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Dr. Sabir Hussain---CVS Notes

The document summarizes key aspects of heart anatomy and physiology. It describes the location and layers of the heart walls. It details the four chambers of the heart and the valves that prevent backflow of blood. It explains the pulmonary and systemic blood circulation circuits. It also outlines the specialized conduction system that controls heart rhythm, including the sinoatrial node, atrioventricular node, and Purkinje fibers. In addition, it discusses how sympathetic and parasympathetic nerves regulate heart rate and conduction.

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Notes for CVS Dr. Sabir Hussain Human Physiology
The Heart
Location and Size of Heart • Located in thoracic cavity in mediastinum • About same size as closed fist – base is the wider anterior portion – apex is tip or point
Pericardium: Heart Covering
Fibrous Pericardium • Rests on and is attached to diaphragm • Tough, inelastic sac of fibrous connective tissue • Continuous with blood vessels entering, leaving heart at base • Protects, anchors heart, prevents overstretching
Parietal (Outer) Serous Pericardium • Thin layer adhered to inside of fibrous pericardium • Secretes serous (watery) lubricating fluid
Layers of the Heart Wall • The wall of the heart is composed of three distinct layers. From superficial to deep they are: – The epicardium – The myocardium – The endocardium
Layers of the Heart Wall
Chambers of the Heart • The heart has 4 Chambers: – The upper 2 are the right and left atria. – The lower 2 are the right and left ventricles.
Chambers of the Heart
Chambers of the Heart
Valves of the Heart • Function to prevent backflow of blood into/through heart • Open, close in response to changes in pressure in heart • Four valves
Heart Valves
Valves
Valves
Valves • Surprisingly, perhaps, there are no valves guarding the junction between the venae cavae and the right atrium or the pulmonary veins and the left atrium. As the atria contract, a small amount of blood does flow backward into these vessels, but it is minimized by the way the atria contract, which compresses, and nearly collapses the venous entry points.
Heart Valves
Blood Flow • The body’s blood flow can best be understood as two circuits arranged in series. The output of one becomes the input of the other: – Pulmonary circuit ejects blood into the pulmonary trunk and is powered by the right side of the heart. – Systemic circuit ejects blood into the aorta, systemic arteries, and arterioles and is powered by the left side of the heart.
The right-sided Pulmonary Circulation • Starting with the venous return to the heart, deoxygenated blood flows into the right atrium from 3 sources (the two vena cavae and the coronary sinus). • Blood then follows a pathway through the right heart to the lungs to be oxygenated. Blood Flow
The left-sided Systemic Circulation Blood Flow • Oxygenated blood returns to the left heart to be pumped through the outflow tract of the systemic circulation.
Coronary Vessels – The myocardium (and other tissues of the thick cardiac walls) must get nutrients from blood flowing through the coronary circulation. • Starting at the aortic root, the direction of blood flow is from the aorta to the left and right coronary arteries (LCA, RCA): – LCA to anterior interventricular and circumflex branches – RCA to marginal and posterior atrioventricular branches
Coronary Vessels • The coronary arteries and veins have been painted in this anterior view of a cadaver heart:
• Coronary veins all collect into the coronary sinus on the back part of the heart: Coronary Vessels
Arteries and Veins • Arteries are vessels that always conduct blood away from the heart – with just a few exceptions, arteries contain oxygenated blood. • Most arteries in the body are thick-walled and exposed to high pressures and friction forces.
Arteries and Veins • Veins are vessels that always bring blood back to the heart - with just a few exceptions, veins contain deoxygenated blood. • Most veins in the body are thin-walled and exposed to low pressures and minimal friction forces.
Arteries and Veins View of the front of the heart
Arteries and Veins
• Cardiac muscle, like skeletal muscle, is striated. Unlike skeletal muscle, its fibers are shorter, they branch, and they have only one (usually centrally located) nucleus. • Cardiac muscle cells connect to and communicate with neighboring cells through gap junctions in intercalated discs. Cardiac Muscle Tissue
By: Dr. Sabir Hussain Specialized excitatory and conductive system of the Heart: SA node - Sinus node or sinoatrial node, initiates the cardiac impulse Internodal pathway - SA to AV node AV node - delays impulse from the atria to the ventricles AV bundle - conducts from AV node to the ventricles Purkinje Fibers - conducts impulses to all parts of the ventricles.
The Sinus Node controls the heart rate: The membrane potential of sinus node is -55 to -60 mV The heart rate is caused by following four factors: . The fast sodium channels are inactivated at the normal resting potential, but there is slow leakage of sodium in the fiber. . Between action potentials the resting potential gradually increases because of slow leakage sodium until the potential reaches -40mV
. At this time, the calcium-sodium channels become activated, allowing rapid entry of sodium and calcium and thus causing the action potential. . Greatly increased numbers of potassium channels open, allowing potassium to escape from the cells, within about 100 to 150 ms after the calcium-sodium open. This returns the membrane potential to its resting potential, and the self excitation cycle starts again with sodium leaking slowly into the sinus node fibers.
