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Cardiovascular Anesthesia > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is the first messenger of a GPCR?

A

Ligand that binds the GPCR

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2
Q

What are examples of ligands?

A

NE, Epi, Ach

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3
Q

What does the effector of a GPCR do?

A

activates the 2nd messenger

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4
Q

What are the names of effectors?

A

Adenylate Cyclase, Phospholipase C, Guanylate Cyclase (nitrodilators)

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5
Q

What does a second messenger do?

A

elicits a specific response

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6
Q

What are the second messengers?

A

cAMP, cGMP, inositol triphosphate, diacylglycerol, Ca

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7
Q

Explain the GPCR pathway of Phenylephrine?

A

Phenylephrine binds to a A-1 Gq protein, Increasing phospholipase C, Increase IP3 DAG and Ca, causing muscle contraction

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8
Q

Explain the GPCR pathway of Precedex?

A

Precedex binds to a A-2 Gi protein, decreasing adenylate cyclase , decreasing cAMP, causing contraction and transient HTN

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9
Q

What happens in the Cardiac Myocyte when you give a Beta-1 or Beta-2 drug?

A

Activates adenylate cyclase, increasing cAMP, which increases protein kinase A, which increases calcium release and muscle contraction.

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10
Q

What happens in the smooth muscle when you give a Beta-2 drug?

A

Increases cAMP which inhibits myosin light chain kinase, leading to vasodilation

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11
Q

What are both endogenous and exogenous sympathomimetic drugs?

A

epinephrine, norepinephrine, and dopamine

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12
Q

What sympathomimetic drugs are just exogenous?

A

isoproterenol, and dobutamine

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13
Q

What is the naturally occurring catecholamine synthesized from tyrosine in the adrenal medulla?

A

Epinephrine

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14
Q

What are the catecholamines secreted by the adrenal medulla and their percentages?

A

80% Epi 20 % Norepinephrine

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15
Q

Do endogenous or exogenous catecholamines have a longer effect in the body?

A

Endogenous

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16
Q

What happens if you give MAOIs with Ephedrine?

A

HTN crisis or exaggerated response

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17
Q

What receptors does Epinephrine act on?

A

A-1, A-2, B-1, B-2

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18
Q

What is the Beta-1 effect seen with Epinephrine?

A

positive inotropy, chronotropy, and dromotropy

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19
Q

What is the Beta-2 effect seen with Epinephrine?

A

smooth muscle relaxation, mast cell stabilization

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20
Q

Which receptors does low dose Epi target more?

A

Beta more than alpha

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21
Q

At what dose of Epi do you see just Beta effects?

A

0.01-0.03 mcg/kg/min

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22
Q

At what dose of Epi do you see Beta and a little alpha effects?

A

0.03-0.1 mcg/kg/min

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23
Q

At what dose of Epi do you see Alpha and Beta effects?

A

Greater than 0.1 mcg/kg/min

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24
Q

What is epinephrine used to treat?

A

low CO, anaphylaxis, bronchospasm

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25
Q

If your patient is on Epi what lab value do you need to monitor?

A

blood sugar

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26
Q

Where is NE synthesized?

A

inside the nerve axon and stored in vesicles

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27
Q

What is the rate limiting step in NE synthesis?

A

conversion of tyrosine to dopa by tyrosine hydroxylase

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28
Q

What receptors does NE bind to?

A

A-1 > A-2 > B-1 > B-2

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29
Q

Does NE produce increased inotropy?

A

yes, it is not purely alpha selective

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30
Q

What is the dose range of NE?

A

0.01-0.4 mcg/kg/min or 1-20mcg/min

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31
Q

What vasopressor is not a great choice for someone with Right sided heart failure with hypotension? Why

A

NE, it causes pulmonary vasoconstriction, it increases right heart afterload. Choose Vasopressin instead.

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32
Q

What receptors does dopamine bind to?

A

Dopamine, alpha and beta

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33
Q

Dopamines beta-1 stimulation, indirectly stimulates the release of what catecholamine?

A

norepinephrine

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34
Q

What is considered low dose dopamine and what does low dose mainly affect?

