can eventually cause ischemia.

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2
Q

How do you calculate CI? Why is it significant?

A

CI = CO/BSA = (SVxHR)/BSA

Range 2.6-4.2

Below 2.2 may indicate cardiac shock

Index is useful because it takes an absolute number (CO) and relates it to the size of the individual. Each person should get 2.2 of cardiac output per body surface area.

Of note, weight is not used, because BSA takes height into account, limiting the contribution of adipose to the equation. This better determine perfusion needs.

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3
Q

How do you calculate SVRI?

A

SVR x BSA

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4
Q

what percentage of CO does the brain, kidney, heart get?

A

Brain 15% Kidney 25% Heart 5%

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5
Q

Preload is linearly related to what?

A

end diastolic volume and filling pressure

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6
Q

What is afterload?

A

resistance against the ventricle contracting

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7
Q

What is stroke volume determined by?

A

preload, contractility, and afterload

SV = EDV - ESV

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8
Q

How do you calculate ejection fraction?

A

stroke volume/end diastolic volume

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9
Q

What is end systolic volume determined by?

A

contractility and afterload

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10
Q

At what heart rate does CO start to decrease?

A

150 - decreased diastolic filling time

This is the point where a hypotensive patient will likely improve BP by decreasing heart rate.

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11
Q

What % of LVEDV does atrial kick account for?

A

15-30%

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12
Q

What is the Anrep effect?

A

Automatic increase in myocardial contractility (inotropy) secondary to increased afterload.

This allows the heart to compensate for vascular resistance, otherwise output would decrease proportionally to increased resistance.

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13
Q

What is the Bowditch effect?

A

Automatic increase in contractility secondary to heart rate increase.

Increasing heart rate does not allow the Na/Ca exchange to efficiently eliminate intracellular Ca. The resulting Ca buildup leads to increased inotropism.

The Bowditch is an effect of the healthy heart. It does not occur in the failing heart - an engine out of fuel. The clinical result is that beta-blockers improve survival in heart failure.

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14
Q

What is the radial diastolic and systolic pressure in relationship to aortic mean pressures?

A

diastolic slightly lower, systolic slightly higher

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15
Q

How do you calculate O2 consumption (VO2)

A

VO2 = (CO x CaO2) - (CO x CvO2) = CO x (CaO2 - CvO2)

  • CaO2 - concentration of arterial O2 measured at pulm vein
  • CvO2 - concentration of venous O2 measured at pulm artery
  • (CaO2 - CvO2) is known as AV O2 difference
  • VO2 can actually be measured allowing CO to be calculated
    • CO = VO2/(CaO2 - CvO2)
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16
Q

What is the normal O2 delivery to consumption ratio?

A

5:1

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17
Q

Is O2 consumption supply dependent?

A

No, does not change until levels of delivery are very low

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18
Q

What causes a right shift in the O2 dissociation curve?

A

Increased CO2, increased temperature, increased ATP production, increased 2,3-DPG production, increased H+ (decreased pH).

The curve describes the relationship between the partial pressure of oxygen (x) and oxygen saturation (y). Increases in these states causes an offloading effect where at lower PO2, the O2 will be less saturated. For temp, acid, this is because of denaturing. Initially more O2 binding increases affinity, increasing O2 sat. Above PO2 60, the effect dampens, and increasing PO2 has a more minimal effect on O2 sat (PO2 60 correlates w/ O2 sat 90%). O2 delivery then relies on Hgb, meaning more transfusions would be needed.

This produces two points in critical states (increased ATP, temperature, acidosis, CO2): Hgb will offload more O2 b/c tissues need more energy, and a higher PO2 is required for a greater O2 sat - eg PO2 80 for O2 sat of 90%.

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19
Q

What is the normal p50 (PO2 at which 50% of O2 receptors are saturated)?

A

27mmhg

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20
Q

When does SvO2 go up?

