Electrical activity of heart PDF

Preview

Summary

HDT lecture notes...

Description

Electrical activity of heart • Some cardiac muscle cells are self-excitable or autorhythmic/myogenic. • These cells generate an action potential that spreads throughout the myocardium, causing the heart to contract as a single unit Structure of cardiac muscle:    



Cardiac muscle consists of interlacing bundles of cardiomyocytes (cardiac muscle cells). cardiac muscle is striated with narrow dark and light bands, due to the parallel arrangement of actin and myosin filaments that extend from end to end of each cardiomyocyte. Cardiomyocytes are often branched, and contain one nucleus but many mitochondria, which provide the energy required for contraction. A prominent and unique feature of cardiac muscle is the presence of irregularly-spaced dark bands between cardiomyocytes. These bands are known as intercalated enable contractile force to be transmitted from one cardiomyocyte to another A second feature of cardiomyocytes is the sarcomere, which is also present skeletal muscle. The sarcomeres give cardiac muscle their striated appearance and are the repeating sections that make up myofibrils.

Phases of ventricular action potential: (phase 0) (depolarisation) that is caused increase in fast Na+-channel conductance (gNa+) through fast sodium channels. This increases the inward directed, depolarizing Na+ currents (INa) that are responsible for the generation of these "fast-response" action potentials. At the same time sodium channels open, gK+ and outward directed K+ currents fall as potassium channels close. These two conductance make equilibrium potential for sodium (ENa), which is positive. Phase 1 represents an partial repolarization that is caused by the opening of a special type of transient outward K+ channel (Kto), which causes a short-lived, hyperpolarizing outward K+ current (IKto). However, because of the large increase in slow inward gCa++ occurring at the same time , the repolarization is delayed and there is a plateau phase in the action potential (phase 2). This inward

calcium movement ICa(L) is through long-lasting (L-type) calcium channels that open up when the membrane potential depolarizes to about -40 mV. This plateau phase prolongs the action potential duration and distinguishes cardiac action potentials from the much shorter action potentials found in nerves and skeletal muscle. The extended refractory period allows the cell to fully contract before another electrical event can occur. The action potential for heart muscle is compared to that of skeletal muscle. Repolarization (phase 3) occurs when gK+ (and therefore IKr) increases, along with the inactivation of Ca++ channels (decreased gCa++). Therefore, the action potential in non-pacemaker cells is primarily determined by relative changes in fast Na+, slow Ca++ and K+ conductances and currents. When g'K+ is high and g'Na+ and g'Ca++ are low (phases 3 and 4), the membrane potential will be more negative (resting state). When g'K+ is low and g'Na+ and/or g'Ca++ are high, the membrane potential will be more positive (phases 0, 1 and 2) when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positivefeedback mechanism of depolarization. This rapid influx of positively charged ions raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. This is due in large part to the opening of the slow Ca2+ channels, allowing Ca2+ to enter the cell while few K+ channels are open, allowing K+ to exit the cell. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca2+ channels close and K+ channels open, allowing K+ to exit the cell. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between 250 and 300 ms (simplified version of membrane potential of contactile cells)



Normal rhythm is determined by pacemaker: Normal cardiac rhythm is established by the sinoatrial (SA) node, a specialized clump of myocardial conducting cells located in the superior and posterior walls of the right atrium in close proximity to the superior vena cava. The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart. It initiates the sinus rhythm, or normal electrical pattern followed by contraction of the heart. (1) The sinoatrial (SA) node and the remainder of the conduction system are at rest. (2) The SA node initiates the action potential, which sweeps across the atria. (3) After reaching the atrioventricular node, there is a delay of approximately 100 ms that allows the atria to complete pumping blood before the impulse is transmitted to the atrioventricular bundle. (4) Following the delay, the impulse travels through the atrioventricular bundle and bundle branches to the Purkinje fibers, and also reaches the right papillary muscle via the moderator band. (5) The impulse spreads to the contractile fibers of the ventricle. (6) Ventricular contraction begin

 



