Heart Physiology

Department of Physiology

SKZMDC

Cardiac Muscle

• Cardiac Muscle• Atrial muscle • Ventricular muscle • Specialized excitatory & conductive muscle fibers

• Cardiac Muscle as a Syncytium• Intercalated disc “communicating” junctions (gap junctions) -

totally free diffusion of ions• Atrial syncytium• Ventricular syncytium

Cardiac Muscle - Histology

Cardiac Muscle Action Potential

• Depolarization• Fast Na+ channels

• Plateau• Slow Ca++ channels

– Slow to open– Slow to close

• After depol. cardiac muscle membrane permeability to K+ decreases

• Ca++ thus pumped in – excitation-contraction coupling

• Repolarization• Slow K+ channels

• Refractory Periods• 0.25 - 0.3 sec (Absolute)

– Corresponds to plateau

• 0.05 sec (Relative)

AP Comparison

Cardiac Muscle Action Potential

Cardiac Muscle Action Potential

Problem

A drug is found to partially inactivate fast sodium channels.

Q: How would this drug alter the action potential in a ventricular myocyte?

Q: How would the drug alter conduction velocity within the ventricle?

Cardiac Cycle• Cardiac events occurring from beginning of one

heartbeat to the beginning of the next beat• Each cycle – INITIATED by SA node

– Spontaneous generation of AP in SA node

– AP travels through both atria

– Through A-V bundle into the ventricles

» AV node delay (more than 0.1 second)

» Hence atria contract ahead of ventricles

• Diastole and Systole– Period of relaxation – Diastole

» Heart fills with blood

– Period of contraction – Systole

» Ejection of blood

Cardiac Cycle - Components• ECG is the event marker1. Atrial Systole

– Follows P wave (electric activation of atria)– Contributes to ventricular filling– Forms the ‘a wave’ in the venous pulse curve– Ventricular filling by atrial systole – 4th heart sound (not

audible in normal adults)

2. Isovolumetric contraction of Ventricle– Occurs after QRS wave (electric activation of ventricles)– Ventricular P raised above atrial P:

» AV valves close (1st heart sound)» Split in 1st heart sound may occur (since mitral valve

closes b/f tricuspid)– Ventricular P rises – NO CHANGE IN VOLUME

» Aortic valve is closed

Cardiac Cycle - Components3. Rapid Ventricular Ejection

– Ventricular P reaches its max.– When it b/c greater than aortic P – aortic valve opens

» Rapid ejection of blood takes place– Ventricular volume decreases rapidly– Atrial filling begins– Onset of “T wave” (ventricular repolarization) – marks

end of vent. contraction & ejection

4. Reduced Ventricular Ejection– Slower ejection of blood from ventricles

– Ventricle P decreases

– Aortic P decreases (runoff of blood from large arteries into smaller arteries)

– Atrial filling continues

Cardiac Cycle - Components5. Isovolumetric Ventricular Relaxation

– Ventricle replorization is complete (end of “T wave”)– Aortic valve closes (followed by pulmonic valve)

» 2nd heart sound» Splitting occurs during inspiration

– AV valves remain closed mostly during this phase– Ventricle P drops rapidly– Ventricle volume remains CONSTANT – all valves are closed– Incisura – When ventricle P b/c < atrial P – mitral valve opens

6. Rapid Ventricular Filling– Post-mitral valve opening – rapid filling of ventricles occurs– Aortic P continues to decrease – more run-off of blood– 3rd heart sound (due to rapid flow from atria to ventricles

» Normally heard in children» Abnormal in adults

7. Reduced Ventricular Filling (Diastasis)– Longest phase of cardiac cycle– Ventricular filling slows down– Diastasis time period depends on heart rate!

