Cardiac conduction system anatomy, cellular action potentials, and surface ECG
the neat, orderly, classic four-phased action potential is seen only in the Purkinje cells of the heart
SA and atria fire first; this is the P wave on the surface ECG
then, the ventricular depolarization leads to QRS complex
repolarization is ventricular T complex
Key points of cellular APs
SA and AV nodes exhibit upsloping phase 4 diastolic action potentials; this is because they exhibit automaticity
phase 0 is due to Na+ channels in most cardiac cells except the AV node, where phase 0 involves Ca++
Normal ionic currents and cellular AP
phase 0 depolarization is Na-dependent
phase 2 is due to Ca and K
phase 3 repolarization is due to K
phase 4 is due to sodium pumps as well as Na/Ca exchanger
altered normal automaticity—for examples, SA node
abnormal automaticity: cells that don’t usually have automaticity exhibit it
triggered activity
Altered normal automaticity
occurs when normal pacemaker cells (SA, AV nodes) begin pacing at a non-physiologic rate
example: junctional tachycardia in the AV node; this can overdrive the pacemaker cells and drive the heart too quickly
Abnormal automaticity
Triggered activity
symptoms are typically caused by atrial-ventricular dissociation or decreased cardiac output
palpitations
lightheadedness
fatigue
dyspnea
syncope
sudden death
cardiac output (CO) is the product of stroke volume (SV) and heart rate (HR)
bradycardias decrease CO by decreasing heart rate
tachycardias decrease CO by decreasing SV (suboptimal filling; increased HR cannot compensate)
bradyarrhythmias
in normal hearts, specialized conduction tissues possess the ability to depolarize spontaneously
intrinsic rates: fast upper, slow lower
SA node 60-100 bpm
AV node 40-60 bpm, which is almost able to sustain life
His-Purkinje system, ventricles <>
AV node and His-Purkinje are less reliable than the SA node and backup rate might be too slow to maintain normal CO
Heparin
this anticoagulates patients right away, unlike coumadin
unfractionated heparin: given intravenously
LWMH: patients can give it themselves with injection at home
Warfarin
used in a majority of patients with atrial fibrillation
even if you go back to sinus rhythm, atrium can still be stunned, so still anticoagulate these patients
one exception is younger patients with no other medical problems (lone atrial fibrillation)
3-5 days to achieve full therapeutic effect; target INR is between 2 and 3
Antiarrhythmic drug therapy is rarely indicated in patients with benign arrhythmias except to relieve debilitating symptoms (e.g.- syncope, dizziness)
Because drug suppression of lethal arrhythmias is only successful in a minority of patients and because the risk of untoward effects (including death) is high, a variety of surgical procedures have been developed:
Radiofrequency (RF) catheter ablation has recently replaced surgical ablation in nearly all cases of ablation for cardiac arrhythmias. It is now a first-line therapy and highly effective in treating:
RF ablation is also useful in treating:
Automatic implantable cardioverter/defibrillator devices (ICDs)
Can now be implanted without thoracotomy
Current generation devices terminate arrhythmias by anticardiac pacing, cardioversion, and defibrillation
Considered by some experts to be the therapy of first choice in patients with ventricular tachycardias based on a number of recent clinical trials comparing ICD therapy to antiarrhythmic drug therapy (both Class I and Class III drugs)
A significant fraction of patients receiving an ICD may still require antiarrhythmic drug therapy to decrease the frequency of arrhythmic episodes (to prolong battery life) and to reduce the number of inappropriate (energy-consuming and painful) shocks. Improvements in ICD design may reduce or eliminate the need for concurrent drug therapy.
reguritation of blood back into atria
huge V wave
murmur heard during ventricular systole (between heard sounds 1 & 2)
increase in atrial pressure during ventricular contraction
In contrast to all of the other heart sounds so far, the gallops are low frequency events. They are much harder to hear and they are uniquely appreciated in the receiving ventricle of the pathology. For example, if you have a failing large LV and the LA is allowing blood to move into the LV causing this sound in the LV, you need to listen to the apex beat. If this is occurring due to a large failing RV, you would need to approximate the position of the RV apex, which is usually at the lower left sternal edge near the xiphoid process, to hear a right sided third heart sound. The other kind of gallop is the fourth heart sound, which is a presystolic sound. It precedes S1. The S3 is usually in the first half of diastole. Remember that S3 is a reflection of a failing ventricle or a volume overloaded ventricle such as in a ventricle of severe mitral regurgitation.
Demo of S3: you listen at the apex of the heart and hear a low frequency sound.
Demo of S4: also low frequency but it occurs right before S1.
Demo of S3 and S4 together: if the heart rate increases enough when you have both an S3 and an S4, you have a summation gallop. That is when S3 and S4 superimpose on each other, producing a loud single diastolic sound.
Hearing a third heart sound is an exceedingly important clinical observation. This is not found in normal individuals with the one exception of pregnancy. It’s found in very diseased ventricles and in very volume overloaded ventricles.
Heart murmurs have been classified in many ways, one of which is based on the timing of the murmur. Systolic murmurs have been divided into four types.
Midsystolic – occurs after S1 and before S2. This murmur usually has a shape of a crescendo/decrescendo pattern. It builds up to a max. intensity and then degrades. It has also been called a diamond shaped murmur or an ejection type systolic murmur b/c most of these murmurs are in fact ejection murmurs; they represent blood flow out of the aorta or out of the pulmonary artery. However, other valvular abnormalities can produce crescendo/decrescendo murmurs so that it is not particularly useful to call something an ejection murmur when it may not be. It’s best to call it a midsystolic murmur. This is the most common type of murmur that is appreciated clinically. It can represent a normal state, a so called innocent or benign murmur, simply due to increased velocity of blood flow or it can represent a structural abnormality of the heart.
Holosystolic (Pansystolic) – The second most common type of murmur. These begin with S1 and end with S2. If they originate in the left side of the heart they end with aortic closure. If they originate in the right side of the heart, they end with pulmonic closure. These murmurs remain relatively constant in intensity. They usually represent murmurs of AV (atrioventricular)valve regurgitation i.e. mitral or tricuspid insufficiency. They may also occur in ventricular septal defects or other congenital heart defects, but they are typically murmurs of AV valve regurgitation.
Early Systolic – Rare event. Begins with S1 and is a decrescendo murmur ending before S2. Usually occurs in one or two very different settings. It occurs in individuals with ventricular septal defects that are small and are physiologically closing. That is, as systole continues, there’s a gradient btwn. the left and right ventricles, hence a murmur is generated due to velocity. As the defect becomes smaller with systole (if it is a muscular VSD vs. a membranous VSD), you get a decrescendo murmur. Paradoxically, you can also hear these murmurs in the opposite extreme case, the so called Eisenmenger syndrome, where you have right sided pressures at systemic levels (almost equal pressure in RV and LV). During systole, these murmurs can abate simply b/c of equalization of pressures in the RV and LV. This is an extreme end- stage condition in patients with large VSDs.
Late Systolic – Also rare. Begins after S1 and goes into S2. This is the murmur of mitral valve prolapse that occurs due to a valve becoming incompetent during systole and allowing a gradient of pressure btwn the LV and LA until the end of systole.
