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Questions and Answers
Which of the following is the primary cation found in extracellular fluid?
Which ion is NOT typically found in high concentrations within extracellular fluid?
What is a key function of the nutrients found in extracellular fluid?
Which combination of substances is predominantly found in extracellular fluid?
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Which nutrient is a key source of energy transported in extracellular fluid?
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What ions are found in large amounts within intracellular fluid?
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How do the concentrations of Potassium and Magnesium ions differ between intracellular and extracellular fluid?
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What role does potassium play in cellular function within intracellular fluid?
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What effect does excess potassium in the extracellular fluids have on the heart?
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What is a direct consequence of high potassium concentration in the extracellular fluids on cardiac muscle fibers?
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How can high levels of potassium affect the conduction of cardiac impulses?
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What potassium concentration can lead to severe weakness of the heart and abnormal rhythms?
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What is a potential outcome of excessive potassium levels in the body?
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Excess calcium ions cause the heart to move toward spastic contraction.
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A deficiency of calcium ions causes the heart to experience increased contractility.
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Calcium ions play a critical role in heart muscle contraction.
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Both excess and deficiency of calcium ions have no significant impact on heart function.
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Normal levels of calcium ions contribute to cardiac stability.
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The sinoatrial node is located at the junction of the superior vena cava and the right ______.
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The blood supply to the sinoatrial node comes from the ______ artery.
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The intrinsic rate of the sinoatrial node is between ______ to _____ beats per minute.
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Pacemaker cells found in the sinoatrial node are known as ______ cells.
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The speed of conduction from the sinoatrial node is approximately ______ m/sec.
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Internodal tracts are located in the ______.
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The cell type found in internodal tracts has large ______ and sparse myofibrils.
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Internodal tracts provide preferential pathways between the SA node and the ______ node.
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Where is the AV Node located and what is its function?
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What is the intrinsic rate of the AV Node and why is this significant?
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Explain the conduction velocity of the AV Node and its importance.
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Discuss the role of the conduction delay provided by the AV Node.
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What anatomical structures are found in close proximity to the AV Node?
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Initial conduction delay is _____ second.
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The total conduction delay before the excitatory signal reaches the contracting muscle of the ventricles is _____ seconds.
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The A-V nodal and A-V bundle conduction delay is _____ second.
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The conduction delays ensure that the heart can effectively pump blood by allowing time for the _____ to fill.
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Before the excitatory signal reaches the ventricles, there is a total conduction delay of _____ seconds.
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What factors contribute to conduction delays in the A-V bundle fibers?
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What role does the A-V node play in the cardiac conduction system?
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The Purkinje system consists of the bundle branch and ______ branches.
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The conduction velocity of the Purkinje fibers is approximately ______ m/sec.
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The Purkinje system extends outward under the ______.
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Cardiac muscle contraction strength is reduced without the calcium from the _____ tubules.
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L-type _____ channels are slow and remain open for several tenths of a second during cardiac action potentials.
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The sarcoplasmic reticulum of cardiac muscle is less well developed than that of _____ muscle.
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Excitation-contraction coupling refers to the process whereby an action potential causes the myofibrils of muscle to _____ .
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Voltage activated fast sodium channels open quickly and are responsible for the initial depolarization during cardiac _____ .
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Match the phases of cardiac muscle action potential with their corresponding voltage changes:
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Match the phase of the cardiac action potential with its membrane potential:
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Match each phase of the cardiac muscle action potential with the main ionic channels involved:
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Match each phase of cardiac muscle action potential to its outcome:
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Match the terms related to the sympathetic nervous system with their correct descriptions:
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Efferent autonomic tone to the heart is initiated in the anterior (PNS) and posterior (SNS) __________.
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Activation of the sympathetic nervous system results in mobilization of myocardial fat-free acids and __________ for energy use by myocardial cells.
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Cardioaccelerator fibers originate from cells in the intermediolateral columns of higher thoracic segment of the spinal cord (T1-T4) and synapse at the 1st - __________ thoracic vertebral ganglia.
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The sympathetic nervous system has a greater distribution of nerves that primarily innervate the __________.
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The activation of the sympathetic nervous system results in increased heart rate, increased myocardial contraction, and increased rate of __________ node discharge.
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The primary neurotransmitter of the parasympathetic nervous system is __________.
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Increased parasympathetic tone leads to a __________ in heart rate.
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The effect of strong parasympathetic stimulation can completely stop rhythmical __________.
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Stimulation of the parasympathetic nervous system increases __________ permeability in cardiac cell membranes.
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During maximum vagal nerve stimulation, contractility can decrease by __________ percent.
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Acetylcholine is the neurotransmitter of the ______ nervous system.
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The release of Acetylcholine during parasympathetic stimulation can decrease the rate of the ______ Node.
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Ventricles may stop beating for ______ to 20 seconds due to strong parasympathetic stimulation.
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The intrinsic rate of the Purkinje fibers is between ______ to 40 beats/min.
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The neurotransmitter of the parasympathetic nervous system is __________.
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Parasympathetic stimulation leads to __________ of cardiac cells' membranes, increasing permeability to potassium.
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In the SA node, acetylcholine decreases the discharge rate, resulting in a resting membrane potential between __________ to __________ mV.
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The ____ and _____ nodes are innervated by the parasympathetic nervous system.
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Rapid leakage of potassium from conductive fibers due to parasympathetic stimulation causes __________.
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What triggers the transmission of signals from baroreceptors to the central nervous system?
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How do signals from the carotid baroreceptors reach the brain?
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Explain the feedback mechanism involved in baroreceptor function.