A

2mcg/kg/min D1 and D2 receptors, dilating renal and mesenteric vascular beds

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35
Q

What is considered intermediate dose dopamine and what receptors does intermediate dose mainly affect?

A

2-10mcg/kg/min Dopa and beta-1 receptors

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36
Q

What is considered high dose dopamine and what receptors does high dose mainly affect?

A

10-20mcg/kg/min alpa receptors

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37
Q

What is dopamine used to treat?

A

cardiogenic shock, and low CO states

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38
Q

What metabolizes Dopamine? What instances may we see increased circulating levels?

A

MAO People taking psych meds, because they are MAOIs

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39
Q

What synthetic catecholamine increase HR independent of the SA node?

A

isoproterenol

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40
Q

What dose of isoproterenol is used to treat heart block?

A

2-20mcg/min

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41
Q

What is the dose of Isoproterenol for septal myectomy gradient testing?

A

5-10mcg bolus

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42
Q

What receptors does isoproterenol bind to?

A

nonselective Beta

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43
Q

What is Dobutamine?

A

synthetic sympathomimetic amine

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44
Q

What receptors does Dobutamine affect?

A

Beta 1 >> Beta2

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45
Q

Dobutamines Beta1 effects cause what hemodynamic changes?

A

Inotropy, with less effect on SVR

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46
Q

What is the dose of Dobutamine?

A

2-20mcg/kg/min

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47
Q

What is Dobutamine used to treat?

A

cardiogenic shock, septic shock, heart failure, used in stress testing

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48
Q

Which vasopressor is a pure alpha agonist?

A

Phenylephrine

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49
Q

What is the dosage range of Phenylephrine on a pump?

A

0.1-1mcg/kg/min

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50
Q

Why does Phenylephrine cause reflex bradycardia?

A

baroreceptor stimulation.

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51
Q

Where is vasopressin stored and produced?

A

produced in the hypothalamus and stored in the posterior pituitary

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52
Q

What stimulates vasopressin release?

A

increased osmolarity and hypovolemia

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53
Q

What is the action of vasopressin?

A

vasoconstriction, dilates renal afferent, pulmonary and cerebral arteries

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54
Q

What is the classification of Milrinone?

A

PDE 3 inhibitor

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55
Q

What does PDE 3 do? What does inhibiting it do?

A

PDE3 breaks down cAMP into AMP. Inhibiting that breakdown increases the amount of cAMP available for cardiac muscle contraction. In the smooth muscle it decreases SVR.

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56
Q

What are the overall effects of milrinone?

A

increases inotropy

decreases SVR, preload, and PVR

no change in chronotropy

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57
Q

If you start Milrinone on your patient with Left HF, what other medication do you likely need to start?

A

vasopressin

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58
Q

Giving a rapid loading dose of Milrinone will cause what?

A

hypotension

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59
Q

PDE5 drugs are selective for what? what does this cause?

A

cGMP, dilation of vascular and pulmonary beds.

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60
Q

Does NTP or NTG release NO spontaneously?

A

NTP

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61
Q

How does NO cause relaxation?

A

NO yields guanylate cyclase, guanylate cyclase catalyzes the conversion of GTP to cGMP, increased cGMP causes vasodilation

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62
Q

Does NTP reduce preload or afterload?

A

BOTH preload and afterload.

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63
Q

What is the dose range of NTP?

A

0.3-10 mcg/kg/min

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64
Q

How many cyanide molecules are in NTP?

A

5 cyaninde molecules

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65
Q

What doses of NTP causes cyanide toxicity?

A

>500mcg/kg administered faster than 2mcg/kg/min

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66
Q

Describe the highlights of NTP metabolism.

A

metabolism by plasma hemoglobin

1 cyanide molecule binds methemoglobin

other 4 undergo rhodanese conversion to thiocyanate (requires B12)

renal elimination

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67
Q

How does B12 deficiency affect NTP metabolism?

A

not enough B12 leads to anaerobic metabolism

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68
Q

What are S/S of cyanide toxicity?

A

metabolic acidosis, increased SVO2, tachycardia, tachyphylaxis

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69
Q

What are the treatment options for cyanide toxicity?

