Right coronary artery: 15% blocked

Right coronary artery: 15% blocked
Case Study: Heart Chief Complaint:68-year-old man who collapsed during exertion. History :Roger Crockett, a 68-year-old man with a 40-pack-year smoking history and recent complaints of angina (sub-sternal chest pressure) upon exercising, collapsed while mowing his lawn. Paramedics arriving at the scene found him unconscious, not breathing, and without a pulse. CPR was successfully performed and Roger was transported to the hospital. An ECG was suggestive of an anterior wall myocardial infarction, and he was given an intravenous solution of tissue plasminogen activator (TPA)(tPA works by dissolving major clots before tissue dies from lack of oxygen). Elevated blood creatine phosphokinase (CPK) (Creatine phosphokinase (CPK) is an enzyme found mainly in the heart, brain, and skeletal muscle) levels measured over the next 2 days confirmed the diagnosis. Coronary angiography was performed a week later, revealing the following results: Circumflex artery: 20% blocked Right coronary artery: 15% blocked Left anterior descending artery (LAD): 95% blocked ("Anterior intraventricular artery")

An Introduction to the Cardiovascular System
The Pulmonary Circuit Carries blood to and from gas exchange surfaces of lungs The Systemic Circuit Carries blood to and from the body Blood alternates between pulmonary circuit and systemic circuit

Three Types of Blood Vessels Arteries Carry blood away from heart Veins Carry blood to heart Capillaries Networks between arteries and veins

Capillaries Also called exchange vessels Exchange materials between blood and tissues Materials include dissolved gases, nutrients, waste products

Figure 20-1 An Overview of the Cardiovascular System.
Pulmonary Circuit Systemic Circuit Pulmonary arteries Systemic arteries Systemic veins Pulmonary veins Capillaries in head, neck, upper limbs Capillaries in lungs Right atrium Left atrium Right ventricle Left ventricle Capillaries in trunk and lower limbs

Four Chambers of the Heart Right atrium Collects blood from systemic circuit Right ventricle Pumps blood to pulmonary circuit Left atrium Collects blood from pulmonary circuit Left ventricle Pumps blood to systemic circuit

20-1 Anatomy of the Heart The Heart
Great veins and arteries at the base Pointed tip is apex Surrounded by pericardial sac Sits between two pleural cavities in the mediastinum

Figure 20-2a The Location of the Heart in the Thoracic Cavity.
Trachea Thyroid gland First rib (cut) Base of heart Right lung Left lung Parietal pericardium (cut) Apex of heart Diaphragm a An anterior view of the chest, showing the position of the heart and major blood vessels relative to the ribs, lungs, and diaphragm.

20-1 Anatomy of the Heart The Pericardium
Double lining of the pericardial cavity Visceral pericardium Inner layer of pericardium Parietal pericardium Outer layer Forms inner layer of pericardial sac

20-1 Anatomy of the Heart The Pericardium Pericardial cavity
Is between parietal and visceral layers Contains pericardial fluid Pericardial sac Fibrous tissue Surrounds and stabilizes heart

Figure 20-2c The Location of the Heart in the Thoracic Cavity.
Base of heart Cut edge of parietal pericardium Wrist (corresponds to base of heart) Fibrous tissue of pericardial sac Inner wall (corresponds to epicardium) Parietal pericardium Air space (corresponds to pericardial cavity) Areolar tissue Mesothelium Outer wall (corresponds to parietal pericardium) Cut edge of epicardium Fibrous attachment to diaphragm Apex of heart Balloon c The relationship between the heart and the pericardial cavity; compare with the fist-and-balloon example.

Figure 20-3a The Position and Superficial Anatomy of the Heart.
Base of heart 1 1 Ribs 2 2 3 3 4 4 5 5 6 6 7 7 Apex of heart 8 8 9 9 10 10 a Heart position relative to the rib cage.

