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PowerPoint Lecture Outlines

Chapter

15

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ANATOMY OF THE HEART

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ANATOMY OF THE HEART

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Size of Heart

Size 12 - 14 cm x 8 - 9 cm x 6

Weight, M – 280 to 340 g F – 230 to 280 g

The heart continues to increase in weight and size up to an advanced period of life This increase is more marked in men than in women.

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• The wall of the right ventricle is thinner than that of the left, the proportion between them being as 1 to 3; it is thickest at the base, and gradually becomes thinner toward the apex. The cavity equals in size that of the left ventricle, and is capable of containing about 85 c.c.

Size of Heart

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• The left ventricle is longer and more conical in shape than the right, and on transverse section its concavity presents an oval or nearly circular outline. It forms a small part of the sternocostal surface and a considerable part of the diaphragmatic surface of the heart; it also forms the apex of the heart. Its walls are about three times as thick as those of the right ventricle.

Size of Heart

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Myocardial Thickness and Function

• The thickness of the myocardium of the four chambers varies according to the function of each chamber.– The atria walls are thin because they deliver blood to

the ventricles.– The ventricle walls are thicker because they pump

blood greater distances (Figure 20.4a).– The right ventricle walls are thinner than the left

because they pump blood into the lungs, which are nearby and offer very little resistance to blood flow.

– The left ventricle walls are thicker because they pump blood through the body where the resistance to blood flow is greater.

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Thickness of Cardiac Walls

Myocardium of left ventricle is much thicker than the right.

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Location of Heart

• posterior to sternum• medial to lungs• anterior to vertebral column• base lies beneath 2nd rib• apex at 5th intercostal space• lies upon diaphragm

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Coverings of Heart

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Wall of the Heart

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Wall of the Heart

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Heart Chambers

Right Atrium• receives blood from

• inferior vena cava• superior vena cava• coronary sinus

Left Atrium• receives blood from pulmonary veins

Right Ventricle• receives blood from right atrium

Left Ventricle• receives blood from left atrium

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Chambers and Sulci

Anterior View

15Posterior View

Chambers and Sulci

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Right Atrium

• Receives blood from 3 sources– superior vena cava, inferior vena cava and coronary sinus

• Interatrial septum partitions the atria• Fossa ovalis is a remnant of the fetal foramen ovale• Tricuspid valve

– Blood flows through into right ventricle– has three cusps composed of dense CT covered by

endocardium

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Right Ventricle

• Forms most of anterior surface of heart• Papillary muscles are cone shaped trabeculae carneae (raised bundles

of cardiac muscle)• Chordae tendineae: cords between valve cusps and papillary muscles• Interventricular septum: partitions ventricles• Pulmonary semilunar valve: blood flows into pulmonary trunk

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Left Atrium

• Forms most of the base of the heart• Receives blood from lungs - 4 pulmonary veins (2 right +

2 left)• Bicuspid valve: blood passes through into left ventricle

– has two cusps– to remember names of this valve, try the pneumonic LAMB

• Left Atrioventricular, Mitral, or Bicuspid valve

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Left Ventricle

• Forms the apex of heart • Chordae tendineae anchor bicuspid valve to papillary

muscles (also has trabeculae carneae like right ventricle)

• Aortic semilunar valve: – blood passes through valve into the ascending aorta– just above valve are the openings to the coronary arteries

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Heart Valves

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Coronal Sections of Heart

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Heart Valves

Tricuspid Valve Pulmonary and Aortic Valve

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• A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure– occurs when ventricles are relaxed, chordae tendineae

are slack and papillary muscles are relaxed

Atrioventricular Valves Open

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• A-V valves close preventing backflow of blood into atria – occurs when ventricles contract, pushing valve cusps

closed, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting

Atrioventricular Valves Close

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Semilunar Valves

• SL valves open with ventricular contraction– allow blood to flow into pulmonary trunk and aorta

• SL valves close with ventricular relaxation– prevents blood from returning to ventricles, blood fills

valve cusps, tightly closing the SL valves

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Atria contract, blood fills ventricles through A-V valves

