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Z.Fiser > Fiser.16.CCM > Flashcards

Fiser.16.CCM Flashcards

1
Q

What is a normal cardiac output in L/min?

A

4-8 LPM

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2
Q

What is a normal cardiac index in L/min?

A

2.5-4 L/min

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3
Q

What is a normal systemic vascular resistance (SVR)?

A

800-1400

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4
Q

What is a normal PCWP?

A

11 +/- 4

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5
Q

What is a normal CVP?

A

7 +/- 2

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6
Q

What is a normal pulmonary artery pressure (PAP)?

A

25/10 +/- 5

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7
Q

What is a normal mixed venous O2 sat (SvO2)?

A

75 +/- 5

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8
Q

What is the equation for MAP?

A

MAP = CO x SVR

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9
Q

What is the equation for CI?

A

CI = CO / BSA

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10
Q

What percent of cardiac output goes to the kidney?

A

25%

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11
Q

What percent of cardiac output goes to the brain?

A

15%

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12
Q

What percent of cardiac output goes to the heart?

A

5%

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13
Q

How do you define preload according to the left ventricle?

A

Preload = left ventricular end-diastolic length

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14
Q

What two variables is preload linearly related to?

A

Left ventricular end-diastolic volume and filling pressure

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15
Q

How does preload relate to recruitable stroke volume?

A

preload relates to changes in stroke volume according to recruitable muscles

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16
Q

how does preload relate to the shape of the starling curve?

A

Increased preload at the steep part of the starling curve means you have lots of recruitable muscles and will have large increase in SV versus negligible increase in SV when increased

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17
Q

How do you define afterload according to the ventricle?

A

Resistance against the ventricle contracting (like SVR: systemic vascular resistance)

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18
Q

What are three determinants of stroke volume?

A

LV EDV, contractility, and afterload

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19
Q

What is the equation for stroke volume?

A

LVEDV - LVESV

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20
Q

What is the equation for ejection fraction?

A

Stroke volume / LVEDV

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21
Q

What are two determinants of end-diastolic volume? (EDV)

A

Preload and distensibility of ventricle

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22
Q

What are the two determinants of end-systolic volume? (ESV)

A

Determined by contractility and afterload

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23
Q

What is the heart rate up to which cardiac output increases and then decreases?

A

CO increases with HR up to 120-150 bpm, then starts to go down

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24
Q

Why does this phenomenon between HR and CO occur?

A

Because as HR increases, you get decreased diastolic filling time

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25
Q

What percent of LVEDV is accounted for by atrial kick?

A

20%

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26
Q

Describe the Anrep effect

A

Automatic increase in contractility 2/2 increased afterload

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27
Q

Describe the Bowditch effect

A

Automatic increase in contractility 2/2 increased heart rate

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28
Q

What is the equation for arterial O2 content (CaO2)?

A

CaO2 = Hb x 1.34 x O2sat + (PO2 x 0.003)

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29
Q

What is the equation for O2 delivery?

A

CO x arterial O2 content (CaO2) x 10

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30
Q

What is the equation for O2 consumption? (VO2)

A

VO2 = CO X (CaO2 - CvO2) CvO2 = venous O2 content

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31
Q

What is the normal O2 delivery to consumption ratio?

A

5:1

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32
Q

What measure of cardiac activity increases to keep the O2 delivery:consumption ratio constant?

A

Cardiac output increases to keep this ratio constant

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33
Q

Why is O2 consumption usually supply-independent?

A

O2 consumption does not change until low levels of delivery are reached

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34
Q

What causes right shift of the O2-Hb dissociation curve? (5)

A

Increased O2 unloading via increased CO2; increased temperature; increased ATP; increased 2,3-DPG; decreased pH (increased acidity)

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35
Q

What occurs with a left shift of the O2-Hb dissociation curve?

A

Increased O2 binding

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36
Q

What is a normal venous O2 saturation (SvO2)?

A

75 +/- 5%

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37
Q

What is the pathophys behind increased SvO2? (2)

A

Increased shunting or decreased O2 extraction

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38
Q

Name eight causes of increased SvO2?

A

Sepsis, cirrhosis, cynaide toxicity, hyperbaric oxygen, hypoterhmia, paralysis, coma, sedation

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39
Q

What is the pathophys behind decreased SvO2? (5 possible MOA)

A

Increased O2 extraction; Decreased O2 delivery Decreased O2 saturation Decreased bicarb Malignant hyperthermia

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40
Q

Name six conditions that can alter wedge pressure

A

Pulmonary HTN; high PEEP Aortic regurgitation; poor LV compliance Mitral stenosis; mitral regurgitation

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41
Q

In which zone of the lung should a Swan Ganz catheter be placed?

