Fahim Khan Heart Anatomy and Electrocardiography Purpose The heart is a multivalve organ sequenced activation of muscle electrocardiogram

(EKG/ECG). How dynamical structure of the heart as it Introduction The heart is a sophisticated organ comprised of cardiac muscle tissue (the myocardium), connective tissue, nerve connections (e.g. vagus), and some adipose tissue (e.g. in myocardium). The mammalian heart has four chambers—the right/left atria and right/left ventricles—separated by valves – the tricuspid valve separates right atrium and right ventricle; the pulmonary valve connects the pulmonary artery leading from the right ventricle to the lungs; the bicuspid valve separates the left atrium and left ventricle; the semilunar aortic valve prevents backflow of blood from aorta to left ventricle as blood leaves the heart to the rest of the body. There are several major blood vessels connected to the heart - the vena cavae transport deoxygenated blood to the heart, the pulmonary artery transfers blood from the right ventricle to the lungs for oxygenation, the pulmonary vein takes newly oxygenated blood to the left atrium, and the aorta transports oxygenated blood to the rest of the body. The heart is sheathed in a connective tissue sac called the visceral pericardium. The heart beats by the sinoatrial node (the “pacemaker”) causing the atria to contract and activating the atrioventricular node, which belatedly passes on the electrical impulse branching down the Purkinje fibers to the apex of the heart causing the ventricles to contract a short while after the atria contract (diastole then systole). An EKG records the electrical impulses that allow a heart to beat, printing a graph showing the voltage of the electric impulse as a function of time. The waveform is periodic, as the heart’s pumping is rhythmic – the short P wave represents the SA node firing, then a sharp QRS wave for ventricular contraction (fast depolarization), and a subsequent long T wave as the heart muscles repolarize. Analysis Questions 1. Waveform frequency is a very important EKG datum, as it tells us exactly how hard the heart is working (if we look at an entire PQRST curve segment) or how efficiently the heart is doing its job (if we look at, say, the length of the PQ segment then we can use the information to compute the volume of blood that the ventricles pump) or even if certain structures that pumps blood by a well-defined contractions, as observable by an does the EKG waveform reflect the rhythmically pumps?

of the heart are malfunctioning (if the SA node stops working, then there is no P wave in the EKG). Tachycardia and bradycardia is diagnosed by looking at the rate at which the heart is beating (too fast or too slow, respectively), and that is represented by EKG wave frequency.

2. Since an EKG is only recording the voltage information (of a rather large
surface area), it can fundamentally only provide insight related to electrical phenomena such as cardiac muscle depolarization. An EKG is abnormal when the broad de/repolarization data that is being collected is abnormal. So, problems can be detected when it is something macroscopic, like the SA or AV nodes, malfunctioning and affecting the depolarization rhythm. 3. The Achilles heel of EKG data is that it is necessarily electrical and macroscopic in nature. While such a limitation is not usually problematic, it is also true that the heart’s function is affected by many more things than simply how the muscles work and that small defects can cause big problems. Blood clots in the heart are not always detectable— approximately one in four people who suffer a heart attack do not show any EKG evidence of their compromised heart—because they only hurt a limited sample of cardiac muscle (so the statistics-based EKG data is not dramatically affected). 4. Fibrillation occurs when the SA node is not working properly or at all. Since the SA node is the pacemaker of the heart i.e. it synchronizes the depolarization times of all the cardiac muscle cells, the cells contract and relax with no overall order. The waveform has no detectable pattern because cells are continually and randomly depolarizing. 5. My normal EKG has a PQRST wave frequency of approximately 2 every second. During and right after exercise, the frequency jumps to about 2 and 2/3 every second. This is so because my heart has to pump blood at a faster rate to satisfy my muscles’ higher oxygen and nutrient craving. Wave amplitudes did not change significantly probably because my cardiac muscles are already working at maximum power (sustained tetanus, I would think). The waveform became more noisy i.e. showed a lot of small seemingly random increases and decreases in amplitude, without a change in overall wave shape/behavior. I think this might be for the same reason as to why skeletal muscles twitch when under stress – probably tiny arrhythmias from incomplete summation falloff.

Data

Before Exercise Interval P–R QRS Q–T Time (s) .25 .1 .25

After Exercise Time (s) .2 .06 .22

Heart Rate (Max)

273 beats/min

Conclusion The lab was very engaging – I had a lot of fun. I realized during the dissection that I had forgotten some notable ideas about the heart anatomy, and so I remembered or relearned those things. Furthermore, I had a better understanding and appreciation of the heart’s physiology the second time around. The EKG also went much more smoothly and made a lot more sense than the first time that I had to monitor EKG in AP Biology – I suppose the reason for this is that I have a much better understanding of cardiac muscle function now than I had back then. I was pleasantly surprised when my EKG was chosen as the model for the analysis. I had no idea that my heart is as healthy (or at least normal), and that is a comforting piece of knowledge.

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