The Internodal and interatrial pathways transmit impulses in the atrium. There are three internodal pathways - the anterior, the middle and the posterior internodal pathway - that carry impulses from the SA node to the AV node. Small bundles of atrial muscle fibers transmit impulses more rapidly than the normal atrial muscle -like the anterior interatrial band, conducts impulses from the right atrium to the anterior part of the left atrium.
The AV node delays impulses from the atria to the ventricles. This delayed time allows the atria to empty into the ventricles before ventricular contraction. The delay in the AV node is achieved by slow conduction: (1) membrane potential is much less negative in the AV node and the bundle than in the normal cardiac muscle. (2) Few gap junctions exist between the cells in the AV node and the bundle, so that resistance to ion flow is great.
The transmission of impulses through the Purkinje system and the cardiac muscle is rapid. The action potentials travel at a velocity of 1,5 to 4,0 m/s, which is 6x the velocity of cardiac muscle. The high permeability of the gap junctions at the intercalated discs between the Purkinje fiber cells likely causes the high velocity of transmission.
The atrial and ventricular syncytia are separate and insulated from one another. Separated by a fibrous barrier that acts as an insulator - forcing atrial impulses to enter through the AV bundle. The transmission of impulses through cardiac muscle travel at a velocity of 0.3 to 0.5 m/s. Travel from the endocardium to the epicardium in 0.03ms.
Control of excitation and conduction in the Heart. The sinus node is the normal pacemaker of the heart. The intrinsic discharge rate for the SA node, 70-80bpm, AV-node 40-60bpm, Purkinje system 15-40bpm. An ectopic pacemaker may develop a rhythmic rate faster than the SA node - the most common location would be in the AV node or the AV bundle.
AV block occurs when impulses fail to pass from the aorta to the ventricles. After a sudden block, the purkinje fibers do not emit rhythmic impulses for 5 to 30 seconds because it has been overridden by the sinus rhythm. During this time the ventricles fail to contract, and person may faint because of the lack of cerebral perfusion. This is known as the STOKES-ADAMS SYNDROME.
Control of Heart Rhythmicity and Conduction by the Cardiac Nerves: Sympathetic and Parasympathetic. Parasympathetic (vagal) stimulation slows the cardiac rhythm - through acetylcholine release causes: 1. The rate of sinus node discharge decrease 2. The excitability of the fibers between the atrial muscle and the AV node to decrease.
The heart rate can decrease to half normal, but strong vagal stimulation can temporarily stop the heartbeat. The purkinje fibers then develop their own rhythmicity at 15 to 40 bpm. This is called ventricular escape. The mechanism of vagal effects on the heart are as follows: 1.) Acetylcholine increases the permeability of the sinus node and the AV fibers to potassium; this causes hyperpolarization of these tissues and makes them less excitable. 2.) The membrane potential of the Sinus Node fibers decrease from -55 to 60mV to -65 to -75mV. The normal upward drift in the membrane potential is caused by sodium leakage in these tissues requires a much longer time to reach self-excitation.
Sympathetic Stimulation increases cardiac rhythm. . The rate of Sinus Node discharge increases . The cardiac impulse conductance rate increases in all parts of the heart . The force of contraction increases in both atrial and ventricular muscle. Sympathetic stimulation releases norepinephrine - increasing the permeability to sodium and calcium, increasing the resting membrane potential and makes the heart more excitable, and therefore increasing the heart rate. The greater calcium permeability increases the force of contraction of cardiac muscle. Dr. Sabir Hussain
Rhythmical Excitation of the Heart Rhythmical Excitation of the Heart
The rhythmical electrical impulses in a normal heart allows: • The atria to contract about one sixth of a second ahead of ventricular contraction. • Allows ventricular filling before they pump the blood through the lungs and peripheral circulation. • Allows all portions of the ventricles to contract almost simultaneously.
Sinus (Sinoatrial Node) Strip of specialized cardiac muscle Sinus nodal fibers connect directly with the atrial muscle fibers. Have the capability of self-excitation, a process that can cause automatic rhythmical discharge and contraction
Mechanism of Sinus Nodal Rhythmicity. • R.M.P of the sinus nodal fiber has a negativity of about -55 to -60 millivolts, in comparison with -85 to - 90 millivolts for the ventricular muscle fiber. • Cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions. • At -55 mV, the fast sodium channels already become “inactivated”. • The atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. The inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.
Transmission of the Cardiac Impulse Through the Atria • The A-V node is located in the posterior wall of the right atrium immediately behind the tricuspid valve • Action potentials originating in the sinus node travel outward into the atrial muscle fibers and to the A-V node. • Impulse, after traveling through the internodal pathways, reaches the A-V node about 0.03 second after its origin in the sinus node. One-Way Conduction Through the A-V Bundle.
• The impulse is delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal A-V bundle. • Once it has entered this bundle, it spreads very rapidly through the Purkinje fibers to the entire endocardial surfaces of the ventricles. • Then the impulse once again spreads slightly less rapidly through the ventricular muscle to the epicardial surfaces.
