Download Chapter 19: The Heart

Chapter 19: The Heart
It’s study = Cardiology.
I. Gross Anatomy
(A) Cardiovascular System Overview – includes heart and blood vessels.
-1- pulmonary circuit connects heart and lungs.
-2- systemic circuit connects heart and body’s tissues.
(B) Size, Shape & Position location = mediastinum of thoracic cavity.
Base and apex (tilts to left). Size of fist.
(C) Pericardium – double layered sac, serous membrane. Outer =
parietal, inner = visceral. Between is the pericardial cavity with fluid.
Inflammation is pericarditis, results in friction rub and cardiac tamponade
(interferes with beating).
(D) Heart Wall
-1- epicardium: visceral pericardium. Serous membrane with fat to fill in
grooves.
-2- myocardium: thickest layer, cardiac muscle. Contains fibrous skeleton for
structural support, anchorage for muscle action, and electrical nonconductivity.
-3- endocardium: smooth lining of simple squamous epithelium.
(E) Chambers – two atria with auricles, two ventricles. Sulci on surface
filled with fat and coronary vessels. Interatrial and interventricular septa,
pectinate muscles (line atria) and trabeluae carneae (line ventricles).
(F) Valves – prevent backflow. Their flaps = cusps. AV (atrioventricular)
valves: tricuspid (right) and bicuspid = mitral (left). These cusps attached to
papillary muscles in ventricles by chordae tendinae.
Semilunar valves between ventricles and arteries (aorta, pulmonary
trunk).
Valve malfunctions:
-1- valvular insufficiency (incompetence): results in reflux (regurgitation).
-2- valvular stenosis: due to stiff scar tissue. Associated with Scarlet Fever,
heart murmurs.
-3- mitral valve prolapse (MVP).
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(G) Blood Flow Through Heart – right side with deoxygenated blood, left
side with oxygenated. Normally separated.
Blood from superior and inferior vena cavae and coronary sinus to right
atrium,
Through tricuspid valve, into right ventricle,
Out pulmonary semilunar valve, into pulmonary trunk, to lungs.
Pulmonary veins, with oxygenated blood, to left atrium,
Through mitral valve, into left ventricle,
Out aortic semilunar valve into aorta.
(H) Coronary Circulation through myocardium. Branches of right and left
coronary arteries suseptible to MIs (myocardial infarctions) when oxygen
deprivation extreme. Less intense = angina pectoris (pain from lactic acid
generation). Defense against blockages = anastomoses (connections between
vessels). Cardiac veins lead to coronary sinus, returning deoxygenated
coronary blood to right atrium.
II. Cardiac Muscle and Conduction
(A) Cardiac Muscle Anatomy Cells= myocytes; joined by intercalated
discs – contain gap junctions for electrical communication. Striated and
branched.
(B) Cardiac Muscle Metabolism Mostly aerobic. Abundant myoglobin and
mitochondria.
(C) Cardiac Conduction Autorhythmic. Non-contracting cells form
conduction system. SA (sinoatrial = sinus) node is the pacemaker,
communicates to AV node, ultimately to Purkinje fibers in ventricles.
III. Electrical and Contractile Activity
Contraction = systole; relaxation = diastole. Usually refers to ventricles.
(A) Cardiac Rhythm – normally sinus (from SA node). Vagus inhibition
establishes beat ~ 70-80 BPM. Ectopic focus may be present, e.g. AV nodal
rhythm, ~ 40-50 BPM. Arrythmias = abnormal rhythms, often due to heart
blocks.
-1- atrial flutter – repeated atrial stimulation.
-2- PVCs = premature ventricular contractions.
-3- ventricular fibrillation: “bag of worms”, corrected with defibrillation.
-4- cardiac arrest
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(B) Physiology of SA Node – cells with pacemaker potentials, leaky Na+
channels. Fast Ca++ channels trigger depolarization.
(C) Impulse Conduction to Myocardium Faster in atria than in ventricles.
Delay allows atria to contract first. Papillary muscles are stimulated first in
ventricles to allow AV valve closure before contraction.
(D) Electrical Behavior of Myocardium Action potentials similar to those of
neurons. Stimulation opens voltage-regulated Na+ channels, results in
depolarization, which spreads to ~ +30mV.
Channels then quickly close. Voltage-gated slow Ca++ channels open,
results in Ca++ release from sarcoplasmic reticulum, causing the contraction.
Relaxation when K+ moves out and Ca++ returned to storage.
Long absolute refractory period prevents summation and tetanus, promotes
pumping.
(E) Electrocardiogram = ECG
Electrical currents generated in heart spread to skin.
-1- P Wave: atrial depolarization
-2- QRS Complex: ventricular depolarization.
-3- T Wave: ventricular repolarization.
IV. Blood Flow, Heart Sounds, Cardiac Cycle
Cardiac cycle – one complete contraction and relaxation of all four chambers.
(A) Principles of Pressure & Flow Pressure measured in mm Hg.
Fluid moves down pressure gradients, from high to low.
(B) Heart Sounds Listening = auscultation. “lubb-dup”, corresponds to
blood turbulence caused by valve closures. Triple rhythms common in children.
(C) Phases of Cardiac Cycle all within one second
-1- ventricular filling: AV valves open. Atrial systole towards end. AV valves
close. Ventricles contain EDV (only ~ 1/3 from atrial action).
-2- isovolumetric contraction: atria now relaxed. Ventricles depolarize, AV
valves close, no ejection of blood yet. BP in aorta and pulmonary trunk still
higher than in ventricles.
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-3- ventricular ejection: when pressure in ventricles exceeds that in arteries.
Semilunar valves open. Remaining blood = ESV. SV (stroke volume) = amount
ejected.
EDV – SV = ESV.
Both ventricles with same output – necessary for fluid balance.
-4- Isovolumetric relaxation – corresponds to T wave. Ventricular
repolarization. Semilunar valves close.
Congestive Heart Failure = problems with ventricular ejection. Results in
pulmonary or systemic edema (fluid accumulation).
V. Cardiac Output
Volume/ ventricle/ minute. CO = HR X SV. Works out that heart normally pumps
all blood each minute.
(A) Heart Rate – measured as pulse. Tachycardia when faster,
bradycardia when slower. HR effected by chronotropic factors.
-1- ANS chronotropic factors: medullary cardioacceletory and cardioinhibitory
(via Vagus) centers communicate to Sa and Av nodes. Receive information
from proprioceptors, baroreceptors, chemoreceptors.
-2- chemical chronotropic factors: epinephrine, norepinephrine, caffeine,
nicotine, K+, Ca++….
(B) Stroke Volume
-1- preload: tension in ventricular myocardium. Frank-Starling law: SV related
to EDV. Ventricles must fill to contract sufficiently.
-2- contractility: for a given preload. Influenced by inotropic factors (e.g. vagus
stimulation, Ca++).
-3- afterload: pressure in aorta and pulmonary trunk. When high, SV
diminished.
May be affected by atherosclerosis: fatty plaques in arteries, often coronary.
Linked to LDLs (low density lipoproteins in blood), sedentary lifestyle,
poor diet, obesity and genetics. Treaments = bypass surgery, balloon or laser
angioplasty, stents.
(C) Exercise Increases cardiac output.
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