Cards Review Flashcards
Normal Tricuspid Area =
Symptoms begin @
Normal Tricuspid Area = 4-6cm2
Symptoms begin @ <1.5cm2
Normal Mitral Area =
Symptoms begin @
Normal Mitral Valve Area = 4-6cm2
symptoms begin @ 2-3cm2
Normal Area of Aortic Valve
Symptoms begin @
Normal area of AVA = 3-4cm2
Symptoms begin @ <1.5 cm2
Normal Pulmonic Area =
Symptoms begin @
Normal Pulmonic Valve Area = 4 cm2
Symptoms begin @ 2cm2
First Heart Sound =
Closing of the AV valves after atrial contraction, beginning of isovolumetric systole/contraction.
Second Heart Sound =
Sound of the SL valves closing, end of ventricular systole = isovolumetric diastole
Blood supply to the
- MYOCARDIUM
- EPICARDIUM
- ENDOCARDIUM
Blood supply to the
- MYOCARDIUM - Epicardial arteries (RCA/LCA)
- EPICARDIUM - Epicardial arteries (RCA/LCA)
- ENDOCARDIUM - blood within the chambers
LCA
- branches
- supplies
LCA
Left Coronary Artery arises from the left coronary sinus, LCA is short, left main arteria then bifurcates to
- Left Anterior Descending:
- Diagonal branch,
- septal perforating branch that supplies the anterior of LV, anterior 2/3 of interventricular septum, eventually anastomoses with RCA (right dominant system)
- also called “anterior interventricular branch”
- Also supplies part of RV
- leads V1-V2 = septum
- leads V3-V4 = anterior
2. Left Circumflex:
- supplies the posterior + lateral LV
- leads = I, AVL, V5, V6
LCA typically supplies:
- Most of the left ventricle [LAD, LCx]
- Part of the right ventricle [LAD]
- Anterior 2/3 of interventricule septum [LAD]
- AV bundle of conducting tissue
- SA node in 40% of people
RCA
- branches
- supplies
RCA
Right coronary artery arises from the right aortic ostia, runs along the coronary sulcus and branches into 1. SA nodal branch, 2. AV nodal branch, and 3. right marginal branch, 4. posterior descending artery/posterior intervenricular branch
-
SA nodal branch
* 60% of people supplies the SA node
2. AV nodal branch
- feeds CRUX of the heart, junction of septa and walls of four chambers. Feeds AV node in 90% of people
3. Right Marginal Branch
- feeds right border of heart
4. Posterior Descending Artery/Posterior Interventricular Branch
- In right dominant heart feeds posterior 1/3 of interventricular septum and anastamoses with LAD
- Lead I, II, AVF
RCA typically supplies:
- Right atrium
- Most of the right ventricle (some supplied by LAD)
- Part of left ventricle
- Posterior 1/3 of IV septum in right-dominant heart
- SA node in 60% of people - SA nodal branch
- AV node in 80-90% of people - AV nodal branch
Coronary Dominance Stats
Coronary Dominance Stats
- Which artery crosses the crux o the heart to feed the posterior IV septum*
1. In 50% of people it is the RCA
2. In 20% of people it is the LCA
3. in 30% of people it is a balanced pattern
APEX SAYS THAT 80% OF POPULATION IS RIGHT DOMINANT.