Special Purkinje fibers lead from the A-V node through the A-V bundle into the ventricles. Diminished numbers of gap junctions between successive cells in the conducting pathways allowing resistance to conduction of excitatory ions from one conducting fiber to the next. Distal portion of the A-V bundle passes downward in the ventricular septum for 5 to 15 millimeters toward the apex of the heart. Transmit action potentials at a velocity of 1.5 to 4.0 m/sec Transmission in the Ventricular Purkinje System
Abnormal Pacemakers (Ectopic pacemakers) A pacemaker elsewhere than the sinus node is called an “ectopic” pacemaker. • The discharge rate of the sinus node is considerably faster than the natural self- excitatory discharge rate of either the A-V node or the Purkinje fibers. • Under abnormal conditions, few other parts of the heart can exhibit intrinsic rhythmical excitation in the same way like the sinus nodal fibers (A-V nodes and Purkinje fibres). • The cardiac impulse arrives at almost all portions of the ventricles within a narrow span of time, exciting the first ventricular muscle fiber only 0.03 to 0.06 second ahead of excitation of the last ventricular muscle fiber. Why Sinus node controls heart rhythymicity
Control of Heart Rhythmicity and Impulse Conduction The Sympathetic and Parasympathetic Nerves Parasympathetic Nerves Sympathetic Nerves Releases acetylcholine Decreases heart rhythm and excitability. Excitatory signals are no longer transmitted into the ventricles. Ventricular Escape Increased permeability of the fiber membranes to potassium ions Releases norepinephrine at sympathetic endings. Increases the rate of sinus nodal discharge. Increases the overall heart activity. Increases the permeability of Na+ and Ca2+ ions.
Abnormal Heart Rhythms • Atrial fibrillation • Superventricular tachycardia (Electric impulses travel from ventricle to atria) Ventricular tachycardia (ventricles don’t have time to fill up properly) • Bradycardia (Slow heart beat)
Pacemaker Implantation
Autorhythmicity • The rhythmical electrical activity produced in heart is called autorhythmicity. Because heart muscle is autorhythmic, it does not rely on the central nervous system to sustain a lifelong heartbeat.
• During embryonic development, about 1% of all of the muscle cells of the heart form a network or pathway called the cardiac conduction system. This specialized group of myocytes is unusual in that they have the ability to spontaneously depolarize. Autorhythmicity
Membrane of two cells clearly seen. The spread of ions through gap junctions of the Intercalated discs (I) allows the AP to pass from cell to cell Autorhythmicity • Autorhythmic cells spontaneously depolarize at a given rate, some groups faster, some groups slower. Once a group of autorhythmic cells reaches threshold and starts an action potential (AP), all of the cells in that area of the heart also depolarize.
Cardiac Conduction • The self-excitable myocytes that "act like nerves" have the 2 important roles of forming the conduction system of the heart and acting as pacemakers within that system. • Because it has the fastest rate of depolarization, the normal pacemaker of the heart is the sinoatrial (SA) node, located in the right atrial wall just below where the superior vena cava enters the chamber.
Cardiac Conduction Spontaneous Depolarization of autorhythmic fibers in the SA node firing about once every 0.8 seconds, or 75 action potentials per minute
Frontal plane Right atrium Right ventricle Left atrium Left ventricle Anterior view of frontal section Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE1 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE 1 2 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) 1 2 3 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES 1 2 3 4 Right atrium Right ventricle Frontal plane SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE Left atrium Left ventricle Anterior view of frontal section ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES PURKINJE FIBERS 1 2 3 4 5 Right atrium Right ventricle
• Although anatomically the heart consist of individual cells, the bands of muscle wind around the heart and work as a unit – forming a “functional syncytium” . – This allows the top and bottom parts to contract in their own unique way. Coordinating Contractions
Coordinating Contractions • The atrial muscle syncytium contracts as a single unit to force blood down into the ventricles. • The syncytium of ventricular muscle starts contracting at the apex (inferiorly), squeezing blood upward to exit the outflow tracts.
ANS Innervation • Although the heart does not rely on outside nerves for its basic rhythm, there is abundant sympathetic and parasympathetic innervation which alters the rate and force of heart contractions.
ANS Innervation
• The action potential (AP) initiated by the SA node travels through the conduction system to excite the “working” contractile muscle fibers in the atria and ventricles. • Unlike autorhythmic fibers, contractile fibers have a stable RMP of –90mV. – The AP propagates throughout the heart by opening and closing Na+ and K+ channels. Cardiac Muscle Action Potential
Depolarization Repolarization Refractory period Contraction Membrane potential (mV) Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 11 Depolarization Repolarization Refractory period Contraction Membrane potential (mV) Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open Plateau (maintained depolarization) due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and K+ outflow when some K+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 11 2 Depolarization Repolarization Refractory period Contraction Membrane potential (mV) Repolarization due to closure of Ca2+ channels and K+ outflow when additional voltage-gated K+ channels open Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open Plateau (maintained depolarization) due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and K+ outflow when some K+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 1 3 1 2 3 Cardiac Muscle Action Potential
Cardiac Muscle Action Potential • Unlike skeletal muscle, the refractory period in cardiac muscle lasts longer than the contraction itself - another contraction cannot begin until relaxation is well underway. • For this reason, tetanus (maintained contraction) cannot occur in cardiac muscle, leaving sufficient time between contractions for the chambers to fill with blood. • If heart muscle could undergo tetanus, blood flow would cease!
