atrioventricular node

AV node

cardiac output

CO

electrocardiogram

EKG

the outermost layer of the heart wall

sinoatrial node

SA node

• AV valves (atrioventricular valves)
• tricuspid
• mitral
• pulmonary semilunar valve
• aortic semilunar valve

• Cardiac fibers are connected by gap junctions, allowing excitation to spread throughout the heart by moving from one fiber to another.
• Some cardiac fibers are specialized for roles other than contraction.
• nodal fibers
•  serve as pacemakers, generating regular action potentials
• Nodal fibers of the sinoatrial (SA) node in the right atrium near the opening of the superior vena cava, and the atrioventricular (AV) node, near the junction of atrial and ventricular septa, are spontaneously active, giving the heart a property called automaticity.
• conducting fibers, 
• which form a conducting pathway that can rapidly transmit excitation between the atria and throughout the ventricular mass. 
• The conducting fibers of the ventricular mass are called Purkinje fibers. 

During each heartbeat, all of the cardiac fibers are activated. Each heartbeat is the result of a single action potential in each cardiac fiber.

• blood flows through the atria and into the ventricles under the relatively low pressure of blood in veins (several mm Hg);
•  this is referred to as the period of passive filling. 
• Contraction of the atrium adds a small amount of blood to the ventricle (perhaps 10 percent or so under resting conditions); 
• at this point, the ventricle contains its end-diastolic volume (EDV) of blood.

• the pressure of the ventricular blood immediately exceeds the venous pressure, closing the AV valves. 
• At this point the ventricle is contracting as a closed container, so this phase of the cycle is called the period of isovolumetric contraction. 
• When the ventricle raises its pressure to a value that exceeds the arterial pressure, the bicuspid valve opens and a stroke volume of blood is ejected into the artery, rapidly raising the arterial pressure from the diastolic pressure, the minimum value reached just before ejection, to the systolic pressure, the value achieved at the peak of ejection. 
• After ejection, the bicuspid valve closes and the ventricle undergoes isovolumetric relaxation. 
• At this point, the ventricle contains the end-systolic volume of blood. This phase ends when ventricular pressure falls to the venous value, allowing the AV valves to open and passive filling to begin again.

• The heart can maintain a regular rhythm (automaticity) and also modulate its force to meet demand without any neural input 
• Autonomic inputs can modulate both the heart rate (a chronotropic effect) and the contractility or force-generating potential of the heart (an inotropic effect). 
• The classical neurotransmitter released by the parasympathetic postganglionic neurons is acetylcholine (ACh) and the heart, like most other visceral effectors, has muscarinic receptors for ACh. 
• The sympathetic branch can deliver both norepinephrine from its postganglionic fibers and epinephrine from the adrenal medulla via the bloodstream. 
• The adrenergic receptors of cardiac muscle are primarily of the beta-1 type, which can respond to both norepinephrine and epinephrine.

superior venae cavae

inferior venae cavae

coronary sinus

the tricuspid valve

(right atrioventricular valve)

• blood enters the right atrium
• passes through the tricuspid valve
• enters the right ventricle
• is pumped through the pulmonary simlunar valve that leads to the pulmonary trunk
• the pulmonary trunk branches into the right and left pulmonary arteries that carry blood to the lungs

• blood enters the left atrium from the 4 pulmonary veins which return oxygenated blood to the heart
• blood passes through the mitral or bicuspid valve
• enters the left ventricle
• contraction of the left ventricle forces blood through the aortic semilunar valve into the aorta

circumflex artery

right coronary artery

anterior interventricular artery

posterior interventricular artery

the SA node

about 100 action potentials/minute in the lack of any external input.

the membrane potential is relatively stable during the interval between heartbeats.

at the beginning of a hearbeat, a wave of excitation spreads from pacemakers through the myocardium.

when it reaches each individual myocardial cell and depolarizes it to threshold, this opens voltage-sensitive Na+ channels like those of neurons and skeletal muscle fibers, resulting in a similar rapid upstroke of the membrane potential.

the opening of L Ca++ channels, which remain open for most of the plateau period

a delay in the opening of voltage-sensitive K+ channels.

1. the SA nodal fibers reach threshold and generate an action potential.
2. Teh excitation spreads through atrial contracting fibers and a conducting system that connects the 2 atria, and atrial systole begins
3. in the meantime, the wave of excitation passing through atrial fibers approaches the AV node. 
4. excitation enters the AV node and then spreads into  the bundle of His. The bundle branches give rise to Purkinge fibers that rapidly spread the wave of excitation into the ventricular mass initiating ventricular systole. The wave of excitaiton has been followed by a wave of repolarization in the atria, allowing them to relax.
5. Ventricular repolarization occurs. The ventricles relax and the diastolic phase of a new cycle begins.

P wave

QRS complex

T wave

• atrail depolarization - P wave
• atrial repolarization - QRS complex
• Ventricular depolarization - T wave
• period when the whole mass of the atria is depolarized, when there is no voltage difference between different parts of the atria and no current flows around the tissue - baseline - PQ interval and 
• period when ventricles are completely depolarized - ST segment

low

high

valve closures.

normal sinus rhythm