Cardiovascular Anatomy, Physiology and Pathophysiology Review

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CardiovascularAnatomy, Physiology and
PathophysiologyReview

• Jeffrey Groom, MS, CRNA, ARNP
• Principles of Anesthesia III - Cardiothoracic
  Anesthesia
• FIU Anesthesiology Nursing Program

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Cardiac Anatomy

• Pumbing
• Electrical
• Mechanical

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Heart
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1. Left anterior descending
2.Diagonal
3.Septal
4.Circumflex
5.Circumflex marginal
6.Right 7.Acute
marginal
8.Posterior descending
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ECG and Coronary Anatomy
Anatomic Site ECG Leads Artery
Inferior II, III, aVF Right
Lateral I, aVL, V5, V6 L Circumflex
Anterior V3-V4 (I, aVL) Left
Anteroseptal V1-V2 LAD
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Ionic Basis of Cardiac Action Potentials
4 Resting Potential (- 70 to - 90 mV)
primarily due to iK PUSHED TO THRESHOLD 0
Depolarization Increased iNa decreased iK 1
Early Repolarization Voltage-dependent
decrease in iNa, increase in iK (transient)
iCl 2 Plateau Slow (L-type) Ca channels
open iCa 3 RepolarizationiK increases slow
Ca channels close 4 Resting Potential
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Spontaneous Depolarization and Automaticity

• Automaticity
• fastest rate sets the pace
• non-neurally mediated neurally modified
• Methods of modifying the rate and automaticity
• 1o Change the rate of spontaneous
  depolarization
• Acetylcholine increases K current - slows rate
  of spontaneous depolarization
• Epinephrine increases Ca current (calcium
  channel blockers have an opposite effect)
• Change the resting potential
• Acetylcholine increased K current causes cell
  to reach more negative value upon repolarization

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iCa (T-type)
Time (msec)
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Ionic Basis of Nodal Action Potentials

• Unstable Resting Potential
• -60 mV
• Ion Currents
• K current present, but declining
• increasing Na and Ca (T-type) currents
• SPONTANEOUS DEPOLARIZATION
• Membrane potential reaches threshold ( - 40 mV)
• further, rapid increase in T-type Ca current
• transient fall in iK, then increases again early
  in depolarization
• cell reaches 0 to 5 mV
• Repolarization Increase in iK decrease in iCa

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ECG and Action Potential
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Heart Muscle Mechanics

• TENSION (force) -
• Elements contributing
• Contractile element
• gt Active tension
• Elastic element (functional, not anatomic)
• gt Resting tension

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Heart Muscle Mechanics

• 2) LENGTH of muscle fibers influences Tension
• Starling's relationship (Tension (active
  resting) vs Length)
• Performance-wise this is PRELOAD

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Heart Muscle Mechanics
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Heart Muscle Mechanics

• 3) VELOCITY is influenced by Length and Tension
• Calcium activation
• Total calcium released
• Sarcomere length alters calcium sensitivity

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Cardiac Performance

• Cardiac output HR x Stroke volume
• Stroke Volume affected by
• Preload
• After load
• Contractility
• Law of La Place relates ventricular pressure and
  wall tension
• T Pr
• 2h

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LAPLACEs LAW

• Tension Pressure Gradient X Radius

Tension Radius balance required to overcome
Critical closing pressure
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LAPLACEs LAW
Tension Pressure Gradient X Radius
Aortic Aneurysm Rupture R P T
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LAPLACEs LAW
Tension Pressure Gradient X Radius
Left Ventricle - filling gt wall pressure
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Cardiac Cycle

• Isovolumetric ventricular contraction
• Rapid ejection phase
• Reduced ejection phase
• Isovolumetric relaxation
• Rapid filling phase
• Slow filling period
• (Atrial contribution (20-30 in failing heart))

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Cardiac Cycle
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Determinants of Myocardial Function

• Preload
• Afterload
• Contractility
• Heart Rate

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Preload

• Normal heart - increased venous return results in
  increased cardiac output
• Failing heart - sarcomere length is already
  maximal cardiac output increase requires
  increased contractility or heart rate

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Preload

• 1. Preload is the pressure applied to fill the
  heart and is represented by the "passive"
  pressure-volume curve - clinically the end
  diastolic pressure is the preload
• 2. Typical values for LVEDP are 4-5 mmHg.
• 3. A sudden increase in Filling Pressure
  (increased preload)
• a. EDV increases
• b. Heart contracts more forcefully due to
  enhanced thick and thin filament overlap,
  contracts to the same ESV -Starlings Law of the
  Heart
• c. SV, CO and PA are increased

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Afterload

• Afterload is the pressure in the aorta throughout
  the ejection phase - estimate of which is
  arterial pressure
• 2. An sudden increase in mean arterial pressure
  causes 3 things to happen
• a. pressure in the ventricle must rise to a
  higher level during the isovolumetric contraction
  phase before the aortic valve will open
• b. ejected volume goes down
• c. SV and CO will decrease

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Afterload

• 3. A sustained increase in mean arterial
  pressure
• a. the increased ESV plus normal venous return
  volume leads to increased EDV
• b. due to the increased EDV the heart
  contracts more forcefully (Starlings Law of the
  Heart)
• c. SV, CO and PA are increased
• d. at steady state, the pressure volume curve
  is shifted to the right, reserve is diminished