A

Zone III

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42
Q

How should you treat hemoptysis after flushing the Swan Ganz catheter? (4)

A

Increase PEEP to tamponade the pulmonary artery bleed Mainstem intubate the unaffected side Can attempt to place Fogarty balloon down affected side May need thoracotomy with lobectomy if these interventions do not work

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43
Q

Name two relative contraindications to a Swan-Ganz catheter

A

Previous pneumonectomy, left BBB

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44
Q

What is the distance of the right SCV to the Swan-Ganz catheter wedge?

A

45cm

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45
Q

What is the distance of the right IJ to the Swan-Ganz catheter wedge?

A

50cm

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46
Q

What is the distance of the left SCV to the Swan-Ganz catheter wedge?

A

55cm

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47
Q

What is the distance of the left IJ to the Swan-Ganz catheter wedge?

A

60cm

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48
Q

Does an echo measure pulmonary vascular resistance?

A

nope

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49
Q

What is the only way to measure pulmonary vascular resistance?

A

Swan-Ganz catheter

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50
Q

When in the respiratory cycle should you measure wedge pressure for ventilated patients?

A

End-expiration

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51
Q

When in the respiratory cycle shoul you measure wedge pressure for nonventilated patients?

A

end expiration

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52
Q

What are the two primary determinants (in order) of myocardial O2 consumption?

A

Increased ventricular wall tension (#1) and heart rate

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53
Q

Where do bronchial veins empty?

A

empty into pulmonary veins

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54
Q

How does this anatomy affect O2 saturations in the left ventricle versus pulmonary capillaries?

A

LV PO2 is ~5mmHg lower than pulmonary capillaries

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55
Q

What is a normal alveolar-arterial gradient?

A

10-15mmHg in a normal nonventilated patient

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56
Q

What location has blood with the lowest venous O2 saturation in the body?

A

coronary sinus blood

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57
Q

What is the venous O2 sat in coronary sinus blood?

A

30%

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58
Q

What is the most basic definition of shock?

A

Inadequate tissue oxygenation

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59
Q

Name two S/Sx that occur with progressive shock

A

Tachypnea and altered mental status with progressive shock

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60
Q

What is the MCC of adrenal insufficiency?

A

Withdrawal from exogenous steroids

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61
Q

What are six S/Sx of acute adrenal insufficiency?

A

Cardiovascular collapse unresponsive to fluids and pressors; N/V; abdominal pain; fever; lethargy

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62
Q

Name two lab findings a/w adrenal insufficiency

A

Hypoglycemia, hyperkalemia

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63
Q

How do you treat acute adrenal insufficiency?

A

dexamethasone

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64
Q

How strong is hydrocortisone compared to cortisone?

A

They are equal in strength

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65
Q

Name three steroids that are five times stronger than hydrocortisone or cortisone

A

Prednisone; prednisolone; methylprednisolone

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66
Q

Name one steroid that is thirty times stronger than hydrocortisone or cortisone

A

dexamethasone

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67
Q

What is the underlying cause of neurogenic shock (MOA)?

A

Loss of sympathetic tone 2/2 head or spine injury

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68
Q

What are the three S/Sx a/w neurogenic shock?

A

Low HR, low BP, warm skin

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69
Q

How do you treat neurogenic shock? (2 steps)

A

IVF first, then phenylephrine after resuscitation

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70
Q

What is the first alteration in vital signs a/w hemorrhagic shock?

A

Narrowed pulse pressure 2/2 increased diastolic pressure

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71
Q

What type of shock is caused by cardiac tamponade?

A

Cardiogenic shock

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72
Q

What is the mechanism of hypotension 2/2 cardiac tamponade?

A

Decreased ventricular filling 2/2 fluid accumulation in pericardial sac

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73
Q

What is Beck’s triad?

A

Hypotension, JVD, muffled heart sounds

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74
Q

What is the first sign of cardiac tamponade seen on echo?

A

Impaired diastolic filling of the right atrium is the first sign of cardiac tamponade on echo

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75
Q

What is a unique characteristic of pericardial blood?

A

It does not clot

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76
Q

What is the treatment of cardiac tamponade?

A

Fluid resuscitation to temporize situation, then pericardial window or pericardiocentesis

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77
Q

What is the pattern of CVP/PCWP, CO, and SVR seen with hemorrhagic shock?

A

Low CVP/PCWP; low CO; elevated SVR

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78
Q

What is the pattern of CVP/PCWP, CO, and SVR seen with septic/hyperdynamic shock?

A

low CVP/PCWP; elevated CO; low SVR

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79
Q

What is the pattern of CVP/PCWP, CO, and SVR seen with cardiogenic shock?

A

elevated CVP/PCWP; low CO; elevated SVR

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80
Q

What is the pattern of CVP/PCWP, CO, and SVR seen with neurogenic shock?

A

low CVP/PCWP; low CO; low SVR

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81
Q

What is the pattern of CVP/PCWP, CO, and SVR seen with adrenal insufficiency?

