Slide1 l.jpg
This presentation is the property of its rightful owner.
Sponsored Links
1 / 69

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


  • 198 Views
  • Uploaded on
  • Presentation posted in: General

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)

Download Presentation

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

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Slide1 l.jpg

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


Structure of the heart l.jpg

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


Slide3 l.jpg

Fibrous skeleton of the heart


Cardiac and skeletal muscles similarities l.jpg

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 muscles differences l.jpg

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 fibers contractile or conductile l.jpg

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 system conductile fibers l.jpg

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


Slide8 l.jpg

AV node

(node of Tawara)

irregularly arranged branching fibers

Bundle of His

unbranched fibers


Slide9 l.jpg

endothelium

endocardium

Purkinje fibers

Ventricular myocardium

Purkinje fibers


Nodal cells l.jpg

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 l.jpg

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 l.jpg

Excitation and Contraction of Cardiac Myocyte


Cardiac myocyte l.jpg

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)


Slide14 l.jpg

endothelium

endocardium

Purkinje fibers

Ventricular myocardium

Purkinje fibers


Cardiac myocyte16 l.jpg

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 l.jpg

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


Slide18 l.jpg

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


Sarcomere l.jpg

Sarcomere

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


Slide20 l.jpg

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 l.jpg

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


Slide22 l.jpg

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


Transverse tubular system t tubules l.jpg

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)


Mitochondria l.jpg

Mitochondria

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

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


Sarcoplasmic reticulum sr l.jpg

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


Slide26 l.jpg

JSR: junctional SR

LSR: longitudinal SR


Subsarcolemmal cisternae junctional sr l.jpg

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 l.jpg

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 l.jpg

Cardiac Cycle

  • Systole

    • isovolumic contraction

    • ejection

  • Diastole

    • isovolumic relaxation

    • rapid inflow- 70-75%

    • diastasis

    • atrial systole- 25-30%


Onset of ventricular contraction l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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%


Terms l.jpg

Terms

  • 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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

Valvular dysfunction

  • Valve not opening fully

    • stenotic

  • Valve not closing fully

    • insufficient/regurgitant/leaky

  • Creates vibrational noise

    • aka murmurs


Heart murmur considerations l.jpg

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 l.jpg

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?


Terminology l.jpg

Terminology

  • 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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

Direct Stretch on SA node

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


Extrinsic influences l.jpg

Extrinsic Influences

  • Autonomic nervous system

  • Hormonal influences

  • Ionic influences

  • Temperature influences


Control of heart by ans l.jpg

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 l.jpg

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 ans56 l.jpg

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 l.jpg

Interaction of the SNS & PSNS

  • SNS

  • PARA

Cardiac cell

NE

-

ACh

Gs

Ad. Cycl.

cAMP

Gi

NPY NE

-

ACh

M


Direct vs indirect sns influence l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

Major Hormonal Influences

  • Thyroid hormones

    • + inotropic

    • + chronotropic

    • also causes an increase in CO by  BMR


Ionic influences l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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 l.jpg

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


Ischemia l.jpg

Ischemia

  • 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)


Infarction l.jpg

Infarction

  • 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


  • Login