The Electrocardiogram • An ECG is a recording of the electrical changes on the surface of the body resulting from the depolarization and repolarization of the myocardium. • ECG recordings measure the presence or absence of certain waveforms (deflections), the size of the waves, and the time intervals of the cardiac cycle. – By measuring the ECG, we can quantify and correlate, electrically, the mechanical activities of the heart.
The Electrocardiogram
1 Depolarization of atrial contractile fibers produces P wave 0.20 Seconds Action potential in SA node P 1 Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.20 Seconds 0.20 Seconds Action potential in SA node P P 2 1 Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P 2 3 P 1 Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P 2 3 4 P 1 5Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.2 0.40 Seconds 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T 2 3 4 5 P 1 6Ventricular diastole (relaxation) 5Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.2 0.40 0.8 Seconds 0.60.2 0.40 Seconds 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T P 2 3 4 5 6 P
• Blood Pressure is usually measured in the larger conducting arteries where the high and low pulsations of the heart can be detected – usually the brachial artery. – Systolic BP is the higher pressure measured during left ventricular systole when the aortic valve is open. – Diastolic BP is the lower pressure measured during left ventricular diastole when the valve is closed. Blood Pressure
Blood Pressure • Normal BP varies by age, but is approximately 120 mm Hg systolic over 80 mmHg diastolic in a healthy young adult ( in females, the pressures are often 8–10 mm Hg less.) • It is often best to refer to the blood pressure as a single number, called the mean arterial pressure (MAP) . – MAP is roughly 1/3 of the way between the diastolic and systolic BP. It is defined as 1/3 (systolic BP – diastolic BP) + diastolic BP.
Blood Pressure • In a person with a BP of 120/80 mm Hg, MAP = 1/3 (120-80) + 80 = 93.3 mm Hg. • In the smaller arterioles, capillaries, and veins, the BP pulsations are not detectable, and only a mean BP is measurable (see the purple and blue areas of this figure).
Cardiac Cycle • The cardiac cycle includes all events associated with one heartbeat, including diastole (relaxation phase) and systole (contraction phase) of both the atria and the ventricles. • In each cycle, atria and ventricles alternately contract and relax. – During atrial systole, the ventricles are relaxed. – During ventricle systole, the atria are relaxed.
Cardiac Cycle • Since ventricular function matters most to the body, the two principal events of the cycle for us to understand are ventricular filling (during ventricular diastole), and ventricular ejection (during ventricular systole). – The blood pressure that we measure in the arm is a reflection of the pressure developed by the left ventricle, before and after left ventricular systole. – Pulmonary blood pressure is a result of right ventricular function, but is not easily measured.
Cardiac Cycle Valves AV SL Outflow Ventricular diastole Open Closed Atrial systole Ventricular systole Closed Open Early atrial diastole Ventricular diastole Open Closed Late atrial diastole
Cardiac Cycle • During the cardiac cycle, all 4 of the heart valves have a chance to open and close. Listening (usually with a stethoscope) to the sounds the heart makes is called auscultation. • Valve opening is usually silent. The “lubb dupp” we associate with heart auscultation is produced by valve closure (in pairs – see p. 740 left side).
Cardiac Cycle
Cardiac Cycle • The average time required to complete the cardiac cycle is usually less than one second (about 0.8 seconds at a heart rate of 75 beats/minute). – 0.1 seconds – atria contract (atrial “kick”), ventricles are relaxed – 0.3 seconds – atria relax, ventricles contract – 0.4 seconds – relaxation period for all chambers, allowing passive filling. When heart rate increases, it’s this relaxation period that decreases the most.
Cardiac Output • The stroke volume (SV) is the volume of blood ejected from the left (or right) ventricle every beat. The cardiac output (CO) is the SV x heart rate (HR). – In a resting male, CO = 70mL/beat x 75 beats/min = 5.25L/min. • On average, a person’s entire blood volume flows through the pulmonary and systemic circuits each minute.
Cardiac Output • The cardiac reserve is the difference between the CO at rest and the maximum CO the heart can generate. – Average cardiac reserve is 4-5 times resting value. • Exercise draws upon the cardiac reserve to meet the body’s increased physiological demands and maintain homeostasis.
Cardiac Output • The cardiac output is affected by changes in SV, heart rate, or both. • There are 3 important factors that affect SV – The amount of ventricular filling before contraction (called the preload) – The contractility of the ventricle – The resistance in the blood vessels (aorta) or valves (aortic valve, when damaged) the heart is pumping into (called the afterload)
Cardiac Output • The more the heart muscle is stretched (filled) before contraction (preload), the more forcefully the heart will contract. This phenomenon is known as Starling’s Law of the heart. – Stimulation of the sympathetic nervous system during exercise increases venous return, stretches the heart muscle, and increases CO.
Cardiac Output

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Dr. Sabir Hussain---CVS Notes

  • 1.
    Notes for CVS Dr.Sabir Hussain Human Physiology
  • 2.
  • 3.
    Location and Sizeof Heart • Located in thoracic cavity in mediastinum • About same size as closed fist – base is the wider anterior portion – apex is tip or point
  • 4.
  • 5.
    Fibrous Pericardium • Restson and is attached to diaphragm • Tough, inelastic sac of fibrous connective tissue • Continuous with blood vessels entering, leaving heart at base • Protects, anchors heart, prevents overstretching
  • 6.