A

sodium nitrite, sodium thiosulfate, vitamin B12, methylene blue 1-2mg/kg

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70
Q

Where does NTG work? arteries, veins, both?

A

veins

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71
Q

What happens to filling pressures, wall tension, and MVO2 in someone on NTG?

A

all decrease

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72
Q

Why is NTG the primary treatment for angina?

A

decrease preload and cardiac work

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73
Q

Discuss NTP’s affect on afterload and preload, onset, and duration

A

decrease afterload > preload, rapid onset, duration 1-3 minutes.

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74
Q

Discuss NTG’s affect on afterload and preload, onset, and duration

A

decrease preload, onset 1-2 minutes, duration 10 minutes

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75
Q

Where does hydralazine work?

A

relaxation of arterial smooth muscle

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76
Q

What is the dose, onset and duration of hydralazine?

A

dose: 2.5-20mg onset: 2-20min (5 minutes) duration: 12 hours

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77
Q

Hydralazine’s decrease in afterload may cause increase in what?

A

heart rate

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78
Q

What is the onset, duration, receptor and dose of esmolol?

A

onset 2 min, duration 10-15min, receptor Beta 1, and bolus dose 10-30mg, gtt 100-300mcg/kg/min

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79
Q

What is the onset, duration, receptor and dose of metoprolol?

A

onset 1-2 min, duration 5-8 h, receptor Beta 1, and bolus dose 5-15mg

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80
Q

What is the onset, duration, receptor and dose of labetalol?

A

onset 2-5 min, duration 12-6h, receptor Beta and alpha 7:1, and bolus dose 5-10mg

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81
Q

What induction medications are cardiac stable, and which are cardiac depressive?

A

stable: etomidate 0.3mg/kg, ketamine 0.5-1.5mg/kg, fentanyl 3-10mcg/kg depressive: propofol 1-2mg/kg, inhaled anesthetics

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82
Q

What does Propofol do to blood pressure in healthy adults?

A

decrease blood pressure

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83
Q

What are patient characteristics indicative of propofol induced hypotension?

A

>50yo ASA 3-4, MAP <70, co-administered with fentanyl

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84
Q

Why does propofol cause hypotension?

A

decreases SNS tone, vasodilation

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85
Q

What is the induction dose of Propofol?

A

2mg/kg

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86
Q

What is the mechanism that Etomidate causes adrenocortical dysfunction?

A

inhibition of 11 beta-hydroxylase and 17 alpha hydroxylase

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87
Q

What is the induction dose of etomidate?

A

0.3mg/kg

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88
Q

Explain how Ketamine is cardiac stable?

A

activates the SNS that causes endogenous release of NT and inhibition of NE uptake

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89
Q

How does ketamine affect blood pressure, heart rate, contractility, and CVP?

A

increases BP, increase HR, increase Contractility, and increases CVP

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90
Q

What does ketamine cause in the critically ill patient?

A

negative inotropic effect, due to a decrease in intracellular calcium

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91
Q

What inhaled anesthetic causes the least reduction in SVR?

A

Sevo

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92
Q

Explain the mechanism behind inhaled anesthetics being cardiodepressant?

A

They reduce Ca++ influx through the sarcolemma and depress depolarization-activated Ca++ release from the sarcoplasmic reticulum

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93
Q

Which inhaled anesthetic causes the least effect on HR?

A

sevo

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94
Q

What gases increase HR above 1 MAC?

A

Iso and Des

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95
Q

Coronary steal is greatest with which anesthetic gas?

A

Iso

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96
Q

Which gas produces the least amount of coronary vasodilation?

A

Sevo

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97
Q

Are gases proarrythmic and antiarhythmic?

A

proarhythmic

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98
Q

What are the key events in isovolumetric contraction?

A

LV pressure > LA Pressure 1st heart sound LV pressure increases LV volume constant

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99
Q

What are the key events in ventricular ejection?

A

LV Pressure > aortic pressure, Ejection of SV, Rapid ejection during 1st 1/3, Reduced ejection during last 2/3

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100
Q

What is the only phase of the ventricular pressure volume loop that requires ATP during diastole?