What Vessel Supplies the SA node? (stats)
What Vessel Supplies the SA node? (stats)
- RCA - SA nodal branch (60%)
- LCx - 40%
Table of EKG leads and vessels
Coronary Blood Flow =
Coronary Blood Flow =
- 5% of CO or about 250 mL/min
- Flow is determined by
- duration of diastole
- Cardiac Perfusion Pressure
- LCA - flow mostly occurs during diastole
- RCA - flow occurs during both diastole and systole
Cardiac Venous Saturation
Cardiac Venous Saturation
- is the lowest in the body (30%)
- cardiac myocardial oxygen consumption is very high
Cardiac Perfusion Pressure
- Formula
- Normal Values
Cardiac Perfusion Pressure
- Formula
- Diastolic BP - LV End Diastolic Pressure= CPP
- Normal Values
- 50-120 mmHg
- autoregulated between 50-120 mmHg
Myocardial oxygen demand ALTERS autoregulation - O2 tension acting through adenosine, greatest dilation occurs in smallest vessels
LCA autoregulates more than RCA (LV only perfused during diastole)
What determines HR:
What determines HR:
- Intrinsic firing rate of the dominant pacemaker cells (SA node - P cells)
- “rate of spontaneous phase 4 depolarization of the SA node determines HR”
- Autonomic tone
Cardiac Conduction System:
Cardiac Conduction System:
- SA node - Pacemaker - P cells (spontaneous phase 4 depolarization)
- Internodal Tracts - within the atria, help to synchronize atrium
- Anterior/Bachman’s Bundle = spetum
- Middle/Wenckebach’s tract = SVC
- Posterior/Thorel’s tract = septum
- AV node (moderator band/septomarginal trabeculae)
- Bundle of Hiss
- Left and Right Bundle Branches
- Purkinje Fibers
RMP vs Threshhold Potential
RMP vs Threshhold Potential
RMP:
- Difference in electrical potential between the inside/outside of the cell [[inside of cell is negative r/t outside of cell]]
Threshhold Potential: [[-70mV]]
- Internval voltage at which a cell depolarizes
Phases of Myocardial Action Potential:
Phases of Myocardial Action Potential: Five Phases
1. Phase 0: Depolarization/Upstroke
- Depolarization = activation of Fast Na+ channels
2. Phase 1: Initiral Repolarization
- inactivation of fast Na+ channels
- Opening of K+ channels -> K+ efflux (slow)
- Opening of Cl - channels -> chloride influx
- inactivation of fast Na+ channels
- Cells becomes slightly more negative
3. Phase 2: Plateau
- Activation of slow voltagae-gated Ca+ channels - OPEN
- Counters loss of K+ from open K+ channels
- results in slow repolarization -> plateau
- Na+ channels remain in active - prolongs absolute refractory time
- sustained contraciton is necessary for heart’s pumping action
4. Phase 3: Repolarization
- More K+ channels open (delayed rectifiers)
- Slow Ca+ channels deactivate
- This restores cell to RMP (-90 mV)
5. Phase 4: Resting
- K+ channel leak as cell is permeable to K+
- Na/K-ATPase: removes Na+ gained during AP, replaces K+ lost during repolarization
Absolute Refractory Period of Heart Muscle
Absolute Refractory Period of Heart Muscle
- much longer absolute refractory period in cardiac muscle compared to nerve/skeletal muscle
- limits frequency of AP - built in safety mechanism
- PREVENTS tetanic contractions
- NO tetanus in cardiac myocytes
- prevents ectopic pacemakers from stimulating contraction and allows time for ventricle to fill
Phases of SA node Action Potential:
Phases of SA node Action Potential:
Most of the stroke volume is ejected during
Most of the stroke volume is ejected during:
the first 1/3 of systole
Phases of Cardiac Cycle:
Phases of Cardiac Cycle:
Pressure-Volume Loop Cardiac Cycle
Normal End Diastolic Volume
Normal End Diastolic Volume
~ 50 mL
EF% Formula
EF% Formula
- (ESV - EDV) / EDV
- SV / EDV
normal EF% = 60-70%
Wigger’s Diagram
Preload =
Preload = The ventricular wall tension at the end of diastole
Factors that Affect Contractility
Law of LaPlace as it applies to ventricles (Apex)
Myocardial Oxygen Extraction =
Myocardial Oxygen Extraction = 70%
- therefore increasing O2 extraction is not a viable method of increasing oxygen supply.
- Instead, coronary blood flow must increase to meet an increased metabolic demand.
