Chapter 18, Heart Physiology

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Cardiac muscle

Is striated, short, fat, branched, and interconnected.

Connective tissue endomysium acts as

Both tendon and insertion

Intercalated discs anchor

Cardiac cells together and allow free passage of ions.

Heart muscle behaves as a functional

Syncytium

Heart Muscle

1. Is stimulated by nerves and self-excitable (automaticity)
2. Contracts as a unit
3. Has a long (250 ms) absolute refractory period

Cardiac muscle contraction is similar to

Skeletal muscle contraction

Autorhythmic cells:

1. Initiate action potentials
2. Have unstable resting potentials called pacemaker potentials
3. Use calcium influx (rather than sodium) for rising phase of action potential

Sequence of Excitation

1. Sinoatrial (SA) nodes generates impulses about 75 times/minute
2. Atrioventricular (AV) node delays the impulse approximately 0.1 second
3. Impulses passes from atria to ventricles via the atrioventricular bundle (bundle of His)

AV bundle splits into two pathways in the interventricular septum (bundle branches)

1. Bundle branches carry the impulse toward the apex of the heart
2. Purkinje fibers carry the impulse to the heart apex and ventricular walls

Sequence of Excitation locations

1. Sinoatrial node (pacemaker)
2. Atrioventricular node
3. Atrioventricular bundle (Bundle of His)
4. Bundle branches
5. Purkinje fibers

Heart Excitation related to ECG

1. SA node generates impulse; atrial excitation begins
2. Impulse delayed at AV node
3. Impulse passes to heart apex; ventricular excitation begins
4. Ventricular excitation complete

Extrinsic Innervation of the Heart

1. Stimulated by the sympathetic cardioacceleratory center
2. Inhibited by the parasympathetic cardioinhibitory center

Electrocardiography

1. Electrical activity is recorded by an electrocardiogram (ECG)
2. P wave corresponds to depolarization of SA node
3. QRS complex corresponds to ventricular depolarization
4. T wave corresponds to ventricular repolarization
5. Atrial repolarization record is masked by the larger QRS complex

Cardiac cycle

Refers to all events associated with blood flow through the heart

Systole

Contraction of heart muscle

Diastole

Relaxation of heart muscle

Ventricular filling-mid-to-late diastole

-Heart blood pressure is low as blood enters atria and flows into ventricles
-AV valves are open then atrial systole occurs

Ventricular systole

-Atria relax
-Rising ventricular pressure results in closing of AV valves
-Isovolumetric contraction phase
-Ventricular ejection phase opens semilunar valves

Isovolumeteric relaxation-early diastole

-Ventricles relax
-Backflow of blood in aorta and pulmonary trunk closes semilunar valves

Dicrotic notch

Brief rise in aortic pressure caused by back flow of blood rebounding off semilunar valves

Cardiac Output

The amount of blood pumped by each ventricle in one minute

Cardiac Output is the product of

Heart Rate (HR) and Stroke Volume (SV)

Heart Rate (HR)

The number of heart beats per minute

Stroke Volume (SV)

The amount of blood pumped out by a ventricle with each beat

Cardiac reserve

The difference between resting and maximal Cardiac Output

Cardiac Output calculation

CO (ml/min)=HR (75beats/min) x SV (70ml/beat)
CO= 5250 ml/min (5.25 L/min)

Stroke Volume=

End diastolic volume (EDV) minus end systolic volume (ESV)

EDV=

Amount of blood collected in a ventricle during diastole

ESV=

Amount of blood remaining in a ventricle after contraction

Regulation of Stroke Volume

1. SV
2. EDV
3. ESV

Factors affecting Stroke Volume

1. Preload
2. Contractility
3. Afterload

Preload

Amount ventricles are stretched by containing blood

Contractility

Cardiac cell contractile force due to factors other than EDV

Afterload

Back pressure exerted by blood in the large arteries leaving the heart

Frank-Starling Law

1. Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
2. Slow heartbeat and exercise increase venous return to the heart, increasing SV
3. Blood loss and extremely rapid heartbeat decrease SV

Contractility

The increase in contractile strength, independent of stretch and EDV

Increase in contractility comes from:

-Increased sympathetic stimuli
-Certain hormones
-Ca2+ and some drugs

Agents/factors that decrease contractility include:

-Acidosis
-Increased extracellular potassium
-Calcium channel blockers

Sympathetic stimulation releases

Norepinephrine and initiates a cyclic AMP second-messenger system

Sympathetic nervous system (SNS) stimulation is activated by

Stress, anxiety, excitement, or exercise

Parasympathetic nervous system (PNS) stimulation is mediated by

Acetylcholine and opposes the SNS

PNS dominates the

Autonomic stimulation, slowing heart rate and causing vagal tone

Atrial (Bainbridge) Reflex

A sympathetic reflex initiated by increased blood in the atria
-Causes stimulation of the SA node
-Stimulates baroreceptors in the atria, causing increased SNS stimulation

The hormones that increase heart rate

Epinephrine and Thyroxine

Inta- and extracellular ion concentration must be maintained for

Normal heart function

Hypocalcemia

Reduced ionic calcium depresses the heart

Hypercalcemia

Dramatically increases heart irritability and leads to spastic contractions

Hypernatremia

Blocks heart contraction by inhibiting ionic calcium transport

Hyperkalemia

Leads to heart block and cardiac arrest

Tachycardia

Heart rate over 100 beats/min

Bradycardia

Heart rate less than 60 beats/min

Congestive heart failure (CHF) caused by:

-Coronary atherosclerosis
-Increased blood pressure in aorta
-Successive myocardial infarcts
-Dilated cardiomyopathy (DCM)

Age-related changes affecting the heart

-Sclerosis and thickening of valve flaps
-Decline in cardiac reserve
-Fibrosis of cardiac muscle
-Atherosclerosis

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