5. Cardiac Physiology I Flashcards
Cardiovascular System (function)
Pump blood
Cardiovascular System
Closed circuit 2 sides (pulmonary, systemic)
Ventricular Contraction
Ventricles must be activated to contract
Electrical activation from cardiac action potentials
Venous Return
VR
Rate at which blood is returned to the heart
Cardiac Output
CO
Rate at which blood is pumped from ventricles
Total systemic blood flow
CO and VR
In a steady state, VR=CO
Right Heart
Pulmonary
100% of blood from R ventricle goes to lungs and gets oxygenated
Left Heart
Systemic
100% of ventricular output goes out to body
Distribution varies - different % to different body systems/parts - all adds up to 100%
Conduction Pathway of the Heart
- Cardiac AP originates at SA node (pacemaker)
- Distributed out through internodal tracts to R and L atria
- AV node - conduction slows down to ensure adequate ventricular filling
- Bundle of His
- R and L bundle branch
- Last point of depolarization, L ventricle
SA Node
Pacemaker of the heart
Spontaneously depolarizes
Sets tone of heart rate
Action Potentials from Various Cardiac Cells Differ
Fast response (contractile) v. slow response (pacemaker/conducting)
Slide 8
Pacemaker Cell
Slow response
Display automaticity
- do NOT require CNS input to elicit AP (can be modified by CNS)
- unstable RMP –> rhythmic APs
gNa is greater
gCa is greater
gK is lower than in fast response cells
Cardiac APs: Phase 4
Spontaneous depolarization or pacemaker potential
Longest portion of SA nodal AP
Accounts for automaticity of SA cells
MDP occurs
Slow depolarization (opening of Na channels = funny current (If) = causes rise in MP)
Rate of rise sets heart rate
MDP
Maximum diastolic potential
Point of maximum repolarization
Cardiac APs: Phase 0 (slow response)
Upstroke
Increased gCa via L type channels
(also some T type)
Overshoot potential less positive than fast response (above 0 for a bit)
Cardiac APs: Phase 3 (slow response)
No phase 1 or 2
Cellular repolarization
- inc K (outward) current
- inactivation of Ca current
Similar to fast response
Non-Pacemaker
Fast response
Occur in atria, ventricles, purkinje fibers
Rapid repolarization
Gap Junctions
Found in intercalated disks
Low resistance pathways
- functional syncytium
- directly transmits depolarizing current across the entire heart
Instantaneous, bidirectional - allows functioning as unit
Non-Pacemaker Cardiac APs: Phase 0
Resting membrane potential: -90mv
-gK»_space;gNa
Due to large, transient inc in gNa (-70 mV)
Initial stimulus: Na and Ca movement into cell via gap junctions
Threshold around -70mV
Na and Ca movement from SA nodal cells
Non-Pacemaker Cardiac APs: Phase 1
Decrease gNa (inactivation)
Increase gK (transient outward current - inactivates very quickly)
Non-Pacemaker Cardiac APs: Phase 2
Plateau due to gradual inc in gCa via L type Ca channels (began to open at -35 to -10 mV)
Balanced by dec in normally high resting gK
Holding membrane in depolarized state
Non-Pacemaker Cardiac APs: Phase 3 and 4
Full repolarization due to inc in gK
IRK voltage activation of gNa, gCa
Normal Heart Rate
60-100 = normal 50-70 = ideal
Latent Pacemakers
Cells in other areas of heart have capacity for spontaneous phase 4 depolarization
Intrinsic automaticity
Cells with the fastest rate of phase 4 depolarization control the heart rate
SA node (60-100) –> atrial foci (60-80) –> AV node (40-60) –> ventricular foci (20-40)
Conduction of Cardiac AP
Not the same in all myocardial tissues
- slowest in AV node (adequate filling)
- fastest in His/Purkinje to ensure quick activation of ventricles
Modulation of Pacemaker Activity
Cardiac slow response cells
Changes in Pacemaker Activity
Emotions Blood pressure Drugs Hormones Etc
- change rate of depolarization of phase 4 (change gK, gNa, gCa)
- change threshold potential
- change maximal diastolic potential
ANS Impact on SA node: Acetylcholine
Parasympathetic
Muscarinic receptors
Dec slope of phase 4 (shifted R and down)
Inc gK (hyperpolarize) Dec gCa
MDP dropped more negative (further from threshold - longer to get to threshold - slows down HR)
ANS Impact on SA Node: Norepinephrine
Sympathetic
Beta 1 receptors
Inc slope of phase 4 (inc gNa and gCa (T type channels))
