[PHYSIO]-LC12-Cardiac Muscle_ The Heart as a Pump and Function of the Heart Valves.docx.pdf

A. COMPONENTS AND FUNCTIONS Heart – pumps blood to maintain circulation OUTLINE...

A. COMPONENTS AND FUNCTIONS Heart – pumps blood to maintain circulation OUTLINE Blood Vessels ○ Arteries – carry blood away from the heart I. OVERVIEW ○ Veins – carry blood back to the heart A. Components and Functions Capillaries – where diffusion happens; enable exchange B. Heart as a Double Pump between the tissues and vascular channels II. STRUCTURES OF THE HEART ○ different functions of your circulatory system III. LAYERS OF THE HEART WALL happen mainly in the capillaries where there is IV. PHYSIOLOGY OF CARDIAC MUSCLES exchange of substances. V. CARDIAC MUSCLE IS A SYNCYTIUM Blood – vehicle that carries oxygen and nutrients essential to VI. THE CARDIAC MYOCYTE cell function. A. Transverse Tubular System B. Sarcoplasmic Reticulum B. HEART AS A DOUBLE PUMP C. Sarcomere: Contraction unit Double pump because it consists of two parallel circulation. i. Excitation-Contraction Coupling The heart is actually two separate pumps: RIGHT and LEFT ii. Cardiac Muscle Relaxation iii. Cardiac Muscle Contraction RIGHT HEART that pumps through the lungs VII. THE CARDIAC CYCLE the right side of the heart, which consists of: right atrium and right A. Periods of Cardiac Cycle ventricle B. Phases of Cardiac Cycle o pumps blood through the lungs (which would make up VIII. MECHANICAL EVENTS OF CARDIAC CYCLE your pulmonary circulation) where exchange of gasses A. Atrial Systole would take place. Oxygen would get in, carbon dioxide B. Isovolumetric Contraction would get out, and then it would oxygenate the blood and C. Rapid Ejection move into the left part of your heart D. Reduced Ejection E. Isovolumetric Relaxation LEFT HEART that pumps blood through the systemic circulation F. Rapid Ventricular Filling left part of your heart which is made up of: left atrium and left G. Reduced Ventricular Filling ventricle. H. Effect of Heart Rate o These chambers carry oxygenated blood for circulation to IX. ATRIA: PRIMER PUMPS the different parts of their organs. (which is systemic X. ATRIAL PRESSURE CURVE circulation). XI. AORTIC PRESSURE CURVE o metabolism would take place. XII. LV VOLUME CURVE o The oxygen would be delivered, carbon dioxide would be XIII. THE CARDIAC OUTPUT collected and the veins would now be carrying XIV. MYOCARDIAL CONTRACTILITY deoxygenated blood returning it back to the right part of XV. REGULATION OF HEART PUMPING the heart. XVI. REGULATION OF CARDIAC CYCLE XVII. STRUCTURE OF THE HEART The circulatory system consists of Parallel Sub-circuits and has Unidirectional XVIII. HEART SOUNDS Flow So basically it's parallel circulation consisting of two pumps: the right side and the left side. I. OVERVIEW That is why in your physical diagnosis later on, right sided heart failure would have different symptoms compared to your left sided heart failure. Functions of the Cardiovascular System Circulate blood throughout entire body for: Types of circulation Transport of oxygen to cells Systemic Circulation – brings blood to and from the body Transport of CO2 and other wastes (metabolic Pulmonary Circulation – brings blood to and from the lungs byproduct) away from cells Transport of nutrients (glucose) to cells Movement of immune system components (cells, antibodies) to fight infection Transport of endocrine gland secretions Participate in Homeostatic mechanisms: Regulates body temperature Helps stabilize pH and ionic concentration of body fluids Blood also plays a very important role in your immune system, in your endocrine glands, and the role of temperature and your acidic pH and ionic concentration of your body fluids basically by a renal function. So there are components of your circulatory system which we call the heart - the vascular system, which is made up of your heart Figure 1. Systemic and Pulmonary Circulation Page 1 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo II. STRUCTURES OF THE HEART If you're going to dissect the heart, You can see four chambers, two upper chambers, which we call the atria, the left atrium and the right atrium. The lower chambers would be called your ventricles, which will have left ventricle and right ventricle. CHAMBERS and SEPTUM Chambers Atria - (2) upper chambers Figure 3. Right ventricle, irregular shaped mainly triangular, and the left Thin walled ventricle which has a thicker wall. Receive blood from veins Send blood to ventricles since the left ventricle is the one that pumps circulation to the systemic circulation it is thicker, as compared to Ventricles (2) lower chambers your right atrium. And your right atrium is irregularly Thick walled (thicker walled because there will be pumping blood shaped mainly triangular, whereas the left ventricle is away from the heart: main function used as pumps) conical and circular. Receive blood from atria Pump blood out through arteries Anatomical Landmarks: HEART (heart occupies on the chest) Left ventricle is thicker compared to the right Pumping blood to greater distances = thicker walls VALVES: Left ventricle is usually conical while the right ventricle is slightly prevent backflow of blood off centered keep blood moving in one direction they would guide the flow of blood into one direction; they are Septum located between chambers and the junction of arteries. So there Wall that divides heart into right and left halves are two types. between the two atria and the two ventricles would be a septum Locations: Some congenital anomalies would prevent the closure of septum Between the chambers and they may produce septal defects. It turns into defects or At junctions of artery and chamber ventricular septal defects. 1. Atrio-Ventricular Valves: Those located between chambers are what we call atrioventricular valves. Mitral Valve (left), Tricuspid Valve (right) On the left we have the mitral valve and on the right we have the tricuspid valve. 