heart beats

• Coordinated hearts occur because of:

  • presence of gap junctions
  • Intrinsic cardiac conduction system
• Intrinsic cardiac conduction system:

  • system of autorhythmic (noncontractile) cells
  • spread and distribute impulses to coordinate depolarization and contraction of heart
• Cardiac pacemaker cells:

  • unstable resting membrane potentials called pacemaker potentials or prepotentials
• Sinoatrial (SA) node

  • Pacemaker of heart in right atrial wall
  • Depolarizes faster than rest of myocardium
  • Generates impulses about 75×/minute (sinus rhythm)
  • Inherent rate of 100×/minute tempered by extrinsic factors
  • Impulse spreads across atria, and to AV node
•  Atrioventricular (AV) node

  • In inferior interatrial septum
  • Delays impulses approximately 0.1 second
  • Because fibers are smaller in diameter, fewer gap junctions
  • Allows atrial contraction prior to ventricular contraction

  Inherent rate of 50×/minute in absence of SA node input
• Atrioventricular (AV) bundle (bundle of His)

  • In superior inter ventricular septum
  • Only electrical connection between atria and ventricles
  • Atria and ventricles not connected via gap junctions
• 1. Right and left bundle branches

  • Two pathways in interventricular septum
  • Carry impulses toward apex of heart
• Subendocardial conducting network (Purkinje fibers)

  • Complete pathway through interventricular septum into apex and ventricular walls
  • More elaborate on left side of heart
  • AV bundle and subendocardial conducting network depolarize 30×/minute in absence of AV node input
  • Ventricular contraction immediately follows from apex toward atria
  • Process from initiation at SA node to complete contraction takes ~0.22 seconds
• • Contractile muscle fibers make up bulk of heart and are responsible for pumping action
  • Different from skeletal muscle contraction; cardiac muscle action potentials have plateau
• 1. Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell

  Positive feedback influx of Na+ causes rising phase of AP (from −90 mV to +30 mV)
• 1. Depolarization by Na+ also opens slow Ca2+ channels

  • At +30 mV, Na+ channels close, but slow Ca2+ channels remain open, prolonging depolarization
• After about 200 ms, slow Ca2+ channels are closed, and voltage-gated K+ channels are open

  • Rapid efflux of K+ repolarizes cell to RMP Ca2+ is pumped both back into SR and out of cell into extracellular space
• Difference between contractile muscle fiber and skeletal muscle fiber contractions:

  • AP in skeletal muscle lasts 1–2 ms; in cardiac muscle it lasts 200 ms
  • Contraction in skeletal muscle lasts 15–100 ms;  in cardiac contraction lasts over 200 ms
• • Benefit of longer AP and contraction:
  • Sustained contraction ensures efficient ejection of blood
  • Longer refractory period prevents tetanic contractions
• Electrocardiograph can detect electrical currents generated by heart
• Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity  

  • records every single action potential in the heart not just one
  • electrodes are placed everywhere through the body
• P wave: depolarization of SA node and atria

  QRS complex: ventricular depolarization and atrial repolarization

  T wave: ventricular repolarization

  
• Electrocardiography:

  P-R interval: beginning of atrial excitation to beginning of ventricular excitation

  S-T segment: entire ventricular myocardium depolarized

  Q-T interval: beginning of ventricular depolarization through ventricular repolarization
• Problems that can be detected with ECG:

  • Enlarged R waves may indicate enlarged ventricles
  • Elevated or depressed S-T segment indicates cardiac ischemia
  • Prolonged Q-T interval reveals a repolarization abnormality that increases risk of ventricular arrhythmias
  • Junctional blocks, blocks, flutters, and fibrillations are also detected on ECG
• Systole: period of heart contraction
• • Diastole: period of heart relaxation
• • Cardiac cycle: blood flow through heart during one complete heartbeat
  • Atrial systole and diastole are followed by ventricular systole and diastole
  • Cycle represents series of pressure and blood volume changes 
  • Mechanical events follow electrical events seen on ECG
• Ventricular filling: mid-to-late diastole

  • Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SL valves closed)
  • Atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle
  • Depolarization spreads to ventricles (QRS wave)
  • Atria finish contracting and return to diastole while ventricles begin systole
• End diastolic volume (EDV): amount of blood in a ventricle after diastole
• End systolic volume (ESV): volume of blood remaining in each ventricle after systole
• 1. Ventricular systole

  • Atria relax; ventricles begin to contract 
  • Rising ventricular pressure causes closing of AV valves
  • Two phases

  2a: Isovolumetric contraction phase: all valves are closed

  2b: Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL valves open

  • Pressure in aorta around 120 mm Hg
•  Isovolumetric relaxation: early diastole

  • Following ventricular repolarization (T wave), ventricles are relaxed; atria are relaxed and filling
  • Backflow of blood in aorta and pulmonary trunk closes SL valves
  • Causes dicrotic notch (brief rise in aortic pressure as blood rebounds off closed valve)
  • Ventricles are totally closed chambers (isovolumetric)
  • When atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again
• Heart sounds:

  • Two sounds (lub-dup) associated with closing of heart valves
  • First sound is closing of AV valves at beginning of ventricular systole
  • Second sound is closing of SL valves at beginning of ventricular diastole
  • Pause between lub-dups indicates heart relaxation
• • Mitral valve closes slightly before tricuspid, and aortic closes slightly before pulmonary valve
  • Differences allow auscultation of each valve when stethoscope is placed in four different regions
• • Heart rate can be regulated by:
  • Autonomic nervous system
  • Chemicals
  • Other factors
• • Autonomic nervous system regulation of heart rate
  • Sympathetic nervous system can be activated by emotional or physical stressors
• • Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing:
  • Pacemaker to fire more rapidly, increasing HR
  • EDV decreased because of decreased fill time
  • Increased contractility
  • ESV decreased because of increased volume of ejected blood
• • Because both EDV and ESV decrease, SV can remain unchanged
  • Parasympathetic nervous system opposes sympathetic effects 
  • Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels, which slows HR
  • Has little to no effect on contractility
• • Heart at rest exhibits vagal tone
  • Parasympathetic is dominant influence on heart rate
  • Decreases rate about 25 beats/min

  Cutting vagal nerve leads to HR of ~100
• • Atrial (Bainbridge) reflex: sympathetic reflex initiated by increased venous return, hence increased atrial filling
  • Atrial walls are stretched with increased volume
  • Stimulates SA node, which increases HR
  • Also stimulates atrial stretch receptors that activate sympathetic reflexes
• When sympathetic is activated, parasympathetic is inhibited, and vice-versa
• • Hormones
  • Epinephrine from adrenal medulla increases heart rate and contractility
  • Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine
• • Ions
  • Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function
  • Imbalances are very dangerous to heart
• Pacemaker potentials 


  K+ channels are closed and Na+ slow channels are open making the inside more positive
• depolarization 


  lots of Ca2+ comes in making the action potential rise