A

isovolumetric relaxation

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101
Q

What are the key events in isovolumetric relaxation?

A

Aortic pressure > LV pressure, 2nd heart sound, LV pressure decreases, LV volume constant, Only phase during diastole that requires ATP, Dicrotic notch

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102
Q

What are the key events of rapid ventricular filling?

A

LA pressure > LV pressure, LV volume increases, LV pressure constant, 80% of ventricular filling occurs during rapid and reduced phases

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103
Q

What is occurring during reduced ventricular filling (diastole)?

A

LV fills but at a slow rate

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104
Q

What is final segment of diastole and what is occurring?

A

LA contraction, 20% ventricular filling End of atrial contraction = EDV

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105
Q

Where is EDV and ESV measured?

A

EDV is always the bottom right corner ESV is always the bottom left corner

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106
Q

Complete the Wiggers diagram.

A

.

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107
Q

Complete the pressure volume loop.

A

.

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108
Q

Patients who had Rheumatic fever typically have which valvular abnormalities?

A

AV and MV stenosis

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109
Q

What are risk factors for AV stenosis? (5)

A

older age, male, smoker, HTN, HLD

110
Q

What is the normal AV diameter?

A

2cm

111
Q

What is the normal AV area?

A

2-4cm

112
Q

What is the normal AV gradient?

A

2-5mmHg

113
Q

Symtoms of AV stenosis do not occur until valve area has decreased by how much?

A

50%, 1-2cm

114
Q

What is the triad of symptoms characteristic of AV stenosis?

A

SAD - syncope, angina, dyspnea

115
Q

What is a critical AV area?

A

<0.8cm2

116
Q

What AV area and gradient are considered mild AV stenosis?

A

>1.5cm <20mmHg

117
Q

What AV area and gradient are considered moderate AV stenosis?

A

1-1.5cm 20-40mmHg

118
Q

What AV area and gradient are considered severe AV stenosis?

A

<1cm >40mmHg

119
Q

As AV stenosis worsens what happens to valve area and gradient?

A

valve area gets smaller Gradient gets larger

120
Q

Is AV stenosis a volume or pressure problem? what does it lead to in the muscle?

A

pressure. Concentric hypertrophy, sarcomeres in parallel

121
Q

Is AV stenosis a volume or pressure problem? what does it lead to in the muscle?

A

pressure. Concentric hypertrophy, sarcomeres in parallel

122
Q

What are the resulting effects of AV stenosis causing concentric hypertrophy?

A

increase LV mass -> decrease compliance -> diastolic dysfunction -> increase in late filling = normal SV

123
Q

In AV stenosis what is vital for adequate LV filling?

A

atrial kick

124
Q

In the compensatory phase of AV stenosis, LV mass increases, having what effect on O2 supply and demand?

A

MVO2 is increased (increased demand) Myocardial O2 supply is decreased

125
Q

What causes MVO2 to be increased in AV stenosis?

A

increased mass, isovolumetric contraction requires more energy, prolonged ejection phase (more afterload to overcome)

126
Q

What causes myocardial O2 supply to decrease in AV stenosis?

A

increased LVEDP (decreases CPP), absent systolic coronary flow, prolonged ejection reduces perfusion interval, subendocardial capillaries compressed

127
Q

What causes myocardial O2 supply to decrease in AV stenosis?

A

increased LVEDP (decreases CPP), absent systolic coronary flow, prolonged ejection reduces perfusion interval, subendocardial capillaries compressed

128
Q

How does AV stenosis lead to LV failure?

A

.

129
Q

What happens to pulse pressure, systolic upstroke, and amplitude of the A-line tracing in AV stenosis?

A

pulse pressure narrow systolic upstroke decreased amplitude decreased

130
Q

What pressure volume loop is consistent with AV stenosis?

A

.

131
Q

What happens to pulse pressure, systolic upstroke, and amplitude of the A-line tracing in AV stenosis?

A

pulse pressure narrow systolic upstroke decreased amplitude decreased

132
Q

What are appropriate induction meds for someone with AV stenosis?

