Physiology of the Cardio-Vascular System
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Physiology of the Cardio-Vascular System Lecture 1 / The Myocardium Dr. Sherwan R Sulaiman MD / MSc / PhD 2011-2012 - PowerPoint PPT Presentation

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Physiology of the Cardio-Vascular System Lecture 1 / The Myocardium Dr. Sherwan R Sulaiman MD / MSc / PhD 2011-2012. Structure of the Heart. Adult human heart = 300-350 g Built upon a “ collagenous skeleton ” located at atrioventricular junction (fibrotendinous ring)

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Physiology of the Cardio-Vascular System Lecture 1 / The Myocardium Dr. Sherwan R Sulaiman MD / MSc / PhD 2011-2012

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Physiology of the Cardio-Vascular SystemLecture 1 / The MyocardiumDr. Sherwan R SulaimanMD / MSc / PhD2011-2012

Structure of the Heart

  • Adult human heart = 300-350 g

  • Built upon a “collagenous skeleton” located at atrioventricular junction (fibrotendinous ring)

  • The ring isolates the atria electrically from the ventricles, except at the bundle of His

Fibrous skeleton of the heart

Cardiac and Skeletal MusclesSimilarities

  • Both- Striated muscle

  • Both use proteins actin and myosin

  • Both contract in response to an action potential on the sarcolemmal membrane

Cardiac and Skeletal MusclesDifferences

Skeletal muscle

  • Neurogenic

    (motor neuron-end plate-acetylcholine)

  • Insulated from each other

  • Contracts in all or none fashion

  • Short action potential

Cardiac Muscle

  • Myogenic

    (action potential originates within the muscle)

  • Gap-junctions

  • Action potential is longer

Cardiac Muscle Fiberscontractile or conductile

  • Contractile

    Action potential leads to vigorous force development and/or mechanical shortening

  • Conductile

    initiation or propagation of action potentials

Conduction SystemConductile Fibers

  • Sinoatrial (SA) node 100-110/min

  • Atrioventricular (AV) node 40-60/min

  • AV bundle (Bundle of His) 20-40/min

  • Left and right bundle branch

  • Purkinje fibers(rapid conduction) 20-40/min

Specialised cardiac muscle cells

AV node

(node of Tawara)

irregularly arranged branching fibers

Bundle of His

unbranched fibers



Purkinje fibers

Ventricular myocardium

Purkinje fibers

Nodal Cells

  • Smaller than contractile cells or Purkinje cells

  • Low propagation velocity(0.05m/sec)

  • Reduced density of gap junctions

  • Lack fast Na channels

Purkinje Cells

  • Larger than ordinary cardiac fibers and bundle fibers

  • Conduct action potentials four times faster than a ventricular myocyte(4m/sec)

  • May be binucleate

  • Few myofibrils

  • Vacuous cytoplasm (filled with glycogen)

  • Subendocardial location

  • Linked to cardiac fibers and bundle fibers by gap junctions and desmosomes

Excitation and Contraction of Cardiac Myocyte

Cardiac Myocyte

Myofiber:is a group of myocytes held together by surrounding collagen connective tissue

excess collagen,

may cause LV diastolic dysfunction

(e.g. left ventricular hypertrophy)



Purkinje fibers

Ventricular myocardium

Purkinje fibers

Cardiac Myocyte

  • 10-20 mm in diameter

  • 50-100 mm long

  • Single central nucleus

  • The cell is branched, attached to adjacent cells in an end-to-end fashion (intercalated disc)

    • Desmosomes (proteoglycan glue)

    • Gap junction (region of close apposition)

Gap Junctions

  • Low resistance connections

  • Small pores in the center of each gap junction

  • Allows ions and small peptides to flow from one cell to another

  • Action potential is propagated to adjacent muscle cells

Heart behaves as a single motor unit

Theoretically, An ion inside an SA nodal cell could travel throughout the heart via the gap junctions


