1- heart 2014-15

PHYSIOLOGY OF THE HEART and CIRCULATION

FUNCTIONAL ANATOMY OF THE HEART

CARDIAC MUSCLE
3 MAJOR TYPESAtrial muscleVentricular muscleExcitatory/conductive muscles
** contractions same as skeletal muscle EXCEPT duration of contractions is much longer

** few contractile fibrils; automatic electrical discharge in the form of an AP; conduction of AP through heart

Arranged in latticeworkStriatedMyofibril (actin and myosin)Intercalated disc - cell membranes separating cardiac muscles connected in series and parallelFused together forming gap junctions (rapid ion diffusion)

SyncytiumCardiac muscle cells are interconnected that when one becomes excited, AP travels spreading to entire latticework interconnectionsAtrial syncytiumVentricular syncytium

2 CHAMBERSAtrium Ventricle VALVESAtrioventricular valvesMitral valveTricuspid valveSemilunar valvesPulmonic valveAortic valve

FUNCTIONAL ANATOMY OF THE HEART

ATRIA / ATRIUM
Primer pumps that increases the ventricular pumping effectiveness as much as 20%Normal flow from great veins into atria blood flows around 80% directly into the ventricles

VENTRICLES
Main pumping force that propels the bloodRight ventricle pulmonary circulationLeft ventricle peripheral circulation

VALVES
ATRIOVENTRICULAR VALVE (mitral and tricuspid)Prevents the backflow of blood from the ventricles to the atrium ( during systole )SEMILUNAR VALVES (aortic and pulmonic valve)Prevents the backflow of blood from the aorta and pulmonary arteries into the ventricles ( during diastole)

CARDIAC CYCLE
Cardiac events that occur from the beginning of one heartbeat to the beginning of the nextInitiated by spontaneous generation of an action potential in the sinoatrial node (located superior lateral wall of right atrium near the opening of the superior vena cava)Diastole period of relaxationSystole period of contraction

CARDIAC CYCLE
Total duration (including systole and diastole) is the reciprocal of heart rateNormal HR: 60-80 beats/min72/min = duration of cardiac cycle is 1/72 per minute = 0.0139min/beat = 0.833sec/beatHR increases, duration of each cardiac cycle decreasesHeart beats faster does not remain relaxed long enough to allow complete filling of the cardiac chamber before the next beat

ATRIA / ATRIUM (atrial pressure)
a wave Atrial contractionRAP (4-6mmHg)LAP (7-8mmHg)C waveVentricles begin to contractSlight backflow of blood into the atria at the onset of ventricular contractionBulging of the AV valves backward towards the atria

ATRIA / ATRIUM
v waveTowards the end of ventricular contractionSlow flow of blood into the atria from the veinsAV valves are closed during ventricular contraction

VENTRICLES
Filling of ventricles during diastoleVentricular systole --- large amounts of blood accumulate in the right and left atria because of the closed AV valvesSystole is over --- ventricular pressure falls
pressure from atria pushes AV valves open

allowing blood to flow rapidly into ventricles

(PERIOD OF RAPID FILLING OF VENTRICLES)

VENTRICLES
Emptying of ventricles during systole
Period of isovolumic (isometric) contraction

After ventricular contraction begins ventricular pressure s causing AV valves to close

Contraction in the ventricle is occurring but there is no emptying

Tension s in muscle but no shortening

period of ejection

- LVP rises above 80mmHg; RVP rises 8mmHg

- pushes Semilunar valves to open

- blood pours out of ventricle: 70% 1st 3rd of ejection (PERIOD OF RAPID EJECTION) : 30% 2nd 3rd of ejection (PERIOD OF SLOW EJECTION)

VENTRICLES
Emptying of ventricles during systole
Period of isovolumic (isometric) relaxation

- End of systole, ventricular relaxation allowing both right and left intraventricular pressure to decrease

END DIASTOLIC VOLUME110 to 120mlNormal filling of the ventricles during diastoleEND SYSTOLIC VOLUME40 to 50mlRemaining volume of each ventricleSTROKE VOLUME OUTPUT70mlVentricles empty during systoleEJECTION FRACTIONFraction of the end diastolic volume that is ejected60%

Normal blood pressure120/80 mmHg120 systolic (maximal pressure that occurs in the aorta during ventricular contraction)80 diastolic (AV valves closes pressure in aorta decreases throughout diastole because blood flows thru the peripheral circulation)

