Cardiac Muscle and Electrical Activity Quiz

To explain how force is produced in cardiac muscle, how it differs from skeletal muscle, and how it can be influenced by the extrinsic sympathetic nerves.

Cardiac muscle produces force through a large influx of extracellular calcium, while skeletal muscle produces force through a smaller influx of extracellular calcium.

The T-tubules of cardiac muscle are 5 times greater in diameter and have 25 times more volume than those of skeletal muscle.

Dihydropyridine channels open in response to an action potential, allowing a large influx of extracellular calcium that contributes to cardiac muscle contraction.

Activation of dihydropyridine channels causes release of calcium from the sarcoplasmic reticulum via ryanodine release channels.

Mucopolysaccharides in cardiac T-tubules sequester calcium, ensuring its availability for contraction.

Cardiac contractility and the events of the cardiac cycle.

The autonomic nervous system can influence cardiac contractility.

The refractory period is the period of time during which the cardiac muscle is unresponsive to further stimulation.

Volume/pressure diagrams are used to interpret and compare cardiac function between the left and right sides of the heart.

Arterial pressure = cardiac output x total peripheral resistance

Re = (velocity of flow) x (radius of vessel) / viscosity

High velocity flow, large diameter vessels, low blood viscosity, abnormal vessel wall

Turbulence disrupts flow and increases resistance

Flow affects viscosity, with static blood having 100x the viscosity of flowing blood

T = PR

1. Control of blood flow - Low tension required to oppose blood pressure in arterioles - Smooth muscle control of arteriole and precapillary sphincters are the sites of tissue blood flow regulation
2. Capillaries - Can be extremely thin and still withstand the pressure - Thin walls essential for exchange processes
3. Aneurysm Regulation of blood flow

1. Active and reactive hyperemia
2. Flow autoregulation
3. Myogenic response

Active hyperemia occurs when tissue is highly active and the rate of flow increases. Reactive hyperemia occurs when blood supply is blocked and blood flow increases to 4-7 times normal.

Short-term (acute) mechanisms include vasodilator theory, which is widely accepted and involves factors such as increased PCO2, decreased PO2, increased H+, increased K+, increased lacKc acid, increased adenosine, and increased histamine. Long-term mechanisms involve changes in physical size or number of blood vessels.

The sinoatrial node is responsible for initiating the electrical activity in the heart, serving as the natural pacemaker.

Depolarization spreads through the heart via a functional syncytium, starting from the atria and then moving to the ventricles.

An electrocardiogram measures the spread of electrical activity throughout the heart and provides information about the cellular action potentials.

Observing the electrical activity in an individual fiber provides specific information, while an ECG measures the overall electrical activity of the heart.

The main focus of this lecture is on the depolarization events in the heart.

Phase 0: Rapid depolarisation due to ↑ Na+ permeability (gNa+) as fast Na+ channels open. Phase 1: Start of repolarisation as fast Na+ channels close. Phase 2: Effect of Ca2+ entry via L-type channels. Phase 3: Rapid repolarisation as ↑ [Ca2+]i stimulates K+ channels to open and gK+ ↑ Ca2+ L-type channels close. Phase 4: Stable resting membrane potential where gK+ exceeds gNa+ by 50:1.

Sympathetic stimulation increases the rate of SAN phase 1 depolarisation by ↑ gCa2+ and ↑ gNa+ via “funny” channels. Parasympathetic stimulation reduces the rate of phase 1 depolarisation and hyperpolarises the membrane potential to a lower starting level by ↑ extent and duration of opening of K+ channels, leading to an increase in gK+.

Sinoatrial node (SAN): ~90/min. Atrioventricular node (AV node): ~60/min. Bundle of His: ~50/min. Purkinje fibers: ~40/min. Ventricles: ~30/min. The SAN has the fastest rate and is the intrinsic pacemaker of the heart.

The electrical activity of the heart is measured using an electrocardiogram (ECG), which measures the electrical activity of the heart over time using multiple electrodes. The limb leads measure the sum of the electrical activity of the heart and the direction that electrical activity is moving in. The chest leads provide more specific, localized information about areas of the heart. The ECG can provide information about atrial and ventricular depolarization and repolarization, as well as the timing intervals of the P-R interval, QRS complex width, and Q-T interval.

Many parts of the heart exhibit spontaneous, rhythmical depolarization. The electrical activity spreads in a coordinated fashion. The rate of depolarization is influenced by the autonomic nervous system. The overall net activity of the heart can be observed using an electrocardiogram (ECG).

