Cardiac and Skeletal Muscle

Microscopic Structure of Cardiac Muscle

• Cardiac muscle tissue composes the myocardium
• Cardiac muscle cells area short and branched, containing one or two central nuclei
• Endomysium, a type of areolar connective tissue supports the cardiac muscle
• The sarcolemma (plasma membrane) invaginates to form T-tubules that extend into the sarcoplasmic reticulum
• Bundles of myofilaments surround the sarcoplasmic reticulum
• Myofilaments are arranged in sarcomeres, giving cardiac muscle a striated appearance under a microscope
• The optimal length of myofilaments (maximum overlap) occurs when the heart chamber is filled with blood, allowing for greater force of contraction

Intercellular Structures

• The sarcolemma is folded at connections between cells, increasing myocardial structural stability and facilitating communication
• Intercalated discs connect cells
• Desmosomes mechanically join cells using protein filaments
• Gap junctions electrically join cells, allowing ion flow and creating a functional syncytium, where each heart chamber acts as a functional unit

Cardiac Muscle Metabolism

• Cardiac muscle has a high energy demand requiring extensive blood supply and numerous mitochondria
• Fuel molecules that cardiac muscle use are: fatty acids, glucose, lactic acid, amino acids, and ketone bodies.
• Myoglobin and creatine kinase are present
• Cardiac muscle relies mostly on aerobic metabolism
• Ischemia can lead to failure when oxygen is low
• Cell death can be a result of interference with blood flow to heart muscle

The Heart's Conduction System

• The conduction system initiates and conducts electrical events to regulate timing of contractions
• Specialized cardiac muscle cells that have action potentials but do not contract, these cells have activity influenced by the autonomic nervous system
• The sinoatrial (SA) node (pacemaker) initiates the heartbeat and is located high in the posterior wall of the right atrium
• The atrioventricular (AV) node is located in the floor of the right atrium (near the right AV valve)
• The atrioventricular (AV) bundle (bundle of His) extends from the AV node through the interventricular septum and divides into left and right bundles
• Purkinje fibers extend from the left and right bundles at the heart's apex and course through the walls of the ventricles

Innervation of the Heart

• The cardiac center, located in the medulla oblongata, contains cardioacceleratory and cardioinhibitory centers
• Baroreceptors and chemoreceptors in the cardiovascular system send signals to the cardiac center
• Sympathetic and parasympathetic pathways transmit signals
• It can modify (but cannot initiate) the cardiac activity, influencing rate and force of heart's contractions
• Parasympathetic innervation decreases heart rate. Signals start at medulla's cardioinhibitory center and are relayed via vagus nerves (CN X)
• The right vagus nerve innervates the SA node, and the left vagus nerve innervates the AV node
• Sympathetic innervation increases heart rate and force of contraction; begins at medulla's cardioacceleratory center, relayed via neurons from spinal cord segments T1-T5 Extend to the SA node, AV node, myocardium, and coronary arteries, increasing coronary vessel dilation

Stimulation of the Heart

• Heart contraction needs two events:
• The conduction system that initiates and propagates an action potential
• Further action potentials are initiated to cause cardiac muscle contraction, this happens first in the atria and then the ventricles

Ectopic Pacemaker

• Ectopic pacemaker: Pacemaker other than SA node
• When conduction system cells other than the SA node have the ability to spontaneously depolarize it occurs
• These types of cells depolarize at slower rates than the SA node
• In the event of SA node impairment the AV node is the default pacemaker
• Inherent rhythm for AV node is 40 to 50 beats/min, that is fast enough to sustain life
• if cardiac muscle has a rate of between 20 to 40 beats/min, it is usually too slow to sustain life

Cardiac Muscle Cells at Rest

• Important components of Cardiac muscle cells:
• Contain Na+/K+ pumps, Ca2+ pumps, leakage channels for Na⁺ and K+
• Has a resting membrane potential of -90 mV
• Contain specific voltage-gated channels which are fast voltage-gated Na+ channels, slow voltage-gated Ca2+ channels, and Voltage-gated K+ channels
• Voltage channels are closed when cell is at rest

