Function Cardiac

8/8/2019 Function Cardiac

1/91

Lifes Progression through

Cardiac Physiology

Understanding the Normal

Physiology of the Heart as it Changes

through the Life Span


2/91

Overall Design of the Heart

Atrial fibers are divided into superficial & deep

Superficial fibers spread ov

er both R & L atria Deep fibers are confined to their respective

areas for the R or L atrium

Function of this is to provide a last minute push

of blood into the ventricles near the end of

filling, otherwise known as the Atrial kick


3/91


4/91


5/91


6/91


7/91


8/91

Cardiovascular Re

view

Anatomy - Skeletal vs Cardiac Muscle

Sarcoplasmic/tubular system T tubules = transmit

Action Potential rapidly from the sarcolemma toall fibrils in muscle

Sarcoplasmic reticulum = houses calcium ions.

Action Potential across the T tubules causing

the release of CA++ from reticulum to the

fibrils resulting in a muscle contraction


9/91

CV review

Sarcotubular system

T tubules = transmit AP rapidly from

sarcolemma to all fibrils in mm.

Sarcoplasmic reticulum = houses calcium ions.

Action Potential across the T tubules causes

release of CA++ from reticulum, resulting in acontraction


10/91

Cardiac Rev

iew Contractile unit (Sarcomere). Muscle fibers

composed of fibrils

Each fibril is divided into filament

Each filament is made up of contractile proteins

Contractile proteins consist of

ACTIN, MYOSIN, TROPONIN, TROPOMYOSIN


11/91

Cardiac Muscle Tissue The actual structure of the cardiac muscle is

also unique and represents its function

Muscle cells form attachments either parallel

or obliquely to each other

There is a greater amount of mitochondria

Sarcoplasmic reticulum is less abundant

Cells are much more dependent upon oxygen


12/91

CV Review

Cardiac mm Vs Skeletal mm

Fibers connected by intercalated discs forming

the SYNCYTIUM (one fiber depolorized , APspreads to all fibers, the whole syncytium

contracts not just one fiber)


13/91

Cardiac Muscle Tissue The aerobic dominance shows greater blood

vessel ratios to muscle cells

Aerobic dominance indicates need for good

supply of fatty acids as the fuel for ATP

Most important, is that each cardiocyte possess

the ability for intrinsic spontaneous rhythm

In other words, the heart will beat on its own!


14/91


15/91


16/91


17/91

Ventricle Design is Different

There are 3

layers of cardiac

muscle that will

overlap eachother from the

R to L ventricle

This unique

design is part ofits functional

operation


18/91


19/91

Myogenic Rhythms Some cardiocytes will become differentiated

into becoming the pacing and conducting

cells of the heart They form the Sino-Atrial Node, S-A Node,

other form the Atrio-Ventricular Node, A-VNode, Bundle Branches and Purkinje fibers

The rates will become progressively slowerfrom the S-A to the Purkinje fibers


20/91

Cardio dynamics Afterload pressures is what the ventricles

have to contend with as they evacuate the

blood from the chambers (systolic pressure)

The cardiac muscle is designed to typically

work effectively against those pressures

However, high pressures will strain the heartmuscle over time & weaken heart function


21/91

Cardio dynamics Preload pressures is the degree of stretching

experienced during ventricular diastole

It is significant since it affects the ability ofthe heart muscle to produce tension

Much like the relationship between actin

and myosin in skeletal muscle for tension It is limited to myocardial connectivetissues, cardiac muscle and pericardial sac


22/91


23/91

Cardio Dynamics End diastolic volume (EDV) - amount of

blood in ventricle at the end of diastole

End systolic volume (ESV) amount ofblood remaining at the end ofvent. systole

Stroke Volume (SV) is the amount of blood

pumped out of thev

entricle on each beat,EDV ESV = SV

Ejection Fraction is SV as a % of EDV


24/91

Cardio Dynamics Frank-Starling Principle is the relationship

between the amount ofventricular stretching

and contractile force of the heart muscle Starling basically said, more in = more out

