Podcast
Questions and Answers
When does contraction start after the onset of an action potential?
When does contraction start after the onset of an action potential?
During which phase does contraction reach peak tension?
During which phase does contraction reach peak tension?
What is the primary reason cardiac muscle cannot be tetanized completely?
What is the primary reason cardiac muscle cannot be tetanized completely?
What kind of response characterizes the contractile response of cardiac muscle?
What kind of response characterizes the contractile response of cardiac muscle?
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Which factor is NOT an intrinsic determinant of myocardial force of contraction?
Which factor is NOT an intrinsic determinant of myocardial force of contraction?
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How does sympathetic stimulation affect cardiac contractility?
How does sympathetic stimulation affect cardiac contractility?
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What is the effect of parasympathetic stimulation on cardiac contractility?
What is the effect of parasympathetic stimulation on cardiac contractility?
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Which is NOT an extrinsic factor affecting myocardial contraction force?
Which is NOT an extrinsic factor affecting myocardial contraction force?
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What is the conduction rate of the SAN?
What is the conduction rate of the SAN?
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Which pathway has the fastest conduction rate in the atria?
Which pathway has the fastest conduction rate in the atria?
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What is the main function of the AV node's refractory period?
What is the main function of the AV node's refractory period?
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How long does the A-V nodal delay last?
How long does the A-V nodal delay last?
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Which of the following has a conduction rate of 4-5 m/sec?
Which of the following has a conduction rate of 4-5 m/sec?
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What effect does sympathetic stimulation have on cardiac conduction rate?
What effect does sympathetic stimulation have on cardiac conduction rate?
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Which factor primarily influences the inotropic state of cardiac muscles?
Which factor primarily influences the inotropic state of cardiac muscles?
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What would happen if the conduction through the AV node is impaired?
What would happen if the conduction through the AV node is impaired?
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What effect does acetylcholine have on myocardial contraction?
What effect does acetylcholine have on myocardial contraction?
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What happens during Ca++ infusion if the levels are too high?
What happens during Ca++ infusion if the levels are too high?
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What is the role of digitalis in cardiac function?
What is the role of digitalis in cardiac function?
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Which ion's excessive levels can depress cardiac contractility?
Which ion's excessive levels can depress cardiac contractility?
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What is the primary determinant of myocardial contractile force?
What is the primary determinant of myocardial contractile force?
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What is the relationship described by the Frank-Starling Law?
What is the relationship described by the Frank-Starling Law?
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What happens during isometric contraction in cardiac muscle?
What happens during isometric contraction in cardiac muscle?
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How does sufficient extracellular Ca++ affect myocardial contraction?
How does sufficient extracellular Ca++ affect myocardial contraction?
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What determines the strength of cardiac muscle contraction?
What determines the strength of cardiac muscle contraction?
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How is calcium pumped back for muscle relaxation in cardiac muscles?
How is calcium pumped back for muscle relaxation in cardiac muscles?
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What effect does an increase in intracellular Ca++ concentration have on contraction duration?
What effect does an increase in intracellular Ca++ concentration have on contraction duration?
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What is the most significant physiological factor that enhances cardiac muscle relaxation?
What is the most significant physiological factor that enhances cardiac muscle relaxation?
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What role does the SR Ca++-ATPase pump play during muscle relaxation?
What role does the SR Ca++-ATPase pump play during muscle relaxation?
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Which factor mainly causes impairment in cardiac muscle relaxation?
Which factor mainly causes impairment in cardiac muscle relaxation?
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What occurs when Ca++ ions are released from troponin C?
What occurs when Ca++ ions are released from troponin C?
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What happens to the rate of relaxation during exercise due to increased sympathetic stimulation?
What happens to the rate of relaxation during exercise due to increased sympathetic stimulation?
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What defines isotonic contraction in muscle fibers?
What defines isotonic contraction in muscle fibers?
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How does increased afterload affect the velocity of shortening in cardiac muscle?
How does increased afterload affect the velocity of shortening in cardiac muscle?
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What is Vmax in relation to muscle contraction?
What is Vmax in relation to muscle contraction?
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What effect does increased preload have on afterload capacity?
What effect does increased preload have on afterload capacity?
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How does the frequency-force relationship affect cardiac muscle?
How does the frequency-force relationship affect cardiac muscle?
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What happens to Ca++ ions during physiological acceleration of the heart?
What happens to Ca++ ions during physiological acceleration of the heart?
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What is the role of the vagus nerve on ventricular contractility?
What is the role of the vagus nerve on ventricular contractility?
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What phenomenon describes the stepwise increase in contraction strength at a higher rate of stimulation?
What phenomenon describes the stepwise increase in contraction strength at a higher rate of stimulation?
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What occurs to the intracellular Ca++ concentration with repeated stimuli in cardiac muscle?
What occurs to the intracellular Ca++ concentration with repeated stimuli in cardiac muscle?
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Which statement about the relationship between afterload and velocity is correct?
Which statement about the relationship between afterload and velocity is correct?
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What is the role of troponin C in cardiac muscle contraction?
What is the role of troponin C in cardiac muscle contraction?
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What directly affects the inotropic state of myocardial contractility?