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Signals from the carotid baroreceptors are transmitted through small Hering’s nerves to the glossopharyngeal nerves in the high ______.
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Chemoreceptor cells are sensitive to low __________ or elevated carbon dioxide & hydrogen ion levels.
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The denervated heart following orthotopic heart transplantation still responds to exercise load with __________, due to increased circulating catecholamine levels.
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Myocardial β1-adrenergic receptors can be activated by pharmacologic agonists like __________ and epinephrine.
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Humoral factors, such as _________ __________, also influence heart rate independent of the SNS and PNS.
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High concentrations of local anesthetics depress conduction by binding to fast sodium channels.
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Bupivacaine is the least cardiotoxic among local anesthetics.
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Opioids such as fentanyl decrease AV conduction time.
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Volatile anesthetics have no effect on the automaticity of the SA node.
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Regional anesthesia cause bradycardia and hypotension due to inhibition of sympathetic ganglia.
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Diastole begins with the closing of the aortic valve and ends with the closing of the ______ valve.
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Systole represents ______ contraction, forcing blood into the arteries.
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During which phase does the mitral valve open, allowing blood to fill the ventricles?
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Isovolumic contraction occurs when the blood is actively leaving the ventricle.
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What is the volume of blood in the ventricles after the previous heartbeat referred to as?
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The average end-diastolic volume is approximately ______ ml.
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Match the pressure with its corresponding phase:
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What marks the beginning of systole in cardiac cycle?
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The second heart sound, S2, is associated with the closure of the mitral valve.
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How long does it take for the ventricles to build up enough pressure during isovolumic contraction?
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During rapid ventricular ejection, a healthy ventricle ejects more than ______% of its volume.
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What happens during the last third of diastole?
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What is preload in the context of cardiac function?
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Afterload primarily depends on systemic vascular resistance.
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What is the Frank-Starling law of the heart?
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The amount of blood pumped by the heart with each contraction is known as _____ volume.
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Match the following terms with their definitions:
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Which of the following factors affect venous return?
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Increased afterload requires the heart to work harder to eject blood.
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What happens to cardiac muscle when it is stretched beyond optimal length?
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The intrinsic ability of the heart to adapt to increasing volumes is explained by the -_ mechanism.
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What primarily influences the force of heart muscle contraction?
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What is the primary effect of the Bainbridge Reflex on the heart?
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The left coronary artery supplies blood to the right ventricle.
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Name one factor that depresses myocardial contractility.
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Coronary blood flow during strenuous exercise can increase _____ to _____ times.
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Match the coronary arteries with their primary areas of supply:
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Which of the following primarily impacts coronary perfusion pressure?
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The inner 1/10th millimeter of the endocardial surface obtains significant nutrition directly from blood in the cardiac chambers.
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What is the average resting coronary blood flow per 100g of heart weight?
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During strenuous exercise, cardiac output can increase _____ to _____ times.
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Which factor is NOT a physical factor influencing coronary blood flow?
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What is the primary substance responsible for coronary vasodilation?
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Vagal stimulation has a significant effect on the caliber of coronary arteries.
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What percentage of oxygen does the myocardium extract from hemoglobin?
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An increase in heart rate by 50% will increase myocardial oxygen consumption by ______.
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Match the determinants of myocardial consumption with their contribution level:
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What effect does increasing afterload by 50% have on myocardial oxygen demand?
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Sympathetic cholinergic innervation exists within coronary arteries.
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Name one vasodilatory substance released from the myocardium in response to decreased oxygen delivery.
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A contraction force increase by 50%, when measured by dP/dT, results in a ______% increase in myocardial oxygen consumption.
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What contributes to the basal cardiac metabolism and influences oxygen consumption?
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List the intrinsic factors that determine heart rate.
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List extrinsic factors that affect heart rate.
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Action potentials are conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue
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Match the following to its corresponding definition.
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Match each internodal pathway to its corresponding anatomical location.
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Study Notes
Composition of Extracellular Fluid
- Contains high concentrations of sodium, crucial for maintaining fluid balance and nerve function.
- Rich in chloride ions, which play a role in regulating osmotic pressure and maintaining pH levels.
- Bicarbonate ions are present, acting as a buffer to maintain acid-base balance in the body.
- Supplies essential nutrients for cells, facilitating metabolic processes and energy production.
- Oxygen is a vital component, necessary for cellular respiration and energy (ATP) production.
- Glucose provides a primary energy source for cells, particularly during metabolic processes.
- Fatty acids serve as building blocks for cell membranes and are vital for energy storage.
- Amino acids are the building blocks of proteins, essential for growth, repair, and overall function of cells.
Composition of Intracellular Fluid
- Contains large amounts of potassium, important for cellular function and maintaining membrane potential.
- Rich in magnesium ions, which are essential for numerous biochemical reactions and enzyme function.
- Phosphate ions are abundant, critical for energy production (ATP), cellular signaling, and bone health.
Composition of Extracellular Fluid
- Major components include sodium, chloride, and bicarbonate ions, which maintain osmotic balance.
- Nutrients such as glucose, fatty acids, and amino acids are present, providing energy and building blocks for cells.
- Oxygen is dissolved in extracellular fluid, essential for cellular respiration and energy production.
Composition of Intracellular Fluid
- Rich in potassium ions, crucial for cellular function, nerve impulse transmission, and muscle contraction.
- Contains magnesium ions, which play a role in enzymatic reactions and energy production.
- High levels of phosphate ions, important for energy storage (ATP) and cellular signaling.