A

Narcotic based Etomidate or Ketamine Consider having esmolol easily accessible

133
Q

What is the most important pre-CPB goal if your patient is having a AVR for AV stenosis?

A

maintain CPP

134
Q

How do you treat HoTN in a patient with AV stenosis?

A

Phenylephrine

135
Q

In AV stenosis what is your SVR goal to help perfuse the subendocardium?

A

high SVR

136
Q

In AV stenosis what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload, afterload maintain contractility and PVR decrease rate

137
Q

How do symptoms of acute vs chronic AR differ?

A

acute: sudden dyspnea, CV collapse chronic: asymptomatic for years

138
Q

What is the vena contracta?

A

narrowest point of AR and corresponds to the size of the regurgitant orifice

139
Q

What vena contracta area and regurgitant volume are considered mild AV regurg?

A

<0.3cm <30mL/beat

140
Q

What vena contracta area and regurgitant volume are considered mild AV regurg?

A

<0.3cm <30mL/beat

141
Q

What vena contracta area and regurgitant volume are considered severe AV regurg?

A

>0.6cm >60mL/beat

142
Q

Is AV regurg a volume or pressure problem? what does it lead to in the muscle?

A

volume, eccentric hypertrophy, sarcomeres in series

143
Q

What are the compensatory mechanisms of acute AV regurg?

A

increased SNS tone (HR and contractility, fluid retention via aldosterone)

144
Q

Acute AV regurg causes what changes to LVEDP, LVEDV, and SV?

A

increases LVEDV, LVEDP and decreases SV

145
Q

Acute AV regurg causes what changes to LA wall tension and contractility?

A

increased wall tension, decrease contractility

146
Q

Does acute or chronic AV regurg cause systolic and diastolic failure leading to cariogenic shock?

A

acute

147
Q

What happens to MVO2 demand in acute AV regurg?

A

increased, due to increased compensatory SNS tone leading to ischemia

148
Q

Chronic AV regurg causes what changes to LVEDP, LVEDV, and SV?

A

increased LVEDV, no change to LVEDP (essentric hypertrophy compensation), increased SV (but not pumping well)

149
Q

Does AV regurg cause a narrow or wide pulse pressure on A-line tracing?

A

wide

150
Q

Does chronic Lv regurg cause a HF?

A

systolic HF, due to increased LV systolic pressure but decreased LV systolic function

151
Q

What happens to ESV, EDV and isovolumetric relaxation tracing on a pressure volume loop in AV regurg?

A

increased ESV and EDV isovolumetric relaxation is sloped to the right

152
Q

What is the bunny ears on A-line tracing called in a patient with AV regurg?

A

pulsus bisferiens

153
Q

In AV regurg what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload and rate maintain contractility, and PVR decrease afterload

154
Q

What is the main anesthetic goal of AV regurg?

A

prevent further increases in LV wall stress

155
Q

What is the basic management of AV regurg? (3 words)

A

Full, Fast, and Forward

156
Q

What pressure volume loop is consistent with AV regurg?

A

.

157
Q

Hypotension in a patient with AV regurg should be treated with which vasopressor?

A

Ephedrine

158
Q

What gas is preferential to use in AV regurg?

A

Iso - increases HR and decreases SVR

159
Q

After bypass what drug may be needed in someone with AV regurg? Why?

A

Inotrope due to essentric hypertrophy

160
Q

What is the overall most common cause of MV stenosis?

A

rheumatic fever, endocarditis and calcification in the US

161
Q

What symptoms are seen with MV stenosis?

A

pulmonary congestion, decreased CO (LV under filled). RV failure/overload

162
Q

What valve area and mean gradient are consistent with mild MV stenosis?

A

>1.5cm area <5 mmHg gradient

163
Q

What valve area, mean gradient, and symptoms are consistent with moderate MV stenosis?

A

1-1.5cm area 5-10 mmHg gradient

164
Q

What valve area, mean gradient, and symptoms are consistent with severe MV stenosis?

A

<1cm area >10 mmHg gradient

165
Q

What happens to valve area and mean gradient as Mv stenosis gets worse?

A

valve area decreases, and mean gradient increases

166
Q

What MV area is consistent with symptoms of tachycardia and increased CO?