    Parietal (Outer) SerousPericardium • Thin layer adhered to inside of fibrous pericardium • Secretes serous (watery) lubricating fluid
  • 7.
    Layers of theHeart Wall • The wall of the heart is composed of three distinct layers. From superficial to deep they are: – The epicardium – The myocardium – The endocardium
  • 8.
    Layers of theHeart Wall
  • 9.
    Chambers of theHeart • The heart has 4 Chambers: – The upper 2 are the right and left atria. – The lower 2 are the right and left ventricles.
  • 10.
  • 11.
  • 12.
    Valves of theHeart • Function to prevent backflow of blood into/through heart • Open, close in response to changes in pressure in heart • Four valves
  • 13.
  • 14.
  • 15.
  • 16.
    Valves • Surprisingly, perhaps,there are no valves guarding the junction between the venae cavae and the right atrium or the pulmonary veins and the left atrium. As the atria contract, a small amount of blood does flow backward into these vessels, but it is minimized by the way the atria contract, which compresses, and nearly collapses the venous entry points.
  • 17.
  • 18.
    Blood Flow • Thebody’s blood flow can best be understood as two circuits arranged in series. The output of one becomes the input of the other: – Pulmonary circuit ejects blood into the pulmonary trunk and is powered by the right side of the heart. – Systemic circuit ejects blood into the aorta, systemic arteries, and arterioles and is powered by the left side of the heart.
  • 19.
    The right-sided PulmonaryCirculation • Starting with the venous return to the heart, deoxygenated blood flows into the right atrium from 3 sources (the two vena cavae and the coronary sinus). • Blood then follows a pathway through the right heart to the lungs to be oxygenated. Blood Flow
  • 20.
    The left-sided SystemicCirculation Blood Flow • Oxygenated blood returns to the left heart to be pumped through the outflow tract of the systemic circulation.
  • 22.
    Coronary Vessels – Themyocardium (and other tissues of the thick cardiac walls) must get nutrients from blood flowing through the coronary circulation. • Starting at the aortic root, the direction of blood flow is from the aorta to the left and right coronary arteries (LCA, RCA): – LCA to anterior interventricular and circumflex branches – RCA to marginal and posterior atrioventricular branches
  • 23.
    Coronary Vessels • Thecoronary arteries and veins have been painted in this anterior view of a cadaver heart:
  • 24.
    • Coronary veinsall collect into the coronary sinus on the back part of the heart: Coronary Vessels
  • 25.
    Arteries and Veins •Arteries are vessels that always conduct blood away from the heart – with just a few exceptions, arteries contain oxygenated blood. • Most arteries in the body are thick-walled and exposed to high pressures and friction forces.
  • 26.
    Arteries and Veins •Veins are vessels that always bring blood back to the heart - with just a few exceptions, veins contain deoxygenated blood. • Most veins in the body are thin-walled and exposed to low pressures and minimal friction forces.
  • 27.
    Arteries and Veins Viewof the front of the heart
  • 28.
  • 29.
    • Cardiac muscle,like skeletal muscle, is striated. Unlike skeletal muscle, its fibers are shorter, they branch, and they have only one (usually centrally located) nucleus. • Cardiac muscle cells connect to and communicate with neighboring cells through gap junctions in intercalated discs. Cardiac Muscle Tissue
  • 30.
    By: Dr. SabirHussain Specialized excitatory and conductive system of the Heart: SA node - Sinus node or sinoatrial node, initiates the cardiac impulse Internodal pathway - SA to AV node AV node - delays impulse from the atria to the ventricles AV bundle - conducts from AV node to the ventricles Purkinje Fibers - conducts impulses to all parts of the ventricles.
  • 31.
    The Sinus Nodecontrols the heart rate: The membrane potential of sinus node is -55 to -60 mV The heart rate is caused by following four factors: . The fast sodium channels are inactivated at the normal resting potential, but there is slow leakage of sodium in the fiber. . Between action potentials the resting potential gradually increases because of slow leakage sodium until the potential reaches -40mV
  • 32.
    . At thistime, the calcium-sodium channels become activated, allowing rapid entry of sodium and calcium and thus causing the action potential. . Greatly increased numbers of potassium channels open, allowing potassium to escape from the cells, within about 100 to 150 ms after the calcium-sodium open. This returns the membrane potential to its resting potential, and the self excitation cycle starts again with sodium leaking slowly into the sinus node fibers.
  • 33.
    The Internodal andinteratrial pathways transmit impulses in the atrium. There are three internodal pathways - the anterior, the middle and the posterior internodal pathway - that carry impulses from the SA node to the AV node. Small bundles of atrial muscle fibers transmit impulses more rapidly than the normal atrial muscle -like the anterior interatrial band, conducts impulses from the right atrium to the anterior part of the left atrium.
  • 34.
    The AV nodedelays impulses from the atria to the ventricles. This delayed time allows the atria to empty into the ventricles before ventricular contraction. The delay in the AV node is achieved by slow conduction: (1) membrane potential is much less negative in the AV node and the bundle than in the normal cardiac muscle. (2) Few gap junctions exist between the cells in the AV node and the bundle, so that resistance to ion flow is great.