Extracellular Fluid Composition
- High levels of Sodium, crucial for nerve transmission and muscle contraction.
- Dominated by Chloride, which helps maintain osmotic pressure and fluid balance.
- Contains Bicarbonate ions, essential for maintaining acid-base homeostasis.
- Rich in nutrients like glucose and fatty acids, providing energy for cellular metabolism.
- Supplies oxygen, vital for aerobic respiration.
- Contains amino acids needed for protein synthesis and various metabolic processes.
Intracellular Fluid Composition
- Predominantly contains Potassium, which is critical for maintaining membrane potential and cellular function.
- Rich in Magnesium, important for many enzymatic reactions and energy production.
- Abundant in Phosphate ions, crucial for energy transfer (ATP), signaling, and structural functions in cells.
Effect of Potassium Ions on Heart Function
- Excess potassium in extracellular fluids leads to dilation and flaccidity of the heart muscle, negatively affecting cardiac performance.
- Elevated potassium levels slow heart rate and can disrupt normal heart rhythm.
- High potassium concentration diminishes the resting membrane potential within cardiac muscle fibers, impairing their excitability.
- Increased potassium can obstruct the conduction of the cardiac impulse from atria to ventricles, particularly at the A-V bundle, affecting normal heartbeat coordination.
- Potassium levels between 8 to 12 mEq/L—two to three times higher than normal—can result in severe cardiac weakness, arrhythmias, and potentially fatal outcomes.
Extracellular Fluid Composition
- Contains high levels of sodium, chloride, and bicarbonate ions.
- Nutrients for cellular functions include oxygen, glucose, fatty acids, and amino acids.
Intracellular Fluid Composition
- Characterized by significant amounts of potassium, magnesium, and phosphate ions.
Effects of Potassium Ions on the Heart
- Excess potassium in extracellular fluid leads to heart dilation, flaccidity, and a decreased heart rate.
- Elevated potassium levels reduce resting membrane potential in cardiac muscle fibers.
- High potassium concentrations can obstruct cardiac impulse conduction from atria to ventricles via the A-V bundle.
- Potassium levels of 8 to 12 mEq/L (2-3 times normal) may induce severe heart weakness, abnormal rhythms, and potentially lead to death.
Effects of Calcium Ions on the Heart
- Excess calcium ions result in spastic contractions of the heart.
- A deficiency in calcium ions can lead to cardiac weakness and impaired function.
Sinoatrial Node Overview
- Located at the epicardial surface where the superior vena cava meets the right atrium.
- Blood supply is primarily through a notable branch of the right coronary artery (RCA).
Cell Composition
- Consists of P cells, which serve as pacemaker cells responsible for initiating heartbeats.
- Contains transitional cells that assist in the conduction of electrical impulses.
Functional Characteristics
- The intrinsic firing rate ranges from 60 to 100 beats per minute, determining the baseline heart rate.
- Conduction speed through the sinoatrial node is approximately 0.5 meters per second, influencing the timing and rhythm of heart contractions.
Extracellular Fluid Composition
- Major components include sodium, chloride, bicarbonate ions, nutrients, oxygen, glucose, fatty acids, and amino acids.
- These elements are essential for the functioning and nourishment of cells.
Intracellular Fluid Composition
- Rich in potassium, magnesium, and phosphate ions.
- Plays a crucial role in cellular processes and maintaining cell health.
Effects of Potassium Ions on the Heart
- High extracellular potassium levels lead to heart dilation, flaccidity, and a slowed heart rate.
- Increases in potassium concentration reduce the resting membrane potential in cardiac muscle fibers.
- Excessive potassium (8-12 mEq/L) can severely impair heart rhythm and function, potentially resulting in death.
Effects of Calcium Ions on the Heart
- Elevated calcium levels can cause spastic contractions in the heart muscle.
- Conversely, calcium deficiency leads to weakened cardiac function.
Sinoatrial Node (SA Node)
- Located at the epicardial surface at the junction of the superior vena cava and right atrium.
- Blood supply comes from a prominent central artery branch of the right coronary artery (RCA).
- Comprised of pacemaker (P) cells and transitional cells, facilitating heart rhythm.
- Intrinsic firing rate of 60 to 100 beats per minute.
- Conduction speed through the node is approximately 0.5 m/sec.
Internodal Tracts
- Located within the atria, these tracts serve as preferential pathways between the SA node and the atrioventricular (AV) node.
- Characterized by large nuclei and sparse myofibrils, facilitating rapid signal transmission in the heart.
AV Node
- Located on the posterior aspect of the right atrium, positioned behind the tricuspid valve, and near the opening of the coronary sinus.
- Functions to delay conduction between the atria and ventricles, providing time for the atria to effectively empty blood into the ventricles.
- Maintains an intrinsic rate of 40 to 60 beats per minute, which is crucial for pacing if higher nodes fail.
- Conducts electrical impulses at a velocity of 2 meters per second, slower than other cardiac conduction pathways, allowing for adequate filling of the ventricles.
Cardiac Conduction System
- Initial conduction delay is 0.03 seconds.
- A-V nodal and A-V bundle delay totals 0.13 seconds.
- Overall conduction delay before excitation reaches ventricular muscle is 0.16 seconds.
Extracellular Fluid Composition
- High concentrations of sodium, chloride, and bicarbonate ions.
- Contains essential nutrients such as oxygen, glucose, fatty acids, and amino acids.
Intracellular Fluid Composition
- Rich in potassium, magnesium, and phosphate ions.
Effects of Potassium Ions on the Heart
- Excess extracellular potassium leads to a dilated, flaccid heart and a slowed heart rate.
