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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