Heart Physiology- Gonsalves

Cardiac muscle cells are:

mechanically, chemically, and electrically connected to one another

Characteristics of cardiac cells

fairly shorty

semi-spindle shape

branched and interconnected

connected via intercalated discs

have an elecrical link via gap junctions

common contraction called among cells called syncytium

1 or 2 central nuclei

dense endomysium

high vasculature

many mitochondria (25%)

almost all aerobic

myofibers fuse at the ends

T tubules are wider and fewer than muscle cells

Mechanism of Contraction of Contractile Cardiac Muscle Fibers

1. Sodium ion influx from extracellular spaces which causes a positive feedback opening of voltage gated sodium channels. Membrane potential quickly depolarizes and (-90 to +30 mV). NA channels close within 3 ms of opening.

2. Depolarization causes release of calcium ions from the sarcoplasmic reticulum, allowing sliding actin and myosin to proceed.

3. Depolarization also causes opening of slow calcium ion channels on the membrane, further increasing calcium influx and activation of filaments. This causes more prolonged depolarization than in skeletal muscle, resulting in a plateau action potential, rather than a spiked action potential as in muscle.

Differences between skeletal and cardiac muscle contraction

1. All-or-none law

2. Automicity (Autorhythmicity)

3. Length of absolute refractory period

The All-or-None Law

Gap junctions allow all cardiac muscle cells to be linked electrochemically, so that action of a small group of cells spreads like a wave throughout the entire heart. This is essential for a synchronistic contraction of the heart.

Automicity (Autorhythmicity)

Some cardiac muscles are self excitable allowing for rhythmic waves of contraction to adjacent cells throughout the heart.

(Skeletal muscle cells must be stimulated by independent motor neurons as part of a motor unit)

Length of Absolute Refractory Period

The absolute refractory period of cardiac muscle is much longer than skeletal muscle cells. This prevents wave summation and tetanic contractions which would cause the heart to stop pumping rhythmically.

Length of cardiac muscle absolute refractory period vs. skeletal muscle

250 ms vs. 2-3 ms

General properties of conduction:

1. Heart can beat rhythmically without nervous input

2. Nodal System (cardiac conduction system)

3. Gap Junctions

Nodal System (cardiac conduction system)

Special autorythmic cells of the heart that initiate impulses for wave-like contraction of entire heart (no nervous stimulation needed for these)

Gap Junctions of the heart

Electrically couple all cardiac muscles so that depolarization sweeps across the the heart in sequential fashion from atria to ventricles. (Atria above, ventricles below- AA, BV)

Pacemaker potentials

"autorhythmic cells" of the heart muscle create action potentials in rhythmic fashion; this is due to unstable resting potentials which slowly drift back toward threshold voltage after repolarization from a previous cycle.

Theoretical Mechanism of Pacemaker Potential pathway:

1. K+ leak channels allow K+ out of the cell more slowly than in skeletal muscle

2. Na+ slowly leaks into the cell, causing the membrane potential to slowly drift up to threshold to trigger Ca++ influx from outside (-40 mV)

3. When -40 mV (threshold) is reached, fast calcium channels open, permitting explosive entry of Ca++ from the cell, causing a sharp rise in level of depolarization.

4. When peak depolarization is achieved, voltage gated K+ channels open, causing repolarization to the unstable resting potential.

Autorhythmic Cell location & Order of Impulses

1. Sinoatrial node (SA) (right atrium

2. Atrioventricular node (AV) (right AV valve)

3. Atrioventricular bundle (bundle of His)

4. Right and left bundle of His branches

5. Purkinje fibers of ventricular walls

Sinoatrial node is the

pacemaker of the heart

SA node characteristics

Has the fastest autorhythmic rate (70-80) beats per minute, and sets the pace for the entire heart. This is called the sinus rhythm. Located in the right atrial wall, just inferior to the vena cava.

Atrioventricular node characteristics

impulses pass from SA via gap junctions in a bout 40 ms. Impulses are delayed 100 ms to allow completion of the contraction of both atria. Located just above the tricuspid valve between the right atrium and ventricle

Atrioventricular bundle (bundle of His)

in the interATRIAL septum (connects L and R atria)

Purkinje fibers

within the lateral walls of both the left and right ventricles. The left ventricle is much larger= p. fibers more elaborate here. Innervate papillary muscles before ventricle walls so AV valves can prevent backflow

The initial SA node excitation causes _________ of both the ____ and ______ _______.

