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APEX/BOARD STUDY > Unit 3 - CV > Flashcards

Unit 3 - CV Flashcards

1
Q

What properties do myocardial cells share with neural and skeletal tissues?

A

They initiate and propagate action potentials that trigger coordinated myocardial contraction.

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2
Q

What are intercalated discs in cardiac myocytes?

A

Specialized junction complexes that transfer mechanical forces and contain gap junctions for action potential spread.

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3
Q

How many mL of O2 do cardiac myocytes consume at rest?

A

8-10 mL O2/100g/min.

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4
Q

Define automaticity in cardiac cells.

A

The ability to generate an action potential spontaneously.

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5
Q

What does excitability refer to in cardiac cells?

A

The ability to respond to an electrical stimulus by depolarizing and firing an action potential.

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6
Q

What is conductance in the context of cardiac cells?

A

The ability to transmit electrical current through ion channels.

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7
Q

What determines the resting membrane potential (RMP)?

A

Serum K+ is the primary determinant of RMP.

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8
Q

What happens to RMP when serum K+ decreases?

A

RMP becomes more negative, making myocytes more resistant to depolarization.

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9
Q

What is threshold potential (TP)?

A

The voltage change required to initiate depolarization.

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10
Q

How does increased serum Ca++ affect threshold potential?

A

TP becomes more positive, and cells become more resistant to depolarization.

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11
Q

What is depolarization in cardiac cells?

A

The movement of a cell’s membrane potential to a more positive value.

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12
Q

What is the refractory period?

A

The time when a cell is resistant to subsequent depolarization.

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13
Q

What is hyperpolarization?

A

The movement of a cell’s membrane potential to a more negative value beyond the baseline RMP.

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14
Q

What is the primary function of the Na+/K+ ATPase in excitable tissue?

A

To restore ionic balance towards RMP.

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15
Q

What is the effect of digoxin on Na+/K+ ATPase?

A

It inhibits the Na+/K+ ATPase.

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16
Q

What are the phases of the cardiac action potential (AP) in myocytes?

A

Phase 0, Phase 1, Phase 2, Phase 3, Phase 4.

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17
Q

What occurs during Phase 2 of the cardiac action potential?

A

Plateau phase where Ca++ enters and K+ exits.

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18
Q

What is the intrinsic firing rate of the SA node?

A

70-80 BPM.

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19
Q

How does the sympathetic nervous system affect heart rate?

A

Increases HR by increasing Na+ and Ca++ conductance.

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20
Q

What is the equation for oxygen content (CaO2) in arterial blood?

A

CaO2 = (Hgb • SaO2 • 1.34) + (PaO2 • 0.003).

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21
Q

What does the O2 extraction ratio (EO2) indicate?

A

How much O2 is extracted by the tissues.

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22
Q

What is Poiseuille’s Law used to understand?

A

The relationship between blood flow, vessel diameter, viscosity, and tube length.

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23
Q

What is the normal value for cardiac output (CO)?

A

5-6 L/min.

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24
Q

What does the Frank-Starling mechanism describe?

A

The relationship between end-diastolic volume (preload) and stroke volume (SV).

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25
Q

What is the effect of decreased preload on stroke volume?

A

It leads to a lower stroke volume.

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26
Q

What is contractility (inotropy)?

A

The ability of myocardial sarcomeres to perform work independently of preload and afterload.

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27
Q

What factors increase contractility?

A
  • SNS stimulation
  • Catecholamines
  • Ca++
  • Digitalis
  • PDEi
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28
Q

What is afterload?

A

The force that the ventricle must overcome to eject its stroke volume.

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29
Q

What is the normal range for systemic vascular resistance (SVR)?

A

800-1,500 dynes•sec•cm-5.

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30
Q

How does wall stress relate to myocardial oxygen consumption?

A

Increased wall stress also increases myocardial O2 consumption.

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31
Q

What happens during the cardiac cycle?

A

It involves the sequence of events in the heart during one complete heartbeat.

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32
Q

What is stress in the context of cardiac function?

A

Force that holds the heart together

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33
Q

How is wall stress reduced?

A

By:
* ↓ Intraventricular pressure
* ↓ Radius
* ↑ Wall thickness

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34
Q

What is the relationship between wall stress and myocardial O2 consumption?

