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Cardiac Physiology CWRU SOM > Cardiac Exam 1 > Flashcards

Cardiac Exam 1 Flashcards

1
Q

Atria

A

Conduits and priming chambers

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2
Q

Ventricles

A

Pumps

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3
Q

Septum

A

Divides right and left sides

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4
Q

AV Valves

A

Tricuspid (right) and Mitral (left)

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5
Q

Semilunar valves

A

Pulmonary (right) and Aortic (left)

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6
Q

Phase 0

A

Depolarization: Fast Na+ channels open, membrane potential becomes more positive, Na+ rapidly flows into the cell and depolarizers it.

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7
Q

Phase I

A

Initial Repolarization: Fast Na+ channels close, cell begins to depolarize, and K+ ions leave the cel through open K+ channels.

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8
Q

Phase II

A

Plateau: Ca+2 channels open and fast K+ channels close. Ca+2 enters the cell. Action potential reaches a plateau. Sustained cardiac contraction occurs here.

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9
Q

Phase III

A

Rapid Repolarization: Ca+2 channels close and slow K+ channels open. K+ ions rapidly exit the cell, ends the plateau and returns cell membrane potential to its resting level.

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10
Q

Phase IV

A

Resting Membrane Potential: About -90 mV, established by Na+ - K+ pump.

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11
Q

Refractory Period

A

0.25 - 0.3 sec where cardiac muscles cannot be re-excited.

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12
Q

Systole

A

Ventricular contraction, heart squeezes

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13
Q

Diastole

A

Ventricular relaxation, heart fills

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14
Q

Percentage of ventricular filling due to atrial contraction?

A

20-30%

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15
Q

S1

A

Closing of AV valves

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16
Q

S2

A

Closing of semilunar valves

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17
Q

Phases of Cardiac Cycle

A 
Atrial Systole
Isometric Contraction
Ejection
Isometric Relaxation
Filling
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18
Q

Papillary muscles

A

Attached to AV valve leaflets by chordate tendinae , which prevent valvular regurgitation

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19
Q

S2 Split

A

Pulmonic closes after Aortic

Normally more pronounced during inspiration

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20
Q

Cause of heart sounds?

A

Vibration of taut valve leaflets after closing

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21
Q

3rd Heart Sound

A

Ken-tuck-Y
“Y” = 3rd sound

Often associated with systolic heart failure

May be normal in children, teens, young adults.

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22
Q

4th Heart Sound

A

Right before 1st Sound
TEN-nes-see

Atrial contraction Sound

Associated with left ventricular hypertrophy

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23
Q

Grade 1 Systolic Murmur

A

Very faint

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24
Q

Grade 2 systolic murmur

A

Quiet, but heard immediately after placing stethoscope on chest

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25
Q

Grade 3 systolic murmur

A

Moderately loud

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26
Q

Grade 4 systolic murmur

A

Loud, with palpable thrill

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27
Q

Grade 5 systolic murmur

A

Very loud, with thrill. May be heard with stethoscope partly off of chest

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28
Q

Grade 6 systolic murmur

A

Very loud with thrill. May be heard with stethoscope entirely off chest

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29
Q

Normal aortic valve area

A

2-4 cm^2

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30
Q

Mild aortic stenosis

A

<25 mmHg 1.5-2 cm^2

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31
Q

Moderate Aortic stenosis

A

25-40 mmHg 1-1.5 cm^2

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32
Q

Severe Aortic stenosis

A

40-55 mmHg <1 cm^2

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33
Q

Critical aortic stenosis

A

> 50 mmHg <0.7 cm^2

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34
Q

Sound of aortic stenosis

A

Harsh systolic murmur during diastole, radiating to neck

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35
Q

AS Anesthetic Goals

A

SLOW, SINUS, SVR

Avoid spinal and epidural in moderate and severe AS

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36
Q

Aortic Regurgitation

A

Eccentric LVH and dilation due to high ventricular volumes

Lowered diastolic BP can reduce coronary flow

MR may occur

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37
Q

Sounds of Aortic Regurgitation

A

Blowing high-pitched murmur during diastole

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38
Q

Anesthetic goals for AR/AI

A

FAST, FORWARD, FULL

Consider PA catheter in acutely AR or pts on vasodilators

Epidural and spinal OK if volume maintained

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39
Q

Mitral Stenosis

A

Symptoms: Pulmonary edema, dyspnea, paroxysmal nocturnal dyspnea, chest pain, palpitations, a-fib, hemoptysis, hoarseness

Pulmonary venous pressures increase, potential pHTN (LA pressure>25 mmHg)