A

low CVP/PCWP; low CO; low SVR

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82
Q

What is the early sepsis triad?

A

Hyperventilation, confusion, hypotension

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83
Q

What are the insulin and glucose findings with early gram negative sepsis and why?

A

Low insulin, hyperglycemia 2/2 impaired glucose utilization

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84
Q

What are the insulin and glucose findings in late gram-negative sepsis and why?

A

Elevated insulin and hyperglycemia 2/2 insulin resistance

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85
Q

When does hyperglycemia present in the septic patient?

A

Usually presents just before the patient becomes clinically septic

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86
Q

What is the rapid neurohormonal response to hypovolemia? (2)

A

Release of epinephrine and norepinephrine

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87
Q

Where are epinephrine and norepinephrine released from?

A

Adrenals (adrenergic release)

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88
Q

What are the effects of the release of epinephrine and norepinephrine in response to hypovolemia?

A

Results in vasoconstriction and increased cardiac activity

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89
Q

What is the sustained neurohormonal response to hypovolemia? (3)

A

Renin, ADH, ACTH

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90
Q

Where is renin released from and what is its effect?

A

Released from kidney, activated renin-angiotensin-aldosterone system for vasoconstriction and H2O reabsorption

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91
Q

Where is ADH released from and what does it do?

A

Released from pituitary and causes reabsorption of water

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92
Q

Where is ACTH released from and what is its effect?

A

reabsorption of water Released from pituitary and increases cortisol

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93
Q

What are the three S/Sx a/w fat emboli?

A

Petichiae, hypoxia, and confusion (similar to presentation of PE)

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94
Q

What pathology test can be used to confirm presence of fat emboli?

A

Sudan red stain may show fat in sputum and urine

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95
Q

What is the MCC of fat emboli?

A

Lower extremity fractures or orthopedic procedures (hip / femur)

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96
Q

What are the 6 S/Sx a/w PE?

A

CP; SOB; tachycardia; tachypnea; hypotension/shock if massive PE

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97
Q

What are three ABG findings a/w PE?

A

Respiratory alkalosis, low PO2, low PCO2

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98
Q

What is the MC source of PE?

A

Iliofemoral region

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99
Q

What are the two medical treatments for PE?

A

Heparin to coumadin

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100
Q

When is surgery indicated for PE?

A

Patient in shock despite massive pressors and inotropes

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101
Q

What approach should you use when operating for PE?

A

Open or percutaneous (suction catheter) embolectomy

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102
Q

What are the steps to manage an air embolism?

A

Patient head down and LLD to keep air in the RV and RA; aspirate air out with central line or PA catheter to RA/RV

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103
Q

When in the cardiac cycle does the intra-aortic balloon pump inflate and deflate?

A

Inflates on diastole and deflates on systole

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104
Q

When on the EKG cycle does the intra-aortic balloon pump inflate and deflate?

A

Inflates on T-wave and deflates on P-wave

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105
Q

What cardiac condition is a contraindication to intra-aortic balloon pump use?

A

Aortic regurgitation

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106
Q

Where should the tip of the intra-aortic balloon pump catheter be placed?

A

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

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107
Q

Name two indications for intra-aortic balloon pump use

A

Cardiogenic shock s/p CABG or MI Patients with refractory angina awaiting revascularization

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108
Q

How does the intra-aortic balloon pump affect afterload?

A

Decreases afterload by deflation during systole (negative pressure down the aorta)

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109
Q

How does the intra-aortic balloon pump affect diastolic BP and what effect does this have on coronary perfusion?

A

Increases diastolic BP by inflating during diastole leads to improved diastolic coronary perfusion

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110
Q

What do alpha-1 receptors do? (3)

A

Vascular smooth muscle constriction; gluconeogenesis; glycogenolysis

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111
Q

What do alpha-2 receptors do? (1)

A

Venous smooth muscle constriction

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112
Q

What do beta-1 receptors do?

A

Affect myocardial contraction and rate

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113
Q

What do beta-2 receptors do? (5)

A

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

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114
Q

What do dopamine receptors do?

A

Relax renal and splanchnic smooth muscle

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115
Q

what is the initial dose of dopamine in kg/min?

A

2-5ug/kg/min initially

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116
Q

which receptors and where are activated when dopamine is administered at 2-5ug/kg/min?

A

dopamine receptors (renal)

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117
Q

which receptors and what effects are activated when dopamine is administered at 6-10 ug/kg/min?

A

beta adrenergic receptors (heart contractility)

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118
Q

which receptors and what effects are activated when dopamine is administered at >10 ug/kg/min?

A

alpha adrenergic receptors causing vasoconstriction and increased bp

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119
Q

what is the initial starting rate of the dobutamine in kg/min?