A

Anything that increases wall stress also increases myocardial O2 consumption

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35
Q

What therapies can reduce afterload?

A

Arterial vasodilators (Propofol, Clevidipine) & sympathectomy (Regional anesthesia)

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36
Q

What is the cardiac cycle?

A

A sequence of electrical & mechanical events from the beginning of one heartbeat to the next, divided into systole and diastole

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37
Q

What precedes mechanical events in the cardiac cycle?

A

Electrical events

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38
Q

What does the pressure-volume (PV) loop assess?

A

Systolic and diastolic function as well as the integrity of the cardiac valves

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39
Q

What does the height of the PV loop represent?

A

Ventricular pressure

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40
Q

What does the width of the PV loop represent?

A

Ventricular volume

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41
Q

What does the area of the PV loop indicate?

A

Myocardial workload

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42
Q

What are the four phases of the ventricular-volume loop?

A
  1. Period of ventricular filling
  2. Isovolumetric contraction
  3. Ventricular ejection
  4. Isovolumetric relaxation
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43
Q

What is external work in cardiac function?

A

The amount of work the ventricle must do to eject its stroke volume (SV)

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44
Q

How is external work estimated?

A

By multiplying SV (Width) by the mean aortic pressure (Height)

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45
Q

What affects the morphology of the PV loop?

A

Changes in preload, contractility, and afterload

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46
Q

How does an increase in preload affect the PV loop?

A

The PV loop gets wider but returns to the original end-systolic volume

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47
Q

How does a decrease in preload affect the PV loop?

A

The PV loop gets narrower but returns to the original end-systolic volume

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48
Q

How does an increase in contractility affect the PV loop?

A

The PV loop gets wider, taller, & shifts to the left

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49
Q

How does a decrease in contractility affect the PV loop?

A

The PV loop gets narrower, shorter, & shifts to the right

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50
Q

How does an increase in afterload affect the PV loop?

A

The PV loop gets narrower, taller, & shifts the end-systolic volume to the right

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51
Q

How does a decrease in afterload affect the PV loop?

A

The PV loop gets wider, shorter, & shifts the end-systolic volume to the left

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52
Q

Where do the left and right coronary arteries arise from?

A

The aortic root (from the sinus Valsalva)

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53
Q

What does the left anterior descending artery perfuse?

A

Anterolateral & apical walls of the left ventricle and anterior two-thirds of the interventricular septum

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54
Q

What does the circumflex artery supply?

A

Left atrium and lateral & posterior walls of the left ventricle

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55
Q

What does the right coronary artery perfuse?

A

Right atrium, right ventricle, interatrial septum, and posterior third of the interventricular septum

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56
Q

What defines coronary dominance?

A

The origin of the posterior descending artery (PDA), which can arise from RCA, circumflex, or both

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57
Q

What is the role of the coronary sinus?

A

Returns cardiac venous blood to the right atrium

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58
Q

What is coronary reserve?

A

The difference between coronary blood flow at rest and maximal dilation

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59
Q

What are the determinants of O2 delivery?

A

Coronary blood flow, CaO2, & O2 extraction

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60
Q

What are the determinants of O2 demand?

A

Preload, afterload, contractility, & wall stress

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61
Q

What happens during ischemia?

A

Anaerobic metabolism leads to lactic acid production, impairing myocardial performance

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62
Q

What are the classic symptoms of aortic stenosis?

A

Syncope, angina, and dyspnea (SAD)

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63
Q

What is the normal size of the aortic valve orifice?

A

2.5 – 3.5 cm2

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64
Q

What is a diagnostic indicator for severe aortic stenosis?

A

Mean transvalvular pressure gradient >40 mmHg

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65
Q

What compensatory mechanisms occur in aortic stenosis?

A

Increased thickness of the LV wall, decreased compliance, & smaller chamber radius

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66
Q

What is the effect of tachycardia on myocardial O2 supply and demand?

A

↓ Supply & ↑ demand

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67
Q

What is the effect of increased afterload on myocardial O2 demand?

A

Increases myocardial O2 demand

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68
Q

What is the role of adenosine in coronary circulation?

A

It is a potent coronary vasodilator released as MVO2 increases

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69
Q

What causes coronary artery constriction?