A

Shunting or decreased extraction (L shift), ie increased O2 delivery, or decreased demand.

SVO2 is mixed venous blood measured from pulmonary artery - ie the end result of O2 consumption.

Shunt - perfusion w/o ventilation; ie V/Q ratio approaches 0. This can occur when alveoli fills with fluid, preventing ventilation though perfusion continues. Sepsis can cause shunting at a microvascular level such that SvO2 would be high but there is evidence of end organ ischemia.

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21
Q

When does SvO2 go down?

A

increased extraction, decreased delivery

  • decreased Hb
  • decreased SaO2 - hypoxemia
  • decreased Q (shock, arrhythmia)
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22
Q

What can make wedge pressures inaccurate?

A

pulmonary htn, aortic regurg, mitral stenosis/regurg, high peep, poor LV compliance

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23
Q

Where should a swan-ganz catheter be placed?

A

zone III (lower) lung

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24
Q

What do you do with hemoptysis after flushing a swan-ganz catheter?

A

Stop the bleeding: pressure then OR

  • Increase PEEP which will tamponade the pulmonary arter bleed
  • Mainstem intubate non-affected side
  • Can try to place fogarty balloon down the affected side
  • May need thoracotomy and lobectomy
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25
Q

What are contraindications to swan?

A

previous pneumonectomy, left bundle branch block

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26
Q

What is the only way to measure pulmonary vascular resistance?

A

swan

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27
Q

What are the primary determinants of myocardial O2 consumption?

A

ventricular wall tension and HR

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28
Q

what has a higher PO2- pulmonary capillaries or LV?

A

pulmonary capillaries- LV gets unsaturated bronchial blood

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29
Q

what is the normal aa gradient?

A

10-15 mmhg

This is used to delineate the cause of low PaO2. Eg in high altitude areas, the lung and its exchange are normal, but the PAO2 is low. The gradient is normal, but the PaO2 is also low.

Diffusion defects dec PaO2

RL shunting inc PaO2

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30
Q

What blood has the lowest venous saturation?

A

coronary venous (30%)

The heart tissue can pull a lot more O2 than the rest of the body.

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31
Q

What are the signs of acute adrenal insufficiency?

A

cardiovascular collapse unresponsive to fluids and pressors

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32
Q

signs of chronic adrenal insufficiency?

A

hyperpigmentation, weakness, weight loss, GI sx

decreased K, increased Na, fever, hypotension

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33
Q

what steroids are at 1x potency of endogenous?

A

cortisone, hydrocortisone

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34
Q

What steroids are at 5x potency of endogenous?

A

prednisone prednisolone methylprednisolone

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35
Q

What steroids are at 30x strength of endogenous steroids?

A

dexamethasone

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36
Q

What is the pathogenesis and what are the signs/symptoms associated with neurogenic shock?

A

loss of sympathetic tone, decreased HR, decreased BP, warm skin

tx: volume then phenylephrine vs levophed; midodrine can be used out of acute phase

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37
Q

what is the initial alteration in hemorrhagic shock?

A

increased diastolic pressure, then tachycardia, then hypotension

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38
Q

what is beck’s triad?

A

hypotension, jugular venous distention, muffled heart sounds

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39
Q

what does echo show in tamponade?

A
  • decreased RA filling pressures
  • possible pericardial effusion
  • subsequently decreased LVEF
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40
Q

What is the early sepsis triad?

A

hyperventilation, confusion, respiratory alkalosis

41
Q

what glucose derangement do you get in early gram negative sepsis?

A

decreased insulin, increased glucose (impaired utilization)

42
Q

What glucose derangements do you get in late gram negative sepsis?

A

increased insulin, increased glucose (secondary to insulin resistance)

43
Q

What are the signs of fat emboli? where do they usually come from?

A
  • petechia, hypoxia, confusion
  • sudan red may show fat in sputum and urine
  • lower extremity fx
44
Q

What will echo show in pulmonary thromboemboli?