2. Semilunar Valves: The semilunar valves are those which are located between the chamber and an artery. Aortic Valve, Pulmonic Valve Aortic valve located between the left ventricle and aorta Pulmonic valve which is located between the right ventricle and the pulmonic valve. Figure 2. The heart showing the atrium and ventricles, with the septum in between the ventricles. Table 1. Brief summary of the difference of the right and left ventricle. Figure 4. Valves as seen from above. If we're going to dissect further left and right ventricles, we can find two important structures which are essential for contraction and prevention of the inversion of your bulbs. So you have your chordae tendineae, which are called your heart strings, they are called cord like and they connect the Page 2 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo atrioventricular valves into the papillary muscles and they function to prevent the inversion of valves during contraction. Internal Structures: Ventricles Chordae Tendineae ○ ”Heart strings” ○ Cord-like tendons ○ Connect papillary muscles to tricuspid and mitral valves ○ prevent inversion valve Papillary muscles ○ small muscles that anchor the cords ○ the papillary muscles are those small muscles that would hold chordae tendineae to prevent the Figure 7. Layers of the heart wall. inversion of your valves during ventricular contraction. Epicardium: (most superficial layer) visceral layer of serous pericardium This is where your blood vessels are. That's why I had mentioned earlier the coronary arteries are also called epicardial arteries because of their location. Myocardium: (middle layer) Muscle of the heart The layer that ‘contracts’ the thick structure here is myocardium, which contains heart muscles. they function for contraction Endocardium: (inner layer) Lines the chambers of the heart (Endothelial cells) Prevents clotting of blood within the heart Forms a barrier between the Oxygen hungry myocardium and the blood. (blood is supplied via the Figure 5. Chorda tendineae coronary system) So we already know that blood doesn't diffuse directly into the myocardium. They also need a blood or blood supply which we call your coronary system. Three types of circulation: 1. Systemic Circulation 2. Pulmonary Circulation 3. Coronary Circulation - a mini-circulation of your heart Clinical Correlation: - Endocarditis – inflammation of the endocardium (e.g. Bacterial Endocarditis) - Myocarditis – inflammation of the myocardium - Epicarditis – inflammation of the epicardium IV. PHYSIOLOGY OF CARDIAC MUSCLES Figure 6. The structures of the heart. muscles which are responsible for contraction The type of muscle cells that can be found in myocardium is divided into two major types: we have the contractile muscle fibers and we have the III. LAYERS OF THE HEART WALL excitatory and conductive muscle fibers. TYPES OF CARDIAC MUSCLES Deeper into the layers of your heart wall, the outermost layer is your Contractile muscle fibers (99% of myocardium) epicardium, it is actually an extension of your pericardium, the visceral ○ located in the atrium and the ventricles. layer of the serous layer pericardium was actually your epicardium. ○ Atrial muscle fibers and Ventricular muscle fibers both contract same as in skeletal muscle Except duration of contraction much longer than the skeletal muscle They both function for muscle contraction and are very much similar to skeletal muscles, only with some difference such as the duration of contraction. for these heart muscles are longer compared to the skeletal muscles. Page 3 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Excitatory and Conductive muscle fibers (autorhythmic: 1%) Within intercalated discs there are two types of junctions: ○ few contractile fibrils Desmosomes ○ exhibit either automatic rhythmic discharge (AP), or Gap junctions conduction of the AP through the heart ○ They do not function for contraction, thus they allow action potential to spread from one cell to adjacent cells contain only a few contractile fibers. ○ function as the spread your action potential ○ The main function is to produce your action from one cell to the other for a faster spread potential. They are capable of producing your of action potentials automatic rhythmic discharge known as your action potential and for the conduction of your action potential of the heart. Figure 10. Intercalated discs as shown in a histologic preparation (a) and the gap Figure 8. The ventricular myocardium and purkinje fibers. junction and desmosomes as illustrated in (b) CARDIAC MUSCLE CELL: MYOCYTE V. CARDIAC MUSCLE IS A SYNCYTIUM Characteristics: Striated Short branched cells When one cardiac cell undergoes an action potential, the electrical impulse Uninucleate spreads to all other cells that are joined by gap junctions so they become Presence of: excited and contract as a single functional syncytium (theoretically, an ion ○ Intercalated discs inside the SA nodal cell could travel throughout the heart via the gap junctions) they have a distinct striation ○ it's a single functional sensation. because of the presence of your ○ unlike in skeletal muscle, individual muscles can contract intercalated disc ○ a syncytium - would contract in a single entity because of the presence ○ T-tubules (larger and over z-discs) of your gap junctions occupy over z lines ○ Because of the gap junctions, theoretically the ion from the SA node can essential for muscle contraction traverse through the heart by these different gap junctions facilitating Which makes faster transmission of action transmission of action potentials. potential from one cell to another 2 FUNCTIONAL SYNCYTIUM: Atrial syncytium ○ meaning the atrium, left and right, would contract simultaneously and when they relax, it's time for the ventricles to contract — also your ventricular syncytium Ventricular syncytium ○ left and the right ventricles would contract as a single unit. essential for the effectiveness of the heart as a pump so that it would be able to effectively pump the blood that is essential for circulation. Figure 9. Myocyte showing the intercalated discs. HISTOLOGIC PROPERTIES OF CARDIAC MUSCLES Exhibit branching Adjacent cardiac cells are joined end to end by specialized structures known as intercalated discs Page 4 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Figure 13. Structure of a