A

α (Epicardial), Histamine 1

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70
Q

What causes coronary artery dilation?

A

β2 (Endocardial), Histamine 2, Muscarinic

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71
Q

What is aortic insufficiency?

A

Aortic insufficiency leads to volume overload & eccentric hypertrophy. A portion of the previous ejected SV re-enters the left ventricle during diastole.

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72
Q

What causes aortic insufficiency?

A

Causes include incomplete valve or dilation of the aortic root or its supporting structures, endocarditis, and aortic root dissection.

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73
Q

What are the chronic causes of aortic insufficiency?

A
  • Valvular calcification
  • Marfan syndrome
  • Ehler-Danlos syndrome
  • Ankylosing spondylitis
74
Q

What must be done before initiating cardiopulmonary bypass in a patient with aortic regurgitation?

A

Cardioplegia must be injected retrograde or directly into each coronary ostia.

75
Q

What happens if the mitral valve is incompetent in a patient with aortic insufficiency?

A

An elevated LVEDP will reflect to the pulmonary circulation, causing congestion.

76
Q

What are the anesthesia goals for aortic insufficiency?

A
  • Heart rate: Elevate
  • Heart rhythm: NSR
  • Preload: Maintain or increase
  • Afterload: Decrease
  • Contractility: Maintain
  • Pulmonary vascular resistance: Maintain
  • SVR: Prevent increased SVR
77
Q

What characterizes the arterial waveform in aortic insufficiency?

A

Increased pulse pressure, sharp upstroke, low diastolic pressure, and bisferiens pulse.

78
Q

What is the normal mitral valve area?

A

Normal = 4 – 6 cm2; Severe = <1 cm2.

79
Q

What is the most common cause of mitral stenosis in the US?

A

Endocarditis and mitral calcification.

80
Q

What can increased left atrial pressure lead to in mitral stenosis?

A

Pulmonary hypertension and a-fib.

81
Q

What are the anesthetic goals for mitral stenosis?

A
  • Heart rate: Low side of normal w NSR
  • Preload: Maintain
  • Afterload: Maintain
  • Contractility: Maintain
  • SVR: Maintain
  • Pulmonary vascular resistance: Avoid increase
82
Q

What are common causes of mitral insufficiency?

A
  • Mitral valve prolapse
  • Myxomatous degeneration
  • Ischemic heart disease
  • Rheumatic fever
  • Rheumatoid arthritis
  • Endocarditis
  • Lupus
83
Q

What does mitral insufficiency cause in terms of volume changes?

A

Volume overload & eccentric hypertrophy.

84
Q

What should be avoided in patients with mitral insufficiency?

A
  • Slower HR
  • Increased pressure gradient between LV & LA
  • Increased SVR
  • Increases size of valve orifice
85
Q

What are the anesthetic goals for mitral insufficiency?

A
  • HR: Elevated
  • Heart rhythm: NSR
  • Preload: Maintain or increase
  • Afterload: Decrease
  • Contractility: Maintain
  • SVR: Decrease
  • PVR: Avoid increase
86
Q

What is the risk after mitral valve repair?

A

Risk of systolic anterior motion (SAM) of the anterior leaflet, leading to outflow obstruction.

87
Q

What are the locations to listen for pathologic murmurs?

A
  • Aortic Stenosis: Right sternal border
  • Aortic Regurgitation: Right sternal border
  • Mitral Stenosis: Apex & left axilla
  • Mitral Regurgitation: Apex & left axilla
88
Q

What is TAVR?

A

TAVR is a minimally invasive method of replacing the aortic valve in patients with aortic stenosis.

89
Q

What are the approaches for TAVR?

A
  • Transfemoral
  • Transaortic
  • Transapical
90
Q

What complications can occur with TAVR?

A
  • Stroke
  • Perivalvular leak
  • Dysrhythmias
  • Acute hemodynamic instability
  • Tamponade
  • Coronary occlusion
  • Hemorrhage due to vascular injury
91
Q

What are the patient-related conditions that increase cardiac risk?

A
  • History of ischemic heart disease
  • CHF
  • Cerebrovascular disease
  • DM
  • Serum creatinine >2 mg/dL
  • High risk surgeries
92
Q

What is myocardial oxygen imbalance?

A

Myocardial O2 balance is determined by the ratio of O2 supply relative to demand.

