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Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, 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
What are contraindications to swan?
previous pneumonectomy, left bundle branch block
26
What is the only way to measure pulmonary vascular resistance?
swan
27
What are the primary determinants of myocardial O2 consumption?
ventricular wall tension and HR
28
what has a higher PO2- pulmonary capillaries or LV?
pulmonary capillaries- LV gets unsaturated bronchial blood
29
what is the normal aa gradient?
10-15 mmhg ## Footnote 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
30
What blood has the lowest venous saturation?
coronary venous (30%) The heart tissue can pull a lot more O2 than the rest of the body.
31
What are the signs of acute adrenal insufficiency?
cardiovascular collapse unresponsive to fluids and pressors
32
signs of chronic adrenal insufficiency?
hyperpigmentation, weakness, weight loss, GI sx decreased K, increased Na, fever, hypotension
33
what steroids are at 1x potency of endogenous?
cortisone, hydrocortisone
34
What steroids are at 5x potency of endogenous?
prednisone prednisolone methylprednisolone
35
What steroids are at 30x strength of endogenous steroids?
dexamethasone
36
What is the pathogenesis and what are the signs/symptoms associated with neurogenic shock?
loss of sympathetic tone, decreased HR, decreased BP, warm skin tx: volume then phenylephrine vs levophed; midodrine can be used out of acute phase
37
what is the initial alteration in hemorrhagic shock?
increased diastolic pressure, then tachycardia, then hypotension
38
what is beck's triad?
hypotension, jugular venous distention, muffled heart sounds
39
what does echo show in tamponade?
* decreased RA filling pressures * possible pericardial effusion * subsequently decreased LVEF
40
What is the early sepsis triad?
hyperventilation, confusion, respiratory alkalosis
41
what glucose derangement do you get in early gram negative sepsis?
decreased insulin, increased glucose (impaired utilization)
42
What glucose derangements do you get in late gram negative sepsis?
increased insulin, increased glucose (secondary to insulin resistance)
43
What are the signs of fat emboli? where do they usually come from?
* petechia, hypoxia, confusion * sudan red may show fat in sputum and urine * lower extremity fx
44
What will echo show in pulmonary thromboemboli?
RV strain
45
When do you suspect PE?
* 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
Air Emboli - what do you do?
* 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
When does an intra-aortic balloon pump inflate, deflate?
Inflates on T-wave (diastole); deflates on P-wave or start of q wave (systole)
48
What is a contraindication for an IABP?
Aortic regurgitation
49
When is an IABP placed?
Cardiogenic shock after CABG, MI or in patients with refractory angina. Decreases afterload. Improves systolic blood pressure which improves coronary perfusion
50
Where are alpha-1 receptors
Vascular smooth muscle constriction; gluconeogenesis, glycogenolysis
51
What do alpha-2 receptors do?
* Venous smooth muscle constriction * Inhibits release of NE and EPI
52
What do beta-1 receptors do?
Increase myocardial contraction and rate
53
What do beta-2 receptors do?
Relaxes bronchial smooth muscle, relaxes vascular smooth muscle, increases insulin, glucagon, rennin
54
What do dopamine receptors do?
Relax renal and splanchnic smooth muscle
55
What is the rate of low dopamine administration and what does it affect?
05 µg per kilogram per minute acts on dopamine receptors -renal
56
What is the medium dose for dopamine drip and what does it affect?
6 to 10 µg per kilogram per minute-beta-adrenergic acts on heart contractility
57
What is the dose for high-dose dopamine and what does it affect?
Greater than 10 µg per kilogram per minute acts on alpha-adrenergic receptors causes vasoconstriction and increased blood pressure
58
What is the initial drip rates for dobutamine and what does it do?
* 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
What does milrinone do?
Phosphodiesterase inhibitor increases cAMP Results in increased calcium influx and increased myocardial contractility Also causes vascular smooth muscle relaxation and vasodilation
60
What does phenylephrine do?
Acts on alpha-1 receptors causes vasoconstriction
61
What does norepinephrine do?
Low-dose causes beta-1 activation increasing contractility High-dose causes alpha-1 and alpha-2 activation Potent splanchnic vasoconstrictor
62
What does epinephrine do?
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
What does isoproterenol do?
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
What does vasopressin do?
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
What does nipride to do?
Arterial and venous dilator. Can cause cyanide toxicity. Check thiocyanate levels
66
What does nitroglycerin do?
Predominantly veno dilation, modest effect on coronaries; decreased myocardial wall tension by decreasing preload
67
What does hydralazine do?
Alpha blocker
68
How do you measure lung compliance?
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
What does aging do to lungs?
Decreases FEV1 and vital capacity, increases functional residual capacity
70
Where is the V/Q ratio highest?
Highest in upper lobes, lowest in lower lobes
71
What does increasing peep do?
Improves oxygenation through alveoli recruitment. Improves FRC.
72
How do you decrease CO2 on a ventilator?
Increase rate or volume
73
What does pressure support do?
Decreases the work of breathing
74
Why do you want to keep FI O2 below 60%?
Prevent 02 radical toxicity
75
When do you have a risk of barotrauma?
Plateaus greater than 30 and peaks greater than 50
76
What are the complications of hi Peep?
Decreased right atrial filling Decreased cardiac output Decreased renal bloodflow Decreased urine output Increased pulmonary vascular resistance
77
When do you use high-frequency ventilation?
Kids; tracheoesophageal fistula, bronchopleural fistula
78
What does inverse ratio ventilation do?
Helps reduce barotrauma
79
What is total lung capacity?
Lung volume after maximal inspiration. TLC equals FVC plus RV
80
What is forced vital capacity
Maximal exhalation after maximal inhalation
81
What is residual volume
Lung volume after maximal expiration
82
What is tidal volume?
Volume of air with normal inspiration and expiration
83
What is functional residual capacity?
Long volume after normal exhalation. FRC equals ERV plus RV Surgery, sepsis, trauma all decrease FTC
84
What is expiratory reserve volume?
volume of air that can be forcefully expired after normal expiration
85
What is inspiratory capacity
maximum air breathed in from FRC
86
What is FEV1?
forced expiratory volume in 1 second after maximal inhalation
87
What is minute ventilation?
TV x RR
88
What does restrictive lung disease do to lung function tests?
decreased TLC decreased RV Decreased FVC FEV1 can be normal or increased
89
What does obstructive lung disease do to lung function tests?
increased TLC increased RV decreased FEV1 FVC can be normal or decreased
90
What is dead space?
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
What does COPD do to lung function?
increases work of breathing because of prolonged expiratory phase work of breathing normally 2% of total body VO2
92
what is ARDS and what does it do to lungs?
mediated by cellular inflammatory process increased proteinaceous material increased gradient increased shunt most common in sepsis
93
Diagnosis of Acute lung injury?
acute onset bilateral pulmonary infiltrates paO2/FiO2 = 18 or no clinical evidence of LAH
94
Diagnosis of ARDS
acute onset bilateral pulmonary infiltrates PaO2/FiO2 \<200
95
What is SIRS mediated by? Criteria?
TNF alpha and IL-1 temp \>38 or 12 or 90
96
Most potent stimulus for SIRS?
lipopolysacharide (Lipid A)
97
Diagnosis of Sepsis?
SIRS with clinical evidence of infection sepsis with organ disfunction
98
Septic shock?
Sepsis and arterial hypotension despite adequate volume resuscitation
99
Muti organ dysfunction?
progressive but reversible dysfunction of 2 or more organs

Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn (50 decks)

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