Semilunar valves vs AV valves
High pressure in the arteries at the end of the systole causes semilunar valves to snap to close position (AV valves softer closure)Smaller openings of SL valves, velocity of blood ejection is greater (AV larger valves)Rapid closure and rapid ejection edges of semilunar valves subjected to much greater mechanical abrasionNot supported by chordae tendinae (AV valves supported)

STROKE WORK OUTPUTAmount of energy that the heart converts to work during each beat while pumping blood into the arteriesMINUTE WORK OUTPUTTotal amount of energy converted to work in 1 minuteStroke work output x HR

VOLUME-PRESSURE DIAGRAM
PHASE I (Period of filling) Begins at a ventricular volume 50ml (end systolic volume)Amount of blood that remains in the ventricles after the previous heart beat120ml end diastolic volume ( venous blood flows into the ventricle from the left atrium)

PHASE II (period of isovolumic contraction)Volume of ventricles does not changeAll valves are closed

PHASE III ( Period of ejection )Systolic pressure rises even higher because of the greater contraction of ventriclesVolume of the ventricles because aortic valve opens and blood flows out of the ventricle to aorta

PHASE IV (Period of isovolumic relaxation)Aortic valve closesVentricular pressure falls back to diastolic pressure without any changes in volume

PRELOAD degree of tension on the muscle when it begins to contractEnd diastolic pressure when ventricles becomes filledAFTERLOADLoad against which the muscle exerts its contractile forcePressure in the aorta from the ventricleCorresponds to the systolic pressure

HEART SOUNDS
Closure of the valvesVanes of valves and surrounding fluids vibrating due to the sudden pressureS1 First heart soundVentricles contract closure of the AV valvesLow in pitch, relatively low in pitchS2Rapid snapAortic and pulmonic valve closure during end systolicShort period

HEART SOUNDS
S1S2Closure of AV valvesClosure of semilunar valvesVibration of the taut valves immediately after closure along with the vibration of the adjacent walls of the heart and its major vesselsContraction of the ventricles causes sudden backflow against AV valvesDuration: 0.14 sec0.11 sec (SL valves more taut ,vibrate shorter)Low pitchHigher pitchTautness of the valvesGreater elasticity coefficient of the taut arterial walls that provides the principal vibrating chamber

HEART SOUNDS
S3 weak rumblingBeginning of the middle 3rd of diastoleOscillation of the blood back and forth between walls of the ventricles initiated by the in rushing blood from the atriaLow frequency (not heard)S4weakVery low in frequency

Regulation of heart pumping
At rest 4 to 6 litres of blood per minuteExercise : 4 to 7x of 4-6 litresBasic means of regulationIntrinsic cardiac regulation of pumping in response to changes in volume of blood flowing to the heartControl of heart rate and strength of heart pumping by the autonomic nervous system

FRANK STARLING MECHANISM
Intrinsic ability of the heart to adapt to increasing volumes of inflowing bloodThe greater the heart muscle is stretched during filling, the greater is the force of contraction, the greater the quantity of blood pumped into the aortaHeart pumps all the blood that returns to it by the way of the veinsAmount of blood pumped by the heart each minute is determined by venous return

FRANK STARLING MECHANISM

Extra amount of blood flow in the ventricles

Cardiac muscle stretches to greater length

Muscle contracts with increase force

Ventricles increases pumping extra blood to the arteries

PHYSIOLOGIC PROPERTIES OF THE HEART
ExcitabilityAutomaticityConductivitycontractility

Pumping effectiveness controlled by sympathetic and parasympathetic nerves (vagus)Sympathetic nervesIncreases HRIncreases force of contraction Increases volume of blood pumped, increases ejection pressureParasympathetic nervesDecrease or stop the heartbeatDecrease strength of heart contractionVagal fibers distributed to the atria

Effect of potassium Excess in ECF causes heart to dilate and becomes flaccid causing slowing HRLarge amounts can block the conduction of heart impulse from atria to ventricle through AV bundle Decreases the resting membrane potential in the cardiac muscle fibers ----- membrane potential becomes negative --- intensity of AP decreases ---- weaker contractionEffect of calciumExcess heart goes spasticInitiates contractile process

Effect of temperaturetemp, causes HRHeat increases the permeability of the cardiac muscle membrane to ions controlling the HRProlonged elevation of temperature exhausts the metabolic system eventually causes weakness

Conductive system of the Heart

SINUS NODE (Sinoatrial)Small flattened, ellipsoid strip of specialized cardiac muscleSuperior posterolateral wall of the right atrium below the SVCFibers almost no contractile muscle filamentsControls the rate of the beat of the entire heart/pacemaker of the heart
Cardiac fibers : self excitation (process that can cause automatic rhythmical discharge and contraction)