Figure 20-3b The Position and Superficial Anatomy of the Heart.
Left subclavian artery Left common carotid artery Arch of aorta Ligamentum arteriosum Brachiocephalic trunk Ascending aorta Descending aorta Left pulmonary artery Superior vena cava Pulmonary trunk Auricle of right atrium Right atrium Auricle of left atrium Fat and vessels in anterior interventricular sulcus Right ventricle Fat and vessels in coronary sulcus Left ventricle b Major anatomical features on the anterior surface.

Figure 20-3d The Position and Superficial Anatomy of the Heart.
Arch of aorta Left pulmonary artery Right pulmonary artery Left pulmonary veins Fat and vessels in coronary sulcus Superior vena cava Left atrium Coronary sinus Right pulmonary veins (superior and inferior) Right atrium Left ventricle Inferior vena cava Right ventricle Fat and vessels in posterior interventricular sulcus d Major landmarks on the posterior surface. Coronary arteries (which supply the heart itself) are shown in red; coronary veins are shown in blue.

20-1 Anatomy of the Heart The Heart Wall Epicardium Myocardium
Endocardium

20-1 Anatomy of the Heart Epicardium (Outer Layer)
Visceral pericardium Covers the heart

20-1 Anatomy of the Heart Myocardium (Middle Layer)
Muscular wall of the heart Concentric layers of cardiac muscle tissue Atrial myocardium wraps around great vessels Two divisions of ventricular myocardium Endocardium (Inner Layer) Simple squamous epithelium

Figure 20-4a The Heart Wall.
Myocardium (cardiac muscle tissue) Pericardial cavity Parietal pericardium Dense fibrous layer Cardiac muscle cells Areolar tissue Connective tissues Mesothelium Artery Vein Endocardium Epicardium (visceral pericardium) Endothelium Areolar tissue Mesothelium Areolar tissue Heart wall a A diagrammatic section through the heart wall, showing the relative positions of the epicardium, myocardium, and endocardium. The proportions are not to scale; the thickness of the myocardial wall has been greatly reduced.

Figure 20-4b The Heart Wall.
Atrial musculature Ventricular musculature b Cardiac muscle tissue forms concentric layers that wrap around the atria or spiral within the walls of the ventricles.

20-1 Anatomy of the Heart Cardiac Muscle Tissue Intercalated discs
Interconnect cardiac muscle cells Secured by desmosomes Linked by gap junctions Convey force of contraction Propagate action potentials

Figure 20-5a Cardiac Muscle Cells.
Mitochondria Intercalated disc (sectioned) Nucleus Cardiac muscle cell (sectioned) Bundles of myofibrils Intercalated discs a Cardiac muscle cells

Figure 20-5c Cardiac Muscle Cells.
Intercalated discs Cardiac muscle tissue LM x 575 c Cardiac muscle tissue

20-1 Anatomy of the Heart Characteristics of Cardiac Muscle Cells
Small size Single, central nucleus Branching interconnections between cells Intercalated discs

Figure 20-6a The Sectional Anatomy of the Heart.
Left common carotid artery Brachiocephalic trunk Left subclavian artery Ligamentum arteriosum Superior vena cava Pulmonary trunk Aortic arch Pulmonary valve Right pulmonary arteries Left pulmonary arteries Ascending aorta Left pulmonary veins Fossa ovalis Left atrium Opening of coronary sinus Interatrial septum Aortic valve Right atrium Cusp of left AV (mitral) valve Pectinate muscles Conus arteriosus Left ventricle Cusp of right AV (tricuspid) valve Chordae tendineae Interventricular septum Papillary muscles Trabeculae carneae Right ventricle Inferior vena cava Moderator band Descending aorta a A diagrammatic frontal section through the heart, showing major landmarks and the path of blood flow (marked by arrows) through the atria, ventricles, and associated vessels.

Figure 20-6b The Sectional Anatomy of the Heart.
Chordae tendineae Papillary muscles b The papillary muscles and chordae tendineae support the right AV (tricuspid) valve. The photograph was taken from inside the right ventricle, looking toward a light shining from the right atrium.

