Cardiac Exam 1 Flashcards
Atria
Conduits and priming chambers
Ventricles
Pumps
Septum
Divides right and left sides
AV Valves
Tricuspid (right) and Mitral (left)
Semilunar valves
Pulmonary (right) and Aortic (left)
Phase 0
Depolarization: Fast Na+ channels open, membrane potential becomes more positive, Na+ rapidly flows into the cell and depolarizers it.
Phase I
Initial Repolarization: Fast Na+ channels close, cell begins to depolarize, and K+ ions leave the cel through open K+ channels.
Phase II
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.
Phase III
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.
Phase IV
Resting Membrane Potential: About -90 mV, established by Na+ - K+ pump.
Refractory Period
0.25 - 0.3 sec where cardiac muscles cannot be re-excited.
Systole
Ventricular contraction, heart squeezes
Diastole
Ventricular relaxation, heart fills
Percentage of ventricular filling due to atrial contraction?
20-30%
S1
Closing of AV valves
S2
Closing of semilunar valves
Phases of Cardiac Cycle
Atrial Systole Isometric Contraction Ejection Isometric Relaxation Filling
Papillary muscles
Attached to AV valve leaflets by chordate tendinae , which prevent valvular regurgitation
S2 Split
Pulmonic closes after Aortic
Normally more pronounced during inspiration
Cause of heart sounds?
Vibration of taut valve leaflets after closing
3rd Heart Sound
Ken-tuck-Y
“Y” = 3rd sound
Often associated with systolic heart failure
May be normal in children, teens, young adults.
4th Heart Sound
Right before 1st Sound
TEN-nes-see
Atrial contraction Sound
Associated with left ventricular hypertrophy
Grade 1 Systolic Murmur
Very faint
Grade 2 systolic murmur
Quiet, but heard immediately after placing stethoscope on chest
Grade 3 systolic murmur
Moderately loud
Grade 4 systolic murmur
Loud, with palpable thrill
Grade 5 systolic murmur
Very loud, with thrill. May be heard with stethoscope partly off of chest
Grade 6 systolic murmur
Very loud with thrill. May be heard with stethoscope entirely off chest
Normal aortic valve area
2-4 cm^2
Mild aortic stenosis
<25 mmHg 1.5-2 cm^2
Moderate Aortic stenosis
25-40 mmHg 1-1.5 cm^2
Severe Aortic stenosis
40-55 mmHg <1 cm^2
Critical aortic stenosis
> 50 mmHg <0.7 cm^2
Sound of aortic stenosis
Harsh systolic murmur during diastole, radiating to neck
AS Anesthetic Goals
SLOW, SINUS, SVR
Avoid spinal and epidural in moderate and severe AS
Aortic Regurgitation
Eccentric LVH and dilation due to high ventricular volumes
Lowered diastolic BP can reduce coronary flow
MR may occur
Sounds of Aortic Regurgitation
Blowing high-pitched murmur during diastole
Anesthetic goals for AR/AI
FAST, FORWARD, FULL
Consider PA catheter in acutely AR or pts on vasodilators
Epidural and spinal OK if volume maintained
Mitral Stenosis
Symptoms: Pulmonary edema, dyspnea, paroxysmal nocturnal dyspnea, chest pain, palpitations, a-fib, hemoptysis, hoarseness
Pulmonary venous pressures increase, potential pHTN (LA pressure>25 mmHg)
Sounds of MS
Low-pitched crescendo-decrescendo rumbling systolic murmur, heard best @ apex
Anesthetic goals for MS
SLOW, SINUS
maintain preload, contractility, SVR, PVR
LA pressures>25 mmHg will lead to acute pulmonary edema
Mitral Regurgitation
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%
Anesthetic goals for MR
Maintain HR 80-100
Avoid high preload and after load
Neuraxial Anesthesia OK, but avoid bradycardia
Sounds of MR
Holosystolic (during systole) murmur continuing to S2
Heard best @ apex, radiates to axilla
Normal CO
5L/min, but varies widely with metabolic level, activity, size, age
Cardiac Index (CI)
CO/BSA (body surface area, m^2)
Normal CI: 2.5-4.2L/min/m^2
Frank-Starling Mechanism
When venous return increases, heart will stretch:
Increased contractile force, increased HR vis sinus node, increased HR due to sympathetic inputs (Bainbridge Reflex)
Preload
LVEDV
Depends on V filling
Frank-Starling Law
Relationship b/w CO and LVEDV
When HR and contractility remain constant, CO is proportional to preload until excessive volumes are reached
Compliance
Relationship between pressure and volume
Factors Affecting Ventricular Compliance?
Intrinsic Factors: hypertrophy, ischemia, fibrosis
Extrinsic Factors: pericardial dz, distinction of other ventricle, increased airway pressures, tumors, surgical compression
Afterload
Arterial Pressure
Pressure the ventricle must overcome to eject blood
SVR
Right side of heart: PVR
Normal = 50-150 dub-sec-cm^-5
Contractility
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.