  • 35.
    The transmission ofimpulses through the Purkinje system and the cardiac muscle is rapid. The action potentials travel at a velocity of 1,5 to 4,0 m/s, which is 6x the velocity of cardiac muscle. The high permeability of the gap junctions at the intercalated discs between the Purkinje fiber cells likely causes the high velocity of transmission.
  • 36.
    The atrial andventricular syncytia are separate and insulated from one another. Separated by a fibrous barrier that acts as an insulator - forcing atrial impulses to enter through the AV bundle. The transmission of impulses through cardiac muscle travel at a velocity of 0.3 to 0.5 m/s. Travel from the endocardium to the epicardium in 0.03ms.
  • 37.
    Control of excitationand conduction in the Heart. The sinus node is the normal pacemaker of the heart. The intrinsic discharge rate for the SA node, 70-80bpm, AV-node 40-60bpm, Purkinje system 15-40bpm. An ectopic pacemaker may develop a rhythmic rate faster than the SA node - the most common location would be in the AV node or the AV bundle.
  • 38.
    AV block occurswhen impulses fail to pass from the aorta to the ventricles. After a sudden block, the purkinje fibers do not emit rhythmic impulses for 5 to 30 seconds because it has been overridden by the sinus rhythm. During this time the ventricles fail to contract, and person may faint because of the lack of cerebral perfusion. This is known as the STOKES-ADAMS SYNDROME.
  • 39.
    Control of HeartRhythmicity and Conduction by the Cardiac Nerves: Sympathetic and Parasympathetic. Parasympathetic (vagal) stimulation slows the cardiac rhythm - through acetylcholine release causes: 1. The rate of sinus node discharge decrease 2. The excitability of the fibers between the atrial muscle and the AV node to decrease.
  • 40.
    The heart ratecan decrease to half normal, but strong vagal stimulation can temporarily stop the heartbeat. The purkinje fibers then develop their own rhythmicity at 15 to 40 bpm. This is called ventricular escape. The mechanism of vagal effects on the heart are as follows: 1.) Acetylcholine increases the permeability of the sinus node and the AV fibers to potassium; this causes hyperpolarization of these tissues and makes them less excitable. 2.) The membrane potential of the Sinus Node fibers decrease from -55 to 60mV to -65 to -75mV. The normal upward drift in the membrane potential is caused by sodium leakage in these tissues requires a much longer time to reach self-excitation.
  • 41.
    Sympathetic Stimulation increasescardiac rhythm. . The rate of Sinus Node discharge increases . The cardiac impulse conductance rate increases in all parts of the heart . The force of contraction increases in both atrial and ventricular muscle. Sympathetic stimulation releases norepinephrine - increasing the permeability to sodium and calcium, increasing the resting membrane potential and makes the heart more excitable, and therefore increasing the heart rate. The greater calcium permeability increases the force of contraction of cardiac muscle. Dr. Sabir Hussain
  • 42.
    Rhythmical Excitation ofthe Heart Rhythmical Excitation of the Heart
  • 43.
    The rhythmical electricalimpulses in a normal heart allows: • The atria to contract about one sixth of a second ahead of ventricular contraction. • Allows ventricular filling before they pump the blood through the lungs and peripheral circulation. • Allows all portions of the ventricles to contract almost simultaneously.
  • 44.
    Sinus (Sinoatrial Node) Stripof specialized cardiac muscle Sinus nodal fibers connect directly with the atrial muscle fibers. Have the capability of self-excitation, a process that can cause automatic rhythmical discharge and contraction
  • 45.
    Mechanism of SinusNodal Rhythmicity. • R.M.P of the sinus nodal fiber has a negativity of about -55 to -60 millivolts, in comparison with -85 to - 90 millivolts for the ventricular muscle fiber. • Cell membranes of the sinus fibers are naturally leaky to sodium and calcium ions. • At -55 mV, the fast sodium channels already become “inactivated”. • The atrial nodal action potential is slower to develop than the action potential of the ventricular muscle. The inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.
  • 46.
    Transmission of theCardiac Impulse Through the Atria • The A-V node is located in the posterior wall of the right atrium immediately behind the tricuspid valve • Action potentials originating in the sinus node travel outward into the atrial muscle fibers and to the A-V node. • Impulse, after traveling through the internodal pathways, reaches the A-V node about 0.03 second after its origin in the sinus node. One-Way Conduction Through the A-V Bundle.
  • 47.
    • The impulseis delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal A-V bundle. • Once it has entered this bundle, it spreads very rapidly through the Purkinje fibers to the entire endocardial surfaces of the ventricles. • Then the impulse once again spreads slightly less rapidly through the ventricular muscle to the epicardial surfaces.
  • 48.
    Special Purkinje fiberslead from the A-V node through the A-V bundle into the ventricles. Diminished numbers of gap junctions between successive cells in the conducting pathways allowing resistance to conduction of excitatory ions from one conducting fiber to the next. Distal portion of the A-V bundle passes downward in the ventricular septum for 5 to 15 millimeters toward the apex of the heart. Transmit action potentials at a velocity of 1.5 to 4.0 m/sec Transmission in the Ventricular Purkinje System
  • 49.