myocyte. SARCOLEMMA (sarco = flesh; lemma = thin husk) Figure 11. Action potential crossing through the gap junctions in the Each myocyte is bounded by a complex cell membrane intercalated discs. Composed of a lipid bilayer- impermeable to charged molecules (barrier to diffusion) MYOFIBER (Muscle Tissue) ○ Hydrophilic heads and hydrophobic tails A group of myocytes held together by surrounding collagen Contains membrane proteins, which include receptors, pumps connective tissue and channels through which ions would pass through specifically Excess collagen may cause LV diastolic dysfunction (e.g left the calcium which is essential for your muscle contraction - ventricular hypertrophy) - No relaxation contribute to overall calcium levels within the myocyte ○ significance of this clinically is that in some instances ○ play a role in the spread of your action potential and when we have left ventricular hypertrophy as in the in regulating the inflow and outflow of your ions case of hypertensive cardiovascular diseases, we during muscle contraction or action potentials have excess collagen which will now inhibit relaxation of your muscles and they would now cause your LV diastolic dysfunction because of your excess collagen. Figure 14. Sarcolemma containing receptors, pumps, and channels. TRANSVERSE TUBULAR SYSTEM- “T-Tubules” actually invaginations of your sarcolemma. function as extensions of your sarcolemma into the cell The sarcolemma of the myocyte invaginates to form an extensive tubular network Extend the extracellular space into the interior of the cell Transmit the electrical stimulus rapidly The main purpose is to transmit electrical impulses Figure 12. Structure of the myofiber. simultaneously while actual potential is in the sarcolemma. It can also be transmitted inside the cell via the T tubules. VI. THE CARDIAC MYOCYTE INDIVIDUAL PROPERTIES (1 myocyte) 10-20 um in diameter 50-100 um long Figure 15. T-tubules encircled in green. Page 5 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo SARCOPLASMIC RETICULUM (SR) A fine network spreading throughout the myocytes demarcated by its lipid bilayer Close apposition to the T tubules Also demarcated by a lipid bilayer. Very much similar to sarcolemma and T tubules Role: RELEASE AND UPTAKE of calcium during contraction and relaxation Figure 17. Calcium storage via the JSR and calcium uptake via the LSR. MITOCHONDRIA Generate the energy in the form of adenosine triphosphate (ATP) in muscle contraction, you need a battery or an energy this is generated by your mitochondria Figure 16. Sarcoplasmic reticulum during release and uptake of calcium. Maintain the heart's contractile function and the associated ion gradients SARCOPLASMIC RETICULUM (SR): TYPES there are two types of sarcoplasmic reticulum 1. JUNCTIONAL SR aka “Subsarcolemmal Cisternae” bulbous extension of your sarcoplasmic reticulum The tubules of the SR expand into bulbous swellings Contains a store of calcium ions (They function as calcium storage.) ○ During actual potential activation, the calcium that is stored here would be released when the ryanodine receptor or calcium release channels are activated. Release calcium from the calcium release channel (ryanodine receptor) to initiate the contractile cycle ○ So when they are activated open, the calcium will be released into the cytosol via your ryanodine receptors. ○ calcium will now be available for muscle contraction. Figure 18. The mitochondria. 2. LONGITUDINAL SR Network SR The heart has two ways of producing your ATP via oxidation of your glucose Consists of ramifying tubules and beta-oxidation of your fatty acids. Concerned with the uptake of calcium that initiates relaxation Glucose oxidation ○ main function is to uptake the calcium that Provides 10% to 30% of energy has been used during contraction, so uptake More O2-efficient pathway. of calcium during relaxation, via SERCA or ATP/O2=6.4 your sarcoplasmic endoplasmic reticulum producing more molecules of ATP per molecule of oxygen. calcium ATPase Achieved by the ATP- requiring calcium pump (SERCA= Beta-oxidation sarcoendoplasmic reticulum Calcium ATPase) Provides 70% to 90% of energy ○ so calcium will now enter in back into the Consumes more O2 than glucose pathway sarcoplasmic reticulum via SERCA during ATP/O2= 5.6 relaxation and they are now stored in your the major pathway is beta oxidation of fatty acids, which provide junctional SR 70 to 90% of the energy of the heart. ○ goes into your junctional sarcoplasmic reticulum ready to be used again when REMEMBER: the glucose pathway is more efficient, but predominant another action potential happens. So the pathway is the fatty acid pathway cycle continues. REMEMBER: Clinical Correlation: During Ischemia, glucose oxidation is compromised, ○ Junctional sarcoplasmic reticulum stores your calcium, thus, greater oxygen consumed ○ Longitudinal SR would uptake your calcium. Trimetazidine: Drug that inhibit Beta Oxidation during Ischemia Page 6 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Figure 19. Glucose oxidation vs Beta Oxidation SARCOMERE Basic contractile unit within the myocyte Refers to the unit from one Z band to the next Resting length: 1.8-2.4 um Figure 22. The Sarcomere and its filaments. Composed of interdigitating filaments ○ Thick filament- myosin protein The Cardiac Muscle Contraction ○ Thin filament- actin protein Excitation-Contraction Coupling Refers to the mechanism by which the action potential causes the myofibrils of muscle to contract (similar to your Skeletal muscles) (the cells of the heart are excitable and generate action potentials → initiate contraction) To differentiate from the skeletal muscles, the cells of the heart are excitable (remaining one percent) and can generate their own action potentials to initiate contraction by themselves without external force like your nervous system. Differences from skeletal muscle mechanism: (have important effects on the characteristics of heart muscle contraction) Sources of calcium ions that are release into the sarcoplasm 1. Sarcoplasmic reticulum 2. T-tubules Figure 20. Sarcomere showing the interdigitating filaments containing the thin Excitation-Contraction Coupling (Step by step) and thick filaments. 