Atrial Relaxation

Early doctors were researching arrhythmia in heart beat as a result of unknown abnormal neuro-cardio mechanisms of the heart, one of theories was that SA and AV nodes were interfering with each other’s bio-electrical impulses another theory was that the right side of the septum was hypersensitive to electrical impulse, all were more else on the right track because we know now that SVT is a result of a faulty electrical connections of the heart.

4. Atrial hypertrophy would probably have what effect on an electrocardiogram? *spike the p wave

Premature beats that occur in the atria are called premature atrial contractions, or (PACs), premature beats that occur in the ventricles are called premature ventricular contractions or (PVCs). Another type of arrhythmia is tachycardia also known as fast heart rate, there are numerous of arrhythmias that fall under this category such as atrial fibliration, which means that the electrical signal don’t begin at the SA node instead they begin near the atria or nearby the pulmonary veins. The electrical signal will spread throughout the atria in a rapid disorganised way causing it to fibrillate hence tachycardia. Another type of tachycardia arrhythmia is Wolff-Parkinson-White syndrome or (WPW) syndrome is a condition in which the heart's electrical signals travel along an extra pathway from the atria to the ventricles. This extra pathway disrupts the timing of the heart's electrical signals and can cause the ventricles to beat very fast and can be life threatening.

Though data from vagal stimulation was disregarded, it is still important to mention the responses that should have been elicited had the vagus nerve been stimulated properly. The vagus nerve (cranial nerve X) is a part of the parasympathetic nervous system and reduce heart rate when given enough electrical stimulation. Vagal escape occurs when the vagus nerve has been stimulated to the point of the nerve ceasing to repolarize, and then resuming sending action potential for heartbeat. The result is a cease or slowing of heart rate temporarily, and then heart rate starting up again. When atropine is applied to the heart along with vagal stimulation, the atropine blocks any response the vagus nerve should send (Sarnoff et al,

of atria and ventricle. Impulses not being transmitted from atria to the ventricle; no whole number relationship between atrial and ventricular contractions was demonstrated.

Atrial fibrillation is a supraventricular tachyarrhythmia which results in very disorganized contractions of the atria. This disorganization can also be seen has electrical impulses that are fast, and chaotic. This prevents the atria from contracting or pumping blood into the ventricles. When applying what I

“An electrical signal from the ventricles causes an early heart beat that generally goes unnoticed”

Atrial fibrillation (AF) is the most common type of heart dysrhythmia which causes the irregular beating of the two atria in the heart. The cause of AF is multiple atrial ectopic foci firing randomly and chaotically. Atria rhythm can be completely disorganized at a rate of 350 to 600 times per minute by the multiple rapid impulses from numerous atrial foci, so the atria are in a quiver status; the ventricles beat with a rapid rate due to the rapid atrial impulses (Ignatavicius and Workman, 2013). The ventricular contraction rhythm can be 120 to 200 beats per minute. The ECG result shows a chaotic rhythm, no P waves, no atrial contractions, no atrial kick and irregular ventricular contractions. The rapid, irregular ventricular rate decreases

Shortly after the induction agent was given the patient became bradycardic (38 bpm) and hypotensive (75/36) for which he was given one bolus of atropine and one bolus of ephedrine. The rhythm then changed to a supraventricular bigemony with a rate of 120 bpm which continued in to the start of the operation with a rate between 130 and 150 bpm and a rhythm alternating between sinus, bigemonic and atrial fibrillation (AF). He remained in atrial tachycardia during the operation despite the attempted correction of possible causes through the intraoperative administration of fluids, peripheral vasoconstrictors and strong opioids, and the attempted correction of electrolyte

The heart is an organ that pumps blood around the body by using 2 separate pumps side by side. The left side of the pump deals with oxygenated blood from the lungs whereas the right one deals with deoxygenated blood from the body. Each pump has 2 chambers called atrium and ventricle. The walls of the atrium are thinner than the ventricle because the atrium only has to pump blood to a short distance (to the ventricle) whereas the ventricles need to pump blood to the rest of the body. The heart has 3 types of pacemaker cells called; Sino atrial (SA) node, Atrioventricular (AV) node and bundle of His which make up the electrical conduction system. SA node found in the right atrium sends a wave of depolarisation to the neighbouring muscle junction, to the left atrium by the Bachmann’s bundle and also to the AV node by the internodal tract. AV node delays the wave of depolarisation causing the ventricle to contract after the atria. The AV node causes that delay to allow all the blood to fully move from the atria to the ventricle then the ventricle can contract sending the blood out the heart. After the AV node has delayed the wave of depolarisation, the wave continues down by a bundle of His and the fibres split up by the Purkinje fibres allowing the muscle to get involved. The wave of electrical released from the fibres causes the ventricles to contract.

The right atria inter-nodal tracks and Bachmann's bundle conduct the SA-nodal activation throughout the atria initiating a coordinated contraction of the atria walls. Meanwhile, the impulse reaches the AV-node, which is the only electrical connection between atria and ventricles. The AV-node introduces an effective delay, allowing the contraction of the atria to complete before ventricular contraction is initiated.

More recent cases and retrospective reviews suggested that the ST segment elevation or depression, T wave inversion and prolonged QT interval were commonly identified (Chin, Branch & Becker 2005; Malik et al. 2015; Shoukat et al. 2013; Waller et al. 2013). In addition, case studies claimed that these observed abnormalities predominantly occurred in the anterior and lateral leads (Franco et al. 2010; Waller et al. 2013), suggesting impaired ventricular repolarisation in a cardiac cycle. These ECG patterns are commonly seen in patients with acute myocardial infarctions. However, in the setting of SAH, the changes of ECG pattern were not associated with coronary obstruction (Banki et al. 2006), but rather the reflection of autonomic dysfunctions that are induced by the neurological insults.

(2014), states that increased or prolonged PR interval is due to the delay of the conduction in the AV node. Due to this delay, the AV node, or the pacemaker of the heart, controls the electrical signal movement from the AV node to the His-Purkinje system. Prolonging the electrical signals from the AV to the His-Purkinje system, will increase the risk of Atrial Fibrillation. Atrial Fibrillation is the quiver of the atria. This gives rise to heart Arrhythmia, hence why the man's heart was skipping beats. As the heart is not functioning properly, it will not pump enough oxygenated blood back to the systemic circuit. Hence, further seeing that he did not receive enough blood to the lungs to be re-oxygenated. Low amounts of oxygen will further cause shortened breathing

A time that starts with contraction between the atria and ventricular relaxation is known as the cardiac cycle. The relaxation period also known as the diastole this occur when the chambers fills with blood. The blood will flow according to pressure. As the fluid from the vein into the left atrium the pressure gets higher and rises, initially move passively into the ventricles from the atria. As the left ventricle filled to its volume the mitral valves closes to prevent any backflow. The contraction from the left ventricle send the oxygenated blood by the aortic value to aorta as the semilunar valves closes to prevent backflow of blood into the left ventricles.

The signal then quickly passes though the AV bundle and excites the apex and base of the ventricles, beginning contractions.