Cardiac Cycle

• End-diastolic volume (130 ml) • End-systolic volume (50 ml)• Stroke volume (70 to 90 ml - @ rest)• Ejection fraction

– % of end-diastolic ventricular volume that is ejected with each stroke

– Is about 65% – Valuable index of ventricular function

• Preload • Afterload

Cardiac Chamber Pressures

Overall

• Length-tension relationship:• Heart during diastole (preload ‘formation’)• It is the study of effects of cardiac muscle stretch on tension

produced in the muscle during diastole & systole

• Force-velocity relationship:– Ventricular function with regards to afterload

• Side point:– Heart after it starts systole, follows:

• Isometeric dynamics – IVC• Isotonic dynamics – Ejection• Isometeric dynamics – IVR

Length (L) –Tension (T) CurveIsolated Cardiac Muscle

Length (L) –Tension (T) Curve – Skeletal M Fiber

Pressure (‘T’) – Volume (‘L’) Curve – Whole Heart

• PV loops:– Depict cardiac

cycle– Show effects

of Preload, afterload & inotropic state on cardiac pumping ability (SV)

Regulation of Heart Pumping

(1) INTRINSIC cardiac regulation of pumping in response to changes in volume of blood flowing into the heart (Frank-Starling Law)

(2) Control of heart rate and strength of heart pumping by ANS

Frank-Starling Law

• “Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole”

• Underlying principle – Length-tension relationship in cardiac

muscle fibers• SV & CO correlate directly with

EDV• EDV correlates with VR• CO = VR (FS Law ensures this)• Cardiac muscle normally operates

only on the ascending limb of the systolic curve

Explanation of FS Law

Concept of Contractility

• Inherent cardiac M Ca++ based ability – INOTROPISM

• Modified by ANS, catecholamines

• Loading situations of the heart• Preload

– Stretch-induced enhancement in contraction» More overlapping of thick & thin filaments» More Ca++ sensitivity of troponin C» More Ca++ release from SR

• After load

Heart Control by ANS

• Sympathetic • NE via action on Beta-1 receptors

– Positive CHRONOTROPIC» Increased HR (increase Phase-4 depolarization)

– Positive IONOTROPIC» Increased force of contraction (increased inward Ca+

+ current during plateau + increases the ability of SR Ca++ pump)

– Positive DROMOTROPIC» Increased conduction velocity through AV node

(increased inward Ca++ current)» Decreased PR interval

– Positive BATHMOTROPIC » Increased excitability of myocardium

Heart Control by ANS

• Parasympathetic– SA node, atria & AV node have supply,

ventricles don’t!– Ach via muscarinic receptors

• Negative chronotropic» Decreasing phase-4 depolarizations

• Negative dromotropic• Negative ionotropic

• Vagal escape

Determinants of Performance of Heart as a Pump

• 4 factors: ‘Loading’ conditions of the cardiac muscle

(1) Preload, or the initial length to which the muscle is stretched prior to contraction

(2) Afterload, or all the forces against which cardiac muscle must contract to generate pressure and shorten

‘Extrinsic’ factors

(3) Contractility, or inotropic state

(4) Inotropic effect of increased heart rate (beats/min)

S-A Nodal Action Potential– IcaL (long-lasting)

– IcaT (transient)

– Firing potential:

-40 mv– Hyperpolarization

Cardiac Impulse• Initiated in SA node• Spreads radially into atrial muscle mostly @ 0.3 m/sec• Atrial conduction is done via bands of fibres

• Anterior• Middle• Posterior

• Arrives at AV node after 0.03 sec• AV delay of 0.13 sec occurs

• 0.09 in bundle• 0.04 in bundle of HIS• Reason for delay?• Benefit of delay?