Electrical and Mechanical Events of Cardiac Muscle Cells

• Electrical action potentials in cardiac muscle:
• Depolarization: Impulse from conduction system (or gap junctions) opens fast voltage-gated Na+ channels, Na⁺ enters cell changing membrane potential from –90 mV to +30 mV, Voltage-gated Na⁺ channels start to inactivate
• Plateau: Depolarization opens voltage-gated K+ and slow voltage-gated Ca2+ channels, K+ leaves cardiac muscle cell as Ca2+ enters, stimulates sarcoplasmic reticulum to release more Ca2+, membrane remains depolarized
• Repolarization: Voltage-gated Ca2+ channels close while K+ channels remain open and membrane potential goes back to -90 mV
• Electrical events at the Sarcolemma of a Cardiac Muscle Cell:
• Mechanical events (crossbridge cycling): Ca2+ enters sarcoplasm from interstitial fluid and SR leading to contraction
• Ca2+ binds to troponin and initiates crossbridge cycling, that triggers Crossbridge formation, power stroke, release of myosin head, and reset of myosin head
• Ca2+ levels decrease leading to relaxation and channels close and pumps move it into SR and out of cell
• Cardiac muscle cannot exhibit tetany, it also has a long refractory period unlike skeletal muscle
• Myocardial cell’s plateau phase results in a refractory period of around 250ms
• The cell fully contracts and relaxes unlike it can fire again
• Cell is protected agains sustained (tetanic) contraction

Electrocardiogram (ECG)

• Electrocardiogram (ECG/EKG):
• Skin electrodes detect electrical signals of cardiac muscle cells
• A common tool for diagnostic purposes
• Waves:
  • P wave - Electrical change of atrial depolarization originating in SA node
  • QRS complex - Electrical change associated with ventricular depolarization
  • Atria simultaneously repolarize
  • T wave - Electrical change associated with ventricular repolarization
• Segments:
  • P-Q segment Associated with atrial cells' plateau, during atria contracting
  • S-T segment Associated with ventricular plateau, during ventricles contracting
• Electrical events of the heart and an ECG
  • Atria:
    • Atrial depolarization: recorded as the P wave, when muscle cells of atria stimulated to contract
    • Atrial plateau: recorded as PQ segment, when muscle cells of atria contract and relax
    • Atrial repolarization: cannot be seen on ECG
  • Ventricles:
    • Ventricular depolarization: recorded as the QRS wave, muscle cells of ventricles stimulated to contract
    • Ventricular plateau: recorded as ST segment, when muscle cells of ventricles contract and relax
    • Ventricular repolarization: recorded as T wave

Cardiac Arrhythmia

• Any abnormality in heart's electrical activity, heart blocks involve impaired conduction which may result in light-headedness, fainting, irregular heartbeat, chest palpitations
• First-degree AV block: PR prolongation Slow conduction between atria and ventricles
• Second-degree AV block Failure of some atrial action potentials to reach ventricles
• Third-degree AV block: complete Failure of all action potentials to reach ventricles
• Premature ventricular contractions Result from stress, stimulants, or sleep deprivation, and abnormal action potential within AV node or ventricles Not detrimental unless they occur in large numbers
• Atrial fibrillation: chaotic timing of atrial action potentials
• Ventricular fibrillation: chaotic electrical activity in ventricles Uncoordinated contraction and pump failure, Leads to death of heart cells Treated with paddle electrode defibrillator or automated external defibrillator (AED)

Overview of the Cardiac Cycle

• Cardiac cycle: all events in heart from the start of one heart beat to start of the next, includes both systole (contraction) and diastole (relaxation)
• Contraction increases pressure; relaxation decreases it; blood moves down its pressure gradient (high to low), valves ensure that flow is forward (closure prevents backflow)
• Ventricular activity is most important driving force
  • Ventricular contraction raises ventrical pressure which AV valves pushed shut pushing semilunar ones to open thus blood ejected
  • Ventricular relaxation lowers ventricular pressure, where semilunar valves close
  • No pressure pushing closed nor pressure from below keeping them open (AV)