1. Starts with CICR (Calcium induced Calcium release) - AP (action potential) spreads along sarcolemma - T-tubules contain voltage gated L-type calcium channels which open upon depolarization - Calcium entrance into myocardial cell and opens RyR (ryanodine receptors) Calcium release channels - Release of Calcium from SR causes a Calcium “spark” - Multiple sparks form a Calcium signal The first major step starts with your calcium induced calcium release. So action potential spreads in the sarcolemma. Okay, and then the sarcolemma invaginates to your T-tubules, action potential also goes to your t-tubules, which would now open your L type calcium channels, and the L type calcium channels will allow the entry of your calcium into your sarcoplasm. Figure 21. The Sarcomere Contractile Unit. T: T tubules; Mit: Mitochondria; G: As the calcium enters the sarcoplasm it will initiate further release of Glycogen; Z line: the actin filaments are attached; I: band of actin filaments, titin calcium by activating your ryanodine receptors. and Z line; A: band of actin-myosin overlap; H: clear central zone containing only in the sarcoplasmic reticulum, now containing your ryanodine receptors, myosin will open up and release also the stored calcium within them. So calcium from extracellular fluid and calcium from the sarcoplasmic reticulum will now produce your calcium sparks and if this would now Sarcomere and its Filament eventually lead to your cardium signal which would interact with your Muscle contraction consists of interaction between your myocytes myosin and actin for contraction. myosin and actin Page 7 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Figure 23. Excitation-Contraction Coupling mechanism Step 1. Figure 25. Cardiac muscle relaxation. 2. Calcium signal (calcium from SR and ECF) binds to troponin Cardiac Muscle Contraction and Relaxation: Summary of Calcium Flow to initiate myosin head attachment to actin so the calcium signal that is generated binds to the calcium and initiates myosin head attachment. So the calcium now that is within the cytosol would now activate your troponin. To initiate the attachment of your actin and myosin. the thin filaments would slide in white between the thick filaments producing a shortening of your sarcomere manifested as your heart contraction. When contraction is done, and relaxation starts, calcium is released from their attachment Figure 26. Cardiac muscle contraction and relaxation summary. REMEMBER: shortening of the sarcomere leads to contraction and lengthening of the sarcomere leads to relaxation What is the difference between the contraction of your skeletal muscle and the contraction of your heart muscles? You learned that in skeletal muscle contraction sarcomeres follow the all or nothing principle however, for cardiac muscles, sarcomeres do not follow the all or nothing principle because response of the muscles are graded. It is dependent on the amount of calcium that is available. Figure 24. Excitation-Contraction Coupling mechanism Step 2. More calcium = more interaction = more forceful contraction Cardiac Muscle Relaxation - Calcium is transported back into the SR (via SERCA) - Calcium is transported out of the cell by a facilitated Na+/Ca2+ exchanger (NCX) - As ICF Ca2+ levels group, interactions between myosin/actin are stopped - Sarcomere lengthens - Some of the calcium enters back your sarcoplasmic reticulum via SERCA and they are now going to be stored there for a while before the next action potential. Some of the calcium leaves out the cell, goes out extracellularly via NCX or your sodium calcium exchanger. So less calcium less interaction in the myosin there will be longer lengthening of your sarcomere it will now manifest as relaxation. Figure 27. Muscle contraction (shortening) Page 8 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo CARDIAC MUSCLE CONTRACTION tetanus, via repeated stimulation. Cardiac muscle CANNOT Same as skeletal muscle, but strength of contraction varies sum action potentials or contractions and cannot be ○ Sarcomeres are not “all or none” as it is in skeletal muscle tetanized. The response is graded! Low levels of cytosolic Ca2+ will not activate as many myosin/actin interactions and the opposite is true It is dependent on the amount of calcium that is available. More calcium = more interaction = more forceful contraction Less calcium = less interaction = less forceful contraction ○ Length tension relationships exist Strongest contraction generated when stretched between 80% & 100% of maximum (physiological range) The longer the length = more tension build up = stronger contraction The optimum stretch or length (physiologic) that could lead to the strongest contraction of cardiac muscle would be when it is stretched 80-100% of its maximum, beyond that it would fail. Figure 30. Refractory period between skeletal muscle and cardiac muscle. ○ What causes stretching? The filling of chambers with blood (more blood pumped into the left ventricle = stretch and produce greater tension) VII. THE CARDIAC CYCLE The cardiac events that occur from the beginning of one heartbeat to the beginning of the next The pressure, volume and electrical changes that occur in a functional heart between successive heart beats. WIGGERS DIAGRAM: - Coordination of: - Pressure changes in Aorta, Left Ventricle, Left Atria - Left Ventricular Volume Changes (how much volume is contained in the left ventricle during the different periods of the cycle) - Electrical Changes (ECG) Figure 28. The relationship between the initial sarcomere length and the tension - Cardiac Valves (Heart Sounds) of skeletal and cardiac muscle. CARDIAC MUSCLE REFRACTORY PERIOD ○ Long refractory period (250 msec) compared to skeletal muscle (3 msec) ○ During this period membrane is refractory to further stimulation until contraction is over ○ It lasts longer than muscle contraction, prevents tetany (if the heart beats very fast, it would lose its pumping action) ○ Gives time for heart to relax after each contraction, prevents fatigue ○ It allows time for the heart chambers to fill during diastole/relaxation