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78 Cards in this Set

  • Front
  • Back

Heart Anatomy

Fist-sized; Enclosed in pericardium (doubled walled sac)

Superficial Fibrous Pericardium

Protects, anchors, prevents overfilling

Deep 2-Layered Serous Pericardium

Parietal layer lines internal surface of fibrous pericardium; Visceral layer (epicardium) on external surface of heart; Separated by fluid filled pericardial cavity (decreases friction

Epicardium

Visceral layer of serous pericardium

Myocardium

Main wall of heart; Spiral bundles of cardiac muscle cells; Fibrous skeleton of heart anchors cardiac muscle fibers, supports great vessels and valves, limits spread of action potentials to specific paths

Endocardium

Continuous with endothelium

Ventricles

Two; Separated by interventricular septum; Anterior and posterior interventricular sulci mark position of septum externally

Atria

Two; Separated internally by interatrial deptum; Coronary sulcus (atrioventricular groove) encircles junction of atria and ventricles; Auricles increase atrial volume

Blood Pathway through Heart

Heart is 2 side-by-side pumps; Circuits are interconnected; Right ventricle is pump for pulmonary circuit; Left ventricle is pump for systemic circuit; Equal volumes of blood are pumped to both circuits

Pulmonary Circuit

Vessels that carry blood to and from lungs, pumped by the right ventricle; Short, low-pressure circulation

Systemic Circuit

Vessels that carry blood to and from all body tissues, pumped by left ventricle; Long pathways cause resistance, high pressure circuit; Left ventricle has more robust walls due to high pressure demands

Blood Flow

RIght atrium to tricuspid valve to right ventricle; to pulmonary semilunar valve to pulmonary trunk to pulmonary arteries to lung; to pulmonary veins to left atrium; to bicuspid valve to left ventricle; to aortic semilunar valve to aorta; to systemic circulation

Coronary Circulation

Function blood supply to heart muscle; Arterial supply varies considerably and contains many anastomoses (junctions) among branches; Collateral routes provide additional routes for blood deliveries

Atrioventricular (AV) Valves

Prevent backflow into atria when ventricles contract; Tricuspid and mitral valve; Chordae tendineas anchor AV valve cusps to papillary muscles

Semilunar (SL) Valves

Prevent backflow into the ventricles when atrias relax; Aortic and pulmonary semilunar valves

Cardiac Muscle

Cells are striated, short, fat, branched, interconnected; Connective tissue matrix (endomysium) connects to fibrous skeleton; T tubules are wide but less numerous - SR is simpler than in skeletal muscle; Numerous large mitochondria (25-35% of cell vol.)

Intercalated Discs

Junctions between cells anchor cardia cells

Desmosomes

Prevent cells from separating during contraction

Gap Junctions

Allow ions to pass, electrically couple adjacent cells

Cytoskeletal Cardiac Cell Bands

Actin - thin filaments; Myosin - thick filaments

Cardiac Muscle Contraction

Depolarization of heart is rhythmic and spontaneous; About 1& of cardiac cells have automaticity (are self-excitable); Gap junctions ensure heart contracts as a unit; Long absolute refractory period (250 ms) - promotes complete relaxation and opportunity for refilling of heart with blood

Depolarization

Opens voltage gated fast Na+ channels in sarcolemma; Reversal of membrane potential form -90 mV to +30 mV; Depolarization wave causes Ca2+ surge which prolongs depolarization

Repolarization

Ca2+ causes EC coupling as Ca2+ binds to toponin; sliding of filaments begins; Repolarization results from inactivation of Ca2 channels and opening of voltage gated K+ channels

Intrinsic Cardiac Conduction System

Network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate depolarization and contraction of heart

Autorhythmic Cells

Populate SA node; Have unstable resting potentials; At threshold, Ca2+ channels open; Ca2+ influx produces rising phase of action potential; Repolarization results from inactivation of Ca2+ channels and opening of voltage gated K+ channels

SInoatrial (SA) Node

Pacemaker; Generates impulses about 75 times/minute (sinus rhythm)

Atrioventricular (AV) Node

Smaller diameter fibers, fewer gap junctions; Delays impulses approximately .1 second; Depolarizes 50 times per minute in absence of SA node input

Atrioventriucular Bundle

Only electrical connection between atria and ventricles

Right/Left Bundle Branches

Two pathways in interventricular septum carry impulses toward apex of heart

Purkinje Fibers

Complete pathway into apex and ventricular walls; AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

Heart Sequence of Excitation

SA node to AV node to AV bundle to Right/Left bundle branches to Purkinje fibers

Extrinsic Innervation of Heart

Heartbeat modified by ANS; Cardiac centers are located in medulla oblongata

Caridoacceleratory Center

Innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons

Cardioinhibitory Center

Inhibits SA and Av nodes through parasympathetic fibers in vagus nerves

Electrocardiogram (EKG)

Composite of all action potentials generated by nodal and contractile cells at a given time