20-1 Anatomy of the Heart The Heart Valves
Two pairs of one-way valves prevent backflow during contraction Atrioventricular (AV) valves Between atria and ventricles Blood pressure closes valve cusps during ventricular contraction Papillary muscles tense chordae tendineae to prevent valves from swinging into atria

20-1 Anatomy of the Heart The Heart Valves Semilunar valves
Pulmonary and aortic tricuspid valves Prevent backflow from pulmonary trunk and aorta into ventricles Have no muscular support Three cusps support like tripod

20-1 Anatomy of the Heart Aortic Sinuses At base of ascending aorta
Sacs that prevent valve cusps from sticking to aorta Origin of right and left coronary arteries

Figure 20-8a Valves of the Heart (Part 1 of 2).
Transverse Sections, Superior View, Atria and Vessels Removed POSTERIOR Cardiac skeleton Left AV (bicuspid) valve (open) RIGHT VENTRICLE LEFT VENTRICLE Relaxed ventricles Right AV (tricuspid) valve (open) Aortic valve (closed) Pulmonary valve (closed) ANTERIOR a When the ventricles are relaxed, the AV valves are open and the semilunar valves are closed. The chordae tendineae are loose, and the papillary muscles are relaxed. Aortic valve closed

Figure 20-8a Valves of the Heart (Part 2 of 2).
Frontal Sections through Left Atrium and Ventricle Pulmonary veins LEFT ATRIUM Left AV (bicuspid) valve (open) Chordae tendineae (loose) Relaxed ventricles Aortic valve (closed) Papillary muscles (relaxed) LEFT VENTRICLE (relaxed and filling with blood) a When the ventricles are relaxed, the AV valves are open and the semilunar valves are closed. The chordae tendineae are loose, and the papillary muscles are relaxed.

Figure 20-8b Valves of the Heart (Part 1 of 2).
Right AV (tricuspid) valve (closed) Cardiac skeleton Left AV (bicuspid) valve (closed) LEFT VENTRICLE RIGHT VENTRICLE Contracting ventricles Aortic valve (open) Pulmonary valve (open) b When the ventricles are contracting, the AV valves are closed and the semilunar valves are open. In the frontal section notice the attachment of the left AV valve to the chordae tendineae and papillary muscles. Aortic valve open

Figure 20-8b Valves of the Heart (Part 2 of 2).
Aorta LEFT ATRIUM Aortic sinus Left AV (bicuspid) valve (closed) Aortic valve (open) Chordae tendineae (tense) Contracting ventricles Papillary muscles (contracted) Left ventricle (contracted) b When the ventricles are contracting, the AV valves are closed and the semilunar valves are open. In the frontal section notice the attachment of the left AV valve to the chordae tendineae and papillary muscles.

20-1 Anatomy of the Heart The Blood Supply to the Heart
= Coronary circulation Supplies blood to muscle tissue of heart Coronary arteries and cardiac veins

Figure 20-9a The Coronary Circulation.
Aortic arch Left coronary artery Ascending aorta Pulmonary trunk Circumflex artery Right coronary artery Anterior interventricular artery Atrial arteries Great cardiac vein Anterior cardiac veins Small cardiac vein Marginal artery a Coronary vessels supplying and draining the anterior surface of the heart.

Figure 20-9b The Coronary Circulation.
Coronary sinus Circumflex artery Great cardiac vein Marginal artery Posterior interventricular artery Posterior cardiac vein Small cardiac vein Left ventricle Right coronary artery Middle cardiac vein Marginal artery b Coronary vessels supplying and draining the posterior surface of the heart.