A

3ug/kg/min initially

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120
Q

which receptors and what effects are activated with dobutamine? How do these effects differ by dose of dobutamine administered

A

beta-1 receptors, causing increased contractility initially and tachycardia at higher doses

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121
Q

what is the MOA of milrinone?

A

phosphodiesterase inhibitor causing increased cAMP and then increased calcium flux

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122
Q

what is the clinical effect of milrinone? (3)

A

incresaed myocardial contractility, vascular SM relaxation, and pulmonary vasodilation

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123
Q

what is the initial rate of phenylephrine in ug/min?

A

10ug/min initially

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124
Q

what is the receptor activated and effect of phenylephrine?

A

alpha-1 receptor causing vasoconstriction

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125
Q

what is the initial dose of norepinephrein in ug/min?

A

5ug/min

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126
Q

what is the effect of norepinephrine at low doses and high doses and its associated effects

A

low dose: causes beta 1 activation = increased contractility high dose: alpha 1 and alpha 2 activation

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127
Q

what is the relevance of norepinephrine in terms of GI/abdominal surgery?

A

norepinephrine is a potent splanchnic vasoconstrictor

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128
Q

what is the initial dose of epinephrine in ug/min?

A

1-2ug/min initially

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129
Q

what is the effect of epinephrine at low doses (and which receptors are activated)?

A

beta 1 and beta 2 activation, causing increased contractility and vasodilation. Can therefore cause reduced BP at low doses

130
Q

what is the effect of epinephrine at high doses and which receptors are activated?

A

alpha 1 and alpha 2 activation leading to vasoconstriction

131
Q

what are the 2 possible cardiac complications a/w high doses of epinephrine?

A

increased cardiac ectopic pacemaker activity and increased myocardial O2 demand

132
Q

what is the initial dose of isoproterenol in ug/min?

A

1-2ug/min initially

133
Q

with isoproterenol, which receptors are activated and what are their effects?

A

beta 1 and beta 2 are activated, causing increased heart rate and contractility + vasodilation

134
Q

what are 3 adverse cardiovascular side effects a/w isoproterenol?

A

extremely arrhytmogenic, increased heart metabolic demand, rarely actually reduces BP

135
Q

what is the action of V1 (vasopressin) receptors?

A

vasoconstriction of vascular smooth muscle

136
Q

what is the action of intrarenal V2 (vasopressin) receptors?

A

water reabsorption at collecting ducts

137
Q

what is the action of extrarenal V2 (vasopressin) receptors?

A

mediates release of factor VIII and von willebrand factor

138
Q

what is the cardiovascular effect of nipride?

A

arterial vasodilator

139
Q

what is an adverse effect of nipride?

A

cyanide toxicity at high doses

140
Q

at what doses/ duration of nipride should you worry about cyanide toxicity?

A

at doses > 3ug/kg/min x 72 hours

141
Q

what labs should you check to monitor for CN toxicity in patients on nipride gtts?

A

check thiocyanate levels and for signs of metabolic acidosis

142
Q

what are the two treatments for cyanide toxicity and in what order are they administered?

A

amyl nitrite and then sodium nitrite

143
Q

what are the three cardiovascular effects of nitroglycerin?

A

predominantly a venodilator leading to decreased myocardial wall tension 2/2 reduced preload; moderate coronary vasodilator

144
Q

what receptor does hydralazine act on and what is its effect?

A

alpha-blocker causing reduced BP

145
Q

what is the formula for compliance in the lungs?

A

change in volume / change in pressure

146
Q

how easy is it to ventilate a patient with high compliance of the lungs?

A

it is easy to ventilate

147
Q

name 5 comorbidities a/w decreased pulmonary compliance

A

ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectasis

148
Q

define inspiratory reserve volume, expiratory reserve volume, tidal volume, residual volume, total lung capacity, vital capacity, inspiratory capacity, and functional residual capacity

A

see photo

149
Q

what is the effect of aging on FEV1

A

reduces FEV1

150
Q

what is the effect of aging on vital capacity?

A

reduced vital capacity

151
Q

what is the effect of aging on the functional residual capacity?

A

increased functional residual capacity

152
Q

what is the V/Q ratio in the lungs?

A

ventilation to perfusion ratio

153
Q

what is the V/Q ratio in the upper lobes versus lower lobes

A

V/Q ratio highest in upper lobes and lowest in lower lobes

154
Q

what are the two effects of increased PEEP on the vent that causes improved oxygenation?

A

alveoli recruitment that improves functional residual capacity

155
Q

what are two alterations to the vent settings you can do to decrease CO2? (to treat hypercarbia)

A

increase RR or increase volume

156
Q

What is a normal negative inspiratory force (NIF) for vent weaning?

A

> 20

157
Q

what is a normal FiO2 for vent weaning?

A

< or = 40%

158
Q

what is a normal PEEP for vent weaning?

A

5 (physiologic)

159
Q

what is a normal pressure support (PS) for vent weaning?

