Arrhythmia and Hypertension
This is a disruption in the rhythm normally kept by the SAN. Tachycardia is when it is over 100bpm while Bradycardia is when it is under 60. It has a number of causes with the most common being a lack of coronary circulation which causes some of the myocytes to lack oxygen. Myocytes which lack oxygen have altered impulse formation or altered impulse conduction meaning that the heart does not beat correctly. Altered impulse formation is associated with a change in the automaticity due to a problem with the SAN or impulses arising from areas over than the SAN. Altered impulse conduction is associated with a partial or complete block of electrical conduction within the heart. It often leads to reentry (when an impulse fails to die out and continues to propagate and re excite the heart).
Changes in cardiac structure like hypertrophy (when cells increase in size as opposed to hyperplasia when they increase in number), Electrolyte disturbances (Potassium and Calcium mainly) and some drugs can also cause arrhythmia.
Types of Arrythmia
Escape rhythms are for when the SAN or conductance or faulty so another pacemaker takes over to make sure heart does not stop. Can be atrial, junction all or ventricular. Escape beats tend to be later than usual as the pacemakers further down the sequence of contraction from the SAN have lower intrinsic rates (hence why SAN is the dominant pacemaker).
Ectopic focus is when part of the heart is stimulated and spontaneously starts firing in a pathway that you would not express. Can be enhanced automaticity (I.e. Faster). Cells with normal prepotential (pacemakers) can be under the influence of beta receptors. A normal cardiomyocyte can spontaneously fire due to ischaemia. This is due to the altered ionic balance either side of the membrane.
The spontaneous triggers are afterdepolarisations. They are coupled to preceding action potential. Early afterdepolarisations are end of phase 2-3 and delayed are end of phase 3.
Early afterdepolarisations more likely to occur when heart rate is slower as plateau stage is longer, sometimes the calcium ion channels can reactivated during the plateau should the plateau be long enough. L type channels could reactive end phase two, T type channels could reactivated end phase 3. Every additional spike of depolarisation could cause more waves of depolarisations in other adjacent cells and recruit more to make a contraction and trigger arrhythmia.
DADs are seen with increased heart rate. Some calcium is pumped out of cell some pumped back into SR Allowing cell to relax. In this case there is not enough time to pump the calcium back into SR causing even more calcium and increased calcium levels which do not drop. Calcium builds up and cell depolarises and hits threshold level to fire off an action potential at an unanticipated moment.
Usually Na/Ca exchange protein allows 3 sodium ions to flow into the cell to pump one calcium ion out. This pumps more positive ions into the cell and increases depolarisation. Toxic levels of cardiac glycosides can build up due to this.
When a cardiac impulse re excites a region through which the impulse has already passed. An extra systole is an isolated event, re-entry is when the cycle continues and causes more contraction.
Re-entry can be ordered on a fixed pathway in which you need to see if it is an anatomical problem. Random re-entry is continuously changing and can cause fibrillation.
For re-entry to occur you need a unidirectional block. Depolarisation will go round both sides of the block however if one side is less healthy than the other it will reach the other side of the block before the other. This will cause the depolarisation to go up the other side in the opposite direction to what it should do. Essentially damaged muscle does not conduct very well. This is not anatomical it is due to ischaemic damage.
Ischaemic muscle is slower to have an action potential with slower upstroke which may or may not pass on to the neighbouring cell. Muscles become out of sync and can cause fibrillation as they'll start recovering at different times.
Atrial flutter is damage to the heart causes altered conductance in the atria make the wave of depolarisation travel round and round the atria in an ordered fashion causing a "saw tooth" appearance on the base line of an ECG due to multiple p waves. The AV node activates irregularly as well so irregular QRS complexes. Makes ventricular tachycardia. Atrial fibrillation is when parts of atrial muscle switching on and off randomly. Lots of tiny re-entry circuits going round and round causing random twitches. Lots of tiny spikes on base line, no identifiable p waves as this is a disordered contraction.
This is high blood pressure. Blood pressure is defined as normal with systolic as 90-119mmHg and diastolic as 60-79mmHg. There is then prehypertension and stage one and stage 2 hypertension each with increasing blood pressure. The Systolic pressure increases by 20mmHg each stage and the diastolic increases by 10mmHg. There are also two classes of hypertension. Class 1 has an unknown cause when presented, this is primary or essential hypertension. The other class is secondary and has arisen secondarily from another know health problem such as renal or endocrine disease.