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40
Q

Sounds of MS

A

Low-pitched crescendo-decrescendo rumbling systolic murmur, heard best @ apex

41
Q

Anesthetic goals for MS

A

SLOW, SINUS

maintain preload, contractility, SVR, PVR

LA pressures>25 mmHg will lead to acute pulmonary edema

42
Q

Mitral Regurgitation

A

Acute MR: (normal atrial compliance) pulmonary vascular congestion and edema)

Chronic MR (increased atrial compliance): low CO

Mild: <30% of total stroke volume
Moderate: 30-60%
Severe: >60%

43
Q

Anesthetic goals for MR

A

Maintain HR 80-100

Avoid high preload and after load

Neuraxial Anesthesia OK, but avoid bradycardia

44
Q

Sounds of MR

A

Holosystolic (during systole) murmur continuing to S2

Heard best @ apex, radiates to axilla

45
Q

Normal CO

A

5L/min, but varies widely with metabolic level, activity, size, age

46
Q

Cardiac Index (CI)

A

CO/BSA (body surface area, m^2)

Normal CI: 2.5-4.2L/min/m^2

47
Q

Frank-Starling Mechanism

A

When venous return increases, heart will stretch:

Increased contractile force, increased HR vis sinus node, increased HR due to sympathetic inputs (Bainbridge Reflex)

48
Q

Preload

A

LVEDV

Depends on V filling

49
Q

Frank-Starling Law

A

Relationship b/w CO and LVEDV

When HR and contractility remain constant, CO is proportional to preload until excessive volumes are reached

50
Q

Compliance

A

Relationship between pressure and volume

51
Q

Factors Affecting Ventricular Compliance?

A

Intrinsic Factors: hypertrophy, ischemia, fibrosis

Extrinsic Factors: pericardial dz, distinction of other ventricle, increased airway pressures, tumors, surgical compression

52
Q

Afterload

A

Arterial Pressure

Pressure the ventricle must overcome to eject blood

SVR

Right side of heart: PVR
Normal = 50-150 dub-sec-cm^-5

53
Q

Contractility

A

Inotropy: ability of the heart to pump

Rate of myocardial muscle shortening

Sympathetic activity can increase contractility

Reduced by acidosis, hypoxia, ischemia, infarction, most anesthetics, wall motion abnormalities, valvular dysfunction.

54
Q

Ejection Fraction

A

Fraction of blood volume ejected from the ventricular chamber during systole

Common measure of systolic function

EF=(EDV-ESV)/EDV

Normal EF 50-75%

Normally measured with ECHO

55
Q

Ventricular Volume-Pressure Diagram: Phase I

A

Filling: ventricle fills during diastole until it reaches EDV with little change in pressure

56
Q

Ventricular Volume-Pressure Diagram: Phase II

A

Isovolumetric contraction: ventricle contracts but aortic valve is still closed. Volume does not change but pressure increases

57
Q

Ventricular Volume-Pressure Diagram: Phase III

A

Ejection: ventricle continues to contract as aortic valve opens. Volume decreases as pressure first increases and then decreases.

58
Q

Ventricular Volume-Pressure Diagram: Phase IV

A

Isovolumetric relaxation: aortic valve closes and ventricular pressure drops, but mitral valve is still closed so volume does not change

59
Q

Ventricular Volume-Pressure Diagrams

A

Can be used to show the effects of independently changing preload, afterload, or contractility

60
Q

Increased preload (w/afterload and contractility held constant)

A

More blood returning to heart (increased EDV)

Ventricle stretches and able to eject more blood (increased SV) without requiring increased pressures

Increased area = increased work done by heart

CO increased to compensate for increased preload

61
Q

Increased afterload (w/preload and contractility constant)

A

Heart pumping against higher Aortic pressure

Ventricle must generate higher pressures to eject contents

Not as much blood able to leave heart

62
Q

Increased contractility (w/preload and afterload held constant)

A

Heart stimulated to pump stronger (increased rage of pressure development and ejection velocity)

Heart can generate higher pressures and eject more volume

Decreases end Systolic volume, so SV and EF are higher

Slope of ESPVR line becomes steeper

63
Q

High CO due to decreased peripheral resistance

A

Arteriovenous Shunt: any direct connection between a large artery and vein
Decreased resistance, increased venous return, increased CO

Hyperthyroidism: tissue metabolism increased, O2 usage increases, tissue releases vasodilators, peripheral resistance decreases, venous return and CO increase

Anemia: decreased concentration of RBCs
Decreased blood viscosity –> decreased peripheral resistance
Diminished O2 delivery to tissues –> vasodilation