- High potassium decreases the resting membrane potential of cardiac muscle fibers.
- Elevated potassium levels can obstruct conduction from atria to ventricles via the A-V bundle.
- Elevated potassium concentration (8 to 12 mEq/L) can induce severe cardiac weakness, rhythm abnormalities, and possibly death.
Effects of Calcium Ions on the Heart
- Excess calcium triggers spastic contractions of the heart.
- Calcium deficiency results in cardiac weakness.
Sinoatrial Node (SA Node)
- Located at the junction of the superior vena cava and right atrium, on the epicardial surface.
- Blood supply from a prominent branch of the right coronary artery (RCA).
- Composed of pacemaker cells (P cells) and transitional cells.
- Functions with an intrinsic rate of 60 to 100 beats per minute.
- Conduction speed is approximately 0.5 m/sec.
Internodal Tracts
- Located within the atria and serve as preferential pathways between SA and AV nodes.
- Composed of cells with large nuclei and sparse myofibrils.
Atrioventricular Node (AV Node)
- Positioned on the posterior aspect of the right atrium, behind the tricuspid valve, near the coronary sinus opening.
- Conduction delay allows the atria sufficient time to empty into the ventricles.
- Intrinsic rate ranges from 40 to 60 beats per minute.
- Conduction velocity is about 2 m/sec.
Conduction Delays in the Heart
- Initial conduction delay is 0.03 seconds.
- A-V nodal and A-V bundle delay is 0.13 seconds.
- Total conduction delay before the excitatory signal reaches the ventricles is 0.16 seconds.
- Causes of conduction delay include slow conduction in transitional, nodal, and A-V bundle fibers.
- Diminished gap junctions between successive cells in the conducting pathways contribute to delays.
Extracellular Fluid Composition
- Contains high levels of sodium, chloride, and bicarbonate ions.
- Nutrients present include oxygen, glucose, fatty acids, and amino acids.
Intracellular Fluid Composition
- Rich in potassium, magnesium, and phosphate ions.
Effects of Potassium Ions on Cardiac Function
- High potassium levels in extracellular fluid lead to a dilated and flaccid heart and a slowed heart rate.
- Increases in extracellular potassium concentration decrease the resting membrane potential in cardiac muscle fibers.
- Excessive potassium can block conduction of cardiac impulses through the A-V bundle, impairing atrial to ventricular communication.
- Potassium levels between 8 to 12 mEq/L (2-3 times normal) can cause heart weakness, abnormal rhythms, and potentially lead to death.
Effects of Calcium Ions on Cardiac Function
- Excess calcium induces spastic contractions of the heart.
- Calcium deficiency results in cardiac weakness.
Sinoatrial Node (SA Node)
- Located along the epicardial surface at the junction of the superior vena cava and right atrium.
- Supplied by a prominent artery from the right coronary artery (RCA).
- Composed of pacemaker cells (P cells) and transitional cells.
- Exhibits an intrinsic rate of 60 to 100 beats per minute.
- Conducts impulses at a speed of 0.5 m/sec.
Internodal Tracts
- Located in the atria, characterized by large nuclei and sparse myofibrils.
- Serve as preferential pathways between the SA and AV nodes.
Atrioventricular Node (AV Node)
- Positioned on the posterior aspect of the right atrium, behind the tricuspid valve and near the coronary sinus opening.
- The conduction delay in the AV node allows for complete emptying of the atria into the ventricles.
- Displays an intrinsic rate of 40 to 60 beats per minute.
- Conducts impulses at a velocity of 2 m/sec.
Purkinje System Overview
- Comprises the bundle branch and terminal branches, integral to cardiac conduction.
- Located beneath the endocardium, facilitating the spread of electrical impulses in the heart.
Key Characteristics
- Contains pacemaker cells that can spontaneously fire at a rate of 20 to 40 beats per minute, acting as a backup to the primary pacemaker (sinoatrial node).
- Exhibits a conduction velocity of 4 meters per second, which is essential for coordinated heart contractions.
Cardiac Fascicles Overview
- Three primary fascicles: Anterior, Posterior, and Septal, responsible for innervating specific regions of the left ventricle (LV).
Anterior Fascicles
- Innervates the anterolateral wall of the left ventricle.
- Provides innervation to the anterior papillary muscle, facilitating proper function during the cardiac cycle.
Posterior Fascicles
- Innervates the lateral and posterior walls of the left ventricle.
- Supplies the posterior papillary muscle, contributing to coordinated ventricular contractions.
Septal Fascicles
- Innervates the lower part of the ventricular septum.
- Also affects the apical wall of the left ventricle, ensuring effective contraction and structural integrity.
Membrane Properties of Cardiac Muscle
- Cardiac muscle cells utilize two key types of ion channels for electrical signaling: voltage-activated fast sodium channels and L-type calcium channels.
- Fast sodium channels open quickly during depolarization, allowing a rapid influx of sodium ions, which initiates the action potential.
- L-type calcium channels, known as slow calcium channels, open more gradually and remain open for several tenths of a second, contributing to the plateau phase of the cardiac action potential.
- In the absence of calcium ions from T tubules, the strength of cardiac muscle contraction significantly decreases, highlighting the importance of extracellular calcium.
- The sarcoplasmic reticulum in cardiac muscle is less developed than in skeletal muscle; thus, it does not store sufficient calcium ions to support maximum contraction strength.
- Excitation-contraction coupling describes the process where an action potential triggers the contraction of muscle myofibrils, playing a crucial role in cardiac function.