Autoregulation is the net effect of:
Autoregulation is the net effect of:
- Local Metabolism - most important
- as MVO2 increases, coronary endothelium release adenosine as well as other vasodilatory substances.
- Vasodilation decreases vascular resistance - leading to increased blood flow, increases coronary perfusion
- Myogenic Response
* “Myogenic refers to the vessels innate ability to maintain a constant vessel diamete” - Autonomic Nervous system:
- causes of coronary constriction = alpha1(prinzmetal’s angina), histamine-1 - increase intracellular Ca++
- causes of coronary artery dilation = beta 2, histamine 2, (decrease intracellular Ca++), muscarinic (increase NO)
At rest, the myocardium consumes oxygen at rate of
At rest, the myocardium consumes oxygen at rate of :
8-10 mL/min/100g with an extraction ratio of 70%
The coronary sinus oxygen saturation is 30%
“Because of this, the myocardium cannot meaningfully increase its extraction ratio when oxygen demand increases. Instead, coronary blood flow and CaO2 must increase to be able to satisfy the demand.”
most perioperative myocardial infarctions occur
24-48 hours following a surgery
Aortic Stenosis Triad
Aortic Stenosis Triad
- Angina
- Due to increased O2 demand and decreased delivery r/t compression of subendothelial vessels r/t hypertrophy
- DOE
- due to decrease CO
- Syncope
- likely the result of exercise induced drop in SVR and uncompensated decrease in CO due to low SVR, SV is relatively fixed (r/t hypertrophy)
Goals for Anesthesia with AORTIC STENOSIS
Goals for Anesthesia with AORTIC STENOSIS
-
Preload: FULL - very SV dependent
- avoid hypotension r/t reflex tachycardia, decrease DBP = decrease CPP
-
Heart Rate: NORMAL / low normal
- tachycardic -not enough time for perfusion
- A.Fib - very dependent on atrial kick
- bradycardic - decreases CO, cannot compensate bc SV is fixed
- Afterload: Keep high because need DBP to be high enough to perfuse coronaries
- Contractility: maintain
- Rhythm: maintain NSR r/t atrial kick
Avoid decreases in SVR, etomidate > propofol
Avoid drugs that induce tachycardia (ketamine, pancuronium)
High opioid technique, half N2O, half volatile
Careful with DVL r/t catecholamine an tachycardia
Hypotension - tx with alpha agonist, avoid beta stim
Hemodynamic Implications with AORTIC STENOSIS
Hemodynamic Implications with AORTIC STENOSIS
- DECREASED ventricular compliance r/t hypertophy r/t pressure
- Sensitivity to volume depletion, SV is fixed
- Depend heavily on atrial kick for adequate ventircular filling pressure
- Wide swings in ventricular filling pressure
- PCWP will underesimate LVEDP
- INCREASED LVEDP r/t hypertrophy, this will decrease CPP
Adequate diastolic time + perfusion pressure are key
- maintain HR - avoid ischemia, SV is fixed so ensure adequate CO
- maintain DBP - LVEDP is elevated, ensure adqueate CO
Magnitude of Regurg in Aortic Regurg depends on
Magnitude of Regurg in Aortic Regurg depends on
- HR - amount of time available for backward flow to occur
- SVR -pressure gradient across arotic valve
Magnitude of aortic regurg is DECREASED by tachycardia and peripheral vasodilation
Symptoms of Aortic Regurg
Symptoms of Aortic Regurg
- symptoms usually minimal if regurg fraction <40%
- severe with regurg fraction >60%
- widened pulse pressure
- decreased diastolic BP
- bounding pulses
Aortic Regurg can be either chronic or acute
Aortic Regurg can be either chronic or acute
- Chronic:
* such as in rheumatic heart failure, persistent systemic HTN, or bicuspid aortic valve - Acute:
- infective endocarditis, trauma, dissection of thoracic aneurysm