Ventricles contract, blood pumped into aorta and pulmonary trunk through SL valves

Valve Function Review

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Skeleton of Heart

• fibrous rings to which the heart valves are attached

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Fibrous Skeleton of Heart

• (Figure 20.5). Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum– Support structure for heart valves– Insertion point for cardiac muscle bundles– Electrical insulator between atria and ventricles

• prevents direct propagation of AP’s to ventricles

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Path of Blood Through the Heart

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Path of BloodThrough the Heart

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Blood Supply to Heart

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Blood Supply to Heart

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Heart Actions

Atrial Systole/Ventricular Diastole Atrial Diastole/Ventricular Systole

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Cardiac Cycle

Atrial Systole/Ventricular Diastole

• blood flows passively into ventricles

• remaining 30% of blood pushed into ventricles

• A-V valves open/semilunar valves close

• ventricles relaxed

• ventricular pressure increases

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Cardiac Cycle

Ventricular Systole/Atrial diastole

• A-V valves close

• chordae tendinae prevent cusps of valves from bulging too far into atria

• atria relaxed

• blood flows into atria

• ventricular pressure increases and opens semilunar valves

• blood flows into pulmonary trunk and aorta

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Heart Sounds

Lubb• first heart sound • occurs during ventricular systole• A-V valves closing

Dupp• second heart sound• occurs during ventricular diastole• pulmonary and aortic semilunar valves closing

Murmur – abnormal heart sound

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Heart Sounds

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Cardiac Muscle Fibers

Cardiac muscle fibers form a functional syncytium

• group of cells that function as a unit• atrial syncytium• ventricular syncytium

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Cardiac Conduction System

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Cardiac Conduction System

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Muscle Fibers in Ventricular Walls

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Muscle Bundles of the Myocardium

• Cardiac muscle fibers swirl diagonally around the heart in interlacing bundles

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Electrocardiogram

• recording of electrical changes that occur in the myocardium• used to assess heart’s ability to conduct impulses

P wave – atrial depolarizationQRS wave – ventricular depolarizationT wave – ventricular repolarization

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Electrocardiogram

• Impulse conduction through the heart generates electrical currents that can be detected at the surface of the body. A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is called an electrocardiogram (ECG or EKG).

• The ECG helps to determine if the conduction pathway is abnormal, if the heart is enlarged, and if certain regions are damaged.

• Figure 20.12 shows a typical ECG.

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Electrocardiogram---ECG or EKG

• EKG– Action potentials of all active

cells can be detected and recorded

• P wave– atrial depolarization

• P to Q interval– conduction time from atrial to

ventricular excitation

• QRS complex – ventricular depolarization

• T wave– ventricular repolarization

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ECG

• In a typical Lead II record, three clearly visible waves accompany each heartbeat It consists of:.

• P wave (atrial depolarization - spread of impulse from SA node over atria)

• QRS complex (ventricular depolarization - spread of impulse through ventricles)

• T wave (ventricular repolarization).• Correlation of ECG waves with atrial and

ventricular systole (Figure 20.13)

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ECG

• As atrial fibers depolarize, the P wave appears.• After the P wave begins, the atria contract (atrial systole).

Action potential slows at the AV node giving the atria time to contract.

• The action potential moves rapidly through the bundle branches, Purkinje fibers, and the ventricular myocardium producing the QRS complex.

• Ventricular contraction after the QRS comples and continues through the ST segment.

• Repolarization of the ventricles produces the T wave.• Both atria and ventricles repolarize and the P wave

appears.

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THE CARDIAC CYCLE

• A cardiac cycle consists of the systole (contraction) and diastole (relaxation) of both atria, rapidly followed by the systole and diastole of both ventricles.

• Pressure and volume changes during the cardiac cycle

• During a cardiac cycle atria and ventricles alternately contract and relax forcing blood from areas of high pressure to areas of lower pressure.