Phases of Cardiac Muscle Action Potential
- Phase 0 – Depolarization: Initiates when fast sodium channels open, leading to a rapid increase in membrane potential from around -70mV to a positive value.
- Phase 1 – Initial Repolarization: Fast sodium channels close, resulting in a decrease in membrane potential. Fast potassium channels open, allowing potassium ions to exit the cell.
- Phase 2 – Plateau: Characterized by the opening of calcium channels, which allows calcium ions in, while fast potassium channels close, creating a balanced state that sustains depolarization.
- Phase 3 – Rapid Repolarization: Calcium channels close, and slow potassium channels open, resulting in a significant outflux of potassium and leading to a return toward resting potential.
- Phase 4 – Resting Membrane Potential: The membrane stabilizes at an average value between -80 to -90 millivolts, ensuring the cell is ready for the next action potential cycle.
Autonomic Tone to the Heart
- Efferent autonomic tone to the heart is initiated in the anterior (parasympathetic) and posterior (sympathetic) hypothalamus.
- Cardiac tone is modulated by the cardiac acceleration and cardiac slowing centers located in the medulla.
Sympathetic Nervous System Effects
- Chronotropic Effect: Increases heart rate.
- Inotropic Effect: Enhances myocardial contraction strength.
- Dromotropic Effect: Accelerates the discharge rate of the AV node.
Cardioaccelerator Fibers
- Originate in the intermediolateral columns of the spinal cord from higher thoracic segments (T1-T4).
- Fibers synapse at the 1st to 5th thoracic vertebral ganglia.
Postganglionic Fibers
- Comprised of superior, middle, and inferior cardiac nerves alongside thoracic visceral nerves.
- Greater distribution of sympathetic nerves focuses on ventricular innervation.
Metabolic Effects of Sympathetic Activation
- Activation leads to the mobilization of myocardial fat-free acids and glycogen, providing energy for myocardial cells.
Efferent Autonomic Tone to the Heart
- Initiated in the anterior (parasympathetic) and posterior (sympathetic) hypothalamus.
- Modulated by cardiac centers in the medulla: acceleration and slowing centers.
Sympathetic Nervous System (SNS) Effects
- Chronotropic effect: Increases heart rate.
- Inotropic effect: Enhances myocardial contraction strength.
- Dromotropic effect: Boosts the rate of discharge at the AV node.
Cardioaccelerator Fibers
- Origin from intermediolateral columns in the higher thoracic segments of the spinal cord (T1-T4).
- Synapse at thoracic ganglia between the 1st and 5th vertebrae.
Postganglionic Fibers
- Include superior, middle, and inferior cardiac nerves.
- Involve thoracic visceral nerves for broader effect.
Ventricular Innervation
- A greater number of sympathetic nerves specifically innervate the ventricles of the heart.
Energy Mobilization
- Activation of the sympathetic nervous system triggers the release of myocardial fat-free acids and glycogen, providing energy for myocardial cells.
Physiological Origins
- Parasympathetic nervous system originates in the dorsal motor nucleus of the medulla.
- It innervates the sinoatrial (SA) node, atrioventricular (AV) node, and atrial muscle fibers.
- Increased parasympathetic tone leads to decreased heart rate (HR).
Functions
- Primary role: Slow down the heart rate.
- Secondary role: Decrease contractility; maximum vagal nerve stimulation can reduce contractility by 30%.
Acetylcholine Mechanism
- Acetylcholine is the key neurotransmitter for the parasympathetic nervous system.
- It binds to muscarinic receptors affecting cardiac function.
- Decreases discharge rate of the SA node.
- Slows conduction velocity via the AV node.
Impact of Parasympathetic Stimulation
- Release of acetylcholine decreases the sinus node rate.
- Weak to moderate stimulation can halve the heart rate.
- Strong stimulation can completely stop rhythmic excitation.
- Complete blockage can occur in transmission from atria to ventricles through the AV node.
- Ventricle contractions may cease for 5 to 20 seconds.
- Purkinje fibers may attempt to initiate their rhythm, resulting in a ventricular escape rate of 15 to 40 beats per minute.
Cellular Effects
- Stimulation increases potassium permeability in cardiac cell membranes, leading to hyperpolarization.
- Rapid potassium leakage from conductive fibers contributes to the hyperpolarization effect.
- The resting membrane potential in the SA node becomes more negative, ranging from -65 to -75 mV.
Parasympathetic Nervous System Overview
- Originates from the dorsal motor nucleus of the medulla.
- Innervates the Sinoatrial (SA) and Atrioventricular (AV) nodes, along with atrial muscle fibers.
- Increased parasympathetic tone leads to decreased heart rate (HR).
Functions of Parasympathetic Nervous System
- Primary function: Slows the heart rate.
- Secondary function: Reduces contractility; maximal vagal nerve stimulation can decrease cardiac contractility by 30%.
Role of Acetylcholine
- Acts as the main neurotransmitter for the parasympathetic nervous system.
- Binds to muscarinic receptors, leading to a decrease in SA node discharge.
- Slows conduction velocity through the AV node.
Effects of Parasympathetic (Vagal Nerve) Stimulation
- Triggers the release of acetylcholine, resulting in decreased sinus node activity:
- Weak to moderate stimulation can halve the heart rate.
- Strong stimulation can completely halt rhythmical excitation.
- Can block conduction between atria and ventricles via the AV node:
- May cause ventricles to temporarily cease beating for 5 to 20 seconds.
- Purkinje fibers may initiate their own rhythm (ventricular escape) at a rate of 15 to 40 beats per minute.