64
Q

Low CO due to decreased effectiveness of cardiac pump

A

Coronary vessel blockage –> MI
Severe valvular dz
Myocarditis
Cardiac tamponade or pericardial effusion
Pulsus paradoxus: decreased SBP >10 mmHg during inspiration

65
Q

Low CO due to decreased venous return

A

Decreased blood volume
Acute venous dilation (fainting)
Obstruction of large veins (pneumothorax, mediastinal mass)
Decreased tissue mass or metabolic rate (aging, bed rest, hyperthyroidism)

66
Q

Oxygen Fick Method

A

Measure O2 concentration in blood both before and after it passes through the lungs

Mixed venous return from pulmonary artery
Systemic arterial blood from any artery

Measure rate of O2 absorption by lungs

CO = pulmonary O2 absorption (mL/min)/ AV O2 difference (mL/min)

67
Q

Indicator Dilution Method

A

Indicator due injected into RA

Concentration measured continuously at some distal point

68
Q

Thermodilution Method

A

Known volume of cold saline injected into RA

Change in blood temperature measured in distal pulmonary artery

69
Q

Echocardiography

A

Measurement of Heart chambers and velocity of blood flowing into the aorta and the aorta cross-sectional area

70
Q

Coronary Artery Anatomy

A

Lie on the surface of the heart, smaller arteries penetrate into cardiac muscles

Originate from coronary aortic sinuses behind aortic valve leaflets

71
Q

Coronary Blood Flow

A

Fill During diastole

LCA and RCA supply myocardium

Blood returns to the heart via coronary sinus, cardiac veins, thebesian veins

Perfusion intermittent due to compression during ventricular systole

Arterial diastolic pressure determines myocardial blood flow more than MAP

72
Q

Left CA

A

Supplies LA and LV

Bifurcates into left anterior descending (LAD) and circumflex (Cx)

LAD supplies ventricular septum, anterior wall

Cx supplies lateral wall

73
Q

Right CA

A

Supplies RA, RV, inferior left ventricle

74
Q

Posterior Descending Artery

A

Supplies Interventricular septum, inferior wall

Is branch of RCA (85%) and LCA (15%)

75
Q

SA node arterial supply

A

RCA or LCA

76
Q

AV Node Arterial Supply

A

RCA or Cx

77
Q

Control Of Coronary Blood Flow

A

Hypoxia –> coronary vasodilation (adenosine, nitric oxide, other substances)

Indirect autonomic effect: sympathetic –> increased HR, contractility –> increased metabolism –> coronary dilation

Direct autonomic effect: B2 receptors > a1 receptors

78
Q

Myocardial Oxygen Balance

A

Most O2 consumption due to pressure work

Myocardium extracts 65% of O2 in blood

HR determines both O2 supply and demand in heart

79
Q

Anesthetic Effects on Myocardial O2 Balance

A

Coronary vasodilation and reduction of metabolic requirements

Reduction of arterial BP, decrease preload and afterload

Protection against repercussion injury after ischemia

80
Q

Myocardial O2 Supply

A

HR

Coronary perfusion pressure: Aortic diastolic pressure, ventricular end-diastolic pressure

Arterial oxygen content: hemoglobin concentration, PaO2

Coronary vessel diameter

81
Q

Myocardial O2 Demand

A

HR

Basal metabolic requirements

Wall tension: preload and afterload

Contractility

Shivering

82
Q

Ischemic Heart DZ

A

CAD

83
Q

CAD Pathophysiology

A

Myocardial O2 demand > supply

Atherosclerosis: cholesterol deposits beneath vascular endothelium –> calcification –> plaques that obstruct blood flow

Plaques can lead to a thrombus that occluded artery
Can rupture and flow until they block artery (coronary embolus)
Can irritate vascular wall –> vasospasm

84
Q

CAD Signs and Symptoms

A

Angina: pain in chest, left arm/shoulder, neck, face when coronary O2 demand exceeds supply

Can be exacerbated by increased activity, stress, emotions, cold temps, full stomach

Treated acutely with nitrate vasodilators (nitroglycerin)

Treated chronically with ACE inhibitors, ARBs, Ca channel blockers

Beta blockers decrease cardiac sympathetic activity, thus decreasing O2 demand

Stable: comes on with exercise
Unstable: comes on at rest

Dyspnea (SOB)

Can be silent angina: no symptoms despite myocardial ischemia

85
Q

Treatment of significant coronary blockage

A

CABG: vessel from arm or leg grafted from aortic root –> side of coronary artery beyond area of occlusion

Angioplasty: (percutaneous coronary intervention, PCI) balloon-tipped catheter advanced from peripheral artery –> coronary artery, inflated to stretch artery

Stents: steel mesh tubes that hold artery open
Risk of restenosis due to formation of scar tissue
Lower risk when using drug-eluting (DES)