A

5

160
Q

what is a normal RR for vent weaning

A

24 breaths per minute

161
Q

what is a normal heart rate for vent weaning?

A

< 120 beats per minute

162
Q

what is a normal PO2 on ABG for vent weaning?

A

> 60mmHg

163
Q

what is a normal PCO2 on ABG for vent weaning?

A

<50mmHg

164
Q

what is a normal pH on ABG for vent weaning?

A

pH 7.35-7.45

165
Q

what is a normal O2 saturation for vent weaning?

A

>93% O2 sat

166
Q

what are three clinical (bedside) indicators that a patient is ready to be weaned off the vent?

A

off pressors, follows commands, can protect airway

167
Q

how does increased pressure support make breathing on the vent easier?

A

decreases the work of breathing with inspiratory pressure held constant until minimum volume is achieved

168
Q

at what level should try to keep FiO2 at or below and why?

A

keep FiO2 at or below 60% to prevent O2 radical toxicity

169
Q

At what plateaus and peaks are you at risk for barotrauma?

A

plateaus > 30 and peaks > 50

170
Q

what two changes to the ventilator can you make to reduce the risk of barotrauma?

A

reduce tidal volumes and consider pressure control ventilation

171
Q

What is the best vent setting to alter to improve oxygenation and why?

A

increase PEEP because it increases functional residual capacity and compliance by keeping alveoli open = improved oxygenation

172
Q

define total lung capacity

A

lung volume after maximal inspiration

173
Q

what is the equation for total lung capacity?

A

TLC = FVC + RV = forced vital capacity + residual volume

174
Q

what is the definition of forced vital capacity?

A

FVC is maximal exhalation after maximal inhalation

175
Q

what is the definition of residual volume?

A

lung volume after maximal expiration

176
Q

what percent of total lung capacity is residual volume?

A

20% TLC = RV

177
Q

define tidal volume

A

the volume of air with normal inspiration and expiration

178
Q

define functional residual capacity

A

lung volume after normal exhalation

179
Q

**PHOTO** what is the equation for functional residual capacity

A

FRC = expiratory reserve volume + residual volume

180
Q

define expiratory reserve volume

A

voluem of air that can be forcefully expired after normal expiration

181
Q

what lung pathology can be caused by surgery and how does it affect functional residual capacity?

A

surgery can cause atelectasis, leading to reduced FRC

182
Q

what lung pathology can be caused by sepsis and how does this affect functional residual capacity?

A

sepsis can cause ARDS leading to reduced functional residual capacity

183
Q

what lung pathologies (3) can be caused by trauma and how does this affect functional residual capacity?

A

trauma can cause lung contusion, atelectasis, and ARDS that all reduce FRC

184
Q

define inspiratory capacity

A

maximum air breathed in from FRC

185
Q

what is FEV1

A

forced expiratory volume in 1 second after maximal inhalation

186
Q

what is the equation for minute ventilation?

A

MV = RR x TV = respiratory rate x tidal volume

187
Q

how does restrictive lung disease affect total lung capacity, residual volume, and forced vital capacity?

A

reduces TLC, RV, and FVC

188
Q

how does restrictive lung disease affect FEV1?

A

can be normal or increased

189
Q

how does obstructive lung disease affect total lung capacity, residual volume, and FEV1?

A

increased TLC and RV, decreased FEV1

190
Q

how does obstructive lung disease affect forced vital capacity?

A

FVC can be normal or decreased

191
Q

to what level of the lung is considered “dead space”

A

to the level of the bronchiole

192
Q

what is a normal volume of lung dead space?

A

150 mL

193
Q

what is the definition of lung dead space in terms of ventilation and perfusioN?

A

it is the region of the lung that is ventilated but not perfused

194
Q

name 5 comorbidities that can cause increase in lung dead space

A

reduced cardiac output, PE, pulmonary hypertension, ARDS, and excessive PEEP

195
Q

what alteration in ABG occurs with increased dead space?

A

elevated CO2 (hypercarbia)

196
Q

what is the underlying abnormality in the breathing cycle that causes increased WOB in COPD?

A

prolonged expiratory phase in COPD causes increased WOB

197
Q

what is the underlying pathophysiology of ARDS

A

mediated primarily by PMNs, get increased proteinaceous material, increased A-a gradient, increased pulmonary shunting

198
Q

what is the MCC of ARDS?

A

pneumonia

199
Q

name six other cuases of ARDS

A

sepsis; multitrauma; severe burns; pancreatitis; aspiration; DIC

200
Q

name the four criteria for diagnosis of ARDS

A

acute onset; bilateral pulmonary infiltarations; PaO2/FiO2 < or = 300; absence of heart failure with wedge pressure < 18mmHg

201
Q

what pH and volume of aspiration are associated with increased lung damage?

