Blood flow through the heart

Right side(lungs)

Right Side: receives blood body--pumps blood to lungs

*Blood from body through IFV & SVC, to Right atrium...

*Through Tricuspid Valve to Right ventricle...

*Through pulmonary vavle, to pulmonary artery..

*Into LUNGS

Blood flow through the heart

Left side (to body)

Left side: Pumps blood to body- receives from lungs.

*From Lungs, through pulmonary veins..

*To LEFT atrium..

*Through mitral(bicuspid) valve, to left ventricle..

*Through Aortic valve, To aorta..

*To BODY.

Systole Cardiac Cycle

*Ventricle contraction=

Eject blood from LEFT ventricle into AORTA

Eject blood from RIGHT ventricle into PULMONARY ARTERY

*Emptying of atria and ventricles.

Diastole Cardiac Cycle

*Ventricle Relaxation=

ventricles relax

Atria contract: moving blood into ventricles

*Filling of heart chambers

*2/3 of cardiac cycle

*AV valves open

*semilunar valves close

Ventricular Contraction and Heart sounds

**S1 (lubb)

*AV valve closure

*ventricular contraction forces mitral & tricuspid valves to close.

**S2 (dubb)

*ventricles emptying the pressure in ventricles decreases aortic & pulmonic(semilunar) valves to close.

*Blood flows from RIGHT to LEFT ventricles to the lungs & body.

Valves of the Heart

*ATRIOVENTRICULAR*

*Tricuspid (right heart)

*Mitral (left heart)

function to prevent backflow of blood from ventricles to atria during systole (contraction of heart). The valves keep blood flowing in a forward direction.

Valves of heart continued

A valve that does not close tightly causes backflow of blood= insufficiency or regurgitation)

A valve that does not open wide enough causes a turbulent flow (secondary to obstruction or narrowing, i.e., stenosis)

SEMILUNAR Heart Valves

*AORTIC (in aorta)

*PULMONIC (in pulmonary artery)

Open during systole and close during diastole.

HEART SOUNDS REVIEW

S1 & S2

*S1= lubb

Closure of AV valves(mitral 1st)

Beginning of ventricular systole

Best heard @ 5th ICS.

*S2= dubb

Closure of semilunar valve(aorta 1st)

End of ventricular systole or beginning of diastole

Best heard @ 2nd ICS.

Heart sounds Review

S3

*S3=

Right ventricle= heard @4th ICS @left sternal boarder.

Left ventricle= heard @apex

Ventricular gallop, >40yrsold=pathological (more normal in younger)

Hear a close after S2 in early diastole while ventricles relax & fill w/blood.

Commonly heard w/heart failure(ventricle has not completely emptied so blood is returning an already partially filled ventricle).

Heart Sounds Review

S4

*S4= late diastole, pre systolic gallop before S1 sound

Heard best @apex of heart

When pathologic- produced by atrial contraction vs. stiff noncompliant ventricles

Due to or R/T scarring of MI or Ventricular hypertrophy (hypertension and pulmonic stenosis).

HEART

MURMERS

Extra sounds during systole or diastole

Turbulent sounds in heart or vesssels

Occur B/T normal sounds

DUE TO or R/T valve disorders & abnormal blood flow patterns.

CORONARY CIRCULATION

Coronary Artery blood flow to the myocardium occurs almost exclusively during DIASTOLE

Left & right arteries & their branches supply arterial blood to the heart.

Originate from aorta above aortic valve leaflets.

Arteries perfused during DIASTOLE.

Right side of heart= right coronary artery

Left side of heart= left coronary artery

AORTIC DIASTOLIC PRESSURE

Pressure by which blood enters the coronary arteries.

IF DIASTOLE (relaxation of heart) is shortened (i.e., increased HR) so is myocardial perfusion.

DIASTOLIC B/P of @ least 60 to maintain adequate blood flow.

Conduction System

AUTOMATICITY

Ability of the heart to initate impulses regularly & spontaneously.