Essentially, the ventricles are in a series with a

balance between the R & Lventricular filling The body will retain fluids to increase this

effect for stretching the heart from more CO


25/91


26/91

CardiacO

utput (CO

) CO is precisely regulated so that peripheral

tissues receive an adequate circulation under

various conditions cardiac reserve

SV can almost triple & HR can increase 250%

Cardiac output can increase 600 700 %

CO = 80 ml X 75 bpm = 6000 ml/min

That is an increase to 36,000 to 42,000 ml/min


27/91

Additional Factors Contractility is the force produced during a

contraction

Drugs or factors that increase this force isreferred to as a positive inotropic action

Those factors that decrease this force is

referred to as a negativ

e inotropic action This is caused by assisting or blocking CA++movement & metabolism of the cardiac cells


28/91

Changes in Ion Concentrations Hypercalcemia elevated CA++ will cause

cardiac cells to be highly excitable

Hypocalcemia low levels of CA++ willcause weaker contractions & slower HR

Hyperkalemia elevated K+ cause weak

contractions and irregular heart beats Hypokalemia low K+ lowers the rate ofcontractions and hyperpolarizes the cells


29/91

Changes in the HeartOv

er Time There are a lower number of cardiocytes

Gradual invasion of fat & collagen tissues

This tends to make the heart less efficient

This will limit the potential for expansion

Pericardium may shrink with infections Endocardium will thicken to reduce filling

Heart valves will calcify & restrict flow


30/91

Changes in the HeartOv

er Time Conductive system progressively looses SA

node cells & allows other cites to pace

Normal 1 capillary to 1 muscle ratio changes

CAD begins to show early in life (20s-30s)

Higher blood pressures create more afterload

Weaker atriums create less preload

Arteries become more rigid as we age also !!!


31/91

Understanding Cardiac Conditions The overall normal structure of the heart is

well designed for its function

There is both a mechanical and electricalcomponent of the normal heart

Aging and various disease processes can

effect the ultimate function of the heart Understanding these components is neededto successfully implement physical therapy


32/91

Structures of the Heart Endocardium: inner surface

Pericardium = fibroserous sac encloses the

heart and roots of great vessels in fluid.Protects heart from friction

Epicardium = Visceral layer of pericardium,

COVERS heart and great vessels


33/91

Structures Continued Mediastinum, base heart occupies the right chest

and apex lies primarily in the left chest

Papillary mm: arise from myocardial surface ofventricles & attach to chordae tendin.

Chordae tendineae: tendinous attachments frompapillary muscle to tricuspid and mitral valves.Helps prevent eversion ofvalves into the atriaduring systole


34/91

Heart Chambers

Atria (thin, low pressure)

RT = venous blood from superiorvena cava, inferior

vena cava & coronary sinus

LT = oxygenated blood heart from lungs via 4

pulmonary veins

70% flows passively from atria into

ventricle

Atrial contract forcefully (atrial kick) supplying

another 10-20% of blood forventricular output


35/91

Heart Chambers Ventricles

RV = Deoxygenated blood into PA

LV = high pressure, ejects blood into systemic

circulation

Valves

AV = mitral (bicuspid), tricuspid (3 leaflets) Aortic = 3 valve cusps Pulmonic = 3 semilunar cusps


36/91

CV Rev

iew Cardiac conduction system

SA node (pacemaker) = possesses fastest

inherent rate ofAUTOMATICITY Internodal atrial pathways (SA node through

RA to AV node)

Anterior tract (Bachmanns)

Middle tract (Wenckebachs)

Posterior tract (Thorels)


37/91

CV Rev

iew Bachmans bundle (SA to LA)

AV node (40-60 beats)

Bundle of His

Bundle branch system = Rt. Lt

Purkinje system


38/91

Cardiac Plumbing Coronary vasculature

RCA = SA node in 55% and AV node in 90%

of pts. RA and RV mm, inferiorpost wall ofLV, 80% hearts provides branch - Posterior

descending artery (located in interventricular

groove, supplies RV and inferior wall of LV

and posterior septum)


39/91

Plumbing (continued) Left main coronary artery (LMCA)

LAD = anterior part of intervent. septum, ant.