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Contractility

• 1. Altered contractile force due to change in the
  rate or quantity of calcium delivered to the
  myofilaments, or a change in the affinity of the
  filaments for calcium.
• 2. A sudden increase in contractility causes
• a. the heart to contract more forcefully from
  any initial length
• b. the heart to contract more forcefully
  during the ejection phase, leading to a reduced
  ESV and increased SV
• c. increased SV increases CO and PA

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Contractility

• 3. Effect of a sustained increase in
  contractility
• a. the reduced ESV plus normal venous return
  volume leads to a reduced EDV
• b. the heart contracts less forcefully due to
  the reduced EDV
• c. at steady sate, the pressure volume curve
  is shifted to the left, heterometric reserve is
  enhanced

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Cardiac Cycle and Pressure Volume Loops
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Phases of the Cardiac Cycle

• Diastole
• Isovolumic relaxation
• Filling
• Atrial kick
• Systole
• Isovolumic contraction
• Ejection
• Rapid and reduced ejection

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Cardiac Pressure-Volume Loop

• Filling Phase (A-B) radius increases at constant
  filling pressure causing increased wall tension

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Cardiac Pressure-Volume Loop

• Isovolumetric ContractionPhase (B-C) Tension
  increases at constant radius causing increased
  pressure.

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Cardiac Pressure-Volume Loop

• Ejection Phase (C-D) Radius decreases at
  constant tension causing further increase in
  pressure

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Cardiac Pressure-Volume Loop

• Isovolumetric Relaxation Phase (D-A) Tension
  decreases at constant radius causing decreased
  pressure.

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Cardiac Pressure-Volume Loop

• 1. Filling phase AV valve opens, ventricular
  volume increases to its maximum - EDV, pressure
  rises only slightly to EDP.
• 2. Isovolumetric contraction phase Mitral valve
  closes, ventricular pressure rises dramatically
  without change in volume.
• 3. Ejection phase When ventricular pressure
  exceeds aortic pressure aortic valve opens, and
  ejection begins (volume decreases). Initially
  pressure continues to rise then begins to fall.
• 4. Isovolumetric relaxation phase Aortic valve
  closes, volume in ventricle is end systolic
  volume. Pressure in ventricle falls until AV
  valve opens (back to step 1)

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PV Loop RV vs LV
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Effects of Changing Preload on Stroke Volume
Ç Increase
ä Decrease
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Effects of Changing Afterload on Stroke Volume
Cycle 1
Cycle 2
Cycle 3
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Nitroglycerin (Decreased Preload in Ischemic
Heart)
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Factors Affecting Cardiac Output

• RATE
• RHYTHM
• PRELOAD
• AFTERLOAD
• CONTRACTILITY

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Cardiac Output

• CO is the product of heart rate (HR) and stroke
  volume (SV) HR X SV CO
• SV is the difference between end diastolic
  volume and end systolic volume
• Ejection fraction is the amount of blood ejected
  in each beat, SV, divided by end diastolic volume
  (EDV)
• Typical ejection fraction is 60-65, lt40
  indicative of severe cardiac disease

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Control of Stroke Volume

• As ventricular volume increases, ventricular
  circumference increases and lengths of individual
  cells increases
• At constant volume, increased intraventricular
  pressure causes increased tension in the
  individual cells of the ventricular muscle
• As ventricular volume increases, a larger force
  from each muscle cell is required to produce any
  given intraventricular pressure
• Pressure (P) 2 x tension (T) x Wall thickness
  (H) intraventricular radius (r)

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Control of Cardiac Output

• Intrinsic Control rapidly compensate for
  changing conditions and equalize R L outputs
• Heart rate
• Stroke volume Starlings Law of the Heart
• Extrinsic Control Changes in contractility
  (inotropic state)
• inotropic state the relative capability to
  generate tension at a given preload

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Frank-Starling Curve
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Ventricular Performance
End-Diastolic Volume
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Factors Influencing Myocardial Oxygen Consumption

• A. Stroke work is the area within the pressure
  volume loop approximated by SV x PA
• B. Cardiac efficiency is defined as SW divided by
  oxygen consumption (QO2)
• C. Cardiac efficiency is typically between 5-15,
  most energy is dissipated as heat in
  isovolumetric contraction.

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Factors Influencing Myocardial Oxygen Consumption

• D. Factors causing increased oxygen consumption
• 1. increased afterload or contractility
• 2. dilation of the ventricular chamber
• 3. increased heart rate
• 4. increased stroke volume the least
  expensive way to increase CO

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Determinants of Mean Arterial Pressure

• A. The product of cardiac output (CO) and total
  peripheral resistance (TPR) determines MAP
• B. Pressure difference between beginning (aorta)
  and end (right atrium) of the systemic
  circulation must be sufficient to overcome
  resistance of the vessels for flow (cardiac
  output) to occur
• C. CO is proportional to pressure difference
  between aorta and right atrium
• D. CO is inversely proportional to resistance of
  the circulatory system

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Intrinsic Regulation of Myocardial Function
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Indicators of Cardiac Performance

• Cardiac index CO / BSA
• LVEDP (or approximation)
• mean left atrial pressure
• mean pulmonary wedge pressure
• pulmonary artery diastolic pressure
• CI and LVEDP together are better indicators of
  contractility than either alone
• Ejection fraction SV / EDV

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QUESTIONS
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Cardiac Function Alterations
EDV ESV LV SV MAP SVR PCWP HR
ÇPL
ÈPL
ÇAL
ÈAL
ÇCT
ÈCT
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Explain the phases of a Pressure-Volume Loop
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mmHg
Pressure Afterload
ml