Cardiac Physiology

The Heart: A Functional Syncytium

• By that, I mean that the heart consists of many different cell types that must work together as a single unit in a very specific way in order to efficiently pump blood through the body and keep us alive. The electrical and mechanical portions of the heart must work concurrently, or else there is pathology.
  • For example, a benign arrhythmia (an electrical problem) over the course of many years can lead to heart failure (a mechanical problem).
• There are 3 different types of tissue. They show differences in structure and in function.
  • Nodal tissue – seen in the SA and AV nodes. These are the pacemakers of the heart and are able to generate electrical impulses by themselves.
    • The SA node lies in the wall of the right atrium near the opening of the SVC. The AV node lies in the interatrial septum.
  • Conductile tissue – the His-Purkinje systems. These fibers are modified cardiac muscles cells that are specialized for conduction. This is non-pacemaker tissue because the cells do not show automaticity like the SA or AV nodes.
    • The bundle of His begins at the AV node and runs along the membranous part of the interventricular septum. It splits into right and left bundle branches, which branch into Purkinje fibers that supply ventricular walls. This system allows for cardiac muscles to contract together and expel blood out of the ventricles.
  • Contractile tissue – the actual cardiac muscle cells that generate the force to expel blood.

The EKG Actually Means Something 

• The EKG is helpfully clinicially because:
  • It tells you about the health of the heart.
  • It shows the heart’s response to drugs.
  • It can show different pathologies.
• The EKG (P—QRS—T waves) is a clinical tool that allows us to visualize the sequence of depolarization (NOT CONTRACTION) in a normal electrical cascade.
• Only depolarization in large structures of the heart is noted. Thus, we can see where the atria and ventricles are depolarized, but depolarization of smaller structures such as the SA node is not usually visualized as a waveform.
  • The signal starts at the SA node. The SA node is the dominant pacemaker of the heart and determines the heart rate in normal cases. In SA nodal cells we see the unique feature of Phase IV diastolic depolarization (which we will visit a bit later).
  • Next comes atrial depolarization (this is the P-wave of the EKG)
  • The PQ interval represents depolarization of the AV node, bundle of His, left and right bundle branches and Purkinje fibers.
  • The QRS complex represents synchronous ventricular depolarization. Lost somewhere in the QRS waveform is atrial repolarization.
  • The ST segment represents systole or ventricular contraction. Remember that ventricular contraction follows ventricular depolarization.
  • The T wave represents ventricular repolarization.
    • Will be changed in pathological states and in response to certain drugs.
    • Cardiac glycosides affect the Na/Ca exchanger involved in ventricular repolarization. Thus, T-wave changes are noted in response to administration of these drugs.
    • The T wave represents the vulnerable period of EKG. Basically, it is a point where not all heart cells are repolarizing at the same rate(the heart is in a sense heterogeneous at this time). If an ectopic beat falls on a T wave (known as the “R on T” phenomenon) it can lead to ventricular tachycardia or fibrillation. This is commonly seen in toxicity to cardiac glycosides.
       

• Passage of the electrical signal through the AV node is the rate limiting step of getting impulses to the ventricles. It is the point of slowest conduction (see figure). It protects the ventricles in the case that the SA node has set a rhythm that is too fast or too irregular (A-fib, or A-flutter).
   
• It is the site of action of many drugs.
  • Ach (from the vagus nerve) and cardiac glycosides function in and increasing the time of passage through the AV node. This is reflected in a lengthened PQ interval on the EKG.

• There is homogeneity of activity in the healthy heart (except during a short period during the T-wave) . I.e., things work together. There is coordinated electrical and mechanical activity. In pathological states, there is heterogeneity of activity. Electrical and mechanical events may not be perfectly coordinated.
• EKG is limited in that there are so many different cell types involved that it cannot explain phatophysiology and drug action.

Autonomic innervation of the heart

• Supraventricular  tissues have both sympathetic and parasympathetic (vagal) innervation. Sympathetic innervation causes positive chronotropic (increase in heart rate) and positive ionotropic (increase in contractility due to increased intracellular Ca++) effects. Parasympathetic innervation causes negative chronotropy and inotropy.
• Ventricular tissue has only sympathetic innervation leading to a positive ionotropic effects. It makes sense that there are no chronotropic effects in ventricular tissue because the SA and AV nodes are located in supraventricular tissue.

Mechanical Physiology 

• Calcium entry into the non-automatic cell leads to contraction.
• The sarcoplasmic reticulum is an intracellular store of Ca++.
• The mitochondria is a long term regulator of Ca++.
•  The Na/Ca exchanger and Ca-ATPase are involved in getting rid of intracellular calcium. The Na/Ca exchanger is bidirectional (remember this for lecture on cardiac glycosides).

Cardiac Muscle Contraction

•  Tropomyosin covers the binding site and prevents actin-myosin interaction.
• Ca++ in the cell binds to troponin, which moves tropomyosin from the binding site.
• Actin and myosin then cross-bridge and shorten leading to muscle contraction.

Frank –Starling Mechanism 

• The Frank – Starling relationship basically says that at a certain sarcomere length (2.5 micrometers) there is optimal cross linking between actin and myosin and optimal force of contraction.
• If ventricular end diastolic pressure is high (too much stretching), due to the Frank-Starling relationship, Cardiac output will not be optimal.
• The graph also shows that in cases of heart failure, there is an altered cardiac function curve due to a defect in the cardiac machinery.

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