HEART

Lecture Notes:

I. Heart anatomy/flow A. Pericardial cavity
Heart is eveloped by fibrous layer (dense irregular CT) called the Pericardium. Functions to protect heart from physical damage. Fused to this layer is serous membrane (parietal serous pericardium) that produces lubricating serous fluid. Between the parietal serous pericardium and visceral serous pericardium is cavity.
B. Heart wall layers1. Epicardium (parietal pericardium ) protecting heart from damage due to friction.

2. Myocardium (= cardiac muscle)

a. Atria (Left and right)
LA drains veins from lungs
RA drains veins from body

b. Ventricles (Left and right)
Much larger
RV fills from RA pumps to lungs
fills from LA pumps to body \ LV larger than RV)

3. Endocardium lines inner wall and continues on as vessels' innermost layer providing a smooth surface for blood flow.
C. Valves - allow blood flow only one way 1. Atrioventricular valves (AV)
tricuspid, between RA & RV
bicuspid, between LA & LV (= mitral valve)

2. Semilunar valves
pulmonary between RV & lungs
aortic between LV & body

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II. Circulatory routes A. Pulmonary circulation (flow of blood through lungs) 1. Vena cava , RA, tricuspid valve, RV, pulmonary semilunar valve, pulmonary artery, lungs, pulmonary veins, LA, bicuspid valves, LV, aortic semilunar valve, aorta, vena cava

2. Oxygenated vs unoxygenated blood
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B. Cardiac circulation -a. R/L coronary arteries branch off aorta with oxygenated blood and service heart capillaries

b. Coronary veins drain heart capillaries into coronary sinus which empties into R atrium

List the vessels, valves, chambers and organs (lung) that blood must travel through from the Right atrium to the Aorta.


II. Heart Physiology

A. Cardiac muscle histology 1. Striated; uninucleated (usually) with many mitochondria

2. Short, branched and intercalated disks (gap junctions that allow communication between cells)

B. Cardiac muscle physiology 1. Cardiac muscle cells act as electrically interconnected units via gap junctions (i.e., all atrial cells contract as once, same with ventricular mycardium) unlike independent skeletal muscle cells

2. Cardiac cells are self-excitable and rhythmic (contract in definite self-induced pattern) \ heart has own pacemaker to set heart rate.
= autorhythmicity
each part of heart has an intrinsic rate
intrinsic contraction rates vary by position
 
 

3. Cardiac depolarization is about 250x as long as skeletal muscle depolarization \ heart muscle does not undergo summation and tetany like skeletal muscle
due to very long ca++ inflow time (plateau)

4. Both contractile and conductile cardiac muscle cells

Compare and contrast histology and physiology of cardiac muscle vs skeletal muscle cells. Compare functions of conductile vs contractive cardiac muscle.

C. Conduction System - dependent on ability of muscle cell membranes to depolarize & carry signal
 
  1. Nodes - noncontractile cardiac muscle cells that initiate contractions in orderly manner a. SA (sinoatrial) node in wall depolarizes spontaneously
SA node determines normal sinus rhythm (= pacemaker)
intrinsic rate 60-100 bpm

b. AV (atrioventricular) node in RA floor
picks up depolarizing wave from SA node sending signal to ventricles
intrinsic rate 40-60 bpm

c. Bundle of His, bundle branches and fibers
depolarize most of ventricles
intrinsic rate < 40 bpm

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Describe the pathway that an muscle action potential follows to excite the entire heart (atria to ventricles).

D. Electrocardiography - way of monitoring electrical currents through heart (and body) via electrocardiogram (ECG) 1. Normal sinus rhythm
waves represent depolarization and repolarization of atria and ventricles, respectively a. P wave - atrial depolarization from SA node

b. QRS wave atria repolarized (masked)
Septal and ventricular depolarizations

c. T wave - ventricular repolarization

d. Each cycle is alternating pumping rhythm (atria first then ventricles)

2. Defects in cardiac cycle
irregular wave shapes and abnormal heart rates a. Too few "normal" cycles (<60) sinus bradycardia
elderly, elite athelete

b. Too many "normal" cycles (100) sinus tachycardia
fear, anxiety, nicotine, caffeine

c. Long PR interval--slow, intermittent or no conduction from SA node. (AV) heart block.
atria & ventricles separated by damage to AV node cells

d. More P waves than QRS waves. Rate 200-300 atrial tachycardia
hyperthyroidism

e. Irregular P waves with saw edge, very rapid rate (>400) atrial fibrillation
mitral stenosis, hypertension, coronary heart disease

f. Rapidly occurring QRS waves, no P waves visible, rate 100-200 ventricular tachycardia
stress, pregnancy, acidosis, ectopic pacemakers

g. Irregular ventricular activity (no waves) ventricular fibrillation
myocardial infarction

Describe which parts of the heart are undergoing electrical activity during the progress through one ECG cycle. Identify arrhythmias.