• Total delay at this point is 0.16 sec

Cardiac Impulse

• After AV node – Velocity is maximum– Bundle of HIS – 1 m/sec– Purkinje system – 4 m/sec

• From the top of septum – via purkinje system – all of ventricle – 0.06 – 0.1 sec

• Total duration: 0.22 sec• Parts that are last depolarized

• Posterobasal portion of left ventricle• Pulmonary conus• Upper most part of septum

Normal ECG

• ECG is produced only when current flows through the heart and this occurs only when the heart is partially depolarized/polarized

Normal ECG

• P wave• Atria depolarize before

contraction• 0.08 - 0.10 sec

• QRS complex• Ventricles depolarize before

contraction• 0.06 – 0.10 sec

• T wave• Ventricles repolarize• Atrial T wave is obscured by

QRS• Duration normally not taken

• U wave• Inconstant finding• Slow repolarization of

papillary muscles

Normal ECG• PR interval – 0.16 sec

• Time b/w beginning of P wave and beginning of QRS complex

– Interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles

» Prolonged: Vagal stimulation, AV block

» Shortened: Accelerated AV conduction, sympathetic stimulation

• ST interval (QT minus QRS) – 0.32 sec• Ventricular repolarization

• Q-T interval – 0.2-0.40 sec • Ventricular depolarization and ventricular repolarization• Corresponds to AP duration

» Prolonged: ventricular extrasystole

Dipole

• The electric dipole consists of two equal and opposite charges, +q and –q, separated by a distance d

• Dipole vector:• Vector whose magnitude is equal to the dipole

moment [voltage] and that points from –ve charge to + one

• Direction of dipole is from –ve towards +ve

1. A wave of depolarization heading toward the +ve electrode is recorded as a +ve voltage

• Represents Atrial & Vent. Depol.2. A wave of repolarization moving away from a +ve electrode

produces a +ve voltage difference• T-wave (Vent. Repol.)

3. A wave of repolarization moving toward a +ve electrode produces a –ve voltage deflection

• Atrial Repol.

Mean Electrical Vector/s

• Individual waves of depol. – electrical vectors

• Summation of electrical vectors at any instance – mean electrical vector (MEV)

• Direction of MEV determines its polarity & magnitude*

Mean Electrical Axis

• 1-4 are individual MEVs during ventricle depol.

• Give rise to QRS

• 1-4 summed up in time:

• Mean Electrical Axis– It is the average ventricle

depolarization vector over time

– Deviation is clinically imp*

Rules of ECG Interpretation

1. A wave of depolarization traveling toward a +ve electrode results in a +ve deflection in ECG

• [Corollary: A wave of depolarization traveling away from a positive electrode results in a negative deflection.]

2. A wave of repolarization traveling toward a +ve electrode results in a -ve deflection

• [Corollary: A wave of repolarization traveling away from a positive electrode results in a positive deflection.]

Rules of ECG Interpretation

3. A wave of depolarization or repolarization oriented perpendicular to an electrode axis has no net deflection.

4. The instantaneous amplitude of the measured potentials depends upon the orientation of the +ve electrode relative to the mean electrical vector

Rules of ECG Interpretation

5. Voltage amplitude (+ve or -ve) is directly related to the mass of tissue undergoing depolarization or repolarization

ECG Written Competition 2011

• “Vectors in ECG”• Based on supplimental material.doc uploaded on:

– Physiologylectures @ hotmail.com (facebook or slideshare.com)

– Reward:• Top written essay: ECG Cup + Box of (delicious) chocolates• 1st runner up: Certificate + Single chocolate bar• 2nd runner up: Certificate + Candy bag

– Assignments are to be turned in by 30th April• No late submissions will be entertained

– Assignments HAVE to be Original• The department may ask a student to defend his/her essay in verbal • Simple copy/paste submissions are discouraged

ECG Leads• Recorded by placing an array of electrodes at

specific locations on the body surface

• Electrodes are placed on:• Each arm & leg• 6 electrodes placed on chest

• Three basic types of ECG leads are recorded by these electrodes:

• Standard limb leads (Bipolar) • Augmented limb leads (Unipolar)• Chest leads (Unipolar)

ECG Standard Limb Leads:

Einthoven’s Triangle

• Einthoven’s triangle– Wave of depolar. -

toward left arm - +ve deflection (lead I*)

– Wave of depolar. - away from left arm - deflection is –ve

– Wave of depolar. - toward left leg - +ve deflection (leads II and III)