A

RV strain

45
Q

When do you suspect PE?

A
  • SX: chest pain, cough, dyspnea; postop, non-amb
  • VS: tachycardia, tachypnea, decreased BP if massive PE
  • PE: single swollen leg
  • ABG: decreased PO2 and PCO2, respiratory alkalosis
  • CXR: clear if nothing else going on
  • Underlying physiology: PA systolic >40
46
Q

Air Emboli - what do you do?

A
  • place pt. head down and roll to left
  • may need to secure airway
  • usually resolves w/ positioning and hi-flow O2
  • if unstable/neuro sx - tx is hyperbaric O2
  • aspirate air out w/ central line/PA catheter to RA/RV
47
Q

When does an intra-aortic balloon pump inflate, deflate?

A

Inflates on T-wave (diastole); deflates on P-wave or start of q wave (systole)

48
Q

What is a contraindication for an IABP?

A

Aortic regurgitation

49
Q

When is an IABP placed?

A

Cardiogenic shock after CABG, MI or in patients with refractory angina. Decreases afterload. Improves systolic blood pressure which improves coronary perfusion

50
Q

Where are alpha-1 receptors

A

Vascular smooth muscle constriction; gluconeogenesis, glycogenolysis

51
Q

What do alpha-2 receptors do?

A
  • Venous smooth muscle constriction
  • Inhibits release of NE and EPI
52
Q

What do beta-1 receptors do?

A

Increase myocardial contraction and rate

53
Q

What do beta-2 receptors do?

A

Relaxes bronchial smooth muscle, relaxes vascular smooth muscle, increases insulin, glucagon, rennin

54
Q

What do dopamine receptors do?

A

Relax renal and splanchnic smooth muscle

55
Q

What is the rate of low dopamine administration and what does it affect?

A

05 µg per kilogram per minute acts on dopamine receptors -renal

56
Q

What is the medium dose for dopamine drip and what does it affect?

A

6 to 10 µg per kilogram per minute-beta-adrenergic acts on heart contractility

57
Q

What is the dose for high-dose dopamine and what does it affect?

A

Greater than 10 µg per kilogram per minute acts on alpha-adrenergic receptors causes vasoconstriction and increased blood pressure

58
Q

What is the initial drip rates for dobutamine and what does it do?

A
  • 3 µg per kilogram per minute initially
  • 5 to 10 µg/kg/min - beta-1 activation increasing contractility
  • >15 µg/kg/min - alpha adrenergic activation
  • vasodilation and increased heart rate
59
Q

What does milrinone do?

A

Phosphodiesterase inhibitor increases cAMP Results in increased calcium influx and increased myocardial contractility Also causes vascular smooth muscle relaxation and vasodilation

60
Q

What does phenylephrine do?

A

Acts on alpha-1 receptors causes vasoconstriction

61
Q

What does norepinephrine do?

A

Low-dose causes beta-1 activation increasing contractility High-dose causes alpha-1 and alpha-2 activation Potent splanchnic vasoconstrictor

62
Q

What does epinephrine do?

A

Low-dose causes beta-1 and beta-2 activation causing increased contractility and vasodilation. Can decrease blood pressure at low doses High-dose causes activation of alpha-1 and alpha-2 causing vasoconstriction. Increased cardiac ectopic pacer activity and myocardial O2 demand

63
Q

What does isoproterenol do?

A

Beta-1 and beta-2 activation, increases heart rate and contractility, vasodilates. Side effects are extremely arrhythmogenic, increased heart metabolic demand, may actually lower blood pressure

64
Q

What does vasopressin do?

A

V1 receptors cause vasoconstriction of vascular smooth muscle V2 receptors are intrarenal and cause water reabsorption at collecting ducts V2 receptors are extrarenal and mediate release of factor VIII and von Willebrand factor

65
Q

What does nipride to do?