Mechanism of Hyperpolarization
- Stimulation increases permeability of cardiac cell membranes to potassium ions, leading to hyperpolarization.
- Potassium leaks rapidly out of conductive fibers, causing a more negative resting membrane potential in the SA node (-65 to -75 mV).
Parasympathetic Nervous System
- Originates in the dorsal motor nucleus of the medulla.
- Innervates sinoatrial (SA) and atrioventricular (AV) nodes, as well as atrial muscle fibers.
Acetylcholine
- Acts as the primary neurotransmitter for the parasympathetic nervous system.
- Binds specifically to muscarinic receptors.
- Decreases the discharge rate of the SA node.
- Slows down conduction velocity through the AV node.
Parasympathetic (Vagal Nerve) Stimulation
- Triggers the release of acetylcholine, leading to a decreased rate of the sinus node.
- Weak to moderate stimulation can slow the heart rate to as low as half its normal rate.
- Strong stimulation can result in a complete halt of rhythmic excitation.
- Can fully block transmission from the atria to the ventricles via the AV node.
- Ventricle activity may cease for a duration of 5 to 20 seconds during strong stimulation.
- Purkinje fibers can take over with an escape rhythm of 15 to 40 beats per minute if ventricular activity stops.
Effects on Cardiac Cell Membranes
- Vagal stimulation enhances potassium permeability in cardiac cell membranes, leading to hyperpolarization.
- This causes a rapid outflow of potassium from conductive fibers, resulting in hyperpolarization.
- In the SA node, this hyperpolarization adjusts the resting membrane potential from -65 mV to -75 mV, making it more negative.
Parasympathetic Nervous System
- Originates in the dorsal motor nucleus of the medulla.
- Innervates the sinoatrial (SA) and atrioventricular (AV) nodes, as well as atrial muscle fibers.
Acetylcholine
- Acts as the primary neurotransmitter for the parasympathetic nervous system.
- Binds specifically to muscarinic receptors.
- Decreases the discharge rate of the SA node.
- Slows conduction velocity through the AV node.
Parasympathetic (Vagal Nerve) Stimulation
- Increases the permeability of cardiac cell membranes to potassium ions, leading to hyperpolarization.
- Rapid potassium leakage from conductive fibers significantly contributes to hyperpolarization.
- Causes the resting membrane potential of the SA node to become more negative, shifting from -65 mV to -75 mV.
Baroreceptors and Their Function
- Baroreceptors detect changes in arterial pressure through mechanical stretching.
- Increased arterial pressure results in the transmission of signals to the central nervous system (CNS).
- Feedback signals are sent back through the autonomic nervous system to lower arterial pressure as a response to stretching.
Signal Transmission Pathways
- Carotid baroreceptors send signals via Hering’s nerves to the glossopharyngeal nerves.
- These signals reach the nucleus tractus solitarius located in the medulla of the brainstem.
- Aortic baroreceptors, located in the arch of the aorta, transmit signals through vagus nerves to the same nucleus tractus solitarius in the medulla.
Baroreceptors and Their Function
- Baroreceptors detect changes in arterial pressure through mechanical stretching.
- Increased arterial pressure results in the transmission of signals to the central nervous system (CNS).
- Feedback signals are sent back through the autonomic nervous system to lower arterial pressure as a response to stretching.
Signal Transmission Pathways
- Carotid baroreceptors send signals via Hering’s nerves to the glossopharyngeal nerves.
- These signals reach the nucleus tractus solitarius located in the medulla of the brainstem.
- Aortic baroreceptors, located in the arch of the aorta, transmit signals through vagus nerves to the same nucleus tractus solitarius in the medulla.
Chemoreceptor Reflexes Overview
- Chemoreceptor cells detect low oxygen and elevated levels of carbon dioxide and hydrogen ions.
- They stimulate nerve fibers that travel through Hering’s nerves and the vagus nerve to the vasomotor center in the brainstem.
Locations of Chemoreceptors
- Carotid bodies: Found at the bifurcation of each common carotid artery (two in total).
- Aortic bodies: Located adjacent to the aorta (three in total).
Activation Mechanism
- A critical drop in arterial blood flow triggers chemoreceptors due to decreased oxygen levels and increased carbon dioxide and hydrogen ion concentrations.
- These receptors excite the vasomotor center, resulting in increased arterial pressure to restore normal levels.
Influence of Humoral Factors
- Circulating catecholamines affect heart rate independently from the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS).
- In denervated hearts after orthotopic heart transplantation, exercise stimuli still induce tachycardia due to elevated circulating catecholamine levels.
Activation of Myocardial β1-Adrenergic Receptors
- Heart rate can be increased by direct pharmacologic agonists that activate myocardial β1-adrenergic receptors.
- Key pharmacological agents include:
- Isoproterenol
- Epinephrine
- Indirect agents that can cause the release of endogenous catecholamines include ephedrine.
- Certain drugs that impair catecholamine metabolism or reuptake, such as cocaine, also influence heart rate.
Local Anesthetics
- High concentrations inhibit conduction by binding to fast sodium channels.
- Depress the sinoatrial (SA) node function, affecting heart rhythm.
- Bupivacaine is identified as the most cardiotoxic local anesthetic.
- Local anesthetics bind to inactivated fast sodium channels, leading to suppression or blockade in regional anesthesia.
- Result in bradycardia and hypotension due to inhibition of sympathetic ganglia, promoting parasympathetic dominance.
Opioids
- Fentanyl and sufentanil are commonly used opioids in anesthesia.