    Abnormal Pacemakers (Ectopicpacemakers) A pacemaker elsewhere than the sinus node is called an “ectopic” pacemaker. • The discharge rate of the sinus node is considerably faster than the natural self- excitatory discharge rate of either the A-V node or the Purkinje fibers. • Under abnormal conditions, few other parts of the heart can exhibit intrinsic rhythmical excitation in the same way like the sinus nodal fibers (A-V nodes and Purkinje fibres). • The cardiac impulse arrives at almost all portions of the ventricles within a narrow span of time, exciting the first ventricular muscle fiber only 0.03 to 0.06 second ahead of excitation of the last ventricular muscle fiber. Why Sinus node controls heart rhythymicity
  • 50.
    Control of HeartRhythmicity and Impulse Conduction The Sympathetic and Parasympathetic Nerves Parasympathetic Nerves Sympathetic Nerves Releases acetylcholine Decreases heart rhythm and excitability. Excitatory signals are no longer transmitted into the ventricles. Ventricular Escape Increased permeability of the fiber membranes to potassium ions Releases norepinephrine at sympathetic endings. Increases the rate of sinus nodal discharge. Increases the overall heart activity. Increases the permeability of Na+ and Ca2+ ions.
  • 51.
    Abnormal Heart Rhythms •Atrial fibrillation • Superventricular tachycardia (Electric impulses travel from ventricle to atria) Ventricular tachycardia (ventricles don’t have time to fill up properly) • Bradycardia (Slow heart beat)
  • 52.
  • 53.
    Autorhythmicity • The rhythmicalelectrical activity produced in heart is called autorhythmicity. Because heart muscle is autorhythmic, it does not rely on the central nervous system to sustain a lifelong heartbeat.
  • 54.
    • During embryonicdevelopment, about 1% of all of the muscle cells of the heart form a network or pathway called the cardiac conduction system. This specialized group of myocytes is unusual in that they have the ability to spontaneously depolarize. Autorhythmicity
  • 55.
    Membrane of twocells clearly seen. The spread of ions through gap junctions of the Intercalated discs (I) allows the AP to pass from cell to cell Autorhythmicity • Autorhythmic cells spontaneously depolarize at a given rate, some groups faster, some groups slower. Once a group of autorhythmic cells reaches threshold and starts an action potential (AP), all of the cells in that area of the heart also depolarize.
  • 56.
    Cardiac Conduction • Theself-excitable myocytes that "act like nerves" have the 2 important roles of forming the conduction system of the heart and acting as pacemakers within that system. • Because it has the fastest rate of depolarization, the normal pacemaker of the heart is the sinoatrial (SA) node, located in the right atrial wall just below where the superior vena cava enters the chamber.
  • 57.
    Cardiac Conduction Spontaneous Depolarization ofautorhythmic fibers in the SA node firing about once every 0.8 seconds, or 75 action potentials per minute
  • 58.
    Frontal plane Right atrium Rightventricle Left atrium Left ventricle Anterior view of frontal section Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE1 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE 1 2 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) 1 2 3 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES 1 2 3 4 Right atrium Right ventricle Frontal plane SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE Left atrium Left ventricle Anterior view of frontal section ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES PURKINJE FIBERS 1 2 3 4 5 Right atrium Right ventricle
  • 59.
    • Although anatomicallythe heart consist of individual cells, the bands of muscle wind around the heart and work as a unit – forming a “functional syncytium” . – This allows the top and bottom parts to contract in their own unique way. Coordinating Contractions
  • 60.
    Coordinating Contractions • Theatrial muscle syncytium contracts as a single unit to force blood down into the ventricles. • The syncytium of ventricular muscle starts contracting at the apex (inferiorly), squeezing blood upward to exit the outflow tracts.
  • 61.
    ANS Innervation • Althoughthe heart does not rely on outside nerves for its basic rhythm, there is abundant sympathetic and parasympathetic innervation which alters the rate and force of heart contractions.
  • 62.
  • 63.
    • The actionpotential (AP) initiated by the SA node travels through the conduction system to excite the “working” contractile muscle fibers in the atria and ventricles. • Unlike autorhythmic fibers, contractile fibers have a stable RMP of –90mV. – The AP propagates throughout the heart by opening and closing Na+ and K+ channels. Cardiac Muscle Action Potential
  • 64.
    Depolarization Repolarization Refractory period Contraction Membrane potential(mV) Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 11 Depolarization Repolarization Refractory period Contraction Membrane potential (mV) Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open Plateau (maintained depolarization) due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and K+ outflow when some K+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 11 2 Depolarization Repolarization Refractory period Contraction Membrane potential (mV) Repolarization due to closure of Ca2+ channels and K+ outflow when additional voltage-gated K+ channels open Rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open Plateau (maintained depolarization) due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and K+ outflow when some K+ channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 1 3 1 2 3 Cardiac Muscle Action Potential
  • 65.
    Cardiac Muscle ActionPotential • Unlike skeletal muscle, the refractory period in cardiac muscle lasts longer than the contraction itself - another contraction cannot begin until relaxation is well underway. • For this reason, tetanus (maintained contraction) cannot occur in cardiac muscle, leaving sufficient time between contractions for the chambers to fill with blood. • If heart muscle could undergo tetanus, blood flow would cease!