Figure 20-10 Heart Disease and Heart Attacks (Part 2 of 4).
Normal Artery Narrowing of Artery Tunica externa Lipid deposit of plaque Tunica media Cross section Cross section

20-1 Anatomy of the Heart Heart Disease – Coronary Artery Disease
Coronary artery disease (CAD) Areas of partial or complete blockage of coronary circulation Cardiac muscle cells need a constant supply of oxygen and nutrients Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance Reduced circulatory supply, coronary ischemia, results from partial or complete blockage of coronary arteries

Usual cause is formation of a fatty deposit, or atherosclerotic plaque, in the wall of a coronary vessel The plaque, or an associated thrombus (clot), then narrows the passageway and reduces blood flow Spasms in smooth muscles of vessel wall can further decrease or stop blood flow One of the first symptoms of CAD is commonly angina pectoris

Myocardial infarction (MI), or heart attack Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen The death of affected tissue creates a nonfunctional area known as an infarct Heart attacks most commonly result from severe coronary artery disease (CAD)

Myocardial infarction (MI), or heart attack A crisis often develops as a result of thrombus formation at a plaque (the most common cause of an MI), a condition called coronary thrombosis A vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall Individuals having an MI experience intense pain, similar to that felt in angina, but persisting even at rest

Myocardial infarction (MI), or heart attack Pain does not always accompany a heart attack; therefore, the condition may go undiagnosed and may not be treated before a fatal MI occurs A myocardial infarction can usually be diagnosed with an ECG and blood studies Damaged myocardial cells release enzymes into the circulation, and these elevated enzymes can be measured in diagnostic blood tests The enzymes include: Cardiac troponin T, Cardiac troponin I, A special form of creatinine phosphokinase, CK-MB

Treatment of CAD and myocardial infarction About 25 percent of MI patients die before obtaining medical assistance 65 percent of MI deaths among those under age 50 occur within an hour after the initial infarction

Treatment of CAD and myocardial infarction Risk factor modification Stop smoking High blood pressure treatment Dietary modification to lower cholesterol and promote weight loss Stress reduction Increased physical activity (where appropriate)

Treatment of CAD and myocardial infarction Drug treatment Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin Drugs that block sympathetic stimulation (propranolol or metoprolol) Drugs that cause vasodilation, such as nitroglycerin Drugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers) In a myocardial infarction, drugs to relieve pain, fibrinolytic agents to help dissolve clots, and oxygen

Treatment of CAD and myocardial infarction Noninvasive surgery Atherectomy Blockage by a single, soft plaque may be reduced with the aid of a long, slender catheter inserted into a coronary artery to the plaque

Treatment of CAD and myocardial infarction Noninvasive surgery Balloon angioplasty The tip of the catheter contains an inflatable balloon Once in position, the balloon is inflated, pressing the plaque against the vessel walls Because plaques commonly redevelop after angioplasty, a fine tubular wire mesh called a stent may be inserted into the vessel, holding it open

Treatment of CAD and myocardial infarction Coronary artery bypass graft (CABG) In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery As many as four coronary arteries can be rerouted this way during a single operation The procedures are named according to the number of vessels repaired, so we speak of single, double, triple, or quadruple coronary bypasses

Advanced Coronary Artery Disease A color-enhanced DSA scan showing advanced coronary artery disease. Blood flow to the ventricular myocardium is severely restricted. Normal Heart A color-enhanced digital subtraction angiography (DSA) scan of a normal heart.

Occluded Coronary Artery Damaged Heart Muscle

20-2 The Conducting System
Heartbeat A single contraction of the heart The entire heart contracts in series First the atria Then the ventricles

Cardiac Physiology Two types of cardiac muscle cells Conducting system Controls and coordinates heartbeat Contractile cells Produce contractions that propel blood

The Cardiac Cycle Begins with action potential at SA node Transmitted through conducting system Produces action potentials in cardiac muscle cells (contractile cells) Electrocardiogram (ECG or EKG) Electrical events in the cardiac cycle can be recorded on an electrocardiogram

A system of specialized cardiac muscle cells Initiates and distributes electrical impulses that stimulate contraction Automaticity Cardiac muscle tissue contracts automatically

Structures of the Conducting System Sinoatrial (SA) node – wall of right atrium Atrioventricular (AV) node – junction between atria and ventricles Conducting cells – throughout myocardium

Conducting Cells Interconnect SA and AV nodes Distribute stimulus through myocardium In the atria Internodal pathways In the ventricles AV bundle and the bundle branches

Figure 20-11a The Conducting System of the Heart.
Sinoatrial (SA) node Internodal pathways Atrioventricular (AV) node AV bundle Bundle branches Purkinje fibers a Components of the conducting system.