contraction, right, left, atria

Contraction of R and L _____________ begins at the ___________ of heart, ejecting blood supply superiorly to ___________ and _________ artery

ventricles, Apex, aorta, pulmonary

The bundle of __________ is the _________ link between __________ and ____________ contraction. (AV node and bundle must work for ventricular contractions)

His, only, atrial, ventricular

Since cells in the ___________ have the fastest autorhythmic rate (70-80 per minute), it ____________ all other autorhythmic centers in a _____________

SA node, drives, normal heart

Arrythmias are

uncoordinated (abnormal) heart contractions

Fibrillation

rapid and irregular contractions of the heart chambers; reduces efficiency of heart

Defibrillation

application of electric shock to heart in attempt to retain SA node rate

Ectopic focus

autorhythmic cells other than SA node take over heart rhythm

Nodal rhythm

When AV node takes over pacemaker function (40-60 per minute)

Extrasystole

when outside influence (such as drugs) leads to premature contraction

Heart block

when AV node or bundle of His is not transmitting sinus rhythm to ventricles

How does the parasympathetic decrease heart rate? Pathway

Decreases rate of contractions via acetylcholine

Cardioinhibitory center (medulla) - Vagus nerve (cranial X) - heart

How does the sympathetic increase rate of contractions? Pathway

Increases rate of contraction via norepinephrine

Cardioacceleratory center (medulla) - lateral horn of the spinal cord to preganglionics T1-T5 - Postganglionic cervical/thoracic ganglia - heart

Deflection waves of ECG (electrocardiograph)

P-wave, QRS complex, T wave, PR Interval, QT interval

P wave

The initial wave that demonstrates the depolarization from SA node through both atria. The atria contract about 0.1 s after the start of the P wave

QRS complex

Demonstrates the depolarization of the AV node through both ventricles. The ventricles contract throughout the period of the QRS complex with a short delay after the end of atrial contraction. Repolarization of atria is also obscured.

T wave

repolarization of the ventricles (0.16s)

PR Interval

time period from beginning of atrial contraction to beginning of ventricular contraction (0.16 s)

QT interval

time of ventricular contraction from depolarization and repolarization (0.36 s)

The period of chamber contraction

Systole

Period of chamber relaxation

Diastole

Cardiac cycle

all events of systole and diastole during one heart flow cycle

Events of the Cardiac Cycle

1. Mid to late ventricular diastole- ventricles filled

2. isovolumetric contraction phase

3. ventricular systole- blood ejected from heart

4. isovolumetric relaxation- early ventricular diastole

MId-to-Late ventricular diastole (ventricular filling) steps

1. AV valves are open

2. Pressure is low in chambers and high in aorta/pulmonary trunk

3. Aortic/pulmonary semilunar valves closed

4. Blood flows from vena cava/ pulmonary vein into atria

5. Blood flows through AV valves into ventricles (70%)

6. Atrial systole propels more blood into the ventricles (30%)

7. atrial diastole returns through the end of the cycle

Ventricular systole (blood ejected from heart)

1. filled ventricles begin to contract, AV valves close

2. Isovolumetric contraction phase- ventricles closed

3. Contraction of closed ventricles increases pressure

4. Ventricular ejection phase- blood forced out

5. Semilunar valves open blood goes to the aorta and pulmonary truck

Isovolumetric Relaxation (early ventricular diastole)

1. ventricles relax ventricular pressure becomes low'

2. semilunar valves close aorta and pulmonary trunk backflow

3. Dicrotic notch, brief increase in aortic pressure

Total cardiac cycle time

0.8 seconds

atrial systole (contraction) time

0.1 second

ventricular systole (contraction) time

0.3 second

atrial systole (contraction time)

0.1 second

Quiescent period (relaxation)

0.4 seconds

lub-dub - lub-dub

1. lub- closure of AV valves, onset of ventricular systole

2. dub- closure of semilunar valves, onset of diastole

3. pause- quiescent period of cardiac cycle

4. Tricuspid valve (lub)- RT 5th intercostal, medial

5. Mitral valve or bicuspid (lub) - LT 5th intercostal, lateral

6. Aortic semilunar valve (dub)- RT 2nd intercostal

7. Pulmonary semilunar valve (dub) LT 2nd intercostal

The LUB sound is caused by

The first sound LUB is produced when the atrioventricular valves i.e. tricuspid and bicuspid (mitral) valves close at the start of ventricular systole.

The DUB sound is caused by

The second sound DUB is produced at the beginning of ventricular diastole when the pulmonary and aortic semilunar valves close.