- These opioids can depress cardiac conduction but simultaneously increase atrioventricular (AV) conduction.
- They enhance the refractory period of the heart, allowing for better control of heart rhythm.
- Prolonged duration of action potential in Purkinje fibers can affect overall cardiac output.
Volatile Anesthetics
- Volatile anesthetics lower the automaticity of the SA node, impacting heart rate.
- Exhibit a moderate depressant effect on the AV node, potentially altering conduction pathways.
- The use of anticholinergics during general anesthesia can lead to junctional tachycardia, a specific heart rhythm disturbance.
Diastole
- Initiated by the closure of the aortic valve (or pulmonic valve).
- Ends with the closure of the mitral valve (or tricuspid valve).
- Involves ventricular relaxation and filling with blood.
- Allows blood vessels to return blood to the heart, preparing for the next contraction of the ventricles.
Systole
- Begins with the closure of the mitral valve (or tricuspid valve).
- Ends with the closure of the aortic valve (or pulmonic valve).
- Characterized by ventricular contraction, pushing blood into the arteries.
- During contraction, ventricular pressure exceeds that of adjacent blood vessels, enabling blood flow through the valves into circulation.
Phases of the Cardiac Cycle
- Ventricular Filling: Blood enters the ventricles; mitral valve opens due to high pressure from blood vessels, leading to ventricular expansion.
- Isovolumic Contraction: Ventricular contraction begins; pressure rises without blood ejection as both mitral and aortic valves are closed.
- Ventricular Ejection: Blood is expelled from the ventricles when pressure exceeds arterial pressure; aortic and pulmonary valves open.
- Isovolumic Relaxation: Follows ventricular contraction; both valves are closed while ventricle pressure decreases, allowing for new filling.
Ventricular Volume
- End-Systolic Volume: Amount of blood remaining after ventricular contraction is approximately 50 ml.
- End-Diastolic Volume: Volume of blood in the ventricles at the end of filling, approximately 120 ml.
Diastolic Pressure
- Begins around 2 to 3 mmHg and rises to about 5 to 7 mmHg by the end of the diastolic phase.
Diastole Phases
- First Third: Rapid filling of the ventricles as blood flows in quickly.
- Middle Third: A small amount continues entering the ventricles from the atria.
- Last Third: Atrial contraction adds additional inflow, accounting for roughly 20% of total ventricular filling.
Ventricular Filling Mechanics
- The opening of the mitral valve initiates ventricular filling; closure of the mitral valve marks the start of systole.
- S1 heart sound occurs with the closure of the mitral and tricuspid valves.
Isovolumic Contraction Details
- The period immediately following ventricular contraction; pressure builds up slightly before the aortic valve opens.
- A duration of 0.02 to 0.03 seconds is needed for sufficient pressure buildup.
Ventricular Ejection Process
- Left ventricular pressure peaks at approximately 80 mmHg while right ventricular pressure is around 8 mmHg.
- Healthy ventricles typically eject more than 60% of blood volume.
- Ejection period: first third (rapid ejection, 70%) and last two thirds (slow ejection, 30%).
- The closing of the aortic valve produces the S2 heart sound.
Isovolumic Relaxation Overview
- Occurs immediately after ventricular systole, lasting 0.03 to 0.06 seconds.
- Intraventricular pressure drops rapidly as distended arteries push blood back towards ventricles, closing aortic and pulmonary valves.
- Very low pressure in the ventricles creates a gradient that facilitates mitral valve reopening for the next filling phase.
Preload
- Preload indicates ventricular stretch at the end of diastole, directly linked to the volume of blood in the ventricles before contraction.
- Influenced by factors such as venous return and ventricular compliance.
- Venous return can be affected by variations in PPV (Positive Pressure Ventilation), changes in posture, tachycardia (heart rates exceeding 120 beats/min), ineffective atrial contraction seen in supraventricular arrhythmias, and pericardial pressure.
Afterload
- Afterload is the resistance the heart faces when pumping blood, critical for understanding cardiac function.
- Primarily determined by systemic vascular resistance and the resistance in the aorta the left ventricle must overcome.
- Left ventricular afterload typically equals systemic vascular resistance, which is influenced by arteriolar tone.
Frank-Starling Law
- Describes the relationship between stroke volume (SV) and end-diastolic volume (EDV), emphasizing the heart's intrinsic ability to adapt to varying blood inflow.
- As blood volume increases in the ventricles, the heart muscle fibers stretch, enhancing the heart's pumping effectiveness.
Stroke Volume (SV)
- SV represents the volume of blood pumped with each heartbeat, influenced by preload, afterload, and contractility.
- Increased preload (ventricular filling) generally leads to increased stroke volume.
End-Diastolic Volume (EDV)
- EDV refers to the blood volume in the ventricles right before contraction, primarily defining preload.
- A greater volume in the ventricles results in more stretch of cardiac muscle fibers, enhancing the force of contraction.
Mechanism of Cardiac Contraction
- Ventricular filling causes stretching of the cardiac muscle, increasing contraction force within physiological limits.
- The stretching of heart muscle aligns actin and myosin filaments to an optimal degree of overlap, allowing for enhanced force during contraction.
- Increased blood flow leads to greater stretch and, consequently, stronger contractions.
Bainbridge Reflex and Myocardial Function
- Increased blood volume triggers afferent signals via the vagus nerve to the medulla.
- Efferent signals from the medulla enhance heart rate (HR) and myocardial contractility.
- Myocardial contractility can be reduced by factors such as anoxia, acidosis, catecholamine depletion, and loss of functional muscle mass due to ischemia or infarction.