The Sinoatrial (SA) Node In posterior wall of right atrium Contains pacemaker cells Connected to AV node by internodal pathways Begins atrial activation (Step 1)

Figure 20-12 Impulse Conduction through the Heart (Part 1 of 5).
SA node activity and atrial activation begin. SA node Time = 0

The Atrioventricular (AV) Node In floor of right atrium Receives impulse from SA node (Step 2) Delays impulse (Step 3) Atrial contraction begins

Stimulus spreads across the atrial surfaces and reaches the AV node. AV node Elapsed time = 50 msec

There is a 100-msec delay at the AV node. Atrial contraction begins. AV bundle Bundle branches Elapsed time = 150 msec

The AV Bundle In the septum Carries impulse to left and right bundle branches Which conduct to Purkinje fibers (Step 4) And to the moderator band Which conducts to papillary muscles

The impulse travels along the interventricular septum within the AV bundle and the bundle branches to the Purkinje fibers and, by the moderator band, to the papillary muscles of the right ventricle. Moderator band Elapsed time = 175 msec

Purkinje Fibers Distribute impulse through ventricles (Step 5) Atrial contraction is completed Ventricular contraction begins

The impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium. Atrial contraction is completed, and ventricular contraction begins. Elapsed time = 225 msec Purkinje fibers

Abnormal Pacemaker Function Bradycardia – abnormally slow heart rate Tachycardia – abnormally fast heart rate Ectopic pacemaker Abnormal cells Generate high rate of action potentials Bypass conducting system Disrupt ventricular contractions

The Electrocardiogram (ECG or EKG) A recording of electrical events in the heart Obtained by electrodes at specific body locations Abnormal patterns diagnose damage

Features of an ECG P wave Atria depolarize QRS complex Ventricles depolarize T wave Ventricles repolarize

Time Intervals between ECG Waves P–R interval From start of atrial depolarization To start of QRS complex Q–T interval From ventricular depolarization To ventricular repolarization

Figure 20-13b An Electrocardiogram.
800 msec +1 R R P wave (atria depolarize) T wave (ventricles repolarize) S–T segment +0.5 P–R segment Millivolts Q S S–T interval P–R interval Q–T interval QRS interval (ventricles depolarize) −0.5 b An ECG printout is a strip of graph paper containing a record of the electrical events monitored by the electrodes. The placement of electrodes on the body surface affects the size and shape of the waves recorded. The example is a normal ECG; the enlarged section indicates the major components of the ECG and the measurements most often taken during clinical analysis.

20-3 The Cardiac Cycle Two Phases of the Cardiac Cycle
Within any one chamber Systole (contraction) Diastole (relaxation)

Figure 20-16 Phases of the Cardiac Cycle.
Start a Atrial systole begins: Atrial contraction forces a small amount of additional blood into relaxed ventricles. b Atrial systole ends, atrial diastole begins 0 msec 800 msec 100 msec Cardiac cycle c Ventricular systole— first phase: Ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. f Ventricular diastole—late: All chambers are relaxed. Ventricles fill passively. 370 msec d Ventricular systole— second phase: As ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected. e Ventricular diastole—early: As ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves and forces them closed. Blood flows into the relaxed atria.

Left ventricular volume (mL)
Figure Pressure and Volume Relationships in the Cardiac Cycle (Part 3 of 4). ATRIAL DIASTOLE ATRIAL SYSTOLE ATRIAL DIASTOLE VENTRICULAR DIASTOLE VENTRICULAR SYSTOLE 120 5 Aortic valve opens Aorta 90 1 Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. 2 Pressure (mm Hg) 60 3 Left ventricle 4 4 5 6 7 30 Left atrium Left AV valve closes 8 2 1 3 130 End-diastolic volume 3 2 Left ventricular volume (mL) 1 Stroke volume 50 100 200 300 Time (msec)