Murmur

sounds other than the typical "lub-dub" typically caused by disruptions in flow

Incompetent valve

swishing sound after the normal lub or dub is due to valve not completely closing and there is some regurgitation of blood

Stenotic valve

high pitched swishing sound when blood should be flowing through the valve, narrowing of outlet in the open state

(narrowing of the pulmonary valve= restricts blood flow)

Variables of Cardiac Output

1. Cardiac output (CO)- blood amount pumped per minute

2. Stroke Volume (SV)- ventricle blood pumped per beat

3. Heart Rate (HR)- cardiac cycles per minute

CO (ml/min)

SV (mL/beat) x HR (beats/min)

Normal CO

75 beats/min X 70 ml/beat = 5.25 L/min

End Diastolic Volume (EDV)

total blood collected in the ventricle at and of diastole; determined by the length of diastole and venous pressure (120 ml)

End Systolic Volume (ESV)

blood that is left remaining in the ventricle at the end of a contraction- determined by the force of ventricle contraction and arterial blood pressure (50 ml)

SV (ml/beat)=

EDV (ml/beat) - ESV (ml/beat)

Normal SV

120 ml/beat - 50 ml/beat = 70 ml/beat

Frank-Starling Law of the Heart

the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.

critical factor for stroke volume is the degree of stretch of cardiac muscle cells, more stretch = more contraction force

Increased EDV =

More contraction force

Reasons for Frank-Starling Law of the Heart

slower heart rate= more time to fill, more blood in the cardiac muscle

exercise= more venous blood to return

Systems and receptors involved in autonomic regulation of the heart

Sympathetic, Parasympathetic, Vagal Tone, Baroreceptors and Pressoreceptors

Sympathetic regulation of the heart

Norepinephrine increases the heart rate but maintains the stroke volume which leads to increased cardiac output

Parasympathetic regulation of the heart

acetylcholine decreases the heart

Vagal tone in regulation of the heart

parasympathetic inhibition of inherent rate of SA node, allowing for normal heart rate

Basoreceptors and Pressorrecptors in regulation of the heart

monitor changes in the blood pressure and allow reflex activity with the autonomic nervous system

Hormone that is released by adrenal medulla during stress and increases the heart rate

epinephrine

Hormone released by the thyroid that increases the heart rate in large quantities and amplifies the effect of epinephrine

Thyroxine

These cation levels are very important in the regulation of the heart

Ca++, K+, Na+

Hyperkalemia

increased levels of potassium and can induce deadly cardiac arryhthmias. KCl is used to stop the heart by lethal injection

Hypokalemia

lower potassium levels that leads to abnormal heart rate rhythms

Hypocalcemia

low calcium in blood, depresses heart function

Hypercalcemia

abnormally high levels of calcium in the blood and increases the contraction rate (affects electrical impulses that regulate heart beat)

Hypernatremia

High sodium concentration that can block Na+ transport and muscle contraction

Other factors affecting heart rate

age, gender, exercise, body temperature, tachycardia, bradycardia

Normal heart rates

Fetus: 140-160 beats/min

Female: 72-80 beats/min

Male: 64-72 beats/min

Exercise on the heart

lowers the resting heart rate (40-60)

Heat on the heart

increases heart rate significantly

Cold on the the heart

decreases heart rate significantly

Tachycardia

higher than normal resting heart rate (over 100) that may lead to fibrillation

Bradycardia

Lower than normal resting heart rate (below 60) this can be due to parasympathetic effects, physical conditioning, is a sign of pathology in a non-healthy patient

Congestive Heart Failure

heart cannot pump sufficiently to meet needs of the body

Coronary atherosclerosis

leads to gradual occlusion of heart vessels, reducing oxygen nutrient supply to cardiac muscle cells; (fat & salt diet, smoking, stress)

High blood pressure

when aortic pressure gets too large and the left ventricle cannot pump properly, increasing ESV and lowering SV

Myocardial infarct

Heart cell death due to numerous factors, including coronary artery occlusion

Pulmonary congestion

failure of LEFT heart; leads to buildup of blood in the lungs

Peripheral congestion

failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers)

Diseases of the heart

1. Congenital heart defects

2. Sclerosis of AV valves

3. Decline in cardiac reserve

4. Fibrosis and conduction problems

Congenital heart defects

heart problems that are present at the time of birth includes patent ductus arteriosus

Patent ductus arteriosus

bypass hole between pulmonary trunk and aorta that does not close (may eventually close) can cause extra blood flow to the lungs

Sclerosis of AV valves

fatty deposits on valves; particularly the mitral valve of LEFT side; leads to heart murmur

Decline in cardiac reserve

heart becomes less efficient with age

Fibrosis and conduction problems

nodes and conduction fibers become scarred over time; may lead to arrhythmias