A

1.5-2.5cm

167
Q

What MV area is consistent with symptoms at rest?

A

<1cm

168
Q

When the PA systolic pressure reaches ___ in MV stenosis, repair is needed?

A

>50mmHg

169
Q

What is the normal MV valve area?

A

4-6cm

170
Q

Severe MV disease is diagnosed when valve area is how much?

A

<1cm

171
Q

How does MV stenosis affect LVEDV?

A

decreases

172
Q

How does tachycardia in MV stenosis affect LVEDV?

A

decreases

173
Q

What is the pathway for tachycardia in MV stenosis leading to pulmonary edema?

A

increased HR -> increased LAP -> increase PAP -> pulm. edema

174
Q

Does PAOP overestimate or underestimate actual LVEDV/LVEDP in MV stenosis?

A

overestimate (remember stenosis is a increased PRESSURE problem)

175
Q

MV stenosis is most likely to cause which dysrhythmias?

A

A-fib

176
Q

What are the pathways for MV stenosis leading to decreased lung compliance and increased work of breathing, tricuspid regurg, and vasoconstriction

A

.

177
Q

What pressure volume loop is consistent with MV stenosis?

A

.

178
Q

What happens to EDV, ESV and SV on a V. pressure volume loop of MV stenosis?

A

decreased EDV, slight decrease in ESV, decreased SV very minimal changes

179
Q

Which wave on a PAC (a,c,v,x,y) is affected in MV stenosis?

A

cannon A wave

180
Q

What is the basic three word management for MV stenosis?

A

Slow, full and constructed

181
Q

In MV stenosis what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload maintain afterload, contractility, decrease rate and PVR

182
Q

You are waking a patient up with MV stenosis during a non cardiac surgery, what do you want to avoid? Why?

A

Apnea, increases PVR (hypercarbia and hypoxia)

183
Q

What is really important to pay attention to during induction for a patient with MV stenosis?

A

HR, because CO is fixed, they are

184
Q

Do you manage pre-CPB hypotension with volume or pressors in a patient with Mv stenosis?

A

pressors, usually not hypovolemic

185
Q

Does MV regurg occur during systole or diastole?

A

systole

186
Q

What are causes of acute MV regurg?

A

papillary muscle dysfunction, MI, trauma

187
Q

MV regurg causes fluid overload in which chamber?

A

LV

188
Q

What vena contracta area and regurgitant volume are considered mild MV regurg?

A

<0.3cm <30mmHg

189
Q

What vena contracta area and regurgitant volume are considered moderate MV regurg?

A

0.3-0.6cm 30-60mmHg

190
Q

What vena contracta area and regurgitant volume are considered severe MV regurg?

A

>0.7cm >60

191
Q

In acute MV regurg what happens to LVDP, SV, and LA pressure?

A

increased LV diastolic pressure decreased SV increased LA pressure -> pulm edema

192
Q

Which wave on a PAC (a,c,v,x,y) is affected in MV regurg?

A

large V waves

193
Q

In chronic MV regurg what happens to LV compliance, EF, and LV pressure?

A

increased LV compliance normal EF decreased LV pressure

194
Q

Is MV regurg a volume or pressure problem? what does it lead to in the muscle?

A

volume, essentric hypertrophy (sarcomeres in series)

195
Q

What pressure volume loop is consistent with MV regurg?

A

.

196
Q

What changes are seen in EDV and isovolumetric contraction in a MV regurg pressure volume loop waveform?

A

EDV increased, sloping left isovolumetric contraction

197
Q

What is the basic three word management for MV regurg?

A

Full, Fast, Forward

198
Q

In MV regurg what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase rate maintain preload, contractility decrease afterload, PVR

199
Q

What are the goals of MV regurg management?

A

decrease regurg volume to increase CO avoid Pulm congestion

200
Q

What mediations are potentially required after MVR for regurg?

A

inotropes

201
Q

What symptoms are seen with TV stenosis?

A

JVD, liver congestion, volume overload in the LE

202
Q

What is the valve area of the TV?

A

7-9cm

203
Q

What is the normal gradient across the TV?