Left ventricular volume (mL)
Figure Pressure and Volume Relationships in the Cardiac Cycle (Part 4 of 4). ATRIAL SYSTOLE ATRIAL DIASTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE 120 Aortic valve closes 6 90 Dicrotic notch 1 Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric ventricular contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. 2 Pressure (mm Hg) 60 3 4 7 5 6 7 30 Left AV valve opens 8 8 130 Left ventricular volume (mL) End-systolic volume 6 50 300 400 500 600 700 800 Time (msec)

20-3 The Cardiac Cycle Heart Sounds S1 S2 Loud sounds
Produced by AV valves S2 Produced by semilunar valves

20-3 The Cardiac Cycle S3, S4 Heart Murmur Soft sounds
Blood flow into ventricles and atrial contraction Heart Murmur Sounds produced by regurgitation through valves

Semilunar valves close
Figure 20-18b Heart Sounds. 120 Semilunar valves open Semilunar valves close 90 Aorta Pressure (mm Hg) 60 Left ventricle Left atrium AV valves close AV valves open 30 S1 S2 S4 S3 S4 Heart sounds “Lubb” “Dupp” b The relationship between heart sounds and key events in the cardiac cycle

20-4 Cardiodynamics Cardiodynamics
The movement and force generated by cardiac contractions End-diastolic volume (EDV) End-systolic volume (ESV) Stroke volume (SV) SV = EDV – ESV Ejection fraction The percentage of EDV represented by SV

20-4 Cardiodynamics Cardiac Output (CO)
The volume pumped by left ventricle in one minute CO = HR  SV CO = cardiac output (mL/min) HR = heart rate (beats/min) SV = stroke volume (mL/beat)

20-4 Cardiodynamics Factors Affecting Cardiac Output Cardiac output
Adjusted by changes in heart rate or stroke volume Heart rate Adjusted by autonomic nervous system or hormones Stroke volume Adjusted by changing EDV or ESV

Figure 20-20 Factors Affecting Cardiac Output.
Factors Affecting Heart Rate (HR) Factors Affecting Stroke Volume (SV) Autonomic innervation End-diastolic volume End-systolic volume Hormones HEART RATE (HR) STROKE VOLUME (SV) = EDV − ESV CARDIAC OUTPUT (CO) = HR × SV

Figure 20-21 Autonomic Innervation of the Heart.
Vagal nucleus Cardioinhibitory center Cardioacceleratory center Medulla oblongata Vagus (N X) Spinal cord Sympathetic Parasympathetic Parasympathetic preganglionic fiber Sympathetic preganglionic fiber Synapses in cardiac plexus Sympathetic ganglia (cervical ganglia and superior thoracic ganglia [T1–T4]) Parasympathetic postganglionic fibers Sympathetic postganglionic fiber Cardiac nerve

20-4 Cardiodynamics Effects on the SA Node
Sympathetic and parasympathetic stimulation Greatest at SA node (heart rate) ACh (parasympathetic stimulation) Slows the heart NE (sympathetic stimulation) Speeds the heart

20-4 Cardiodynamics Atrial Reflex Also called Bainbridge reflex
Adjusts heart rate in response to venous return Stretch receptors in right atrium Trigger increase in heart rate Through increased sympathetic activity

20-4 Cardiodynamics Hormonal Effects on Heart Rate
Increase heart rate (by sympathetic stimulation of SA node) Epinephrine (E) Norepinephrine (NE) Thyroid hormone

20-4 Cardiodynamics Factors Affecting the Stroke Volume
The EDV – amount of blood a ventricle contains at the end of diastole Filling time Duration of ventricular diastole Venous return Rate of blood flow during ventricular diastole

20-4 Cardiodynamics Preload
The degree of ventricular stretching during ventricular diastole Directly proportional to EDV Affects ability of muscle cells to produce tension

20-4 Cardiodynamics The EDV and Stroke Volume At rest With exercise
EDV is low Myocardium stretches less Stroke volume is low With exercise EDV increases Myocardium stretches more Stroke volume increases