Coronary Blood Supply
- Nutrition for the inner 0.1 mm of the endocardium comes directly from blood in cardiac chambers.
- Remaining cardiac tissue nutrition is solely from right and left coronary arteries.
Right Coronary Artery (RCA)
- Supplies right atrium, most of right ventricle, and parts of left ventricle.
- In 85% of individuals, RCA branches into the posterior descending artery (PDA), supplying the superior-posterior intraventricular septum and most of the left ventricle.
Left Coronary Artery (LCA)
- Supplies left atrium, most of intraventricular septum, and majority of left ventricle.
- Bifurcates into left anterior descending artery (LDA) and left circumflex artery (CX).
- LDA supplies septum and anterior wall.
- CX supplies lateral wall.
Coronary Blood Flow
- Average resting coronary blood flow is 70 mL/100g of heart weight, equivalent to 250 mL/min (~5% of total cardiac output).
- During strenuous exercise, cardiac output (CO) can increase by 4 to 7 times, with coronary blood flow rising 3 to 4 times.
Coronary Perfusion Pressure (CPP)
- Calculated as CPP = Diastolic Blood Pressure (DBP) - Left Ventricular End-Diastolic Pressure (LVEDP).
Factors Affecting Coronary Blood Flow
-
Physical Factors:
- Coronary perfusion pressure is the key factor, impacted by aortic pressure and LV/RV pressures.
- Myocardial contraction can compress coronary arteries and affect flow.
-
Neural Factors:
- Sympathetic nervous system (SNS) activity increases coronary blood flow when aortic pressure is high enough.
- Vagal stimulation has little effect on coronary artery caliber.
- β2-adrenergic receptors mediate vasodilation in small arterioles, contributing to ~25% of exercise-induced coronary vasodilation.
-
Metabolic Factors:
- Increased myocardial metabolism drives most coronary vasodilation.
Myocardial Oxygen Demand Determinants
- Heart Rate: Primary determinant; a 50% increase in HR raises oxygen consumption by 50%.
- Preload: Minor contributor; a 50% increase in preload raises demand by only 4%.
- Contractility: Major contributor; a 50% increase in contractility raises demand by 45%.
- Afterload: Major contributor; a 50% increase in afterload raises demand by 50%.
- Electrical Conduction: Contributes 0.5-5% of total cardiac oxygen demand.
- Basal Cardiac Metabolism: Influenced by temperature (hypothermia lowers metabolic rate and oxygen consumption).
Increased Oxygen Demands
- The myocardium extracts 65% to 70% of available oxygen from hemoglobin.
- During high oxygen demand, coronary arteries vasodilate, leading to a 3-4 fold increase in blood flow.
Vasodilatory Substances
- Decreased oxygen delivery prompts release of vasodilatory substances such as:
- Adenosine (primary vasodilator)
- Adenosine phosphate compounds
- Potassium ions
- Hydrogen ions
- Carbon dioxide
- Bradykinin
- Prostaglandin
Lung Volumes
- Tidal Volume (TV): The volume of air inhaled and exhaled during normal breathing, typically around 500 mL.
- Inspiratory Reserve Volume (IRV): The additional volume of air that can be inhaled beyond the normal tidal volume with a forceful inspiration, typically around 3000 mL.
- Expiratory Reserve Volume (ERV): The additional volume of air that can be exhaled beyond the normal tidal volume with a forceful expiration, typically around 1100 mL.
- Residual Volume (RV): The volume of air remaining in the lungs after a forceful expiration, typically around 1200 mL. This volume ensures the lungs remain expanded and alveoli open.
Lung Capacities
- Inspiratory Capacity (IC): The total volume of air that can be inhaled, including both tidal volume and inspiratory reserve volume (TV + IRV), typically around 3500 mL.
- Functional Residual Capacity (FRC): The volume of air remaining in the lungs after a normal expiration, including expiratory reserve volume and residual volume (ERV + RV), typically around 2300 mL. This volume can be indirectly measured using helium dilution and represents the alveolar gas used for oxygenation between breaths or during apnea.
- Vital Capacity (VC): The total volume of air that can be forcefully exhaled after a maximal inhalation, including tidal volume, inspiratory reserve volume, and expiratory reserve volume (TV + IRV + ERV), typically around 4600 mL.
- Total Lung Capacity (TLC): The maximum volume to which the lungs can be expanded with maximal effort, including residual volume and vital capacity (RV + VC), typically around 5800 mL.
Other Measures
- Minute Respiratory Volume (MRV): The total amount of new air moved into the respiratory passages each minute, calculated by multiplying tidal volume by respiratory rate (TV x RR), typically around 6 L/min.
- Closing Volume: The point during exhalation when small airways collapse. Closing capacity is the sum of closing volume and residual volume. Closing volume is usually below residual volume but increases with age, especially after 70. Conditions such as supine position, pregnancy, obesity, COPD, CHF, and any factor decreasing residual volume can increase closing volume.
- Alveolar Ventilation: The volume of fresh air reaching the alveoli per minute. It's calculated by subtracting the anatomic dead space from tidal volume, and then multiplying by the respiratory rate ((TV - anatomic dead space) x RR), typically around 4200 mL/min.
- Perfusion: The blood flow to the lungs, which is equal to cardiac output (CO), calculated by multiplying heart rate by stroke volume (CO = HR x SV), typically around 5000 mL/min.
Spirometry
- Spirometry: Measures the volume of air movement into and out of the lungs. Spirometry involves using a device called a spirometer, which is used to measure the volume of air inhaled and exhaled by a person.
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