Self excitation --- action potential --- recovery from action potential --- hyperpolarization --- resting membrane potential

INTERNODAL PATHWAYSSinus nodal fibers connecting directly with the atrial muscle fibersWhere AP travel from SA node to AV nodeAV NODEDelay of impulse from atria to ventricles (allowing time for atria to empty before ventricular contraction)Posterior wall of the RA behind the tricuspid valveSlow conduction mainly by diminished number of gap junctions between conducting pathways

PURKINJE FIBERSVery large fiberstransmits cardiac impulse throughout the remaining ventriclesRapid transmission caused by high levels of permeability of gap junctions at the intercalated discInability of AP to travel backward from the ventricles to atria

ELECTROCARDIOGRAM (ECG)

P wave Atrial depolarizationQRSVentricular depolarization
P and QRS wave are depolarization waves
T wave
Ventricles recover from state of depolarization

repolarization wave

P-Q or P-R intervalBeginning of the P wave and beginning of QRS0.16secQ-T interval0.35 secVentricular contraction to the end

ECG LEADS
3 BIPOLAR LIMB LEADSLEAD ILEAD IILEAD IIIPRECORDIAL LEADSV1,V2,V3,V4,V5,V6AUGMENTED UNIPOLAR LIMB LEADSaVr, aVL,aVF

ECG LEADS
LEAD I(-) right arm(+) left armLEAD II(-) right arm(+) left legLEAD III(-) left arm(+) left leg

ECG LEADS
V1 to V6 anterior chest wallV1 and V2 QRS negativeV4, V5, V6 positive

CIRCULATION
Transport nutrients to the body tissuesTransport waste products awayTransport hormones from one part of body to anotherMaintain an appropriate environment in all tissues

TWO DIVISIONS OF CIRCULATION
SYSTEMIC CIRCULATIONSupplies blood flow to all tissues of the body except lungsGreater circulationPeripheral circulationPULMONARY CIRCULATIONBlood supply to the lungs

FUNCTIONAL PARTS OF THE CIRCULATION
ARTERIESTransport blood under high pressure to the tissuesStrong vascular wallBlood flows at high velocityARTERIOLESLast small branches of the arterial systemAct as control conduits through which blood is released into capillariesStrong muscular walls

CAPILLARIESExchange of fluids, nutrients, electrolytes, hormones and other substances between the blood and interstitial fluidVery thin wallsNumerous capillary pores permeable to water and other molecular substancesVENULESCollect blood from capillariesGradually coalesce into progressively larger veins

VEINSConduits for transport of blood from venules back to the heartMajor reservoir of extra bloodPressure is low, walls are thin

BASIC PRINCIPLES OF CIRCULATORY FUNCTION
Rate of blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue needTissues active, need an increase supply of nutrients requiring more blood flow ---- microvessels acting directly on local blood vessels either to dilate or constrict in controlling blood flow

The cardiac output is controlled mainly by the sum of all the local tissue flowsBlood returns by the way of veins back to the heartHeart responds automatically to the needs of the tissues

Arterial pressure regulation is generally independent of either local blood flow control or cardiac output controlExtensive system for controlling arterial pressurePressure falls below normal--- nervous reflexes elicits series of circulatory changesIncrease force of heart pumpingContraction of large venous reservoir to provide more blood to the heart

Factors determining blood flow
Pressure differencePressure gradient along the vesselForce that pushes the blood through the vesselVascular resistanceImpediment to blood flow through the vesselOccurs as a result of friction between the flowing blood and the intravascular endothelium OHMS LAW
F = P F blood flow P pressure R resistance

R

BLOOD FLOWQuantity of blood that passes a given point in the circulation in a given period of timeOverall blood flow in the circulation 5000ml/min Cardiac output > amount of blood pumped into the aorta by the heart each minuteLaminar flow of bloodBlood flows at a steady rate through a smooth blood vessel flowing in streamlinesLayer of blood remain in same distance of vessel wallTurbulent flow of bloodBlood flows in all direction; forming whorls in the blood directly with velocity, diameter of vessel, inversely with viscosity

BLOOD PRESSURE
Force exerted by the blood against any unit area of the vessel wallmmHgSystolic (top of the pulse) and diastolic pressure (lowest point of pulse)Pulse pressure difference between systolic and diastolicKorotkoff sound sound heard during each pulsation

1- heart 2014-15

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