20-4 Cardiodynamics The Frank–Starling Principle Physical Limits
As EDV increases, stroke volume increases Physical Limits Ventricular expansion is limited by: Myocardial connective tissue The cardiac (fibrous) skeleton The pericardial sac

20-4 Cardiodynamics End-Systolic Volume (ESV)
Is the amount of blood that remains in the ventricle at the end of ventricular systole

20-4 Cardiodynamics Three Factors That Affect ESV Preload
Ventricular stretching during diastole Contractility Force produced during contraction, at a given preload Afterload Tension the ventricle produces to open the semilunar valve and eject blood

20-4 Cardiodynamics Contractility Is affected by: Autonomic activity
Hormones

20-4 Cardiodynamics Effects of Autonomic Activity on Contractility
Sympathetic stimulation NE released by postganglionic fibers of cardiac nerves Epinephrine and NE released by adrenal medullae Causes ventricles to contract with more force Increases ejection fraction and decreases ESV

20-4 Cardiodynamics Effects of Autonomic Activity on Contractility
Parasympathetic activity Acetylcholine released by vagus nerves Reduces force of cardiac contractions

20-4 Cardiodynamics Hormones Many hormones affect heart contraction
Pharmaceutical drugs mimic hormone actions Stimulate or block beta receptors Affect calcium ions (e.g., calcium channel blockers) blocking the “beta receptors” that bind epinephrine. Among other things, blocking the beta receptors slows the heart rate, reduces the force of contraction of the heart muscle, reduces the amount of oxygen the heart muscle needs to do its work, reduces stress on the vascular system, and tends to lower the blood pressure.

20-4 Cardiodynamics Afterload (Tension the ventricle produces to open the semilunar valve and eject blood) Is increased by any factor that restricts arterial blood flow As afterload increases, stroke volume decreases

Figure 20-23 Factors Affecting Stroke Volume.
Factors Affecting Stroke Volume (SV) Venous return (VR) Filling time (FT) Increased by sympathetic stimulation Decreased by parasympathetic stimulation Increased by E, NE, glucagon, thyroid hormones VR = EDV FT = EDV VR = EDV FT = EDV Contractility (Cont) of muscle cells Preload Cont = ESV Increased by vasoconstriction Decreased by vasodilation Cont = ESV Afterload (AL) End-diastolic volume (EDV) End-systolic volume (ESV) AL = ESV AL = ESV STROKE VOLUME (SV) EDV = SV ESV = SV EDV = SV ESV = SV

20-4 Cardiodynamics Summary: The Control of Cardiac Output
Heart rate control factors Autonomic nervous system Sympathetic and parasympathetic Circulating hormones Venous return and stretch receptors

20-4 Cardiodynamics Summary: The Control of Cardiac Output
Stroke volume control factors EDV Filling time and rate of venous return ESV Preload, contractility, afterload

20-4 Cardiodynamics Cardiac Reserve
The difference between resting and maximal cardiac outputs

20-4 Cardiodynamics The Heart and Cardiovascular System
Cardiovascular regulation Ensures adequate circulation to body tissues Cardiovascular centers Control heart and peripheral blood vessels Cardiovascular system responds to: Changing activity patterns Circulatory emergencies

Figure 20-24a A Summary of the Factors Affecting Cardiac Output.
Maximum for trained athletes exercising at peak levels 40 35 30 Normal range of cardiac output during heavy exercise 25 Cardiac output (L/min) 20 15 10 Average resting cardiac output 5 Heart failure a Cardiac output varies widely to meet metabolic demands

Figure 20-24b A Summary of the Factors Affecting Cardiac Output.
Factors affecting heart rate (HR) Factors affecting stroke volume (SV) Skeletal muscle activity Blood volume Changes in peripheral circulation Atrial reflex Venous return Filling time Autonomic innervation Hormones Vasodilation or vasoconstriction Preload Contractility Autonomic innervation Hormones End-diastolic volume End-systolic volume Afterload HEART RATE (HR) STROKE VOLUME (SV) = EDV − ESV CARDIAC OUTPUT (CO) = HR × SV b Factors affecting cardiac output

Right coronary artery: 15% blocked

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