  • 66.
    The Electrocardiogram • AnECG is a recording of the electrical changes on the surface of the body resulting from the depolarization and repolarization of the myocardium. • ECG recordings measure the presence or absence of certain waveforms (deflections), the size of the waves, and the time intervals of the cardiac cycle. – By measuring the ECG, we can quantify and correlate, electrically, the mechanical activities of the heart.
  • 67.
  • 68.
    1 Depolarization ofatrial contractile fibers produces P wave 0.20 Seconds Action potential in SA node P 1 Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.20 Seconds 0.20 Seconds Action potential in SA node P P 2 1 Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P 2 3 P 1 Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P 2 3 4 P 1 5Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.2 0.40 Seconds 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T 2 3 4 5 P 1 6Ventricular diastole (relaxation) 5Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.2 0.40 0.8 Seconds 0.60.2 0.40 Seconds 0.2 0.40 Seconds 0.2 0.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T P 2 3 4 5 6 P
  • 69.
    • Blood Pressureis usually measured in the larger conducting arteries where the high and low pulsations of the heart can be detected – usually the brachial artery. – Systolic BP is the higher pressure measured during left ventricular systole when the aortic valve is open. – Diastolic BP is the lower pressure measured during left ventricular diastole when the valve is closed. Blood Pressure
  • 70.
    Blood Pressure • NormalBP varies by age, but is approximately 120 mm Hg systolic over 80 mmHg diastolic in a healthy young adult ( in females, the pressures are often 8–10 mm Hg less.) • It is often best to refer to the blood pressure as a single number, called the mean arterial pressure (MAP) . – MAP is roughly 1/3 of the way between the diastolic and systolic BP. It is defined as 1/3 (systolic BP – diastolic BP) + diastolic BP.
  • 71.
    Blood Pressure • Ina person with a BP of 120/80 mm Hg, MAP = 1/3 (120-80) + 80 = 93.3 mm Hg. • In the smaller arterioles, capillaries, and veins, the BP pulsations are not detectable, and only a mean BP is measurable (see the purple and blue areas of this figure).
  • 72.
    Cardiac Cycle • Thecardiac cycle includes all events associated with one heartbeat, including diastole (relaxation phase) and systole (contraction phase) of both the atria and the ventricles. • In each cycle, atria and ventricles alternately contract and relax. – During atrial systole, the ventricles are relaxed. – During ventricle systole, the atria are relaxed.
  • 73.
    Cardiac Cycle • Sinceventricular function matters most to the body, the two principal events of the cycle for us to understand are ventricular filling (during ventricular diastole), and ventricular ejection (during ventricular systole). – The blood pressure that we measure in the arm is a reflection of the pressure developed by the left ventricle, before and after left ventricular systole. – Pulmonary blood pressure is a result of right ventricular function, but is not easily measured.
  • 74.
    Cardiac Cycle Valves AV SLOutflow Ventricular diastole Open Closed Atrial systole Ventricular systole Closed Open Early atrial diastole Ventricular diastole Open Closed Late atrial diastole
  • 75.
    Cardiac Cycle • Duringthe cardiac cycle, all 4 of the heart valves have a chance to open and close. Listening (usually with a stethoscope) to the sounds the heart makes is called auscultation. • Valve opening is usually silent. The “lubb dupp” we associate with heart auscultation is produced by valve closure (in pairs – see p. 740 left side).
  • 76.
  • 77.
    Cardiac Cycle • Theaverage time required to complete the cardiac cycle is usually less than one second (about 0.8 seconds at a heart rate of 75 beats/minute). – 0.1 seconds – atria contract (atrial “kick”), ventricles are relaxed – 0.3 seconds – atria relax, ventricles contract – 0.4 seconds – relaxation period for all chambers, allowing passive filling. When heart rate increases, it’s this relaxation period that decreases the most.
  • 78.
    Cardiac Output • Thestroke volume (SV) is the volume of blood ejected from the left (or right) ventricle every beat. The cardiac output (CO) is the SV x heart rate (HR). – In a resting male, CO = 70mL/beat x 75 beats/min = 5.25L/min. • On average, a person’s entire blood volume flows through the pulmonary and systemic circuits each minute.
  • 79.
    Cardiac Output • Thecardiac reserve is the difference between the CO at rest and the maximum CO the heart can generate. – Average cardiac reserve is 4-5 times resting value. • Exercise draws upon the cardiac reserve to meet the body’s increased physiological demands and maintain homeostasis.
  • 80.
    Cardiac Output • Thecardiac output is affected by changes in SV, heart rate, or both. • There are 3 important factors that affect SV – The amount of ventricular filling before contraction (called the preload) – The contractility of the ventricle – The resistance in the blood vessels (aorta) or valves (aortic valve, when damaged) the heart is pumping into (called the afterload)
  • 81.
    Cardiac Output • Themore the heart muscle is stretched (filled) before contraction (preload), the more forcefully the heart will contract. This phenomenon is known as Starling’s Law of the heart. – Stimulation of the sympathetic nervous system during exercise increases venous return, stretches the heart muscle, and increases CO.
  • 82.