What directly affects the inotropic state of myocardial contractility?
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Which factor is considered a positive inotropic factor?
Which factor is considered a positive inotropic factor?
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What is the primary effect of myocardial infarction on cardiac muscle?
What is the primary effect of myocardial infarction on cardiac muscle?
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During skeletal muscle contraction, which complex prevents actin-myosin interaction at rest?
During skeletal muscle contraction, which complex prevents actin-myosin interaction at rest?
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What happens to the length of the sarcomere when myosin heads pull the actin filaments?
What happens to the length of the sarcomere when myosin heads pull the actin filaments?
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Study Notes
BMS 204: Cardiac Properties Part 2
- The lecture covers the spread of excitation waves, AV node characteristics, excitation-contraction coupling, and factors affecting cardiac muscle inotropy.
- Students should be able to describe the spread of excitation waves and its importance.
- Students should be able to describe the characteristics of the AV node.
- Students should be able to explain excitation-contraction coupling.
- Students should be able to identify the factors affecting cardiac muscle inotropy.
3) Conductivity
- All cardiac muscle cells are conductive, but at differing rates.
- Vagal stimulation decreases conduction rate, while sympathetic stimulation increases it.
- SAN (Sinoatrial node) conduction is very slow (0.05 m/sec). This slow conduction prevents ectopic foci from depolarizing and maintains the normal pacemaker as the primary.
2. Atrial Conduction of Excitation Wave (EW)
- EWs rapidly spread through the atria, converging on the AV node (atrioventricular node) within 0.1 seconds.
- Specialized atrial pathways (internodal pathways) facilitate rapid conduction (1 m/sec) from the SA node to other atrial regions and the AV node.
3. AVN Conduction
- The AV node has the slowest conduction rate in the heart (0.02-0.05 m/sec.).
- It has three functional zones: A-N zone (maximum delay due to long path length), N zone (slowest conduction velocity), and N-H zone.
- A-V nodal delay (100-150 msec) occurs between the atria and ventricles. This delay helps prevent ventricular overload.
- A-V nodal block (refractoriness) protects ventricles from high atrial rhythms, allowing only 180-200 bpm to pass. This prevents rapid atrial rhythms from overwhelming the ventricle.
- The AV node's decreased chance of retrograde conduction safeguards the sinoatrial node (SAN) from ventricular ectopic foci.
4. Ventricular Conduction
- Ventricular conduction involves the A-V bundle, bundle branches, and Purkinje fibers.
- The A-V bundle branches into right and left bundle branches, with conduction rates of 1-2 m/sec.
- Purkinje fibers exhibit high conduction velocities (4-5 m/sec), synchronizing ventricular activation.
- The final Purkinje fiber ramifications reach about 2/3 of the ventricular muscle thickness.
5. Ventricular Myocardial Conduction
- Ventricular muscle activation begins in the mid-portion of the septum on the left ventricle
- Activation spreads through the left and right ventricular walls.
- The last part to be activated is the epicardial surface of the left ventricle.
4th Cardiac Property is Contractility
- Contractility is the heart's inherent ability to contract and generate force in response to stimulation.
- This capability is independent of muscle length.
Sources of Ca++ for Contraction
- Depolarizing Ca++ enters the cell during the plateau phase.
- SR Ca++ is released by the depolarizing Ca++.
Mechanism of Muscle Contraction
- Ca++ binds to troponin C, leading to conformational changes in the troponin-tropomyosin complex.
- Myosin binding sites on the actin molecules are exposed.
- Cross-bridge cycles between actin and myosin occur (binding, bending, detaching).
- Sliding of actin over myosin produces muscle contraction.
Mechanism of Cardiac Muscle Relaxation
- Ca++ is pumped back into the sarcoplasmic reticulum (SR) by Ca++ pumps.
- Ca++ is extruded outside the cell by membrane Ca++ pumps and Na+-Ca++ exchangers.
- The release of Ca++ from troponin C stops, and tropomyosin moves back to cover actin binding sites.
- Muscle relaxation (diastole) occurs when actin and myosin interactions cease.
3] The Duration of Contraction
- The duration of contraction directly correlates to the intracellular Ca++ concentration and is directly proportionate.
- Higher intracellular Ca++ concentrations lead to prolonged contractions because of the increased time needed by the Ca++ pump to remove Ca++.
Regulation of Relaxation
- Catecholamines (E, NE) increase sarcoplasmic reticulum Ca++-ATPase pump activity and reuptake of Ca++.
- This accelerates relaxation, particularly important during rapid heart rates like exercise.
4] The Most Important Physiological Factor
- Sympathetic stimulation enhances relaxation by accelerating Ca++ reuptake into the sarcoplasmic reticulum via a beta-adrenergic mechanism that is mediated by cAMP.
- Important during exercise or increased heart rates.
- The pathological implications for relaxation in ischemia heart disease.
Time Relations & Characteristics Of The Contractile Response
- Contraction begins 20 msec after action potential onset.
- Peak tension is reached during the plateau of the action potential.
3 - The Cardiac Muscle cannot be tetanized
- The long absolute refractory period (ARP) prevents tetanus.