Standard Limb Leads:

Normal ECGs

ECG Standard Limb Leads:

Axial Reference System

• Wave of depolar. oriented @ 60º produces greatest +ve deflection in lead II

• Wave of depolar. Oriented @ 90º produces equally +ve deflections in both leads II & III

ECG Augmented Limb Leads

• aVL (+ve on left arm; -ve rest*)

• aVR (+ve on right arm; -ve rest*)

• aVF (+ve on left leg; -ve rest*)

• Standard + Augmented = 6 limb leads of ECG

ECG Chest Leads

• V1 – V6• V1 overlies right

ventricular free wall, • V6 overlies left

ventricular lateral wall

Cardiac Arrhythmias & ECG

• Five things to be read:– Rate– Rhythm– Axis– Hypertrophy– Infarction

• Cardiac arrhythmias reflect disturbances in:• Impulse initiation (S-A nodal cause/ectopic focus)• Impulse propagation (conduction blocks/re-entry rhythm)

• Normal sinus rhythm (NSR)– Normal heart– Each heart beat originates in S-A node

Cardiac Arrhythmias & ECG

• Abnormal sinus rhythms– Sinus Tachycardia

– Rate change is gradual– Fast HR – more than 100 beats/min– Causes: increased body temperature, sympathetic stimulation

of heart or toxic conditions of heart

– Sinus Bradycardia– Rate change is gradual– Slow HR – less than 60 beats/min– Bradycardia in athletes– Sick sinus syndrome

» Excessively sensitive baroreceptors» Mild external pressure on neck – strong vagal stimulation –

heart may stop!

Cardiac Arrhythmias & ECG

• Heart Blocks• Sinoatrial block

– Blockage of impulse before entry into atrial muscle» Disappearance of P waves

• AV block– Conditions decreasing rate of impulse

conduction/complete block:» Ischemia» Compression» Inflammation» Extreme vagal stimulation

AV BLOCKS

• First Degree Block– Delay in conduction from atria – PR interval increases to > 0.2 sec

• Second Degree Block– PR interval increases to 0.25 – 0.45 sec – some APs

pass through, some don’t!– “Dropped beats” – P wave present, no QRS– 2:1, 3:2, 3:1 rhythms

• Mobitz-I: – Repeated sequence of beats in which PR interval

lengthens progressively until a ventricular beat is dropped (also called Wenckebach Phenomenon)

• Mobitz-II: – Prolongation of PR interval is constant, but there are

some P waves which are not followed by QRS

AV BLOCKS

• Third Degree Block - Complete AV block

• Serious conduction abnormality at AV node• No conduction of impulses • Ventricles establish their own rhythm • P waves dissociate from QRS complexes

AV BLOCKS - ECG

Stokes-Adam Syndrome

• Ventricular escape• AV block “comes and goes”• Occurs in borderline ischemia of conductive

system• Block duration: secs to weeks (or longer)• Ventricles ‘escape’ after a delay of 5-30 secs

(overdrive suppression)• Clinically

– Patients faint due to lack of blood supply to brain– Recovers due to ventricular escape– Repeated fainting spells (Stokes-Adams Syndrome)

Wolff-Parkinson-White Syndrome

• Accessory pathway b/w atria & ventricles• Ordinarily, no functional abnormality • AV node + Bundle of Kent

• Bundle of Kent conducts faster than AV node• Excites one ventricle early – circus movement

» Paroxysmal atrial tachycardia

• ECG– Short P-R interval

– Prolonged QRS (slurred upstroke)

ECTOPIC PACEMAKERS• Ectopic foci may become pacemakers when:

– Their own rhythmicity becomes enhanced

– Rhythmicity of the higher-order pacemakers becomes depressed

– All conduction pathways b/w ectopic focus & those regions with greater rhythmicity become blocked

– May be safety net – when higher pacemaker fail

– May cause problems – when fires in presence of normal pacemaker

» Sporadic rhythm disturbances, such as premature depolarizations/beats – atrial/nodal/ventricular beats 