A

pH < 2.5 and volume > 0.4cc/kg

202
Q

Define Mendelson’s syndrome

A

chemical pneumonitis from aspiration of gastric secretions

203
Q

What is the most frequent site of aspiration?

A

superior segment of RLL

204
Q

define atelectasis

A

collapse of alveoli resulting in reduced oxygenation, usually caused by poor inspiration postop

205
Q

what are the S/Sx of atelectasis (3)

A

fever, tachycardia, hypoxia

206
Q

what is the MCC of fever 48 hours postop?

A

atelectasis

207
Q

name three risk factors for postop atelectasis

A

COPD, upper abdominal surgery, obesity

208
Q

name three treatments for atelectasis

A

incentive spirometer; pain control; ambulation

209
Q

name 6 underlying causes of inaccurate transcutaneous pulse ox reading

A

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

210
Q

what is the effect of hypoxia on pulmonary vasculature?

A

pulmonary vasoconstriction

211
Q

what is the effect of alkalosis on pulmonary vasculature?

A

pulmonary vasodilation

212
Q

what is the effect of acidosis on pulmonary vasculature?

A

pulmonary vasoconstriction

213
Q

what is the effect of prostacyclin (PGI2) on pulmonary vasculature?

A

pulmonary vasodilation

214
Q

what is the effect of nitric oxide on pulmonary vasculature?

A

pulmonary vasodilation

215
Q

what is the effect of histamine on pulmonary vasculature

A

pulmonary pulmonary vasoconstriction

216
Q

what is the effect of serotonin on pulmonary vasculature?

A

pulmonary vasoconstriction

217
Q

what is the effect of nipride/nitroprusside on oxygenation?

A

causes pulmonary shunting

218
Q

what is the effect of bradykinin on pulmonary vasculature?

A

pulmonary vasodilation

219
Q

what is the effect of nitroglycerin on pulmonary oxygenation?

A

causes pulmonary shunting

220
Q

what is the effect of TXA2 on pulmonary vasculature?

A

causes pulmonary vasoconstriction

221
Q

what is the effect of nifedipine on pulmonary oxygenation?

A

causes pulmonary shunting

222
Q

what is the MCC of postop renal failure?

A

intraop hypotension

223
Q

what percentage of nephrons need to be damaged before renal dysfunction occurs?

A

70%

224
Q

what is the best lab test for azotemia?

A

FeNa

225
Q

what is azotemia?

A

elevated BUN

226
Q

what is the formula for FeNa?

A

U need to pee [(urine Na*plasma Cr)/(urine Cr * plasma Na)]

227
Q

What are the labs / maneuvers you should initially do when you suspect renal failure?

A

check Foley for kinks / blockage; flush Foley; get serum and urine lytes; check FeNa

228
Q

What is the urine osmolarity in prerenal renal failure?

A

>500

229
Q

what is the urine osmolarity in parenchymal renal failure?

A

250-350

230
Q

what is the Urine:Plasma osmolarity ratio in prerenal failure?

A

>1.5

231
Q

what is the Urine:Plasma osmolarity ratio in parenchymal renal failure?

A

<1.1

232
Q

what is the Urine:Plasma creatinine ration in prerenal failure?

A

>20

233
Q

what is the Urine:Plasma creatinine ration in parenchymal renal failure?

A

<10

234
Q

what is the Urine sodium in prerenal failure?

A

<20

235
Q

what is the Urine sodium in parenchymal renal failure?

A

>40

236
Q

what is the FeNa in prerenal failure?

A

<1%

237
Q

what is the FeNa in parenchymal renal failure?

A

>3%

238
Q

What is your first intervention for oliguria and goal CVP?

A

make sure patient is volume loaded with CVP 11-15mmHg

239
Q

What is your second intervention for oliguria?

A

try diuretic trial, usually Lasix/furosemide

240
Q

what is the third intervention for oliguria

A

HD if needed

241
Q

name six indications for dialysis

A

fluid overload, hyperkalemia, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning

242
Q

what are the major pro and con for HD over CVVH?

A

pro: rapid / con: causes large volume shifts

243
Q

what are the pros of CVVH over HD

A

pro: slower, good for ill patients who cannot tolerate large volume shifts (ex: septic shock)

244
Q

What is the expected change in Hct with each liter taken off with HD?

A

expect Hct to increase by 5-8 with each liter removed

245
Q

what is the MoA of renin release by the juxtoglomerular apparatus?

A

renin released in response to decreased pressure sensed by the JGA in the kidney

246
Q

what is the MOA of renin release by the macula densa?

A

renin released in response to increased sodium concentrations sensed by the macula densa in the distal convoluted tubule

247
Q

how does beta adrenergic stimulation affect renin release?

A

causes renin release

248
Q

how does potassium affect renin release?

A

hyperkalemia causes renin release

249
Q

where is the angiotensin converting enzyme located?