- Ventricular relaxation is necessary for adequate filling.
4 - The Contractile Response is all- or none
- Cardiac muscle contractions are all-or-none, not graded.
- Each atrial and ventricular muscle sheet functions as a single unit (functional syncytium).
Factors Affecting Myocardial Force Of Contraction
- Intrinsic factors (Determinants): Initial length (preload), frequency of stimulation, contractility
- Extrinsic factors (Inotropic Factors): Nervous (sympathetic, parasympathetic), neurohormonal (epinephrine, norepinephrine, acetylcholine), ECF ions , drugs.
EC coupling as target of contractility regulation
- Parasympathetic NS reduces heart rate and contractile force.
- Sympathetic NS increases heart rate and contractile force.
Extrinsic Factors Affecting Myocardial Contraction Force
- Sympathetic stimulation increases Ca++ entry and release from the SR.
- There are multiple mechanisms for increasing intracellular Ca++ including the mechanisms of the frequency of action potentials and the relationship between Ca++ and force of contraction.
- Sympathetic stimulation increases the rate of relaxation.
Neurohormones
- Epinephrine and norepinephrine act as positive inotropic factors.
- Acetylcholine acts as a negative inotropic factor, opposing sympathetic effects.
ECF Ions
- Ca++ infusion can cause heart stoppage (Ca++ rigor).
- Insufficient extracellular Ca++ has a negative inotropic effect.
- High K+ (hyperkalemia) depresses contractility and can stop the heart in diastole.
Drugs
- Ca++ entry blockers are negative inotropic agents (e.g., nifedipine).
- Drugs that increase intracellular Ca++ are positive inotropic agents(e.g., cardiac glycosides).
- Digitalis inhibits Na+-K+-ATPase, leading to Na+ accumulation, activating the Na+-Ca+ exchange mechanism, and increasing intracellular Ca++.
1) Initial Length (Preload)
- Preload is the degree of passive stretch exerted by blood volume in the ventricle before contraction.
- End-diastolic volume (EDV) is used instead of muscle length.
- A direct relationship between preload and contraction strength up to a point. Beyond that point further increases in preload reduce contractility.
2) Afterload
- Afterload is the resistance the heart must overcome to eject blood.
- Isometric contractions result in increased tension without ventricular volume change.
- In isotonic contraction, the tension developed allows muscle shortening.
- Increased afterload (e.g., high blood pressure) reduces the velocity of shortening of the cardiac muscle.
The relation between afterload & Velocity (Force-Velocity relationship)
- Heavier loads are lifted slower.
- Lighter loads result in higher velocities until the maximum velocity is reached at zero load.
- The maximum velocity is independent of preload.
- Increased preload allows the muscle to overcome larger afterloads, however this does not change Vmax which is related to contractility.
3) Frequency of Stimulation
- Increased rates of stimulation result in progressively greater contraction forces.
- This phenomenon is known as the frequency-force relationship and is caused by changes in intracellular Ca++ concentration during repeated stimulation.
Examples & Explanations
- Increased heart rate leads to greater contractility (more Ca++ triggers).
- Vagus nerve stimulation decreases contractility through decreased heart rate.
2] Stair-case phenomenon (= Treppe = Bodwitch effect)
- Increased stimulation frequency leads to stepwise increases in the force of each contraction until a plateau is reached.
- This occurs because the SR cannot remove all Ca++ quickly enough before the next action potential.
Summary of Cardiac Muscle Contraction
- The troponin-tropomyosin complex prevents actin-myosin interactions at rest.
- Increased intracellular Ca++ causes conformational changes in troponin, allowing actin-myosin interactions.
- The binding, bending, and detachment of actin-myosin cross-bridges cause muscle shortening.
- ATP is needed for detachment.
- The cycle repeats.
Sources of Ca+2
- Ca++ comes from the extracellular and intracellular compartments; the SR at the T-Tubules.
- Extracellular Ca++ plays an important role in contraction and is regulated by numerous intrinsic and extrinsic factors.
To Sum up: Myocardial Contractility
- The intrinsic ability of the cardiac muscle to generate force at a constant length.
- Myocardial contractility depends on the integrity of the muscle elements.
- Contractility changes are related to sarcoplasmic Ca++ concentration.
- Factors raising intracellular Ca++ are positive inotropic agents.
- Factors decreasing intracellular Ca++ are negative inotropic agents.
Ca2+ signaling in cardiac muscle
- Numerous intrinsic and extrinsic factors affect Ca2+ signaling in the heart.
- This signaling process underlies myocardial contractility and relaxation.
- Several sources of Ca2+ contribute to the needed Ca2+ for contraction.
References.
- Ganong's Review of Medical Physiology, Kim E. Barrett, 2019
- Guyton and Hall textbook of Medical Physiology
- Fox, Stuart Ira.
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Description
This quiz covers the key concepts from BMS 204 related to cardiac properties, including the spread of excitation waves, characteristics of the AV node, and excitation-contraction coupling. Students are assessed on their understanding of these mechanisms and factors influencing cardiac muscle inotropy. Prepare to explore the intricacies of cardiac conductivity and its regulation.