Accelerates phase 3 repolarization
- shortens AP duration
- inc discharge frequency
Chronotropic Effects
Effects of ANS on heart rate
Dromotropic Effects
Effects of ANS on conduction velocity
Inotropic Effects
Effects of ANS on contractility
Pos –> greater force of contraction of ventricles –> more blood out
Electrocardiogram
Surface recording of the entire heart
Based on conductile system (APs traveling through the heart activating muscle to contract)
NOTE THE RELATION OF AP CONDUCTION TO ECG
Recording the EKG
Electrodes on surface of body
Pos wave of depolarization advances toward pos electrode, upward deflection recorded on EKG
Active (exploring) Electrode
Senses the electrical field
Passive (indifferent) Electrode
Reference electrode (not sensing the field - almost like a ground)
Considered to be at 0mV
Lead
Combination of 2 electrodes
Unipolar Lead
Active plus passive electrode
Measure the voltage only at active electrode
Bipolar Lead
Two active electrodes
Measure the voltage difference bt the two electrodes
Standard Limb Leads
Bipolar limb leads
3 bipolar leads make up Einthoven’s Triangle - heart in center
Lead 1: RA -, LA +
Lead 2: RA -, LL +
Lead 3: LA -, LL +
Lead 2: in line with normal conduction system of heart
Augmented Limb Leads
Unipolar leads
aVR, aVL, aVF
Bisecting corners of Einthoven’s triangle
Frontal and Horizontal Plane Leads
Chest leads (6)
SLIDE 28
10 electrodes on patient …
12 leads!
Standard: I, II, III
Augmented: aVR, aVL, aVF
Precordial: V1-V6
ECG Intervals and Waves
P wave QRS complex ST segment T wave U wave (sometimes)
PR
QT
P Wave
Atrial depolarization
QRS Complex
Ventricular depolarization
T Wave
Ventricular repolarization
Upright wave form - repolarize backwards - outside (epi) to inside (endo)
Normal Sinus Rhythm
Rate: 60-100 bpm
Rhythm originates at SA node and reflects normal electrical activity
Measure Heart Rate
P-P interval = atrial rate
R-R interval = ventricular rate
Sympathetic Activation
Increased heart rate
-shorten P-P, R-R intervals
Increased conduction through AV node
-dec P-R interval (inc speed)
Parasympathetic Activation
Decreased heart rate
-inc P-P, R-R interbals
Decreased conduction through AV node
-inc P-R interval
No vagal innervation of ventricles
Atrial excitation and contraction should be …
completed before the onset of ventricular contraction
Ensures complete ventricular filling
Excitation of cardiac muscle should be …
coordinated to ensure that each heart chamber contracts as a unit
Ensures efficient pumping
The pair of atria and ventricles should be …
functionally coordinated so that both members of the pair contract simultaneously
Cardiac Muscle Contraction (steps)
Contractile or autorhythmic cell connected to contractile cell by gap junctions
- Current spreads through gap junctions to contractile cell
- AP travel along plasma membrane and T tubules
- Ca channels open in plasma membrane (external) and SR (internal)
- Ca induces Ca release from SR
- Ca binds to troponin, exposing myosin binding sites
- Crossbridge cycle begins (muscle fiber contracts)
- Ca is actively transported back into SR and ECF
- Tropomyosin blocks myosin binding sites (muscle fiber relaxes)
Tension
Proportional to ICF Ca concentration
More Ca –> greater tension
Skeletal Muscle
Voluntary
Striated
Multinucleated
Non-branching
Ca from SR
Cannot contract w/out nerve stimulation
Muscle fiber stimulated independently (no gap junctions)
Nerve
Neuromuscular junction
Muscle cell
Cardiac Muscle
Involuntary
Striated
Single nucleus
Branching
Ca from SR, ECF
Can contract w/out nerve stimulation - AP originate in pacemaker cells
Gap junctions present as intercalated discs
Autorhythmic cells
Gap junctions
Contractile cell
The Cardiac Cycle
Diastole + Systole
The mechanical and electrical events that define one phase of cardiac filling and emptying
Duration=60(s/min)/HR
Diastole
Ventricular relaxation and filling
Perfusion of coronary arteries
Systole
Ventricular contraction and ejection
Phases of Cardiac Cycle
Atrial systole (D) Isovolumic contraction (S) Rapid ejection (S) Reduced ejection (S) Isovolumic relaxation (D) Rapid filling (D) Reduced filling (D)
Atrial Systole
Preceded by P wave