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One Cardiac Cycle - Vocabulary

• At 75 beats/min, one cycle requires 0.8 sec.– systole (contraction) and diastole (relaxation) of

both atria, plus the systole and diastole of both ventricles

• End diastolic volume (EDV)– volume in ventricle at end of diastole, about 130ml

• End systolic volume (ESV)– volume in ventricle at end of systole, about 60ml

• Stroke volume (SV)– the volume ejected per beat from each ventricle,

about 70ml– SV = EDV - ESV

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Phases of Cardiac Cycle• Isovolumetric relaxation

– brief period when volume in ventricles does not change--as ventricles relax, pressure drops and AV valves open

• Ventricular filling– rapid ventricular filling:as blood flows from full atria– diastasis: as blood flows from atria in smaller volume– atrial systole pushes final 20-25 ml blood into

ventricle• Ventricular systole

– ventricular systole– isovolumetric contraction

• brief period, AV valves close before SL valves open – ventricular ejection: as SL valves open and blood is

ejected

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Regulation of Cardiac Cycle

Autonomic nerve impulses alter the activities of the S-A and A-V nodes

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Regulation of Cardiac Cycle

• physical exercise• body temperature• concentration of various ions

• potassium• calcium

• parasympathetic impulses decrease heart action• sympathetic impulses increase heart action• cardiac center regulates autonomic impulses to the heart

Additional Factors that Influence HR

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CARDIAC OUTPUT• Cardiac output (CO) is the volume of blood ejected

from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute.– Cardiac output equals the stroke volume, the

volume of blood ejected by the ventricle with each contraction, multiplied by the heart rate, the number of beats per minute.

– CO = SV X HR• Cardiac reserve is the ratio between the maximum

cardiac output a person can achieve and the cardiac output at rest.

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Cardiac Output

• CO = SV x HR– at 70ml stroke volume & 75 beat/min----5 and

1/4 liters/min– entire blood supply passes through circulatory

system every minute

• Cardiac reserve is maximum output/output at rest– average is 4-5x while athlete’s is 7-8x

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Influences on Stroke Volume

• Preload (affect of stretching)– Frank-Starling Law of Heart– more muscle is stretched, greater force of

contraction– more blood more force of contraction results

• Contractility– autonomic nerves, hormones, Ca+2 or K+ levels

• Afterload– amount of pressure created by the blood in the way– high blood pressure creates high afterload

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Stroke Volume and Heart Rate

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Preload: Effect of Stretching• According to the Frank-Starling law of the heart,

a greater preload (stretch) on cardiac muscle fibers just before they contract increases their force of contraction during systole.– Preload is proportional to EDV.

– EDV is determined by length of ventricular diastole and venous return.

• The Frank-Starling law of the heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations.

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Contractility• Myocardial contractility, the strength of

contraction at any given preload, is affected by positive and negative inotropic agents. – Positive inotropic agents increase contractility– Negative inotropic agents decrease

contractility.

• For a constant preload, the stroke volume increases when positive inotropic agents are present and decreases when negative inotropic agents are present.

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Afterload• The pressure that must be overcome before

a semilunar valve can open is the afterload.• In congestive heart failure, blood begins to

remain in the ventricles increasing the preload and ultimately causing an overstretching of the heart and less forceful contraction– Left ventricular failure results in pulmonary

edema– Right ventricular failure results in peripheral

edema.

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Chemical regulation of heart rate

• Heart rate affected by hormones (epinephrine, norepinephrine, thyroid hormones).

• Cations (Na+, K+, Ca+2) also affect heart rate.

• Other factors such as age, gender, physical fitness, and temperature also affect heart rate.

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Risk Factors for Heart Disease

• Risk factors in heart disease: – high blood cholesterol level– high blood pressure– cigarette smoking– obesity & lack of regular exercise.