P Wave

Depolarization of SA node

QRS Complex

Ventricular depolarization

T Wave

Ventricular repolarization

Heart Sounds

Two sounds (lub-dup) associated with clsing of heart valves; First sound occurs as AV valves close - signifies beginning of systole; Second sound occurs when SL valves close at beginning of ventricular diastole

Heart Murmurs

Abnormal heart sounds most often indicative of valve problems; Leakage of blood in wrong direction - malformed during embryonic development or disease/mechanical trauma to valve

Cardiac Cycle

All events associated with blood flow through the heart during one complete heartbeat

Systole

Contraction

Diastole

Relaxation

Mechanical Events of Cardiac Cycle

1. Atrial systole and ventricular diastole to 2. Ventricular systole and atrial diastole to 3. Atrial/Ventricular diastole

(1) Atrial Systole with Ventricular Diastole

AV valves open; 80% or more of blood passively flows into ventricles; Atrial systole occurs near end, delivering remaining 20%

End Diastolic Volume (EDV)

Volume of blood in each ventricle immediately before starting ventricular systole, occurs at end of phase 1 of the cardiac mechanical cycle

(2) Ventricular Systole with Atrial Diastole

Atria relax, ventricles begin to contract; Rising ventricular pressure results in closed AV valves; Isovolumetric contraction phase (all valves are closed); IN ejection phase, ventricular pressure exceeds pressure in large arteries, forcing SL valves open

End Systolic Volume (ESV)

Volume of blood remaining in each ventricle at the end of phase 2 of the cardiac mechanical cycle

(3) Atrial and Ventricular Diastole

Isovolumetric relaxation; Ventricles relax; Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure)

Cardiac Output (CO)

Volume of blood pumped by each ventricle in one minute; CO = HR (Heart Rate) x SV (Stroke Volume)

Heart Rate (HR)

number of beats per minute

Stroke Volume (SV)

Volume of blood pumped out by a ventricle with each beat

Cardiac Output Statistics

At rest CO (ml/min) = HR (75 bpm) x SV (70 ml per beat), most adults use 5 to 6 L per circuit; Maximal CO is 4 to 5 times resting CO in nonathletes; Maximal CO may reach 35 L/min in athletes

Cardiac Reserve

Difference between resting and maximal CO

Regulation of Stroke Volume

SV = EDV - ESV; Main factors are preload, contractility, and afterload

Preload

The degree to which cardiac muscle cells can stretch before the contract (Frank Starling law of the heart; Slow heartbeat and exercise increase venous return, which in turn stretches ventricles and increases contraction force

Contractility

Contractile strength at a given muscle length, independent of muscle stretch and EDV

Positive Inotropic Agents of Contractility

Increase contractility (epinephrine and norepinephrine or secondary hormone actions like thyroxine)

Negative Inotropic Agents

Decrease contractility (Acidosis, increased extracellular K+, Calcium channel blockers - propanolol)

Afterload

Pressure that must be overcome for ventricles to eject blood

Hypertension

Increases afterload, resulting in increased ESV and reduced SV; Increases chronic workload of cardiac system; Promotes abnormal ventricular hypertrophy

Heart Rate Regulation

Positive chronotropic factors increase heart rate, negative chronotropic factors decrease heat rate

Autonmic Nervous System Regulation

Sympathetic nervous system activated by emotional/physical stressors; Norephinephrine causes pacemaker to fire more rapidly and increase contractility; Parasympathetic NS opposes sympathetic effects - acetylcholine hyperpolarizes pacemaker cells by opening K+ channels; Heart at rest exhibits vagal tone

Atrial (Bainbridge) Reflex

Sympathetic reflex initiated by increased benous return; Stretch of atrial walls stimulates SA nodes and atrial stretch receptors activating sympathetic reflexes

Epinephrine

Chemical from adrenal medulla that enhances heart rate and contractility

Thyroxine

Increases heart rate and enhances effects of norepinephrine and epinephrine

Intra/Extracelluar Ion Concentration

Ca2+ and K+ concentrations must be maintained for normal heart functions

Other Factors for Heart Rate

Age; Gender; Exercise; Body Temp.

Arrhythmmias

Irregular heart rhythms

Fibrilliation

Rapid, irregular contractions -useless for pumping blood

Uncoordinated Atrial/Ventricular Contractions

Result of defect in intrinsic conduction system

Defective SA Node

Can result in ectopic focus - abnormal pacemaker takes over ; AV node take over - junctional rhythm

Defective AV Node

Can result in heart block; Few or no impulses from SA node reach ventricles

Tachycardia

Abnormall fast heart rate (more than 100 bpm)

Bradycardia

Heart rate slower than 60 bpm - may result in inadequate blood circulation

Angina Pectoris

Thoracic pain caused by fleeting deficiency in blood delivery to myocardium - cells are weakened

Myocardial Infarction (Heart Attack)

Prolonged coronary blockage; Areas of cell death are repaired with noncontractile scar tissue

Congestive Heart Failure (CHF)

Progressive condition where CO is so low that blood circulation is inadequate to meet tissue needs; Caused by coronary atherosclerosis, persistent high blood pressure, multiple myocardial infarcts, dilated cardiomyopathy (DCM)