A

in the lung

250
Q

what does the angiotensin converting enzyme do?

A

converts angiotensin I to angiotensin II

251
Q

what is the effect of angiotensin II on the adrenal cortex?

A

causes adrenal cortex to release aldosterone

252
Q

what is the effect of aldosterone on the kidney? (MOA, pathophysiology)

A

aldosterone acts on the distal convoluted tubule to reabsorb water by upregulating Na/K ATPase on the membrane, causing Na to be reabsorbed and K to be secreted

253
Q

What is the effect of angiotensin II on the cardiovascular system? (3)

A

vasoconstriction, increased HR, increased contractility

254
Q

What is the effect of angiotensin II on glucose balance?

A

causes glycogenolysis and gluconeogenesis

255
Q

what is the effect of angiotensin II on renin?

A

inhibits renin relase

256
Q

what is the MOA / pathophysiology of atrial natriuretic peptide / atrial natriuretic factor release?

A

released from the atrial wall with atrial dstension

257
Q

what is the function of atrial natriuretic peptide (AKA atrial natriuretic factor)?

A

inhibits Na and water resorption in the collecting ducts

258
Q

what is the cardiovascular effect of atrial natriuretic peptide (AKA atrial natriuretic factor)/

A

vasoconstrictor

259
Q

which limb of the nephron (afferent or efferent) controls GFR?

A

efferent limb controls GFR

260
Q

how do NSAIDS cause renal injury?

A

inhibit prostaglandin synthesis, resulting in renal arteriole vasoconstriction

261
Q

how do aminoglycosides cause renal injury?

A

direct tubular injury

262
Q

how does myoglobin cause renal injury?

A

direct tubular injury

263
Q

how do you treat/prevent myoglobin-induced renal injury?

A

alkalinize urine

264
Q

how do contrast dyes cause renal injury?

A

direct tubular injury

265
Q

how do you treat/prevent contrast-induced renal injury?

A

prehydration before contrast exposure, bicarb, N-acetylcysteine

266
Q

what does SIRS stand for?

A

systemic inflammatory response syndrome

267
Q

name 5 causes of SIRS

A

shock, infection, burns, multitrauma, pancreatitis, severe inflammatory responses

268
Q

what is the most potent stimulus for SIRS

A

endotoxin with lipopolysaccharide (lipid A) is the most potent stimulus for SIRS

269
Q

what inflammatory factor is stimulated by lipid A

A

TNF release

270
Q

Name the two molecules that are released in response to inflammation that cause SIRS

A

systemic inflammation causes TNF-alpha and IL1 release, leading to shock and multiorgan dysfunction

271
Q

name four pathophysiological disturbances that occur with SIRS

A

capillary leakage; microvascular thrombi; hypotension; end-organ dysfunction

272
Q

Define sepsis according to SIRS

A

Sepsis = SIRS + infection

273
Q

how many of the SIRS criteria need to be met to diagnose SIRS?

A

need 2 or more SIRS criteria

274
Q

name the four SIRS criteria

A

Temperature: >38C or <36C; HR: >90; RR >20 or PaCO2 < 32; WBC > 12 or <4

275
Q

What is the definition of shock in a patient with sepsis/SIRS?

A

areterial hypotension despite adequate volume resuscitation (inadequate tissue oxygenation)

276
Q

Define multisystem organ dysfunction

A

progressive but reversible dysfunction of 2+ organs arising from an acute disruption of normal homeostasis

277
Q

what are the dignostic criteria for significant organ dysfunction of the pulmonary system? (2)

A

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

278
Q

what are the dignostic criteria for significant organ dysfunction of the cardiovascular system? (2)

A

need for inotropic drugs *OR* CI < 2.5L/min/m2

279
Q

what are the dignostic criteria for significant organ dysfunction of the renal system? (2)

A

creatinine >2x baseline on 2 consecutive days OR need for dialysis

280
Q

what are the dignostic criteria for significant organ dysfunction of the hepatic system? (2)

A

bilirubin >3 mg/dL on two consecutive days OR PT > 1.5 control

281
Q

what are the dignostic criteria for significant organ dysfunction of the nutrition system? (3)

A

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

282
Q

what are the dignostic criteria for significant organ dysfunction of the CNS? (1)

A

GCS < 10 without sedation

283
Q

what are the dignostic criteria for significant organ dysfunction of the coagulation systsem? (3)

A

platelets < 50; fibrinogen < 100; OR need for factor replacement

284
Q

what are the dignostic criteria for significant organ dysfunction of the immunologic/host defenses system (2)

A

WBC < 1 or invasive infection including bacteremia

285
Q

desribe the progression from insult to SIRS to sepsis to septic shock to MODS

A

**FLOWChART**

286
Q

what drugs on board preclude diagnosis of braindeath

A

any drugs but especially phenobarbital, pentobarbital, or EtOH

287
Q

what metabolic derangements preclude diagnosis of brain death?