before next contraction Figure 31. Wigger’s Diagram Figure 29. Refractory period A. Periods of Cardiac Cycle Period of relaxation is termed diastole. AP in skeletal muscle: 1-5 msec Period of contraction is termed systole. AP in cardiac muscle: 200-300 msec – Atrial systole: when atria contract ○ The refractory period is short in skeletal muscle, but very long – Ventricular systole: when ventricles contract in cardiac muscle. ○ This means that skeletal muscle can undergo summation and Page 9 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Ventricular Systole - 1/3 of the cardiac cycle - Contraction of the ventricles Ventricular Diastole - 2/3 of the cardiac cycle - Relaxation and filling of the ventricles (Ventricular) Systole is the period of chamber contraction and blood ejection which corresponds to: - the period between the closure of the mitral/tricuspid valves and the closure of the aortic/pulmonic valves - the period between the QRS complex and the end of the T wave (Ventricular) Diastole is the period of chamber relaxation and cardiac filling which corresponds to: - The period during which the mitral valve/tricuspid valves are open - The period between the end of the T wave and the end of the PR interval Figure 33. Phases of the Cardiac Cycle. VIII. MECHANICAL EVENTS OF THE CARDIAC CYCLE Figure 32. Ventricular Systole and Diastole. B. Phases of Cardiac Cycles Figure 34. Phases of the Cardiac Cycle: In general, seven basic cardiac cycle phases are recognized: a. Atrial contraction causes increased atrial and ventricular pressure. b. Mitral valve closes (1st heart sound), isovolumetric contraction Systolic phases: begins. Isovolumetric contraction c. Aortic valve opens, aortic pressure equals LV pressure. Early ventricular systole: Rapid Ejection d. Systolic pressure Late ventricular systole: Reduced Ejection e. Aortic valve closes (2nd heart sound), isovolumetric relaxation begins f. Mitral valve opens Diastolic phases: Isovolumetric relaxation Phases of the Cardiac Cycle Early ventricular diastole: Rapid Filling Late ventricular diastole: Reduced Filling(Diastasis) A. ATRIAL SYSTOLE (End of Ventricular Diastole) Atrial systole Prior to atrial systole, blood (about 70%) has been flowing passively from the atrium into the ventricle through the open AV valve. CONTRACTION of ATRIA: intraATRIAL PRESSURE increases Blood pushed into ventricle through open AV Valves (about 20-30%) Atrial contraction is complete before the ventricle begins to contract. The "a" wave occurs when the atrium contracts, increasing atrial pressure (yellow). (Refer to figure 35) Page 10 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo ○ Blood arriving at the heart cannot enter the CONTRACTING atrium so it flows back up the jugular vein, causing the first discernible wave in the jugular venous pulse. Atrial pressure drops when the atria stop contracting. Figure 38. Isovolumetric Contraction. Pressure and Volumes (Refer to Figure 38) The AV valves close when the pressure in the ventricles (red) exceeds the pressure in the atria (yellow). Figure 35. Contraction of Atria. As the ventricles contract isovolumetrically -- their volume does not change (white) -- the pressure inside increases (red), approaching the ECG pressure in the aorta and pulmonary arteries (green). An impulse arising from the SA node results in depolarization and Ventricular pressure RISES but volume stays CONSTANT! contraction of the atria (the right atrium contracts slightly before the left atrium). ECG (Refer to Figure 39) The P wave is due to this atrial depolarization. The beginning of this phase corresponds with the peak of the R wave The PR segment is electrically quiet as the depolarization proceeds to This corresponds to Phase 0 (rapid sodium influx) of the ventricular the AV node. myocyte action potential This brief pause before contraction allows the ventricles to fill The QRS complex is due to ventricular depolarization, and it marks completely with blood. the beginning of ventricular systole. It is so large that it masks the underlying atrial repolarization signal. Figure 36. Contraction of Atria as seen in the ECG. Heart Sounds Figure 39. Isovolumetric Contraction as seen on ECG. A fourth heart sound (S4) is abnormal and is associated with the end of atrial emptying after atrial contraction. Heart Sounds It occurs with hypertrophic congestive heart failure, massive The first heart sound (S1, "lub") is due to the closing AV valves. pulmonary embolism, tricuspid incompetence, or cor pulmonale. At end of this stage, LV volume is HIGHEST = End Diastolic Volume (EDV) – approximately 130 ml Figure 40. First heart sound due to closing of AV valves. C. RAPID EJECTION (Early Ventricular Systole) The semilunar (aortic and pulmonary) valves open at the beginning Figure 37. Abnormal fourth heart sound. of this phase. This period corresponds to Phase 2 (plateau, rapid calcium influx) of B. ISOVOLUMETRIC CONTRACTION (Beginning of Ventricular Systole) the cardiac myocyte action potential The atrioventricular (AV) valves close at the beginning of this phase. Mechanically, ventricular systole is defined as the interval between the closing of the AV valves (mitral and tricuspid valves) and the closing of the semilunar valves (aortic and pulmonary valves). ALL VALVES CLOSED! Figure 41. Rapid Ejection Page 11 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Pressure and Volumes (Refer to Figure 41) ECG While the ventricles continue contracting, the pressure in the The end of this period corresponds to the peak of the T wave on the ventricles (red) exceeds the pressure in the aorta and pulmonary surface ECG arteries (green); the semilunar valves open, blood exits the This corresponds to Phase 3 (repolarisation) of the cardiac myocyte ventricles, and the volume in the ventricles decreases rapidly (white). action potential The "c" wave of atrial pressure is not normally discernible in the The T wave is due to ventricular repolarization. The end of the T jugular venous pulse. wave marks the end of the ventricular systole electrically. Right ventricular contraction pushes the tricuspid valve into the atrium and increases atrial pressure, creating