» Continuous rhythm disturbances cause atrial/nodal/ventricular paroxysmal tachycardias

Premature Contractions

• Contraction of the heart b/f normal contraction would have been expected

• Also called extrasystole/premature beat/ectopic beat

• Types: – Premature Atrial Contractions– A-V Nodal or A-V Bundle Premature

Contractions– Premature Ventricular Contractions

Premature Contractions

• Causes:• Local areas of ischemia• Small calcified plaques pressing against adjacent

cardiac muscle - irritation• Toxic irritation of (caused by drugs, nicotine, or

caffeine):» A-V node » Purkinje system» Myocardium

Atrial PC

• P wave of this beat occurred too soon

• P-R interval is shortened• Indicating ectopic origin of the beat to be in atria

near A-V node

• Compensatory pause• Interval between premature contraction & next

succeeding contraction is slightly prolonged*

• Pulse Deficit

A-V Nodal/Bundle PC

• P wave is missing• Instead, the P wave is superimposed onto the

QRS-T complex*

Ventricular PC

• QRS complex is usually considerably prolonged

• QRS complex has a high voltage

• T wave inverts

RE-ENTRY PHENOMENON

• Three conditions necessary for re-entry:

– The impulse loop becomes longer

» Dilated hearts– Conduction velocity is

decreased» Blockage of Purkinje

fibres» Ischemia of muscles» High blood K+

– Relative refractory period of the reentered region must be shorter than the propagation time around the loop

Ventricular Fibrillation• Most serious arrhythmia• If not stopped within 1-3 mins – fatal• Phenomenon of Re-entry “Circus Movements”• Causes

• Sudden electric shock of the heart (moderate voltage)• Ischemia of

– Part of myocardium– Part of conductive system– Both

• ECG• Bizarre• Coarse irregular waves

• Treatment• Strong high voltage AC

Atrial Fibrillation

• Similar to V-Fib

• Due to enlargement of atria secondary to valvular disease

• ECG: – No P waves – QRS, T waves present

• Irregular ventricular rhythm• Due to irregular atrial impulses

Atrial Flutter

Myocardial Infarction & ECG

• Ischemia changes myocardial properties• Become irreversible – death of myocardial fibers –

infarction!

• ECG can detect these changes

• Three main changes in infarcted area:– Rapid repolarization – C.o.I. out of infarct - ST segment

elevation– Decreased RMP - C.o.I. into infarct - ST segment

elevation– Delayed depolarization – C.o.I. out of infarct - ST

segment elevation

ECG Changes in MI - Timeline

• Very early pattern (hrs after infarction)• ST segment elevation – in leads facing infarct• ST segment depression – in reciprocal leads

• Late pattern (many hrs – few days)• Deep & wide Q waves appear

» Normal Q wave: <1/3 of R wave (height), 0.02 sec (wide)

» Deep/wide Q wave:

> 1/3 of R wave, > 0.03 sec

• Q waves: “Window effect”

ECG Changes in MI - Timeline

• Late established pattern (many days – weeks)

• Q waves, QS complexes persist• ST segment – isoelectric• T waves – invert – segments that had ST elevation• T waves – tall – segments that had ST depression• This pattern may persist for the patient’s life

• Very late pattern (months to years)• Abnormal Q waves, QS complexes persist• T wave normalizes

ECF K+ and ECG• Hypokalemia

• +/- 3.5 mEq/L– ST depression– Prominent U wave

• +/- 2.5 mEq/L– PR interval prolonged– ST depression– T wave inverts– Prominent U wave

• Hyperkalemia• +/- 7.0 mEq/L

– Tall slender, peaked T waves present

• +/- 8.5 mEq/L– No evidence of atrial activity– QRS – broad and slurred– QRS interval – wide– T waves remain tall, slender

• Further increase in K+ - ventricular tachycardia or fibrillation

Revision