E. Cardiac cycle 1. ECG depolarizations (P and R waves) stimulate muscle contractions which, in turn, alter blood pressure in chambers.

2. Systole vs diastole (ventricular) are changes in blood pressure

a. Systole occurs when ventricles pump causing higher arterial blood pressure
e.g., 120 mm Hg pressure

b. Diastole occurs when ventricles and atria relax therebycausing lower arterial blood pressure, e.g. 80 mm Hg

Blood pressure monitored on brachial artery is 120/80 mm Hg. Systolic over diastolic pressure ratio

3. Heart sounds a. Lubb (S1) begins at ventricular systole = closing AV valves

b. Dupp (S2) ends at ventricular systole = closing of semilunar valves

4. Filling and ejection of blood
Atria fill during flat line and eject blood upon contraction resulting from P wave depolarization. This ejection fills the ventricles. Ventricles eject during contraction resulting from QRS depolarization (Systole)
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Using an ECG pattern as a background, name the waves, which chambers are depolarizing/repolarizing, locate ventricular systole/diastole, locate ventricular filling/ejection, locate sounds and describe the movement of blood.

F. Cardiac output 1. Output = volume  of blood, in liters,  pumped per minute
CO=HR X SV----If increased stroke volume or heart rate, within normal ranges, then cardiac output goes up a. Typical stroke volume pumped = ~ 70 ml/beat at rest

b. Typical heart rate = 75 beats/min at rest

typical CO = 5 l/min at rest, (i.e., entire blood supply moved every minute)
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2. Regulation of SV a. Amount of returning venous blood (preload)
more return (preload) causes more stretch and therefore more forceful contraction and fluid moved.

b. Amount of blood heart must move to push blood out of heart (afterload)
higher blood pressure increases afterload and reduces stroke volume.

c. Amount of contractility of cardiac muscle
more contraction causes more fluid to be moved

1) Increased sympathetic stimulation to SA and myocardium (Norepinephrine) increases contraction, Increased parasympathetic stimulation (acetylcholine) reduces contraction

2) Increased hormones (NE, Epinephrine) increase contraction

3. Regulation of HR a. Neural regulation

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ANS control through baroreceptor reflex (baroreceptors in carotid arteries and aorta, vagus and glossopharangeal nerve input, cardioaccelerator area in medulla oblongata, nerve output (see below) to SA node and cardiac muscle. Also chemoreceptor reflex (oxygen, carbon dioxide and pH)

1) low bp, low oxygen, low pH or high carbon dioxide triggers increased  sympathetic stimulation (cardioaccelerator nerves and Norepinephrine) promotes increased HR

 2) high bp, high oxygen, high pH or low carbon dioxide triggers increased parasympathetic stimulation (vagus nerve and Acetylchoine) promotes decreased HR

 

b. Chemical regulation

If [K+] is high then decreased HR due to inhibited neural stimulation

Epinephrine and NE-increased hormone therefore increased HR

Thyroid-increased hormone therefore increased HR

Describe the major factors influencing heart rate and the conditions that regulate those factors.


G. Disorders of Heart

1. congestive heart failures (CHF) --less pumping causes more damage causes less pumping so
blood not moved promoting less O2 in blood (positive feedback spiral downwards)a. Right side damaged results in peripheral edema

b. Left side damaged results in pulmonary edema

2. Coronary artery disease (CAD)
narrowed arteries due to plaque causing less O2 promoting cell ischemia.

3. Myocardial ischemia (Angina pectoris))
temporary reduced O2 supply to myocardium via coronary arteries
often associated with chest pain
4. Myocardial infarction (MI or heart attack)
Permanent damage to heart muscle which is replaced by connective tissue. Because coronary arteries are blocked, arterial spasms result in no blood flow and O2 delivery and eventual cell death.

Professor Thomas M. Lancraft

Human Anatomy and Physiology Courses 
at St. Petersburg College
St. Petersburg/Gibbs Campus

5/2008