Cardiac excitation-contraction coupling: Excitation-contraction coupling (ECC) is the process whereby an action potential triggers a myocyte to contract. When a myocyte is depolarized by an action potential, calcium ions enter the cell during phase 2 of the action potential through Ltype calcium channels located on the sarcolemma. Causes release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels ("ryanodine receptors"). Calcium released by the SR increases the intracellular calcium concentration The free calcium binds to troponin-C (TN-C) that is part of the regulatory complex attached to the thin filaments. When calcium binds to the TN-C, this induces a conformational change in the regulatory complex such that troponin-I (TN-I) exposes a site on the actin molecule that is able to bind to the myosin ATPase located on the



myosin head. This binding results in ATP hydrolysis that supplies energy for a conformational change to occur in the actin-myosin complex. actin and myosin filaments slide past each other thereby shortening the sarcomere length. At the end of phase 2, calcium entry into the cell slows and calcium is sequestered by the SR by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase), thus lowering the cytosolic calcium concentration and removing calcium from the TN-C. To a quantitatively smaller extent, cytosolic calcium is transported out of the cell by the sodiumcalcium-exchange pump. The reduced intracellular calcium induces a conformational change in the troponin complex leading, once again, to TN-I inhibition of the actin binding site. At the end of the cycle, a new ATP binds to the myosin head, displacing the ADP, and the initial sarcomere length is restored.

The electrocardiogram: • Measures the heart’s electrical conduction system • Detected by electrodes attached to the surface of the skin • Picks up electrical impulses generated by the polarization and depolarization of cardiac tissue • Current is transformed into waveform • Powerful diagnostic tool:  Rhythm disturbances (arrhythmias) Conduction disturbances (conducting tissue disease e.g. left bundle block) Marked left ventricular hypertrophy  Myocardial infarction e.g. ST elevation myocardial infarction (STEMI)  There are 6 limb leads and 6 chest leads

 Augmented leads are unipolar and use one limb electrode as the positive pole and take average inputs from the other 2 as the zero reference

 

All six leads (I, II, III, AVR, AVL, and AVF) meet to form six intersecting leads that lie in a flat “frontal” plane of the patients chest Each limb lead (I, II, III, AVR, AVL, and AVF) records from a different angle (viewpoint), to provide a different view of the same cardiac activity

Chest readings: 

To obtain the six standard chest leads, a positive electrode is placed at six different positions (one for each lead) on the chest

 ECG uses negative electrode as zero refernce  Leads I, ii, iii are bipolar they measure electrical potential between 2 of the 3 limbs

 chest leads view the heart from horizontal view  Unipolar leads, corresponding chest electrodes serve as positive pole  The reference negative value is the same for all chest leads and is calculated average from th 3 limb electrodes.

 Depolarization towards a lead produces a positive deflection  Depolarization away from lead produces negative deflection.



 

There are five prominent points on the ECG: the P wave, the QRS complex, and the T wave. The small P

wave represents the depolarization of the atria. The atria begin contracting approximately 25 ms after the start of the P wave. The large QRS complex represents the depolarization of the ventricles, which requires a much stronger electrical signal because of the larger size of the ventricular cardiac muscle. The ventricles begin to contract as the QRS reaches the peak of the R wave.



Lastly, the T wave represents the repolarization of the ventricles. The repolarization of the atria occurs during the QRS complex, which masks it on an ECG.

Step 1: calculate the rate  

Count the number of complete R wave to R wave in a 6 second rhythm strip, then multiply by 10. Option 2 – Find a R wave that lands on a bold line. – Count the number of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont)



Have to memorise!!!!!!!!!

Step 2: determine regularity  

Look at the R-R distances (using markings on a pen or paper). • Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?

Step 3: assess the P waves  

Are there P waves? • Do the P waves all look alike? Do the P waves occur at a regular rate? • Is there one P wave before each QRS?

Step 4: determine the PR interval  

PR interval – can reveal AV conduction problems in patients (Heart Block) Normal: 0.12 - 0.20 seconds. (3 - 5 small boxes)

Step 5: QRS interval • Normal: 0.04 - 0.12 seconds. (1 - 3 small boxes)

• Must measure QRS duration – need to check if it is greater than 0.12 seconds...