a small wave into the jugular vein. It is simultaneous with the carotid pulse. ECG On the surface ECG, the end of this phase corresponds to the beginning of the T wave Electrically, ventricular systole is defined as the interval between the Figure 45. Reduced Ejection as seen on ECG QRS complex and the end of the T wave (the Q-T interval). Heart Sounds No Heart sounds Figure 42. Rapid Ejection as seen on ECG Heart Sounds Heart sounds: None (Normal) Figure 46. Heart sounds in Reduced Ejection Systolic murmurs of stenotic semilunar valves Systolic murmurs of regurgitant AV valves E. ISOVOLUMETRIC RELAXATION (Beginning of Ventricular Diastole) At the beginning of this phase the AV valves are closed. The "v" wave is due to the backflow of blood after it hits the closed AV valve. It is the second discernible wave of the jugular venous pulse. Figure 43. Heart sounds in Rapid Ejection D. REDUCED EJECTION (Late Ventricular Systole) At the end of this phase the semilunar (aortic and pulmonary) valves CLOSE. When the pressure in the ventricles falls below the pressure in the arteries, blood in the arteries begins to flow back toward the ventricles and causes the semilunar valves to close. This marks the end of the ventricular systole mechanically. Figure 47. Isovolumetric Relaxation Pressure and Volume (Refer to Figure 47) The pressure in the ventricles (red) continues to drop. Ventricular volume (white) is at a minimum and is ready to be filled again with blood. ECG This period corresponds to the end of the T wave on the surface ECG, and the end of Phase 3 of the action potential No Deflections on ECG Figure 44. Reduced Ejection Pressure and Volumes (Refer to Figure 44) After the peak in ventricular and arterial pressures (red and green), blood flow out of the ventricles decreases and ventricular volume decreases more slowly (white). At the end of this phase, Ventricle volume is LOWEST but never fully Figure 48. Isovolumetric Relaxation as seen on ECG empty: End Systolic Volume (ESV) – amount of blood left in ventricles Heart Sounds (about 50 ml) The second heart sound (S2, "dup") occurs when the semilunar (aortic and pulmonary) valves close. Page 12 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo S2 is normally split because the aortic valve closes slightly earlier than the pulmonary valve. Figure 49. Second heart sound due to the closing of the semilunar valves F. RAPID VENTRICULAR FILLING (Early Ventricular Diastole) Ventricles relax → Ventricular pressure falls below Atrial Pressure → Figure 53. Reduced Ventricular Filling AV valves OPEN Once the AV valves open, blood that has accumulated in the atria Pressure and Volumes (Refer to Figure 53) flows rapidly into the ventricles. Ventricular volume (white) increases more slowly now. The ventricles continue to fill with blood until they are nearly full Ventricular and atrial pressures equilibrate and the atria act as passive conduits for ventricular filling ECG No Deflections on ECG The end of this phase corresponds to the end of the P-wave on the surface ECG Figure 50. Rapid Ventricular Filling Pressure and Volumes (Refer to Figure 50) Figure 54. Reduced Ventricular Filling as seen on ECG Ventricular volume (white) increases rapidly as blood flows from the atria into the ventricles. Heart Sounds 80% of the ventricular end-diastolic volume is achieved during this No Heart sounds phase Coronary blood flow is maximal during this phase ECG No Deflections on ECG Figure 55. Heart sounds in Reduced Ventricular Filling Effect of Heart Rate The total duration of the cardiac cycle is the reciprocal of the heart rate Heart rate increases → duration of each cardiac cycle decreases! Figure 51. Rapid Ventricular Filling as seen on ECG (including the contraction and relaxation phases) The duration of the action potential and the period of contraction Heart Sounds (systole) decrease A third heart sound (S3) is usually abnormal and is due to rapid NOT by as great a percentage as does the relaxation phase (diastole) passive ventricular filling. It occurs in dilated congestive heart failure, severe hypertension, At a normal heart rate of 72 beats/min: myocardial infarction, or mitral incompetence. systole comprises about 0.4 of the entire cardiac cycle At three times the normal heart rate: systole is about 0.65 of the entire cardiac cycle This means that the heart beating at a very fast rate does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction Figure 52. Abnormal third heart sound due to rapid ventricular filling Note: Review again the Rhythmical Excitation of the Heart for its relationship with ECG. G. REDUCED VENTRICULAR FILLING (Diastasis) Rest of blood that has accumulated in the atria flows slowly into the IX. ATRIA: PRIMER PUMPS ventricles. The atria simply function as primer pumps that increase the ventricular pumping effectiveness as much as 20 percent Page 13 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Blood normally flows continually from the great veins into the atria: about 80 percent of the blood flows directly through the atria into the ventricles even before the atria contract atrial contraction usually causes an additional 20 percent filling of the ventricles The heart can continue to operate without this extra 20 percent effectiveness: because it has the capability of pumping 300 to 400 percent more blood than is required by the resting body when the atria fail to function, the difference is unlikely to be noticed unless a person exercises Then acute signs of heart failure occasionally develop, especially shortness of breath. X. ATRIAL PRESSURE CURVE Figure 58. Graph showing atrial contraction simultaneously with right ventricular contraction and the pressure exerted. Events in the left atrium: XI. AORTIC PRESSURE CURVE Pressure in the aorta varies with the cardiac cycle Two pressure readings: Systolic blood pressure = maximum pressure ○ peak pressure reached during the systole of the left ventricle (90-140 mmHg) ○ Due to ejection of blood into aorta Diastolic blood pressure = minimum pressure ○ remaining pressure at the beginning of the diastole of the left ventricle (50-90 mmHg) ○ Not zero due to elastic recoil of aorta