• Other factors include:– diabetes mellitus– genetic predisposition– male gender– high blood levels of fibrinogen– left ventricular hypertrophy

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Plasma Lipids and Heart Disease

• Risk factor for developing heart disease is high blood cholesterol level.– promotes growth of fatty plaques – Most lipids are transported as lipoproteins

• low-density lipoproteins (LDLs)• high-density lipoproteins (HDLs)• very low-density lipoproteins (VLDLs)

– HDLs remove excess cholesterol from circulation– LDLs are associated with the formation of fatty

plaques – VLDLs contribute to increased fatty plaque

formation• There are two sources of cholesterol in the

body:– in foods we ingest & formed by liver

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Desirable Levels of Blood Cholesterol for Adults

• TC (total cholesterol) under 200 mg/dl• LDL under 130 mg/dl• HDL over 40 mg/dl• Normally, triglycerides are in the range of

10-190 mg/dl.• Among the therapies used to reduce

blood cholesterol level are exercise, diet, and drugs.

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EXERCISE AND THE HEART

• A person’s cardiovascular fitness can be improved with regular exercise.– Aerobic exercise (any activity that works large body muscles

for at least 20 minutes, preferably 3 – 5 times per week) increases cardiac output and elevates metabolic rate.

– Several weeks of training results in maximal cardiac output and oxygen delivery to tissues

– Regular exercise also decreases anxiety and depression, controls weight, and increases fibrinolytic activity.

– Sustained exercise increases oxygen demand in muscles

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Blood Vessels

• arteries• carry blood away from ventricles of heart

• arterioles• receive blood from arteries• carry blood to capillaries

• capillaries• sites of exchange of substances between blood and body cells

• venules• receive blood from capillaries

• veins• carry blood toward ventricle of heart

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Arteries and Arterioles

Artery• thick strong wall • endothelial lining• middle layer of smooth muscle and elastic tissue• outer layer of connective tissue• carries blood under relatively high pressure

Arterioles• thinner wall than artery• endothelial lining• some smooth muscle tissue• small amount of connective tissue• helps control blood flow into a capillary

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Walls of Artery and Vein

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Arteriole

• smallest arterioles only have a few smooth muscle fibers• capillaries lack muscle fibers

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Capillaries• smallest diameter blood vessels• extensions of inner lining of arterioles• walls are endothelium only• semipermeable• sinusoids – leaky capillaries

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Regulation of Capillary Blood Flow

Precapillary sphincters

• may close a capillary• respond to needs of the cells• low oxygen and nutrients cause sphincter to relax

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Exchange in the Capillaries• water and other substances leave capillaries because of net outward pressure at the capillaries’ arteriolar ends• water enters capillaries’ venular ends because of a net inward pressure•substances move in and out along the length of the capillaries according to their respective concentration gradients

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Venules and Veins

Venule• thinner wall than arteriole• less smooth muscle and elastic tissue than arteriole

Vein• thinner wall than artery• three layers to wall but middle layer is poorly developed• some have flaplike valves• carries blood under relatively low pressure• serves as blood reservoir

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Venous Valves

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Characteristics of Blood Vessels

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Blood Volumes in Vessels

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Arterial Blood Pressure

Blood Pressure – force the blood exerts against the inner walls of the blood vessels

Arterial Blood Pressure• rises when ventricles contract• falls when ventricles relax• systolic pressure – maximum pressure• diastolic pressure – minimum pressure

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Pulse

• alternate expanding and recoiling of the arterial wall that can be felt

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Factors That InfluenceArterial Blood Pressure

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Regulation of Cardiac Cycle

Autonomic nerve impulses alter the activities of the S-A and A-V nodes

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Control of Blood Pressure

If blood pressure rises, baroreceptors initiate the cardioinhibitory reflex, which lowers the blood pressure

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Control of Blood Pressure

Dilating arterioles helps regulate blood pressure

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Venous Blood Flow

• not a direct result of heart action

• dependent on • skeletal muscle contraction• breathing• venoconstriction

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Central Venous Pressure

• pressure in the right atrium

• factors that influence it alter flow of blood into the right atrium

• affects pressure within the peripheral veins

• weakly beating heart increases central venous pressure

• increase in central venous pressure causes blood to back up into peripheral vein

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Pulmonary Circuit

• consists of vessels that carry blood from the heart to the lungs and back to the heart