93
Q

What factors can lead to decreased O2 delivery?

A
  • Decreased coronary flow
  • Tachycardia
  • Decreased aortic pressure
  • Decreased vessel diameter
  • Decreased CaO2
  • Hypoxemia
  • Anemia
  • Decreased O2 extraction
94
Q

What are the compensatory mechanisms for heart failure?

A
  • Chronic SNS activation
  • Down-regulation of Beta R
  • Excessive vasoconstriction
  • Fluid retention
  • Cardiac remodeling
95
Q

What is the role of BNP in heart failure?

A

BNP is a biomarker for assessing risk in patients with heart failure, promoting natriuresis, diuresis, and vasodilation.

96
Q

What is secondary hypertension?

A

Secondary HTN is an elevated BP that has a definitive cause.

97
Q

What are the causes of secondary hypertension?

A

Causes include conditions such as renal disease, endocrine disorders, and sleep apnea.

98
Q

What is the impact of chronic hypertension on the body?

A
  • LVH
  • CAD
  • CHF
  • Stroke
  • Arterial aneurysm
  • Renal disease
99
Q

What should be done for patients on ACEi/ARB therapy who experience hypotension?

A

Treat with vasopressin, terlipressin, or methylene blue.

100
Q

What is the preferred treatment for hypertensive crisis?

A

Antihypertensive agents that target the SNS or myocardium and vascular smooth muscle.

101
Q

What is the benefit of using mixed alpha 1/Beta 1 & Beta 2 antagonists?

A

Systemic vasodilation due to the alpha-1 component

102
Q

What can happen if a non-selective beta blocker is given to a patient in hypertensive crisis?

A

It can precipitate heart failure

103
Q

What types of drugs target the myocardium and vascular smooth muscle?

A

CCB and vasodilators

104
Q

How do vasodilators promote vasodilation?

A

By increasing nitric oxide

105
Q

What is the effect of hydralazine on afterload?

A

Reduces afterload

106
Q

What is the effect of nitroglycerin on preload?

A

Reduces preload

107
Q

What is the effect of sodium nitroprusside on preload and afterload?

A

Reduces both preload and afterload

108
Q

What do ACE inhibitors and ARBs inhibit?

A

Angiotensin-2-mediated vasoconstriction and aldosterone release

109
Q

How do diuretics decrease blood pressure?

A

By reducing intravascular volume

110
Q

What do aldosterone antagonists block?

A

Aldosterone at mineralocorticoid receptors

111
Q

What is the mechanism of action of calcium channel blockers (CCBs)?

A

Increase vasodilation and decrease inotropy, chronotropy, and dromotropy

112
Q

Which CCBs are effective in reducing heart rate in patients with tachycardia or atrial fibrillation?

A

Verapamil and diltiazem

113
Q

Rank CCBs in order of their impairment of contractility from highest to lowest.

A

Verapamil > Nifedipine > Diltiazem > Nicardipine

114
Q

In a patient with decreased contractility, which CCB is a better choice?

115
Q

Which CCB is proven to reduce morbidity and mortality from cerebral vasospasm?

A

Nimodipine

116
Q

What do all CCBs bind to?

A

The alpha-1-subunit of the L-type calcium channel

117
Q

What is the mechanism of action of Clevidipine?

A

Arterial vasodilation reduces systemic vascular resistance without affecting preload

118
Q

What are the contraindications for Clevidipine?

A

Allergy to eggs, impaired lipid metabolism, severe aortic stenosis

119
Q

What is the role of the pericardium?

A

Surrounds the heart and provides a minimal friction environment

120
Q

What is acute pericarditis usually caused by?

A

Inflammation

121
Q

What does constrictive pericarditis lead to?

A

Reduced diastolic filling due to thickening of the pericardium

122
Q

What is the treatment for constrictive pericarditis?

A

Pericardiotomy

123
Q

What are the anesthetic considerations for constrictive pericarditis?

A
  • Avoid bradycardia * Preserve contractility * Maintain afterload
124
Q

What is pericardial effusion?

A

Accumulation of fluid inside the pericardial sac without increased pericardial pressures

125
Q

What is cardiac tamponade?

A

Fluid accumulation inside the pericardium that compresses the myocardium

126
Q

What is Beck’s triad?

