Question

Explain why there is an absence of electrical activity between the following on an ECG:

1. between the P wave and the Q wave

2. between the S wave and the T wave

Need detailed answers please.
Explain multiple mechanisms for how a tissue that has increased metabolic activity will gain increased blood flow.
Compare and contrast the excitation-contraction coupling mechanisms of skeletal muscle versus contractile cardiac muscle.

Answer 1

1.The flat line between the P wave and the starting of the QRS complex is known as the PR interval, where there is no electrical activity at all due to a slight impulse conduction through atrioventricular node.The PR interval is the time period between the starting of the atrial depolarization to the starting of the ventricular depolarization.It is the used to assess the speed of impulse transmission from atria to the ventricle.It should not be too short or long. The normal time period of a PR interval is 0.12-0.22 sec.It is used to assess the amplitude of the depolarization, acting as the base line.

2.ST segment starts from J point and ends at the starting of the T wave,which is the plateau phase of the action potential. It is flat (parallel to the base) because of two reasons:

• Because of long duration of the plateau phase, most of the contractile cells are in this phase at the same time.
• The membrane potential is unchanged during this phase.

in case of cardiac ischemia or myocardial infarction, there will be an action potential generated in these cells causing an elevation/depression of the line above the base line.(upward elevation/downward displacement of the ST segment). The amount of deviation is measured by the difference in millimeters between J point and the PR segment.

The mechanism of increased blood flow to increased metabolic activity cells. RENIN - ANGIOTENSIN ALDOSTERON SYSTEM

Renin (enzyme secreted by kidney) converts the Angiotensinogen into Angiotensin I (inactive decapeptide). Further conversion of angiotensin I is carried out by an enzyme Angiotensin Converting Enzyme (ACE), which is found in pulmonary circulation., kidney, adrenal gland and heart.ACE converts inactive enzyme angiotensin I to active enzyme Angiotensin II.ACE degrade the bradykinin which is required for the production of major vasodilator Nitric oxide.Thus impairs the vasodilation of the blood vessels.Angiotensin II bind to the AT1-R recetor present on the smooth muscle of the blood vessels and expresses inhibition of the Nitric oxide. Reduced Nitric oxide availability combined with AT1-Receptor causes the vasoconstriction.Stimulation of the AT1 receptor causes the adrenal gland to release Aldosterone which causes vasoconstriction. Finally thus the Blood pressure increases.Thus blood flow increases.

Comparison of the Contraction coupling mechanism of skeletal muscle and Cardiac muscle.

Skeletal muscle   

• Acetyl choline released into synaptic cleft
• Neurotransmittor receptor dependent
• Na+ influx causes end plate potential on motor end plate
• Depolarization of rest of sarcolemma
• Flow of the action potential to T tubules   
• Sarcoplasmic reticulum releases
• Actin - myosin crossbridge mechanism

Cardiac muscles

• Self producing action potential from SA node
• Ca2+ dependent (Ca2+ induced Ca2+ release)
• Ca2+ influx into L type channel into the cell
• Ca2+ binds to Ryanodine receptor on Sarcoplasmic Reticulum
• Ca2+ initiates contraction on binding to troponin
• Ca2+ into cytoplasm Actin - myosin crossbridge mechanism.