Basic contractile unit within the myocyte

  • Refers to the unit from one Z band to the next

  • Resting length:1.8-2.4 mm

  • Composed of interdigitating filaments

    • Thick myosin protein

    • Thin actin protein

T: T tubules

mit: mitochondria

g: glycogen

contractile unit: sarcomere

Z line: the actin filaments are attached

I: band of actin filaments, titin and Z line

A: band of actin-myosin overlap

H: clear central zone containing only myosin

Sarcolemma (sarco = flesh; lemma = thin husk)

  • Each cell is bounded by a complex cell membrane

  • Composed of a lipid bilayer

    • Hydrophilic heads

    • Hydrophobic tails

  • Impermeable to charged molecules (barrier for diffusion)

  • Contains membrane proteins, which include receptors, pumps and channels

Sarcolemma contains a number of ion channels and pumps that contribute to overall Ca2+ levels within the myocyte

Transverse Tubular System(T-tubules)

  • The sarcolemma of the myocyte invaginates to form an extensive tubular network

  • Extends the extracellular space into the interior of the cell

  • Transmit the electrical stimulus rapidly (well developed in ventricular myocytes but is scanty in atrial and purkinje cells)


  • Generate the energy in the form of adenosine triphosphate (ATP)

  • Maintain the heart’s contractile function and the associated ion gradients

Sarcoplasmic Reticulum (SR)

  • A fine network spreading throughout the myocytes

  • Demarcated by its lipid bilayer

  • Close apposition to the T tubules

  • Junctional sr

  • Longitudinal SR

JSR: junctional SR

LSR: longitudinal SR

Subsarcolemmal Cisternae Junctional SR

  • the tubules of the SR expand into bulbous swellings

  • contains a store of Ca2+ ions

  • release calcium from the calcium release channel (ryanodine receptor) to initiate the contractile cycle

Longitudinal or Network SR

  • consists of ramifying tubules

  • concerned with the uptake of calcium that initiates relaxation

  • achieved by the ATP-requiring calcium pump (SERCA= sarcoendoplasmic reticulum Ca2+ -ATPase)

Cardiac Cycle

  • Systole

    • isovolumic contraction

    • ejection

  • Diastole

    • isovolumic relaxation

    • rapid inflow- 70-75%

    • diastasis

    • atrial systole- 25-30%

Onset of Ventricular Contraction

  • Isovolumic contraction

    • Tricuspid & Mitral valves close

      • as ventricular pressure rises above atrial pressure

    • Pulmonic & Aortic valves open

      • as ventricular pressure rises above pulmonic & aortic artery pressure

Ejection of blood from ventricles

  • Most of blood ejected in first 1/2 of phase

  • Ventricular pressure peaks and starts to fall off

  • Ejection is terminated by closure of the semilunar valves (pulmonic & aortic)

Ventricular Relaxation

  • Isovolumetric (isometric) relaxation-As the ventricular wall relaxes, ventricular pressure (P) falls; the aortic and pulmonic valves close as the ventricular P falls below aortic and pulmonic artery P

  • Rapid inflow-When ventricular P falls below atrial pressure, the mitral and tricuspid valves will open and ventricles fill

Ventricular Relaxation (cont)

  • Diastasis-inflow to ventricles is reduced.

  • Atrial systole-atrial contraction actively pumps about 25-30% of the inflow volume and marks the last phase of ventricular relaxation (diastole)

Ventricular Volumes

  • End Diastolic Volume-(EDV)

    • volume in ventricles at the end of filling

  • End Systolic Volume- (ESV)

    • volume in ventricles at the end of ejection

  • Stroke volume (EDV-ESV)

    • volume ejected by ventricles

  • Ejection fraction

    • % of EDV ejected (SV/EDV X 100%)

    • normal 50-60%


  • Preload-stretch on the wall prior to contraction (proportional to the EDV)