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Blood Flow Through Alveoli

• cells of alveolar wall are tightly joined together• the high osmotic pressure of the interstitial fluid draws water out of them

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Systemic Circuit

• composed of vessels that lead from the heart to all body parts (except the lungs) and back to the heart

• includes the aorta and its branches

• includes the system of veins that return blood to the right atrium

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Life-Span Changes• cholesterol deposition in blood vessels

• heart enlargement

• death of cardiac muscle cells

• increase in fibrous connective tissue of the heart

• increase in adipose tissue of the heart

• increase in blood pressure

• decrease in resting heart rate

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Clinical Problems

• MI = myocardial infarction– death of area of heart muscle from lack of O2

– replaced with scar tissue– results depend on size & location of damage

• Blood clot– use clot dissolving drugs streptokinase or t-PA &

heparin– balloon angioplasty

• Angina pectoris----heart pain from ischemia of cardiac muscle

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CAD• Coronary artery disease (CAD), or coronary heart disease

(CHD), is a condition in which the heart muscle receives an inadequate amount of blood due to obstruction of its blood supply.

• It is the leading cause of death in the United States each year.

• The principal causes of obstruction include atherosclerosis, coronary artery spasm, or a clot in a coronary artery.

• Risk factors for development of CAD include:– high blood cholesterol levels, – high blood pressure, cigarette smoking, obesity, diabetes, – “type A” personality, – and sedentary lifestyle.

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CAD

• Atherosclerosis is a process in which smooth muscle cells proliferate and fatty substances, especially cholesterol and triglycerides (neutral fats), accumulate in the walls of the medium-sized and large arteries in response to certain stimuli, such as endothelial damage (Figure 20.18).

• Diagnosis of CAD includes such procedures as cardiac catherization and cardiac angiography.

• Treatment options for CAD include drugs and coronary artery bypass grafting (Figure 20.19).

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Coronary Artery Disease • Heart muscle

receiving insufficient blood supply– narrowing of

vessels---atherosclerosis, artery spasm or clot

– atherosclerosis--smooth muscle & fatty deposits in walls of arteries

• Treatment– drugs, bypass graft,

angioplasty, stent

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By-pass Graft

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Percutaneous Transluminal

Coronary Angioplasty

Stent

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• Update on Digoxin Therapy in Congestive Heart Failure

• SHOWKAT A. HAJI, M.D., and ASSAD MOVAHED, M.D. – East Carolina University School of Medicine,

Greenville, North Carolina

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Digoxin and Other Medications for Congestive Heart Failure

• ACE inhibitors, beta blockers and spironolactone have been shown to improve survival in patients with heart failure.

• Consequently, the role of digoxin in the treatment of heart failure remains secondary

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TABLE 4 Digoxin (Lanoxin) Therapy in

Congestive Heart Failure 1. Digoxin has been shown to improve morbidity

without any benefit on mortality.2. Digoxin may act by decreasing sympathetic

activity.3. Digoxin may not be effective in patients who

have normal left ventricular systolic function.4. The benefits of digoxin therapy are greatest in

patients with severe heart failure, an enlarged heart and a third heart sound gallop.

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TABLE 4 Digoxin (Lanoxin) Therapy in

Congestive Heart Failure 5. Digoxin may be used in patients with mild to

moderate heart failure if they do not respond to an angiotensin-converting enzyme inhibitor or a beta blocker.

6. Low dosages of digoxin can be effective.7. Renal function and possible drug interactions

must be considered in deciding on an appropriate dosage of digoxin.

8. In general, digoxin therapy should be avoided in the acute phase after myocardial infarction

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Digoxin and Other Medications for Congestive Heart Failure

• In the absence of a survival benefit, the goal of digoxin therapy is to improve quality of life by reducing symptoms and preventing hospitalizations

• Digoxin should be used routinely, in conjunction with diuretics, ACE inhibitors, beta blockers and spironolactone,

• In all patients with severe congestive heart failure and reduced systolic function.

• It also should be added to the therapy of patients with mild to moderate congestive heart failure if they have not responded adequately to an ACE inhibitor or a beta blocker.