Ejection Fraction
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
Ventricular Volume-Pressure Diagram: Phase I
Filling: ventricle fills during diastole until it reaches EDV with little change in pressure
Ventricular Volume-Pressure Diagram: Phase II
Isovolumetric contraction: ventricle contracts but aortic valve is still closed. Volume does not change but pressure increases
Ventricular Volume-Pressure Diagram: Phase III
Ejection: ventricle continues to contract as aortic valve opens. Volume decreases as pressure first increases and then decreases.
Ventricular Volume-Pressure Diagram: Phase IV
Isovolumetric relaxation: aortic valve closes and ventricular pressure drops, but mitral valve is still closed so volume does not change
Ventricular Volume-Pressure Diagrams
Can be used to show the effects of independently changing preload, afterload, or contractility
Increased preload (w/afterload and contractility held constant)
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
Increased afterload (w/preload and contractility constant)
Heart pumping against higher Aortic pressure
Ventricle must generate higher pressures to eject contents
Not as much blood able to leave heart
Increased contractility (w/preload and afterload held constant)
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
High CO due to decreased peripheral resistance
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
Low CO due to decreased effectiveness of cardiac pump
Coronary vessel blockage –> MI
Severe valvular dz
Myocarditis
Cardiac tamponade or pericardial effusion
Pulsus paradoxus: decreased SBP >10 mmHg during inspiration
Low CO due to decreased venous return
Decreased blood volume
Acute venous dilation (fainting)
Obstruction of large veins (pneumothorax, mediastinal mass)
Decreased tissue mass or metabolic rate (aging, bed rest, hyperthyroidism)
Oxygen Fick Method
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)
Indicator Dilution Method
Indicator due injected into RA
Concentration measured continuously at some distal point
Thermodilution Method
Known volume of cold saline injected into RA
Change in blood temperature measured in distal pulmonary artery
Echocardiography
Measurement of Heart chambers and velocity of blood flowing into the aorta and the aorta cross-sectional area
Coronary Artery Anatomy
Lie on the surface of the heart, smaller arteries penetrate into cardiac muscles
Originate from coronary aortic sinuses behind aortic valve leaflets
Coronary Blood Flow
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
Left CA
Supplies LA and LV
Bifurcates into left anterior descending (LAD) and circumflex (Cx)
LAD supplies ventricular septum, anterior wall
Cx supplies lateral wall
Right CA
Supplies RA, RV, inferior left ventricle
Posterior Descending Artery
Supplies Interventricular septum, inferior wall
Is branch of RCA (85%) and LCA (15%)
SA node arterial supply
RCA or LCA
AV Node Arterial Supply
RCA or Cx
Control Of Coronary Blood Flow
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
Myocardial Oxygen Balance
Most O2 consumption due to pressure work
Myocardium extracts 65% of O2 in blood
HR determines both O2 supply and demand in heart
Anesthetic Effects on Myocardial O2 Balance
Coronary vasodilation and reduction of metabolic requirements
Reduction of arterial BP, decrease preload and afterload
Protection against repercussion injury after ischemia
Myocardial O2 Supply
HR
Coronary perfusion pressure: Aortic diastolic pressure, ventricular end-diastolic pressure
Arterial oxygen content: hemoglobin concentration, PaO2
Coronary vessel diameter
Myocardial O2 Demand
HR
Basal metabolic requirements
Wall tension: preload and afterload
Contractility
Shivering
Ischemic Heart DZ
CAD
CAD Pathophysiology
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
CAD Signs and Symptoms
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
Treatment of significant coronary blockage
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)
Post-Stent Care
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
Acute Coronary Syndrome (ACS)
Unstable angina, myocardial ischemia, myocardial infarction
Usually due to rupture of atherosclerotic plaque
Could also occur with coronary artery spasm
ACS EKG
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
Cardiac Muscle Function in ACS
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
Cardiac Markers of ACS
Release of enzymes and cell contents
Elevated levels of CK-MB, Troponin I
Treatment of ACS
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
ACS Recovery
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
Preop Eval for PT with CAD
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
High Risk for ischemia during Anesthesia/Surgery
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
Intermediate Risk for ischemia during Anesthesia/Surgery
Hx of CAD, prior MI, mild angina
Compensated or previous heart failure
Hx of cerebrovascular dz
DM (particularly insulin dependent)
Renal insufficiency (Cr>2)
Minor Risk for ischemia during Anesthesia/Surgery
Advanced age (>70)
Abnl EKG (LV hypertrophy, LBBB, ST-T abnl)
Rhythm other than NS
Low functional capacity
Uncontrolled systemic HTN
High Risk SURGERY for CAD Pts
Emergency major surgery, especially >70 years
Aortic or peripheral vascular surgery
Extensive surgery with large fluid shifts
Intermediate Risk SURGERY for CAD Pts
Intraperitoneal or intrathoracic
Carotid endarterectomy
Head and neck
Ortho
Prostate
Risk Straification
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