  • Afterload-the changing resistance (impedance) that the heart has to pump against as blood is ejected. i.e. Changing aortic BP during ejection of blood from the left ventricle

Atrial Pressure Waves

  • A wave

    • associated with atrial contraction

  • C wave

    • associated with ventricular contraction

      • bulging of AV valves and tugging on atrial muscle

  • V wave

    • associated with atrial filling

Function of Valves

  • Open with a forward pressure gradient

    • e.g. when LV pressure > the aortic pressure the aortic valve is open

  • Close with a backward pressure gradient

    • e.g. when aortic pressure > LV pressure the aortic valve is closed

Heart Valves

  • AV valves

    • Mitral & Tricupid

      • Thin & filmy

      • Chorda tendineae act as check lines to prevent prolapse

      • papillary muscles-increase tension on chorda t.

  • Semilunar valves

    • Aortic & Pulmonic

      • stronger construction

Valvular dysfunction

  • Valve not opening fully

    • stenotic

  • Valve not closing fully

    • insufficient/regurgitant/leaky

  • Creates vibrational noise

    • aka murmurs

Heart Murmur Considerations

  • Timing

    • Systolic

      • aortic & pulmonary stenosis

      • mitral & tricuspid insufficiency

    • Diastolic

      • aortic & pulmonary insufficiency

      • mitral & tricuspid stenosis

    • Both

      • patent ductus arteriosis

      • combined valvular defect

Law of Laplace

  • Wall tension = (pressure)(radius)/2

  • At a given operating pressure as ventricular radius  , developed wall tension .

    •  tension   force of ventricular contraction

    • two ventricles operating at the same pressure but with different chamber radii

      • the larger chamber will have to generate more wall tension, consuming more energy & oxygen

    • Batista resection

  • How does this law explain how capillaries can withstand high intravascular pressure?


  • Chronotropic (+ increases) (- decreases)

    • Anything that affects heart rate

  • Dromotropic

    • Anything that affects conduction velocity

  • Inotropic

    • Anything that affects strength of contraction

      • eg. Caffeine would be a + chronotropic agent (increases heart rate)

Control of Heart Pumping

  • Intrinsic properties of cardiac muscle cells

  • Frank-Starling Law of the Heart

    • Within physiologic limits the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins

      • heterometric & homeometric autoregulation

      • direct stretch on the SA node

Mechanism of Frank-Starling

  • Increased venous return causes increased stretch of cardiac muscle fibers. (Intrinsic effects)

    • increased cross-bridge formation

    • increased calcium influx

      • both increases force of contraction

    • increased stretch on SA node

      • increases heart rate

Heterometric autoregulation

  • Within limits as cardiac fibers are stretched the force of contraction is increased

    • More cross bridge formation as actin overlap is removed

    • More ca++ influx into cell associated with the increased stretch

Homeometric autoregulation

  • Ability to increase strength of contraction independent of a length change

    • Flow induced

      • increased stroke volume maintained as EDV decreases

    • Pressure induced

      • increase in aortic BP (afterload) will + force of contraction

    • Rate induced

      • increased heart rate will + force “treppe”

Direct Stretch on SA node

  • Stretch on the SA node will increase Ca++ and/or Na+ permeability which will increase heart rate

Extrinsic Influences

  • Autonomic nervous system

  • Hormonal influences

  • Ionic influences

  • Temperature influences

Control of Heart by ANS

  • Sympathetic innervation-

    • + heart rate

    • + strength of contraction

    • + conduction velocity

  • Parasympathetic innervation

    • - heart rate

    • - strength of contraction

    • - conduction velocity

Interaction of ANS

  • SNS effects on the heart blocked using propranolol (beta blocker) which blocks beta receptors

  • Para effects blocked using atropine which blocks muscarinic receptors

    • HR will increase

    • Strength of contraction decreases

  • What can be concluded?