Wall of LV, RBB, anteriorsuperior LBB

Circumflex (CF) = branch off CF called obtuse

marginal branch (OMB). CF supplies AV node

in 10%, SA node in 45% and lateral post.

Surface of LV via the OMB


40/91

CV Rev

iew Veins = great cardiac vein, small cardiac vein,

thebesian.

Local Control Mechanisms: tissues ability tocontrol their own blood flow calledAUTOREGULATION.

There are 2 major hypotheses

1. Vasdilatory = rate of metabolism increase, O2is consumed higher rate, so decreased PaO2 soincrease in vasodilator substances (lactic acid

adenosine, carbon dioxide) to increase blood


41/91

1. Vasdilatory = rate of metabolism increase, O2 is consumed

higher rate, so decreased PaO2 so increase in vasodilatorsubstances (lactic acid adenosine, carbon dioxide) to

increase blood supply

2. Oxygen demand theory = when O2 decreases, dilation of

vessels occur to increase flow to increase O2. As increasedmetabolism occurs, O2 use increases so decreased amt. O2

available and causes local vasodilatation

Autoregulation of blood flow:

Myogenic theory: arterial pressure rises, vessels stretch,

stimulates contract. of smooth mm. in vessels (feedback

mechanism), reducing blood flow back to normal. As

tension decreases, smooth mm. relax


42/91

CV Rev

iew Metabolic theory: Arterial pressure rises, increase blood

flow brings nutrients to tissues and remove vasodilator

substances. Both cause vessels to constrict.

Autonomic regulation ofvessels

Adrenergic symp. NS fibers secrete norepinephrine to

nerve endings, causing VASOCONSTRICTION

Parasymp. NS secrete ACETYLCHOLINE (cholinergiceffect) so VASODILATION


43/91

CV Rev

iew Stretch receptors: barorecptors

(pressoreceptors) located in aortic arch,

carotid sinus, venae cavae, pulmonary arteriesand atria

Sensitive to arterial pressure > 60 mm Hg

Activated by elevated BP

1. Stretch in artery to aortic arch via vagus to medulla andcarotid sinus via Herings nerve to glossopharyneal nerveto medulla


44/91

CV Rev

iew2. Sympath. action inhibited3. Vagal reflex dominates

4. Results in decreased HR and contract., dilation of peripheral

vessels, decreased SVR, BP lowered to normal

Activated with decreased BP1. Decreased vagal tone

2. Symp. NS dominant

3. Results in increased HR & contract., vasoconstriction (preserving

blood flow to brain and heart)


45/91

CV Rev

iew Factors that affect BP- HR, CO,SVR,arterial

elasticity, blood volume, blood viscosity, age,

body surface area, exercise, Na retention,emotions

Pulse pressure, MAP (calculate)

CO

= SV X HR


46/91

Preload Due to number ofvariables

stretch - fiber length, volume

Increase preload by increasing vol. to ventricles

Increase preload stretches fibers causing more forceful

contraction so increase SV thus increase CO but also

ventricular work

Myocardial fibers reach a point of stretch beyond which it

can contract and SV and CO decreases SO


47/91

Preload changes Increased preload mitral insufficiency, aortic insufficiency

increased volume

vasoconstricting drugs increase atrial kick

Decrease preload mitral stenosis

decreased volume vasodilating drugs

decreased atrial kick


48/91

Frank-Starling Curv

e Intrinsic ability of the heart to adapt to

changing volumes of inflowing blood. The

greater the heart mm. is stretched duringfilling, the greater will be the quantity of

blood pumped into the aorta.


49/91

Afterload

Resistance that must be overcome byventricles in order to open semilunarvalves

and propel blood. SVR = MAP-CVP

CO

Increase afterload- aortic stenosis, arteriolarvasoconstriction, hypertension, polycythemia,vasoconstricting drugs


50/91

Afterload (cont.)

Decreased afterload - arteriolarvasodilators

drugs, septic shock (late phase)

Excessive afterload causes increased LV

stroke work, decrease stroke volume,

increased MI O2 demand and may result in

LV failure


51/91

Contractility

Increase contractility usually there is shift of curve

to the left and up

Increase in contractility Inotropic drugs - digitalis, epinephrine,

dobutamine

Increase HR Symp. stimulation via beta 1 receptors

Hypercalcemia


52/91

Neurologic Control of the Heart

Chemoreceptors = carotid and aortic bodies,

sensitive to changes in pH,PaO2,PaCO2 and

cause changes in HR & RRvia stimulationvasomotor center in medulla

Stretch receptors: Respond to pressure and

volume changes


53/91

Neurologic (cont.)