Figure 56. Atrial pressure curve Normal BP: 120/80 mm Hg a wave - responds to the atrial contraction Higher than normal = hypertension x descent - represents left ventricular contraction Lower than normal = hypotension v wave - represents the backpressure from pulmonary blood flow y descent - represents opening of the mitral valve, releasing the Dicrotic notch shows semilunar valves closing (INCISURA) volume within the chamber - Incisura - short period of backward flow of blood immediately before closure of the valve, followed by a sudden cessation of the backflow. Right Atrial Pressure (RAP) = Central Venous Pressure (CVP) When the valves are open - systole When the valves are closed - diastole a wave - atrial contraction Dicrotic notch represents the 2nd heart sound Right atrial pressure - 4-6 mmHg Left atrial pressure - 7-8 mmHg c-wave - when the ventricles begin to contract; mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles caused partly by slight backflow of blood into the atria v-wave - toward the end of ventricular contraction; it results from slow flow of blood into the atria from the veins while the A-V valves are closed when the A-V valves open, this stored atrial blood flow rapidly into the ventricles causing the v wave to disappear Figure 59. Aortic pressure compared to ventricular pressure and the aortic valve opening and closing. Figure 57. Atrium with its valves during contraction. Page 14 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Clinical Measurement of the Arterial Blood Pressure (BP) Figure 62. LV volume curve showing stroke volume. The difference between the End Systolic Volume (ESV) and End Diastolic Volume (EDV) is what we call your Stroke Volume. How much blood had been ejected in the left ventricle during the contraction. The difference between how much was there and how much is left during contraction. LV VOLUME Curve Parameters Figure 60. Measurement of Arterial Blood Pressure. SV (stroke volume) ○ Volume of blood ejected by each ventricle with each Mean Arterial Pressure (MAP) heartbeat. Average blood pressure in aorta (pressure required to perfuse brain, ○ 70-80 mL coronary arteries and kidneys with blood) EF (ejection fraction) MAP = CO x TPR ○ Stroke volume express in percentage ○ CO - Cardiac Output ○ Percentage of the LVEDV that is ejected from the ventricle ○ TPR - Total Peripheral Resistance with each heartbeat ○ 60-80% Pulse pressure (PP) = SBP-DBP ○ EF = SV/LVEDV x 100 (SBP - systolic blood pressure; DBP - diastolic blood pressure) ○ Measure of effectiveness of ventricular contraction. Difference between SBP and DBP ○ Sometimes, when we say cardiac failure, when there is a Force the heart generates when it contracts decrease in ejection fraction. Use SP, DP, and PP as indicators of cardiovascular health CO (cardiac output) ○ Volume of blood ejected per minute ○ 5-6 L/min ○ CO = HR x SV ○ how much heart rate in 1 minute. CI (Cardiac Index) ○ Cardiac Output in relation to body surface area ○ Cardiac Output / Body Surface Area ○ 4.2 - 3.3 L/m2 Figure 61. Systolic and diastolic blood pressure timing with mean pressure. MAP = (1/3 Pulse Pressure) + DBP MAP = (1/3 [SBP-DBP]) + DBP MAP = (SBP+2[DBP])/3 XII. LV VOLUME CURVE LVEDV/EDV (Left Ventricular End Diastolic Volume) Total volume of blood in the left ventricle at the end of diastole just before contraction (110-120 ml; up to 250 ml during exercise) - “PRELOAD” Figure 63. Stroke Volume Simple Model. LVESV/ESV (Left Ventricular End Systolic Volume) Graphical Analysis of Ventricular Pumping The blood remaining in the ventricle after ejection during systole (40-50 ml) - NOT ZERO! The Diastolic Pressure Curve: Is measured immediately before ventricular contraction occurs Stroke Volume (end-diastolic pressure) volume of blood ejected per beat Does not increase greatly SV = EDV - ESV Limited by fibrous tissue & pericardium The Systolic Pressure Curve Is determined by the systolic pressure achieved during ventricular contraction at each volume filing Page 15 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Increases even with low volume & reaches a peak then decreases The Pressure-Volume LOOP ○ It decreases because the actin and myosin filaments are Describes the maximal end-systolic pressure which can be achieved pulled apart far enough that the strength of each cardiac with that volume. fiber contraction becomes less than optimal. The increase in preload (end-diastolic volume) leads to blood pressure increase The end-systolic volume is also higher The end-systolic pressure and volume point (and the rest of the loop) is shifted to the right Figure 66. Pressure-Volume Loop. Figure 64. Relationship between left ventricular volume and intra-ventricular End-systolic pressure-volume relationship (ESPVR) pressure during diastole and systole. Also shown by the red lines is the "volume-pressure diagram, " demonstrating changes in intraventricular volume The relationship of these end-systolic pressure-volume points plotted as a line and pressure during the normal cardiac cycle. EW, net external work; PE, potential energy. LV Pressure-Volume Loop: Cardiac-Work Output Phase I (A→B): Period of filling (the ventricle fills and pressure increases) Phase II (B→C): Period of isovolumic contraction (pressure then rises sharply) ○ It’s straight up because there is no change in volume. Phase III (C→D): Period of ejection ○ There is a decrease in volume again. Phase IV (D→A): Period of isovolumic relaxation (pressure falls) ○ There is no change in volume but fall in pressure. External Work “EW” ○ net external work output of the ventricle during its Figure 67. End-systolic pressure volume relationship (ESPVR) contraction cycle ○ Used for calculating cardiac work output ○ Correlates with the STROKE VOLUME ○ Whatever is within the square is your stroke volume. Figure 68. Slope of the ESPVR changes as contractility changes. The more "contractile" the ventricle, the greater the change in pressure from a given level of preload. XIII. THE CARDIAC OUTPUT Figure 65. The volume-pressure diagram demonstrating changes in intraventricular volume and pressure during a single cardiac cycle (red line). The Effectivity of the