Prominent property of SA NODE.

Conduction System

EXCITABILITY

Ability of cardiac cells to respond to a stimulus by initating the cardiac impluse.

Conduction System

CONDUCTIVITY

Ability of cardiac cells to respond to a cardiac impulse by transmitting the impulse along cell membranes.

Conduction System

CONTRACTIBILITY

Ability of cardiac cells to respond to an impulse by contracting.

**Contractile cells compose the largest mass of the myocardium.

Conduction system of Heart

SA NODE & AV NODE

SA NODE:

Near Vena Cava in right atrium

PACEMAKER OF HEART

Rate controlled @70-80 (60-100).

AV NODE:

Responsible for .10sec delay in conduction of impulse to ventricles

Composed of dense fibrous tissue that continues into the BUNDLE OF HIS

Conduction System of the heart

BUNDLE OF HIS

Tail of AV NODE

Separates into RIGHT & LEFT BUNDLE BRANCHES which then travel into ventricles

Connects AV NODE to the BUNDLE OF HIS

Separates into RIGHT & LEFT BUNDLE BRANCHES which then travel into ventricles

Conduction System of the Heart

PURKINJIE FIBERS

(network)

On endocardial surface of both ventricles

Aid in accelerated conduction of the impulse.

ECTOPIC BEAT

Beat originating in area other than the SA NODE

CARDIAC OUTPUT

Amount of blood ejected from the LEFT ventricle into the AORTA per min.

**CO= SV X HR

STROKE VOLUME

Amount of blood ejected into the aorta by the LEFT ventricle per beat.

SV= end of DIASTOLIC volume- end SYSTOLIC volume

EJECTION FRACTION

Ratio of stroke volume to end DIASTOLIC volume (EDV)

A measure of LEFT ventricle function

*A decrease in ejection fraction means left ventricular failure

* SV divided by EDV= EJECTION FRACTION

Control of Cardiac Output

Compensatory adjustments to HR or Stroke Volume occur to stabilize Cardiac Output in the normal healthy heart.

MECHANISMA REGULATING STROKE VOLUME

PRELOAD

Refers to the degree of myocardial fiber stretch at the end of DIASTOLE and just before contraction.

*STARLINGS LAW OF THE HEART*

Myocardial fibers respond with a more forceful contraction when stretched.

MECHANISMS REGULATING STROKE VOLUME

AFTERLOAD

Refers to resistance

As AFTERLOAD increases so does the CARDIAC work and O2 consumption.

MECHANISMS REGULATING STROKE VOLUME

CONTRACTILITY

Refers to the FORCE of contraction that myocardial muscle generates

*Inotropic State*

Postive= increased contractility

Negative= decreased contractility

Increased contractility improves ventricular emptying so-- increased STROKE VOLUME.

Control of Heart Rate--ANS

SYMPATHETIC

Increases rate (positive chronotropic)

Increases force (positive inotropic)

Neurotransmitter is NOREPINEPHRINE

Control of Heart Rate--ANS

PARASYMPATHETIC

decreases rate (neg chronotropic)

decreases force of contraction (neg. inotropic)

neurotransmitter is ACETYLCHOLINE

Control of Heat Rate

BARORECEPTORS

specialized nerve cells in aortic and carotid arteries

Sensitive to changes in BP

Hypertension= transmit to medulla to initate a PARASYMPATHETIC RESPONSE

Hypotension= less baroreceptor stimulation-allows for enhances of SYMPATHETIC ACTIVITY.

GERONTOLOGIC CONSIDERATIONS

General aging can result in:

Changes in LEFT ventricle

Decreased elasticity & widening of AORTA

Thickening & rigid cardiac valves

Increased connective tissue in SA & AV NODES & BUNDLE BRANCHES

ELECTROPHYSIOLOGY

of the

HEART

The heart has RHYTHMIC pumping b/c of electrical impulses generated & passed along the conduction system of the heart.

ECG= complexes that make up an electrocradiography image. 