Autonomic

Sympathetic: Release norepin. Elicits 2

types of effects Alpha adrenergic = arteriolarvasoconstriction

Beta adrenergic (B1)

Increase SA node discharge - HR

(+ chronotropic)


54/91

Neuro (cont.)

Increases force of myocardial contraction (+

intropic)

Accelerates AV conduction time (+dromotropic)

Parasympathetic: Rt vagus (affecting SAnode), Lt. Vagus (Affecting AV conduction) =

Release of acetylcholine


55/91

Neuro (cont)

Decrease in SA node discharge - decreased HR can slow

conduction through AV tissue

Bainbridge Reflex: Stretch receptors in atria, large

veins and pulmonary arteries


56/91

Heart

Aerobic organ so can easily undergo

irreversible damage with reduction in O2.

3 factors influencing O2 consumption

1. Tension time index (p. 15)

2. Contractile state of myocardium

3. Heart rate


57/91

Heart (cont.)

Look up:

Pressures in chambers

Blood flow to the heart

Subendocardial region: more vulnerable to

diminished flow than subepicardial region

Collateral vessels


58/91

Myocardial Ischemia

MyocardialO2 deprivation and inadequate

removal of metabolites secondary to decreased

perfusion. Most common pathologic process is narrowing of

coronary arteries (often proximal segments).

Nonatherosclerotic: inflammatory or autoimmune

processes. (Lupus, RA, diabetes)


59/91

Coronary Artery Disease (CAD)

Endothelial cells in the intima are mech. &chemical injured. This changes structure of

cells, making more permeable to circulationlipoproteins (Phase 1 CAD)

Platelets adhere and aggregate to injury andmacrophages migrate to area. Lipoproteins

enter smooth mm. cells of intima andpromote fatty streak ( Phase 2 CAD)


60/91


61/91

Myocardial Ischemia

Also have coronary artery spasms,embolism. Anemia & infections can also

increaseO

2 demand Contractile force & segment shortening are

reduced ABRUPT coronary occlusion.

Reduced high-energy phosphate supply

Cellular acidosis Both cause CA++ binding alterations


62/91

Myocardial Infarction

NECROSIS of myocardial tissue due toloss of blood supply to myocardium

Important to determine: Location, severity

of narrowing, extent of collaterals, size of

vasc. Bed perfused, O2 needs ofmyocardium at risk.


63/91

Myocardial Infarction

Color changes and infarcted mm. Is REMOVED

by mononuclear cells. Becomes scared, white &

firm. Types

Transmural = Full thickness

Subendocardial

Intramural

Subepicardial


64/91

Types of Angina

1. Stable

2. Vasospastic

3. Unstable

ACUTE MIS

The atria and Rt. Vent. less incidence


65/91

Acute MI

90% of transmural MI due toatherosclerosis. Occur most often in

proximal 2 cm of LAD and LCX andproximal and distal thirds of RC.

Nearly all transmural MI affect LV, 15%RV

Reflow to reperfusion to injured cells mayrestore viability but leave cells poorlycontractile (stunned) for up to 1 -2 days


66/91

Cardiomyopathies


67/91

Causes of Cardiac Dysfunction

Cardiomyopathy

Myocardial infarction

Arrhythmias, valve defects

Pulmonary hypertension

Pericardial or myocarditis

Aging


68/91

Secondary causes of Cardiomyopathy

inflammatory

metabolic

toxic

infiltrative

fibroplastic

idiopathic

hematologic

hypersensitive

genetic

physical agents

acquired (misc)


69/91

Prevalence of Cardiac

Dysfunction Greater than 2 million cases CHF

400,000 new cases annually

Costs range $15 to 28 Billion annually

1% prevalence in 50 to 59 year olds

Increases to 10% in 80 to 89 year olds

Left ventricular failure most common


70/91

Break Time


71/91

Pulmonary Heart Disease

RV VOLUME is larger than LV and EF is

lower. Afterload is lower, stroke work is

less ITP falls during inspiration which

INCREASES venous return to RV, shifts

septum toward the LV so decrease inLVEDV.