A

1mmHg

204
Q

Reductions in blood flow are not seen until TV area is reduced to what size?

A

1.5cm, gradient of 3mmHg

205
Q

In TV stenosis what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload, afterload maintain contractility, and PVR decrease rate

206
Q

Which wave on a CVP (a,c,v,x,y) is affected in TV stenosis?

A

cannon A wave

207
Q

How do you manage multiple valvular lesions?

A

manage the most lethal

208
Q

Ebsteins anomaly is seen in which valvular lesion?

A

TV regurg

209
Q

Symptoms of increased RV afterload are consistent with which valve lesion?

A

TV regurg

210
Q

Which wave on a CVP (a,c,v,x,y) is affected in TV regurg?

A

V wave

211
Q

What is the goal in managing TV regurg?

A

maintain adequate right side forward flow

212
Q

How can we decrease PVR in TV regurg?

A

hyperventilate

213
Q

After coming off pump for TVR for regurg which medication may you need to start?

A

Milrinone, Epi, Vaso, NO

214
Q

In TV regurg what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload, rate maintain afterload, contractility decrease PVR

215
Q

Why is NE contraindicated in TV regurg?

A

Pulm vasoconstriction

216
Q

What are symptoms of Pulm stenosis?

A

tachypnea, syncope, angina, hepatomegaly, peripheral edema

217
Q

What is the normal pressure gradient across the pulm valve?

A

5mmHg

218
Q

What pressure gradients are characteristic of mild, moderate, and severe P. stenosis?

A

mild 15-36mmHg moderate 36-64mmHg severe >64mmHg

219
Q

How is P. stenosis managed unlike other stenotic lesions?

A

increased HR

220
Q

In P. stenosis what is your goal for preload, afterload, contractility, rate, and PVR?

A

increase preload, and rate maintain afterload, and contractility decrease PVR

221
Q

What is the most common cause of P. regurg?

A

annular dilation from pulm. HTN

222
Q

In tamponade is diastolic or systolic function affected more?

A

diastolic

223
Q

What is Becks triad?

A

HoTN, JVD, muffled heart tones

224
Q

What is pulsus paradoxus?

A

decreased SBP >10mmHg during inspiration

225
Q

What is kussmals sign?

A

increased CVP and JVD during inspiration

226
Q

Tamponade increases intra-epicardial pressure leading to what?

A

decrease in diastolic filling

227
Q

Tamponade increases intra-epicardial pressure leading to what changes in LV pressure and LV volume?

A

increased LV pressure, decreased LV volume

228
Q

How does increased LV pressure from tamponade affect coronary perfusion and v. filling?

A

decreased coronary perfusion, decreased v. filling

229
Q

How does decreased v. volume from tamponade affect Co and SV?

A

decreased SV and CO (increased contractility, HR and renal fluid retention to compensate)

230
Q

How do you manage a patient with tamponade?

A

give fluids, don’t induce until tamponade is relieved or wait until the patient is draped and everyone is READY

231
Q

Why do you want to keep a patient with tamponade breathing spontaneously?

A

PPV decreases venous return and can lead to cardiac collapse

232
Q

How can you induce the patient with tamponade and prevent decreasing their SNS?

A

Ketamine or inhalation induction (also keeps them breathing spontaneously!)

233
Q

What drugs should you avoid inducing with in someone with tamponade?

A

large doses of gases, propofol, thiopental, high dose opioids, neuraxial

234
Q

What drugs should you induce with in someone with tamponade?

A

ketamine, N2O, benzos, low dose opioids, etomidate

235
Q

In tamponade what is your goal for preload, afterload, contractility, rate?

A

maintain/increase preload, contractility, rate maintain afterload

236
Q

Which cardiomyopathy is characterized by Eccentric left/right ventricle that results in systolic/diastolic dysfunction?

A

Dilated

237
Q

Which cardiomyopathy is characterized by Stiff/noncompliant ventricles and Decrease in EDV despite normal systolic function?

A

restrictive

238
Q

Which cardiomyopathy is characterized by LV hypertrophy resulting in decreased LV chamber size and LVOT obstruction?