86
Q

Post-Stent Care

A

Pts placed on dual antiplatelet therapy (DAPT)- usually clopidodrel (placid) and aspirin

4-6 weeks after BMS
6-12 months after DES
Asa usually continued indefinitely
Stopping APT increases risk of in-stent thrombosis, especially in the perioperative period- should be done in consultation with pt cardiologist

87
Q

Acute Coronary Syndrome (ACS)

A

Unstable angina, myocardial ischemia, myocardial infarction

Usually due to rupture of atherosclerotic plaque

Could also occur with coronary artery spasm

88
Q

ACS EKG

A

ST segment elevation MI (STEMI) > 1mm in 2 contiguous leads
Thrombus –> abrupt decrease in coronary blood flow

Non-ST segment elevation MI (NSTEMI) - no diagnostic EKG changes
Ischemia, infarction, cell damage
Decreased myocardial O2 supply
Plaque rupture –> thrombosis, inflammation, vasoconstriction, embolization of platelets and clot fragments into coronary microvasculature

V-fib: decreased blood supply to infarcted area –> loss of K+ gradient, increased cell irritability, injury currents

Dilated ventricle –> creation of circular currents in ventricular wall

89
Q

Cardiac Muscle Function in ACS

A

Decreased function –> decreased CO

Hypokinetic or Akinetic wall segments

Dead muscle cells lose structural integrity, bulge out during systole

Cardiogenic shock: peripheral ischemia due to low CO

Rupture of infected area of the heart wall can occur

90
Q

Cardiac Markers of ACS

A

Release of enzymes and cell contents

Elevated levels of CK-MB, Troponin I

91
Q

Treatment of ACS

A

O2, asa, nitrates, morphine, beta blockers

Optimize O2 supply/demand Balance

Anticoagulation (heparin) if possible, consider Antiplatelet meds

Cardio consult

Urgent angiography or thrombolytic therapy for NSTEMI

92
Q

ACS Recovery

A

Replacement of dead muscle with fibroid scar tissue

Collateral circulation: anastomoses of tiny branches of coronary arteries
When coronary occlusion occurs, the anastomoses dilate to restore blood flow

93
Q

Preop Eval for PT with CAD

A

Hx angina, dyspnea

Functional capacity: ability to tolerate exercise without symptoms

EKG not indicated in asymptomatic pts undergoing low risk procedures
Recommended for pts with: > or = 1 risk factor and undergoing vascular surgical procedures
Known CAD, peripheral artery dz, cerebrovascular dz undergoing intermediate-risk surgical procedures

Signs of ischemic heart damage: arrhythmias, LBBB,
Q waves, inverted T waves, poor R wave progression

Echo: in pts with dyspnea, known heart failure; to evaluate L ventricular function

Stress test: direct ischemia and functional capacity

Coronary angiography: used when non-invasive testing shows high cardiac risk

94
Q

High Risk for ischemia during Anesthesia/Surgery

A

Unstable coronary syndromes:

  • Acute (<7days) or recent (8-30days) MI
  • Unstable or sever angina

Decompensated heart failure

Significant dysrhythmias:

  • high grade AV block
  • symptomatic ventricular dysrhythmias
  • supraventricular dysrhythmias with ventricular rate> 100bpm

Severe valvular dz

95
Q

Intermediate Risk for ischemia during Anesthesia/Surgery

A

Hx of CAD, prior MI, mild angina

Compensated or previous heart failure

Hx of cerebrovascular dz

DM (particularly insulin dependent)

Renal insufficiency (Cr>2)

96
Q

Minor Risk for ischemia during Anesthesia/Surgery

A

Advanced age (>70)

Abnl EKG (LV hypertrophy, LBBB, ST-T abnl)

Rhythm other than NS

Low functional capacity

Uncontrolled systemic HTN

97
Q

High Risk SURGERY for CAD Pts

A

Emergency major surgery, especially >70 years

Aortic or peripheral vascular surgery

Extensive surgery with large fluid shifts

98
Q

Intermediate Risk SURGERY for CAD Pts

A

Intraperitoneal or intrathoracic

Carotid endarterectomy

Head and neck

Ortho

Prostate

99
Q

Risk Straification

A

Step 1: if emergency surgery -> go

Step 2: of active cardiac condition -> evaluate and treat

Step 3: if low risk surgery -> go

Step 4: if functional capacity adequate -> go

Step 5: if number of risk factors is:

  • None -> go
  • 1 or more -> go to surgery with HR control; testing only if it will change management
  • > or = 3 and vascular surgery; consider testing if it will change management

Cardiac Physiology CWRU SOM (1 decks)

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