72/91

RT Ventricle & Pulmonary

Circulation Decrease in LV preload and increase in

afterload result in insp. Decrease in BP

(Pulsus Paradoxus) PP is usually less than 10 mmHg but

increases with pts with obstructive lung

disease


73/91

Pulmonary Circulation

COMPLIANCE , Proportion ofvessel NOT

perfused. Normal pul circulation can increase

2.5-3 fold before increase in PAP (Fig 7-2) RESISTANCE, PVR is increased with hypoxia

(vasoconstriction), low and high lung volumes.

VENT-PERFUSION MATCHING = normally

there is physiologic dead space. Vent. but under

perfused.


74/91

Cardiovascular Review Items

Normal Electrophysiology

Depolarization, Repolarization, Automaticity,

Bradycardia, Tachycardia

Reentry Barrier, Unidirectional block, slow conduction

Reentrant tachycardia (WPW,MI)


75/91

Normal Electrophysiology

Depolarization, Repolarization,

Automaticity, Bradycardia, Tachycardia


76/91

Reentry

Barrier, Unidirectional block, slow

conduction

Reentrant tachycardia (WPW,MI)


77/91

Types of Angina

1. Stable

2. Vasospastic

3. Unstable

ACUTE MIS

The atria and Rt. Vent. less incidence


78/91

Acute MI

90% of transmural MI due toatherosclerosis. Occur most often in

proximal 2 cm of LAD and LCX andproximal and distal thirds of RC.

Nearly all transmural MI affect LV, 15%RV

Reflow to reperfusion to injured cells mayrestore viability but leave cells poorlycontractile (stunned) for up to 1 -2 days


79/91

Causes of Cardiac Dysfunction

Cardiomyopathy

Myocardial infarction

Arrhythmias, valve defects

Pulmonary hypertension

Pericardial or myocarditis

Aging


80/91

Prevalence of Cardiac

Dysfunction Greater than 2 million cases CHF

400,000 new cases annually

Costs range $15 to 28 Billion annually

1% prevalence in 50 to 59 year olds

Increases to 10% in 80 to 89 year olds

Left ventricular failure most common


81/91


82/91

It All Begins with the Heart Fetal Development

Structural differences of cardiac muscle

Responses to blood volume & growth

Conductive nature of the cardiac tissues

Importance of HR x SV = CO

How does all this respond to the aging process?


83/91

Impact of Growth on Cardiac System

Physical changes due to growth

Changes in stroke volume & blood volume Metabolic tissue changes cardiac response

Dietary & Lifestyle influences on the

cardiovascular system over time


84/91


85/91

Aging Effects on the Cardiac System

Histological changes to the cardiac tissues

Culminating effects of chosen lifestyles Afterload & Preload pressures on the heart

Potential impact on functional tolerances

Overall influences of lifespan modifications


86/91

It Starts with the Hearts

Is the 1st functioning system in the embryo!

Begins to form in the 3rd week of gestation

Due to the fact that as cells divide, simple

diffusion does not work, call the plumber!

Heart begins to pump in a tube fashion the

oxygen, nutrients & remove CO2, wastes


87/91


88/91

Heart Tube beings to Change

As more cells divide and grow, there is needfor more plumbing and pumping of the heart

Lungs begin to develop but very little bloodis sent there, Youre getting 02 from Mom

But, when you leave home, you had betterstart breathing, so lungs, begin to expand !

This causes a lower pressure gradient pullingthe blood into the lung tissues


89/91

Stop the Shunting

The change in pressure gradients stops the

shunting of blood away from the lungs

This causes the patent structures to close, likethe Foreamen Ovale & Ductus Arteriosus

This is usually completed within 3 months

Cardiac tissues are now feeling the full effectof their job with increased blood pressures


90/91


91/91

Break Time

Function Cardiac

Documents

Transcript of Function Cardiac