A
  • Muffled heart tones * Jugular venous distention * Hypotension
127
Q

What is pulses paradoxus?

A

Decreased SBP by >10 mmHg during inspiration

128
Q

What does Kussmaul’s sign indicate?

A

Increased CVP and jugular venous distention during inspiration

129
Q

What are the surgical management options for cardiac tamponade?

A
  • Pericardiocentesis * Pericardiostomy
130
Q

What are complications of pericardiocentesis and pericardiostomy?

A
  • Pneumothorax * Re-accumulation of pericardial fluid * Puncture of coronary vessels
131
Q

What is the preferred anesthetic management for cardiac tamponade?

A

Local anesthesia over general anesthesia for better hemodynamic stability

132
Q

What is the #1 goal in anesthetic management of cardiac tamponade?

A

Preserve myocardial function

133
Q

What type of ventilation is preferred in cardiac tamponade cases?

A

Spontaneous ventilation over positive pressure ventilation

134
Q

What is infective pericarditis (IE)?

A

Typically a bacterial infection of the heart valves & endocardium caused by bacteremia

135
Q

When is antibiotic prophylaxis recommended for infective endocarditis?

A

Only if the patient is at higher risk for developing IE

136
Q

List patient-related factors that increase the risk of infective endocarditis.

A
  • History of IE
  • Prosthetic heart valve
  • Heart transplant with valvopathy
  • Certain congenital heart defects
137
Q

What are surgery-related factors that necessitate antibiotic prophylaxis against endocarditis?

A
  • ‘Dirty’ procedures
  • Dental procedures with gingival manipulation
  • Certain respiratory procedures
  • Biopsies of infected lesions
138
Q

True or False: Antibiotic prophylaxis is required for mitral valve prolapse.

139
Q

What IV antibiotics are used for IE prophylaxis?

A
  • Ampicillin
  • Cefazolin
  • Ceftriaxone
  • Clindamycin
140
Q

What is hypertrophic cardiomyopathy?

A

The most common autosomal dominant cardiovascular disease and cause of sudden cardiac death in young athletes

141
Q

What causes LV outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy?

A
  • Congenital hypertrophy of the intraventricular septum
  • Systolic anterior motion (SAM) of the anterior leaflet of the mitral valve
142
Q

What are the surgical options to correct LVOT obstruction?

A
  • Septal myomectomy
  • Alcohol injection into septal perforator arteries
  • Mitral valve replacement
143
Q

What is required for a patient receiving a coronary stent?

A

Dual antiplatelet therapy (DAPT) to prevent stent thrombosis

144
Q

What are the components of dual antiplatelet therapy?

A
  • Aspirin (irreversible cyclooxygenase inhibitor)
  • Thienopyridine (usually clopidogrel or ticlopidine)
145
Q

When can elective surgery be performed after stent placement?

A

Varies with type of stent: Angioplasty w/o stent = 2-4 weeks, Bare metal stent = 30 days, Drug eluting stent = 6-12 months depending on the situation

146
Q

What is the function of cardiopulmonary bypass (CPB)?

A

Allows the surgeon to operate on an immobile heart by circulating blood through a bypass circuit

147
Q

What type of pump is preferred in CPB and why?

A

Centrifuge pump due to lower risk of high pressure and reduced risk of line rupture

148
Q

What is the primary advantage of a membrane oxygenator over a bubble oxygenator?

A

Safer, as it carries a lower risk of cerebral air embolism

149
Q

What is the primary purpose of cardioplegia during CPB?

A

Arrests the heart in diastole to reduce myocardial oxygen consumption

150
Q

What is the most common cause of awareness during CPB?

A

During sternotomy or rewarming

151
Q

What are the indications for an intra-aortic balloon pump (IABP)?

A
  • Cardiogenic shock
  • Myocardial infarction
  • Intractable angina
152
Q

What are the contraindications for an intra-aortic balloon pump?

A
  • Severe aortic insufficiency
  • Descending aortic disease
  • Severe peripheral vascular disease
  • Sepsis
153
Q

What is the purpose of the intra-aortic balloon pump inflating during diastole?

A

Augments coronary perfusion

154
Q

What is the primary function of a Left Ventricular Assist Device (LVAD)?