CARDIAC ACTION POTENTIAL

Changes in cell membrane potential is described in terms of polarization

POLARIZED= resting state

*Na- extracellualr

*Ka-intracelluar

DEPOLARIZATION

When cell responds to electrical stimulus.

Mechanical contraction of cardiac muscle cell follows depolarization (SYSTOLE)

REPOLARIZATION

When cell is going back into the resting state (polarized)

Corresponds to mechanical relaxation of myocardial muscle (DIASTOLE)

RESTING MEMBRANE POTENTIAL

Cell is at rest

Inside the cell is more neg. charged than outside the cell

Cell is polarized-not participating in electrical events.

Phases of Cardiac Action Potential

(phases 0-4)

PHASE 0= DEPOLARIZATION

The cell responds to an impulse due to rapid entry of Na & Ca, lasts a few millisecs

P wave= atrial depolarization

QRS Complex= ventricular depolarization

Phases of Cardiac Action Potential

PHASE 1= short period of repolarization/early rapid   repolarization

Begins @ ST segment

Phases of Cardiac Action Potential

PHASE 2= PLATEAU

allows completion of contraction

asst. w/slow entry of Ca into cells

longer lasting- 100 millisecs

ST segment

PHASES of Cardiac Action Potential

PHASE 3= RAPID repolarization

electrical recovery of cells

cells regain neg. charge

T WAVE

PHASES of Cardiac Action Potential

PHASE 4= Resting membrane potential

cell prepared for next electrical impulse

REFRACTORINESS

The ability of Cardiac cells to respond

to

sucessive stimuli

ABSOULTE REFRACTORY PERIOD=

No stimulus will produce a response

RELATIVE REFRACTORY PERIOD=

During final stage of repolarization a strong stimulus will produce a response.

EFFECTS OF Ca+ & K+

Hypercalcemia                                  Hypocalemia

increased                                             decreased

contractility                                          contractility

ventricular                                            decreased 

dysrhytmias                                          sensitivity to Dig

                                                          Cardiac

                                                           insufficiencies

Hyperkalemia                              hypokalemia

slowed conduction of impulses          Prolonged cardiac

                                                  repolarization

                                                  decreased strength in

                                                  muscle contraction

                                                  Potentiates Dig

                                                  toxicity

ECG Assessment

HEART RATE=

Count # of complexes in a 6 sec strip & multiply by 10

Count # of large boxes b/t 2 complexes & divide by 300

Count # of small squares b/t complexes & divide that # into1500

RHYTHM & REGULARITY=

Atrial- measure P to P waves w/caliper= <1-3 small boxes (0.8-0.12 secs)

Ventricular- measure R to R intervals

ECG Assessment

Examine P waves-

should be present & look the same in size & shape throughout Sinus Rhythm (SR)

If not the impulse is generated from a focus different from the SA NODE, may be ectopic.

ECG Assessment

P to QRS relationship-

There should be one P for every QRS

ECG- Interval durations

P to R

Measures the time for ATRIAL depolarization & impulse delay & travel through the PURKENJIE FIBERS (0.12-0.20 secs)

Measure beginning of P wave to beginning of QRS

ECG- Interval durations

QRS complex-

Ventricular depolarization

Shape of this complex will depend on the lead selected

Check that ea. is preceded by a P wave

Is it consistant in duration & form?

Duration: 0.06-0.10 secs, normally less than 3 small boxes.

ECG Assessment

S T segment

A flat line having no voltage from end of S wave to beginning of T wave (isoelectic)

Early ventricular repolarization- PHASE 1 & 2.

ECG Assessment

Q  T interval

Represents total ventricular repolarization & depolarization

Less than .4 sec (0.32-0.44) or 8-11 sm boxes

Onset of QRS complex to end of T wave

ECG Assessment

T wave

ventricular repolarization

If an ectopic stimulus excites the ventricles at this time it may cause irritabilty

Look @shape- smooth, round, same direction as QRS

U wave sometimes follows T wave: may represent hypokalemia.