Interaction of ANS

  • From the previous results it can be concluded that under resting conditions:

    • Parasympathetic NS exerts a dominate inhibitory influence on heart rate

    • Sympathetic NS exerts a dominate stimulatory influence on strength of contraction

Interaction of the SNS & PSNS

  • SNS

  • PARA

Cardiac cell





Ad. Cycl.







Direct vs. Indirect SNS influence

  • Direct innervation of Cardiac cells accounts for most of the SNS effect.

    • Norepinephrine acting on -1 receptors. (85%)

  • Indirect effects would be due to circulating catacholamines (epinephrine & norepinephrine) released primarily from the adrenal medulla (blood borne) which would find their way to the cardiac -1 receptors. (15%)

Cardioacclerator reflex

  • Stretch on right atrial wall + stretch receptors which in turn send signals to medulla oblongata + SNS outflow to heart

    • AKA Bainbridge reflex

    • Helps prevents damning of blood in the heart & central veins

Neurocardiogenic syncope

Benzold-Jarisch reflex (Baroreceptors in ventricles)

Stimulation of sensory endings mainly in the ventricles (some in the atria) that reflex via the X CN to the CNS

Inferoposterior wall of LV which is supplied by the circumflex artery is site of majority of receptors

Reflex effects results in hypotension & bradycardia

Reflex stimulated by

Occlusion of circumflex artery (inferior wall infarct)

 in LVP & LV volume (eg. Aortic stenosis)

Major Hormonal Influences

  • Thyroid hormones

    • + inotropic

    • + chronotropic

    • also causes an increase in CO by  BMR

Ionic influences

  • Effect of elevated [K+]ECF

    • dilation and flaccidity of cardiac muscle at concentrations 2-3 X normal (8-12 meq/l)

    • decreases resting membrane potential

  • Effect of elevated [Ca++] ECF

    • spastic contraction

Effect of body temperature

  • Elevated body temperature

    • HR increases about 10 beats for every degree F elevation in body temperature

    • Contractile strength will increase temporarily but prolonged fever can decrease contractile strength due to exhaustion of metabolic systems

  • Decreased body temperature

    • decreased HR and strength

Energy substrate for cardiac cells

  • Heart is versatile & can use many different energy substrates

  • Fatty acids-70% preferred

  • Glucose

  • Glycerol

  • Lactate

  • Pyruvate

  • Amino acids

Relationship of energy to work

  • 75% of energy the heart utilizes is converted to heat

  • The remaining 25% is utilized as work which is broken down into:

    • Pressurization of blood (>99%)

    • Acceleration of blood (<1%)

Work output of the heart

  • Pressurization of the blood (potential energy)

    • Moving blood from low pressure to high pressure (volume pressure work or external work)

      • The majority of the work (>99%)

  • Acceleration of blood to its ejection velocity (kinetic energy)

    • Out the aortic & pulmonic valves normally accounts for less than 1% of the work component

      • Can increase to ~ 50% with valvular stenosis

Blood flow to myocardium

  • The myocardium is supplied by the coronary arteries & their branches.

  • Cells near the endocardium may be able to receive some O2 from chamber blood

  • The heart muscle at a resting heart rate takes the maximum oxygen out of the perfusing coronary flow (70% extraction)

    • Any  demand must be met by  coronary flow


  • Normally the first cells to depolarize are the last to repolarize.

    • Depolarization & repolarization waves are in opposite directions

      • QRS and T wave point in the same direction

  • Ischemia prolongs depolarization & therefore delays repolarization

    • Depolarization & repolarization waves are now in the same direction

      • This will cause an inversion in T wave (opposite deflection compared to QRS)


  • Damaged cells lose ability to repolarize

  • Most of the frank damage occurs upon reperfusion & is associated with free radical damage.

  • Damaged area is in an abnormal state of depolarization

  • When normal myocardium is in a resting polarized state, there is a “current of injury” between damaged & normal myocardium

    • creates a depressed baseline which appears as an elevated ST segment

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