Possible mechanisms of primary hypertension include the sympathetic system, the renin-angiotensin-aldosterone system (RAAS), circulating factors, and genetics.

Consequences of hypertension include increased risk of heart disease, stroke, kidney disease, and other health complications.

Hypertension is typically treated through lifestyle changes such as diet and exercise, as well as medication if necessary.

Hypertension is a complex phenotype with multiple genetic and environmental risk factors. Age, weight, sex, race, education status, and diet are all possible risk factors.

Possible contributors to systemic hypertension include increased sympathetic activity/sensitivity, the renin-angiotensin-aldosterone system (RAAS), and circulating factors.

The kidneys play a critical role in maintaining blood pressure by balancing sodium intake with sodium excretion, which regulates extracellular fluid (ECF) volume and long-term blood pressure. The renin-angiotensin-aldosterone system (RAAS) is also involved in regulating blood pressure.

Increased sympathetic activity/sensitivity, renin-angiotensin-aldosterone system (RAAS), circulating factors (endothelin, nitric oxide, reactive oxygen species), and genetics.

Heart failure, myocardial infarction, accelerated atherosclerosis, stroke, retinopathy, albuminuria, and end stage renal disease.

The sympathetic nervous system can increase blood pressure through increased sympathetic activity and sensitivity. It can directly affect blood pressure through vasoconstriction and increased contractility of cardiomyocytes. Overall, the sympathetic nervous system increases blood pressure by increasing peripheral resistance and cardiac output.

Primary hypertension refers to high blood pressure with no identifiable cause, while secondary hypertension is caused by an underlying condition or factor. An example of secondary hypertension is renal artery stenosis, which can result in decreased blood flow to the kidneys and activation of the renin-angiotensin-aldosterone system (RAAS).

Heart block, Ectopic pacemaker activity, Delayed after-depolarisations, Circus re-entry

Atrial fibrillation, Supraventricular tachycardia (SVT), Ectopic beats, Sustained ventricular arrhythmias (VT and VF)

Atrial (supraventricular), Junctional (associated with the AV node), Ventricular

First degree heart block is characterized by a slightly affected AV node and slowed conduction with an abnormally long P-R interval. Second degree heart block can be further divided into several subtypes, including Mobitz type 2, which involves a constant P-R interval with occasional failure of ventricular depolarization, and 2:1 or 3:1 block, which refers to the ratio of P waves to QRS complexes. Third degree heart block is the most severe, where the AV node is completely blocked and no electrical activity from the atria reaches the ventricles.

Ectopic pacemakers are areas of the heart other than the sinoatrial node (SAN) that can develop pacemaker activity. They can arise due to various factors, including ischemic damage, increased sympathetic activity, increased sensitivity to catecholamines, cardiac glycoside toxicity, and other conditions like ischemia, coronary heart disease, rheumatic heart disease, hypertension, stress, exercise, caffeine consumption, hyperthyroidism, and certain medications.

Circus re-entry movements refer to when an electrical impulse can re-stimulate a region of the heart after its refractory period has passed, creating a re-entry circuit. In the heart, this can occur when there are two branches of conducting fibers connected to a chain of contractile fibers, forming a loop. When the impulse originates in the sinoatrial node (SAN) and is transmitted to the branches, each branch depolarizes. When the impulses meet, there is extinction by collision. However, if the impulse comes from an unusual direction and arrives before the tissue would have been re-stimulated by the next normal impulse from the SAN, circus re-entry movements can occur.

The grey area is an area of damage with no full conduction in the orthodromic direction – cells unable to generate sufficient current to maintain the depolarisation to reach threshold at A.

Circus re-entry movements are short circuits in the heart that result in high frequency impulses. They can be generated by either a unidirectional block or a transient block.

Wolf-Parkinson-White Syndrome is a condition characterized by an additional or "accessory" electrical connection between the atria and ventricles. It is usually on the left side and results in early depolarization reaching the ventricle, leading to a short PR interval and a delta wave in the QRS complex.

The Vaughn-Williams Classification system is a classification system for anti-dysrhythmic drugs based on their mechanisms of action. It categorizes drugs into four main classes - Class I (block fast sodium channels), Class II (block beta-adrenergic receptors), Class III (prolong action potential repolarization), and Class IV (block calcium channels).

Systolic and diastolic dysfunction

Right and left ventricular dysfunction

Vascular resistance and ventricular wall tension

Cardiac output = HR x SV

Increased contractility increases cardiac output independent of preload and afterload

A classification system for heart failure based on patient symptoms

Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath)

Systolic vs. diastolic dysfunction

Impaired cardiac contractility

Impaired ventricular relaxation and filling