- Pts with acute onset regurg experience severe volume overload in a ventricle that has not had time to compensate (dilate). This typically results in coronary ischemia r/t increase wall stress, rapid deterioration in left ventricular function, decrease CO, pulm edema, and heart failure
Anesthetic Implications of Aortic Regurg
Anesthetic Implications of Aortic Regurg
“Fast HR, Full Volume, Forward Flow”
“Normal to elevated HR, normal to low BP“
- Preload: maintain - increase to maximize foward flow/CO
- HR: normal to high normal (>80 bpm)
- Bradycardia will increase the duration of diastole which is when regurg occurs, will increase LVEDV, tx bradycardia promptly
- Contractility: minimize myocardial depression- may disrupt compensation
If LV failure DOES occur -> treat with vasodilator to decrease afterload and inotrope to increase contractility
“overall modest decreases in SVR and modest increases in HR are reasonable goals for aortic regurg + anesthesia”
If using high opioid technique - AVOID bradycardia
Underlying patho of hemodynamic changes in [chronic] aortic regurg:
Underlying patho of hemodynamic changes in [chronic] aortic regurg:
- dilation of aortic root and chronic regurg leads to chronic volume overload
- chamber size [LV] increases gradually
- Increased wall stress r/t increased LVEDV
- decrease in forward left ventricular SV r/t regurg
- eccentric hypertrophic - chamber enlargement + increased wall thickness
- increase in diastolic chamber compliance - dilation - thus LVEDP is maintained - less risk for ischemia in chronic compared to acute
Hemodynamic changes of mitral stenosis
Hemodynamic changes of mitral stenosis
- LV is not subject to pressure or volume overload, actually LV is underloaded.
- Instead, LA pressures rise -> LA enlargement -> prone to a.Fib
- Decreasein CO is from decreased LV filling and also if a.fib develops
- when CO increases - DOE(?) - from increased LA volume
- severe MS can lead to CHF -> pulm edema
- pulm. congestion can lead to RV failure, pulm HTN
Anesthetic Goals of Mitral Stenosis managment
Anesthetic Goals of Mitral Stenosis managment
- slow, tight/HIGH, full
- preload: enough to maintain flow across stenotic valve
- slow: HR, ensure atrial kick is maintained, allow time for ventriuclar filling
- BP: tight control, avoid decreases in BP because CO is already compromised, maintain slightly higher BP r/t this.
- prevention or treatment of events that can decrease CO or lead to pulmonary edema
- AVOID rapid transfusions, careful with lithotomy positions
*
Symptoms of MS
Symptoms of MS
- dyspnea on exertion
- A. Fib
- orthopnea, paroxysmal noctural dyspnea
- P. Mitrale on EKG
most common valve dx in the US: (2)
most common valve dx in the US: (2)
- Aortic stenosis (calcifcication, bicuspid valve)
- Mitral regurg
MR is associated with:
MR is associated with:
- Mitral stenosis, usually in the context of rhuematic heart dx
- ISOLATED MR is associated with IHD, hx of inferior MI, papillary muscle dysfunction
Severe MR is classified as
Severe MR is classified as
MR >60%
<30% = Mild Symptoms
30-60% = Moderate Symptoms
>60% = Severe Symptoms
Chronic MR can develop…
Chronic MR can develop…
- asymptomatically because the LA will expand to accomodate volume.
Acute MR presents as
Acute MR presents as
- Usually in the setting of inferior MI
- papillary muscle rupture
- acute pulm edema
- cardiogenic shock
- holosystolic murmur
Can monitor degree of MR via
Can monitor degree of MR via :
V wave on CVP
Anesthetic Goals of MR
Anesthetic Goals of MR
- Full, Fast, Forward,
- Preload: Full - ensure enough forward flow
- HR: Fast, less time for regurg
- afterload: low, normal, ensure forward flow
- Contractility - maintain
- Rhythm - NSR, normal/fast, less reliant on atrial kick
Avoid sudden decreases in HR - more time for regurg
Prevent bradycardia
