Human Physiology Exam 2 Part 3

What are the top two leading causes of death in the U.S.?

Heart diseases and malignant neoplasms

How does blood flow in coronary circulation?

Oxygenated blood from the left ventricle enters the aorta. The coronary arteries divide into smaller capillaries that penetrate the myocardium. Deoxygenated blood from the capillaries collects in coronary veins. The coronary veins then empty into the right atrium.

What is the principle of coronary bypass surgery?

to reroute blood flow around a blocked or clogged coronary artery using a healthy blood vessel taken from another part of the body

Cardiac muscle cells contract without neural innervation is

myogenic

Pacemaker cells

set the rate of the heartbeat

The conducting system initiates

The heartbeat and helps spread the impulse rapidly throughout the heart

Some cardiac muscle cells do not function in contraction, but constitute a network known as the

conducting system

The Purkinje fibers

transmit electric signals down the atrioventricular bundle (bundle of His) to left and right bundle branches.

Sinoatrial (SA) node

Sets the pace of the heartbeat at 60-100 bpm.

Escape rhythm

when action potentials from the SA node fail to reach ventricles, AV node and Purkinje fibers can act as pacemakers

Internodal pathway from SA to atrioventricular (AV) node

Routes the direction of electrical signals so the heart contracts from apex to base. AV node delay is accomplished by slower conductional signals through nodal cells

P wave

atrial depolarization

QRS complex

Ventricular depolarization. Also atrial repolarization

T wave

ventricular repolarization

Atrial contraction begins 

At the end of P wave.

Ventricular contraction begins 

At the end of Q wave and continues through T wave

Atrioventricular (AV) heart block describes

a type of heart block in which the conduction between the atria and ventricles of the heart is impaired

First degree AV block is

a delay in conduction of the atrial impulse, resulting in an increased PR interval of greater than 200 msec

Second degree AV block has two types

Type I second degree AV block involves progressive PR lengthening until the QRS “drops out,” indicating the previous P wave was not conducted to the ventricles. This is typically a nodal block.

Type II second degree AV block occurs in the setting of a constant PR interval with sudden nonconduction of a P wave. It may present as a single nonconducted P wave or a repetitive pattern of nonconduction. This block is commonly infranodal with a wider QRS complex.

Third degree AV block occurs

when P waves are not conducted to the ventricles and a slow escape rhythm is present. The atrial and ventricular impulses are not synchronized, and the atrial rate is faster than the independent ventricular rate. 

Systole is

The period of ventricular contraction and blood ejection

Diastole

the period of ventricular relaxation and blood filling

 Isovolumetric ventricular contraction

the ventricles are contracting but all valves in the heart are closed, and so no blood can be ejected.

Isovolumetric ventricular relaxation

the ventricles begin to relax, no blood is entering or leaving the ventricles meaning all the valves are closed

The cardiac cycle has four phases

isovolumetric relaxation, ventricular filling, isovolumetric contraction, and ejection

Ejection

The second part of systole is blood moving out of the ventricles.

Blood filling

The second part of diastole is blood moving into the ventricles

“Lub” heart sound

closure of the AV valves at the onset of systole and isovolumetric ventricular contraction

“Dup” heart sound

closure of the pulmonary and aortic valves at the onset of diastole and isovolumetric ventricular relaxation.

Valve does not open fully

Stenosis

Valve doesn't close tightly

Regurgitation

Cardiac output (CO)

The heart is the pump that moves the blood. In reference to the amount of blood moved per unit of time. Cardiac Output = Heart Rate x Stroke Volume

Cardiac cycle is 1/3

systole

Cardiac cycle is 2/3

diastole

Cardiac output is regulated by

Heart rate via sympathetic or parasympathetic nerve and hormone in blood (epinephrine). Also by stroke volume via venous return and ventricular contractility (by nerve and epinephrine)

The sympathetic nerves 

innervate the entire heart and releases norepinephrine

Parasympathetic nerves

innervates node cells only and releases primarily acetylcholine

Both norepinephrine/epinephrine and acetylcholine receptors in the heart are GPCRs but have __________ effects

opposite

Pacemaker potential is caused by

hyperpolarization activated cyclic nucleotide gated (HCN) channels

cAMP activates _____ channels

HCN

Why can caffeine increase heart rate?

Caffeine promotes the accumulation of cAMP. The more cAMP, the higher probability that HCN channel will be open, the stronger pacemaker potential, the faster heart rate.

How does epinephrine/norepinephrine increase heart rate? Molecules involved?

WATCH VIDEO

How does acetylcholine decrease heart rate? Molecules involved

The binding of ACh to mAChR triggers the dissociation of G_α-GTP from G_ßγ, which directly binds to and opens a K⁺ channel

What is the Frank-Starling mechanism?

the stroke volume (SV) of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume, or EDV) when all other factors remain constant