At the end of this phase, the vol of blood in LV is maximal (EDV ~120)
During diastole
Atrial muscle contracting to fill ventricles
Isovolumic Ventricular Contraction
Marks beginning of QRS complex
First heart sound heard (S1) - closure of AV valves close
Rapid Ventricular Ejection
Most of stroke volume ejected now –> dec in ventricular volume
Reduced Ventricular Ejection
T wave begins (starts to repolarize)
Isovolumic Ventricular Relaxation
Begins after ventricles are fully repolarized (end of T wave)
Aortic valve closes slightly before pulmonic valve creating S2
Ventricular blood volume is now at lowest point
Volume remaining = ESV (~50)
Rapid Ventricular Filling
Mitral valve opens as ventricular pressure falls below atrial pressure
LV filling begins
Reduced Ventricular Filling
Diastasis
Longest phase, final ventricular filling
P wave begins during this phase
Pressure Volume Loop
Plot of pressure v. volume for one cardiac cycle
Counterclockwise direction
LAP
Left atrial pressure
Pressure at which mitral valve opens
EDP
End diastolic pressure
End of diastole
DBP
Diastolic blood pressure
Right before ejection
Lowest ARTERIAL pressure of cardiac cycle
SBP
Systolic blood pressure
Greatest pressure in AORTA
Stroke Volume (SV)
Volume of blood ejected from one ventricular contraction each time the heart beats
SV=EDV-ESV
Normal: 75 ml/beat
Cardiac Output (CO)
Amount of blood pumped by the heart each minute
CO=SV x HR
Normal: 5 L/min
Ejection Fraction (EF)
Fraction of EDV ejected with one SV
Effectiveness of ventricles in ejecting blood
Indicator of contractility
EF=SV/EDV x 100%
Normal: 55-75%
Dec = problematic Inc = no problems
Increasing Muscle Length
Inc Ca sensitivity of troponin (more myosin exposed)
Inc Ca release from SR
Length Tension Relationship
The length of a single L ventricular muscle fiber just prior to contraction corresponds to L ventricular end diastolic volume
The tension of a single L ventricular muscle fiber corresponds to the tension/pressure developed by the entire L ventricle
Preload
The resting length from which the muscle contracts
Bigger preload - bigger contraction
Length:tension
Volume:pressure
As volume increases, ventricular pressure increases
Length-Tension Relationship
Inc preload –> inc sarcomere length toward optimum actin myosin overlap
Left Ventricular End Diastolic Volume
aka end diastolic fiber length
preload for the L ventricle
Greater EDV - greater stretch on ventricles - greater force of contraction to get out of SV to get out EF
Afterload
The force against which cardiac muscle shortens
The load on the muscle during contraction
LV: afterload = aortic pressure
Hypertension
Increased afterload - harder to get SV out
Hypotension
Decreased afterload - easier to get blood out
Acute Increased Afterload
= dec SV
blood remaining inc preload = restore SV
Chronic Increased Afterload
aka chronic hypertension
hypertrophy (lay down more sarcomeres in parallel)
Hypertrophy increases the force of contraction at a given preload and helps maintain SV
Contractility
Change in performance at a given preload
Changes due to intracellular dynamics of Ca
- inc contractility = more Ca
- dec contractility = less Ca
Volume ejected in systole is determined by
EDV
Positive Inotropic Effect
Increase in contractility (ie: inc in SV and CO) for a given EDV
- dopamine, dobutamine, digoxin, amiodarone
- drugs provide more Ca and at a faster rate to the contractile machinery
Negative Inotropic Effect
Decrease in contractility (ie: dec in SV and CO) for a given EDV
- beta blockers, Ca channel blockers
- drugs provide less Ca and at a slower rate to the contractile machinery
Factors determining overall force of ventricular contraction
Preload
Contractility
SLIDE 50
Frank Starling Relationship
volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole
- ensures that the volume the heart ejects in systole equals the volume it receives in venous return –> closed system
- CO at 100% should equal venous return at 100%
inc VR –> inc EDV –> bc length tension relationship –> inc SV
Frank
P developed during systole in a ventricle and the vol present in ventricle just prior to systole
Starling
vol the ventricle ejected in systole was determined by EDV