A

Hypertropic

239
Q

Which cardiomyopathy is characterized by Fatty tissue infiltrates and Dilation/outflow tract obstruction of the RV?

A

arrythmogenic right ventricular

240
Q

What is the most common cause of sudden death in peds and young adults?

A

hypertropic cardiomyopathy

241
Q

What are the major changes that occur with hypertropic cardiomyopathy?

A

ventricular hypertrophy, decreased v chamber size, increased v wall thickness, impaired v relaxation

242
Q

What ion channels are affected in hypertropic cardiomyopathy?

A

calcium channels

243
Q

Hypertrophy of the interventricular septum in hypertropic cardiomyopathy leads to what?

A

LVOT obstruction

244
Q

What is the gradient that results from a LVOT obstruction?

A

Ao < LV

245
Q

What is SAM?

A

anterior leaflet of the MV getting sucked into the LVOT due to interventricular hypertrophy and the Venturi effect

246
Q

How does hypertropic cardiomyopathy affect systolic and diastolic function and LVEDP?

A

systolic and diastolic dysfunction, elevated LVEDP

247
Q

How does hypertropic cardiomyopathy affect myocardial O2 demand and supply?

A

decrease in supply increase in demand

248
Q

In hypertropic cardiomyopathy what is your goal for preload, afterload, contractility, and rate?

A

increase preload and afterload low normal heart rate decrease contractility

249
Q

How is increased preload beneficial in managing hypertropic cardiomyopathy?

A

opens the LVOT, prevents SAM

250
Q

How is increased afterload beneficial in managing hypertropic cardiomyopathy?

A

opens LVOT my preventing septum from obstructing flow

251
Q

How is decreased contractility beneficial in managing hypertropic cardiomyopathy?

A

decreases amount of obstruction of the LVOT, increase forward flow

252
Q

What is the most common form of cardiomyopathy?

A

dilated

253
Q

Dilated cardiomyopathy causes essentric or concentric hypertrophy of the right or left ventricle?

A

essentric, both ventricles

254
Q

What happens to MVO2, LVEDV and LVEDP in dilated cardiomyopathy?

A

MVO2 increase as LVEDV and LVEDP increase

255
Q

Dilated cardiomyopathy causes regurg of which valve?

A

aortic

256
Q

Dilated cardiomyopathy decreases EF, causing what alterations in catecholamines, cortisol, and RAAS?

A

increased catecholamines, and cortisol, and activation of RAAS

257
Q

Dilated cardiomyopathy will eventually lead to which type of heart failure?

A

biventricular. Starts with LV failure.

258
Q

How do you manage a patient with dilated cardiomyopathy in the OR?

A

avoid increased afterload and myocardial depression, they rely on SNS activity

259
Q

What is the most sensitive intraoperative monitor for detecting ischemia?

A

TEE

260
Q

Which lead is best for detecting ischemia?

A

V5

261
Q

What are the earliest signs of MI intraop?

A

diastolic dysfunction (increased LVEDP, decreased compliance)

262
Q

What are late signs of MI intraop?

A

ECG changes (ST depression/elevation, T wave inversion)

263
Q

Is systolic dysfunction a supply or demand ischemia?

A

supply

264
Q

Is diastolic dysfunction a supply or demand ischemia?

A

demand

265
Q

Does systolic dysfunction lead to concentric or essentric hypertrophy?

A

essentric to preserve SV

266
Q

Does diastolic dysfunction lead to concentric or essentric hypertrophy?

A

concentric

267
Q

Systolic dysfunction is measured by EF. What EF is mild, moderate, and severe?

A

mild 45-55% moderate 30-44% severe <30%

268
Q

What causes Systolic dysfunction?

A

CAD, DCM, volume overload

269
Q

What causes Diastolic dysfunction?

A

OCM, chronic HTN, obesity

270
Q

Does Systolic HF lead to Diastolic HF or does Diastolic HF lead to Systolic HF?

A

Diastolic HF leads to Systolic HF

271
Q

Which genders are systolic and diastolic HF common in?

A

systolic males diastolic females

Cardiovascular Anesthesia (4 decks)

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