A

Unloads the failing heart by pumping blood from the LV to the aorta

155
Q

What is the most common cause of death in patients with LVAD?

156
Q

What is the mechanism for the development of abdominal aortic aneurysm (AAA)?

A
  • Destruction of elastin & collagen
  • Inflammation
  • Endothelial dysfunction
  • Platelet activation
  • Atherosclerosis
157
Q

What is the classic triad of AAA rupture?

A
  • Hypotension
  • Back pain
  • Pulsatile abdominal mass
158
Q

At what size is surgical correction of AAA recommended?

A

When the aneurysm exceeds 5.5 cm or grows more than 0.6-0.8 cm per year

159
Q

What does the Crawford classification classify?

A

Aortic aneurysms into 4 types based on involvement of the thoracic & abdominal aorta

160
Q

What is anterior spinal artery syndrome?

A

Ischemia or infarction to the anterior spinal cord segments due to interruption of blood flow to the artery of Adamkiewicz

161
Q

What are the symptoms of anterior spinal artery syndrome?

A
  • Flaccid paralysis of the lower extremities
  • Bowel & bladder dysfunction
  • Loss of temperature & pain sensation
162
Q

What is the significance of the artery of Adamkiewicz?

A

It perfuses the anterior two-thirds of the spinal cord in the thoracolumbar region

163
Q

What is the preferred method for carotid endarterectomy (CEA)?

A

Awake status is best for assessing neurologic integrity

164
Q

What glucose level should be treated to reduce stroke risk on the day of surgery?

A

Hyperglycemia (>200 mg/dL)

165
Q

What is the physiological response to aortic cross-clamping?

A

Creates central hypervolemia by increasing venous return and shifts blood volume proximal to the clamp

166
Q

What should be avoided to treat hyperglycemia?

A

Glucose-containing solutions

Hyperglycemia should be treated with insulin.

167
Q

What blood pressure range should be maintained during cross-clamping?

A

Normal to slightly elevated BP

This is because the vessels in ischemic regions are maximally dilated and perfusion is pressure dependent.

168
Q

What should the SBP be kept under after cross-clamping is revoked?

A

145 mmHg

This helps reduce the risk of bleeding at the graft site.

169
Q

What reflex can be activated by surgical stimulation?

A

Baroreceptor reflex

This can lead to hypotension and bradycardia.

170
Q

What can head rotation, flexion, or extension compress?

A

Carotid and/or vertebral arteries

This can reduce cerebral perfusion.

171
Q

What should be maintained regarding carbon dioxide levels?

A

Normocapnia or mild hypocapnia

Hypercapnia can dilate cerebral vessels and create a ‘steal’ phenomenon.

172
Q

What are some postoperative considerations?

A

Hematoma, RLN injury, labile BP, carotid denervation, stroke

Hypertension is the most common postoperative issue and can cause reperfusion injury.

173
Q

What does Carotid Artery Angioplasty (CAS) use for access?

A

Percutaneous trans vascular access

This allows the stent to be passed into the carotid artery.

174
Q

What anticoagulation is maintained during CAS?

A

Heparin (50-100 u/kg)

This is to maintain ACT > 250 seconds.

175
Q

What is the most common complication of CAS?

A

Thromboembolic stroke

This occurs due to atherosclerotic debris that lodges in the cerebral vasculature.

176
Q

What device is used to catch debris during CAS?

A

Distal protection filter

This is placed beyond the angioplasty balloon.

177
Q

How is an embolic stroke treated?

A

TPA

TPA is a thrombolytic agent used in treating strokes.

178
Q

What occurs during Subclavian Steal Syndrome?

A

Occlusion of the subclavian or innominate artery proximal to the vertebral artery

This usually occurs on the left side.

179
Q

What is the effect of Subclavian Steal Syndrome on blood flow?

A

Reverse flow towards the ipsilateral subclavian artery

Arterial blood is ‘stolen’ from the posterior cerebral circulation.

180
Q

What is the treatment of choice for Subclavian Steal Syndrome?

A

Subclavian endarterectomy

This procedure helps restore normal blood flow.

181
Q

What symptom is associated with Subclavian Steal Syndrome?

A

Lower blood pressure in the ipsilateral arm

The pulse may also be diminished.

APEX/BOARD STUDY (5 decks)

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