Events of the Cardiac Cycle

• Beginning: as the cardiac cycle begins, four chambers at rest. Blood returns to atria thus leading to passive filling of ventricles where AV valves opern becuase atrial pressure > ventricular pressure and semilunar valves closed because pressure in ventricles < arterial trunk pressure
• Atrial Contraction and Ventricular filling: SA node starts atrial excitation, the atria contracts pushing all blood into ventricles, which fill to end-diastolic volume (EDV), Atria then relax for remainder of cardiac cycle
• Isovolumic Contraction: Purkinje fivers initiate ventricular excitation, ventricles contract with rising pressure which leads to pushing shut of AV valves and ventricular pressure is still less than arterial trunk pressure, so semilunar valves still closed
• Ventricular Ejection: Ventricles continue to contract so that ventricular pressure rises above arterial pressure, The force from ventricular pressure opens semilunar valves for blood to move from ventricles to arterial trunks, The amount volume of blood ejected is the Stroke volume (SV), Afterwards End systolic volume (ESV) is amount of blood remaining in ventricle after contraction finishes -ESV = EDV – SV: For example, 60 mL = 130 mL – 70 mL
• Isovolumic relaxation: Ventricle starts relaxing thus lowering expanding pressure more, closing all semilunar valves
• Atrial relaxation and ventricular filling: Atrial blood pressure forces AV valves open and allows blood to flow into the ventricles, Semilunar valves remain closed as arterial pressure is greater than ventricular pressure, leads to all heart chambers at a relaxed state
• Ventricular balance: Equal amounts of blood are pumped by left and right sides of the heart where Left heart pumps blood farther and so must be stronger (thicker) But ejected blood volumes must be the same or edema (swelling) can occur

Cardiac Output

• Cardiac output (CO) measured in liters per minutes is the amount of blood pumped by a single ventricle in one minute, that measures effectiveness of cardiovascular system by increases in healthy individuals during excersize
• The main factors determining cardiac output are heart rate (beats per minute) and stroke volume(amount of blood ejected per beat) -HR × SV = CO: For example, 75 beats/min × 70 ml/beat = 5.25 L/min
• Maintainting rest cardiac output is used to meet tissue needs

Variables That Influence Heart Rate and Stroke Volume

• Chronotropic agents change heart rate Alter the activity of nodal cells (SA and/or AV node), working via autonomic nervous system or hormones -Positive chronotropic agents increase heart rate: They enhance the Sympathetic nerve stimulation by release norepinephrine (NE) on heart plus adrenal is caused to release epinephrine (EPI) and NE, increasing thier firing rate -Negative chorontopic agents decrease heart rate: caused by Parasympathetic activity , because Parasympathetic axons release acetylcholine (ACh) onto nodal cells binding muscarinic receptors to open K+ channels, K+ exits cell making it more negative -This process can be manipulated by medications - Beta-blocker drugs interfere with EPI and NE binding to beta receptors - Treat high blood pressure via Autonomic reflexes - Baroreceptors and chemoreceptors by sending signals to cardiac center to alter cardiac output as needed
• Stroke volume is influenced by: venous return, inotropic agents, and afterload : Venous return is volume of blood returned to the heart and determines amount of ventricular blood prior to contraction : That is, end-diastolic volume (EDV)
  • Volume determines preload : Pressure stretching heart wall before shortening : Thus venous return may be increased by increased venous pressure or increased time to fill
  • Inotropic agents change stroke volume and alter contractility : force of contraction and generally due to a changes in Ca2+ available in sarcoplasm
  • Negative Agents : decrease available Ca2+ and thus lower contractility due to Elctrolyte imbalances such as increased K+ or H+ which leads to Ca2+ channel-blocking blood pressure drugs
  • Afterload : Resistance in arteries to ejection of blood by ventricles : It is is known that plaque increases afterload

Explore the comparison of skeletal and cardiac muscles, ECG interpretation with prolonged PR interval, ventricular contraction phases, factors affecting cardiac output, and the parasympathetic nervous system's influence on heart function.