heart to contract and how much stroke volume is shaded area represents the net external work (E) output by the left ventricle expressed out of the heart. during the cardiac cycle. The volume of blood ejected by the heart per unit time [stroke volume x heart rate] in L/min This diagram represents External Work (EW). How much work the heart can “Average” of 5.0 L/min function during 1 heart beat or during 1 cardiac cycle. Cardiac index: cardiac output divided by the surface area of the body. Cardiogenic shock: if the cardiac output falls below 2.5 L/min. Determinants: ○ Heart volume Page 16 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo ○ Stroke volume Preload Afterload Contractility Regulation of the Cardiac Output Anything that affects your stroke volume or heart rate will eventually affect your cardiac output. Examples are: ○ Parasympathetic stimulation ○ Sympathetic stimulation ○ Frank-starling law ○ Contractility ○ Autoregulation Preload Afterload Figure 70. Stroke volume as a determinant of cardiac output during afterload Heart Rate as a Determinant of Cardiac Output and preload. A higher heart rate increases cardiac output as it multiplies by stroke volume Determinants of Stroke Volume An excessively high heart rate decrease cardiac output by depressing Preload - amount ventricles are stretched by contained blood preload Afterload - back pressure exerted by blood in the large arteries For every individual, there will be some maximum heart rate which leaving the heart achieves the best hemodynamic performance (max HR = 220 minus Contractility (Inotropy) - cardiac cell contractile force due to factors age) other than EDV & afterload. Each person will have some optimum heart rate at which cardiac ○ Incurrent contractility of the heart without the effect of output will be maximal, and this value decreases with age. preload and afterload. Figure 69. Heart rate as a determinant of cardiac output Figure 71. Stroke volume during preload, afterload and inotropy. The higher the heart rate the higher the cardiac output, until it reaches a level called Maximum Effective Heart Rate. Beyond that Preload increases stroke volume, afterload decreases stroke volume, there would be a fall of the cardiac output. Maximum Heart Rate contractility increases stroke volume. would depend on your age. As we grow older, Maximum Heart Rate decreases. Younger Factors that Affect STROKE VOLUME individuals would have higher Maximum Heart Rate as compared to Contraction of cardiac muscle is influenced by both preload and elderly. They could tolerate a higher heart rate. afterload. Stroke Volume as a Determinant of Cardiac Output Preload: Factors that affect stroke volumes are: preload, afterload and The degree of tension on the muscle when it begins to contract contractility. Before it begins to contract there is a build up of pressure within the “The volume of blood pumped out of the left ventricle of the heart left ventricle, that is the preload. during each systolic cardiac contraction”= STROKE VOLUME The force that stretches the relaxed muscle fibers (increasing the Stroke volume decreases with increased afterload, in a fairly linear resting length) fashion. Increase in resting length, increase in tension, and more forceful Stroke volume increases with increased preload, up to a plateau, contraction. beyond which it begins to decrease again. The greater the preload, the greater the stretch of the muscle, the Stroke volume increases with increased contractility, for any given greater the tension, the greater the force, the greater the preload and afterload. contraction. Increase in preload, increase in stroke volume. In the left ventricle: the blood filling and stretching of the wall during diastole represents the preload. Can be increased by greater filling of the left ventricle during diastole (i.e., increasing end-diastolic volume (EDV)) How much blood is within the left ventricle. You increase your stroke volume when you increase your EDV. Which is your surrogate marker for your preload. How much blood is present in the left ventricle before it contracts Page 17 of 24 [PHYSIOLOGY] 1.12 Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves - Dr. M. Butardo Degree of myocardial fiber stretch at the end of diastole and just before contraction Determined by LVED pressure and blood return from the venous system (Venous Return) Wall tension at EDV (analogous to EDP) ○ Preload increases = Stroke Volume increases This is a regulatory mechanism, how much you load the heart before it contracts Figure 74. Preload on muscle contraction. MAP as surrogate the pressure that the ventricle must overcome to eject blood the higher the BP, the lower the stroke volume Afterload can be defined as the resistance to ventricular ejection - the "load" that the heart must eject blood against. It consists of two main sets of determinant factors: Figure 72. Preload stretches the relaxed muscle. Myocardial wall stress, which represents intracardiac factors Input impedance, which represents extracardiac factors End-diastolic volume (EDV) as a surrogate. The higher the impedance, the lower the stroke volume and cardiac Myocardial sarcomere length just prior to contraction, for which the output best approximation is end-diastolic volume Tension on the myocardial sarcomeres just prior to contraction, for which the best approximation is end-diastolic pressure Figure 75. Mean arterial pressure and stroke volume direct relationship. Figure 73. Normal stroke volume and Maximum Stroke Volume. Afterload “load” against which the muscle exerts its contractile force in order to eject blood out of ventricles The force added to the muscle against which the contracting muscle must act If preload would increase stroke volume, afterload inhibit the stroke volume to decrease In the left ventricle, afterload is the pressure in the aorta that must be overcome by the contracting left ventricular muscle to open the aortic valve and eject the blood Sometimes, loosely considered to be the resistance in the Circulation or peripheral vascular resistance rather than the pressure A sum of all forces opposing ventricular ejection Figure 76. Preload increased in