A

hyperglycemia, uremia

288
Q

what vital signs preclude diagnosis of brain death (3)

A

temperature < 32C, SBP <90; desaturation with apnea test

289
Q

how is the apnea test for brain death administered?

A

patient is preoxygenated with a catheter delivering O2 at 8LPM at the carina via the ETT and PCO2 should be normal before the start of the test. Patient is then disconnected from the ventilator for 10 minutes

290
Q

What are two findings of the apnea test that are positive for braindeath?

A

CO2 > 60mmHg or increase in CO2 by 20mmHg by the end of the test meets brain death criteria

291
Q

name 8 findings that must be present for 6-12 hours to allow dx of brain death

A

unresponsive to pain; absent cold caloric oculovestibular reflexes; absent oculocephalic (dolls eye/tracking) reflex; no spontaneous respirations; no corneal reflex; no gag reflex; fixed and dilated pupils; positive apnea test

292
Q

what are the EEG findings in brain death?

A

electrical silence

293
Q

what are MRA findings in brain death?

A

no blood flow to brain

294
Q

what are deep tendon reflexes with brain death?

A

you can still have DTRs with brain death

295
Q

what are three findings on the apnea test that are NEGATIVE for brain death?

A

BP drops to <90mmHg, patient desaturates to <85% on pulse ox; or spontaneous breathing occurs

296
Q

what do you do when a patient has a negative apnea test when testing for brain death

A

if negative, terminate the test and put patient back on the ventilator

297
Q

What are the S/Sx of CO poisoning?

A

HA, nausea, confusion, coma, death

298
Q

what are the pulse ox findings with CO poisoning?

A

falsely elevated O2 sat on pulse ox

299
Q

what is the MOA of CO poisoning?

A

CO binds directly to hemoglobin and creates carboxyhemoglobin

300
Q

How do you treat CO poisoning?

A

100% O2 on the ventilator is usually enough to displace the CO molecules, rarely need hyperbaric O2

301
Q

what is an abnormal carboxyhemoglobin level in a non-smoker?

A

>10%

302
Q

what is an abnormal carboxyhemoglobin level in a smoker?

A

>20%

303
Q

what is methemoglobin and how does it affect oxygenation?

A

Hb bound to Fe3+ becomes methemoglobin, which binds more tightly to O2 and has reduced unloading in tissues

304
Q

name two antibiotics associated with methemoglobinemia

A

Bactrim and dapsone

305
Q

name three anesthetics a/w methemoglobinemia

A

locals: articaine, benzocaine, and prilocaine

306
Q

name two sources of nitrates that can cause methemoglobinemia

A

chemicals for patina/leather (bismuth nitrate) and Hurricane spray (topical benzocaine)

307
Q

what are the O2 sats found with methemoglobinemia

A

reduced, O2 sats will read 85% ish

308
Q

how do you treat methemoglobinemia and what is its MOA?

A

methylene blue restores iron in hemoglobin to the normal (reduced) state by acting as an electron acceptor

309
Q

what can happen with patients on SSRIs treated with methylene blue?

A

can cause serotonin toxicity because methylene blue inhibits monoamine oxidase

310
Q

what is critical illness polyneuropathy and how does it affect ventilation?

A

with prolonged sepsis, you can get motor > sensory neuropathy, can lead to failure to wean from ventilation

311
Q

where is xanthine oxidase located?

A

in endothelial cells

312
Q

what does xanthine oxidase do and how is it a/w reperfusion injury?

A

XO forms toxic oxygen radicals with reperfusion

313
Q

how is xanthine oxidase involved with purine metabolism?

A

involved with purine metabolism to breakdown to uric acid

314
Q

which cells are the most important mediators of reperfusion injury?

A

PMNs migrate to reperfused tissue after injury as inflammatory reaction –> damage

315
Q

how does DKA present? (4 S/Sx)

A

N/V, thirst, polyuria

316
Q

what are 4 chemistry findings a/w DKA?

A

elevated glucose, elevated ketones, elevated potassium, low sodium

317
Q

how do you treat DKA initially?

A

NS and insulin gtt initially

318
Q

what are the 4 S/Sx a/w EtOH withdrawal and when do they occur in a hospitalization

A

occurring after 48 hours in the hospital: HTN, tachycardia, delirium, seizures

319
Q

how do you treat EtOH withdrawal? (6 meds)

A

thiamine, folate, B12, Mag, K + PRN Ativan (lorazepam)

320
Q

when does ICU / hospital psychosis occur in a hospitalizaiton / postop?

A

lucid interval to psychosis at POD3

321
Q

what do you need to rule out before you diagnose ICU/hospital psychosis?

A

metabolic causes (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic causes (MI, CVA)

Z.Fiser (22 decks)

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