A

Arterial and venous dilator. Can cause cyanide toxicity. Check thiocyanate levels

66
Q

What does nitroglycerin do?

A

Predominantly veno dilation, modest effect on coronaries; decreased myocardial wall tension by decreasing preload

67
Q

What does hydralazine do?

A

Alpha blocker

68
Q

How do you measure lung compliance?

A

Change in volume divided by change in pressure. High compliance means lungs easy to ventilate. Pulmonary compliance decreases in patients with ARDS, fibrotic lung disease, reperfusion injury, pulmonary edema.

69
Q

What does aging do to lungs?

A

Decreases FEV1 and vital capacity, increases functional residual capacity

70
Q

Where is the V/Q ratio highest?

A

Highest in upper lobes, lowest in lower lobes

71
Q

What does increasing peep do?

A

Improves oxygenation through alveoli recruitment. Improves FRC.

72
Q

How do you decrease CO2 on a ventilator?

A

Increase rate or volume

73
Q

What does pressure support do?

A

Decreases the work of breathing

74
Q

Why do you want to keep FI O2 below 60%?

A

Prevent 02 radical toxicity

75
Q

When do you have a risk of barotrauma?

A

Plateaus greater than 30 and peaks greater than 50

76
Q

What are the complications of hi Peep?

A

Decreased right atrial filling Decreased cardiac output Decreased renal bloodflow Decreased urine output Increased pulmonary vascular resistance

77
Q

When do you use high-frequency ventilation?

A

Kids; tracheoesophageal fistula, bronchopleural fistula

78
Q

What does inverse ratio ventilation do?

A

Helps reduce barotrauma

79
Q

What is total lung capacity?

A

Lung volume after maximal inspiration. TLC equals FVC plus RV

80
Q

What is forced vital capacity

A

Maximal exhalation after maximal inhalation

81
Q

What is residual volume

A

Lung volume after maximal expiration

82
Q

What is tidal volume?

A

Volume of air with normal inspiration and expiration

83
Q

What is functional residual capacity?

A

Long volume after normal exhalation. FRC equals ERV plus RV Surgery, sepsis, trauma all decrease FTC

84
Q

What is expiratory reserve volume?

A

volume of air that can be forcefully expired after normal expiration

85
Q

What is inspiratory capacity

A

maximum air breathed in from FRC

86
Q

What is FEV1?

A

forced expiratory volume in 1 second after maximal inhalation

87
Q

What is minute ventilation?

A

TV x RR

88
Q

What does restrictive lung disease do to lung function tests?

A

decreased TLC decreased RV Decreased FVC FEV1 can be normal or increased

89
Q

What does obstructive lung disease do to lung function tests?

A

increased TLC increased RV decreased FEV1 FVC can be normal or decreased

90
Q

What is dead space?

A

normally to the level of the bronciole (150mL) increases 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

91
Q

What does COPD do to lung function?

A

increases work of breathing because of prolonged expiratory phase work of breathing normally 2% of total body VO2

92
Q

what is ARDS and what does it do to lungs?

A

mediated by cellular inflammatory process increased proteinaceous material increased gradient increased shunt most common in sepsis

93
Q

Diagnosis of Acute lung injury?

A

acute onset bilateral pulmonary infiltrates paO2/FiO2 = 18 or no clinical evidence of LAH

94
Q

Diagnosis of ARDS

A

acute onset bilateral pulmonary infiltrates PaO2/FiO2 <200

95
Q

What is SIRS mediated by? Criteria?

A

TNF alpha and IL-1 temp >38 or 12 or 90

96
Q

Most potent stimulus for SIRS?

A

lipopolysacharide (Lipid A)

97
Q

Diagnosis of Sepsis?

A

SIRS with clinical evidence of infection sepsis with organ disfunction

98
Q

Septic shock?

A

Sepsis and arterial hypotension despite adequate volume resuscitation

99
Q

Muti organ dysfunction?

A

progressive but reversible dysfunction of 2 or more organs

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