Cardiovascular system

Congestive heart failure

weak cardiac muscle

Arrhythmias

disrupted normal electrical activity

— or —— causes an increased work load on the heart

vasoconstriction, heartworms

Drugs can focus on:

• pumping function

• electrical coordination

• vasculature diameter

• or more than one at a time

Narrow therapeutic index

concentrations that work are very close to concentrations that produce toxicity

Through what valve does the left ventricle pump blood out of the body?

Aorta

Through what valve does the right ventricle pump blood out to the lungs?

pulmonic valve

Label A, B, C, D

A - right atrium

B - right ventricle

C - left atrium

D - left ventricle

Which chamber pumps blood TO the body?

left ventricle

Label E, F, G, H

E - aorta

F - cranial vena cava

G - tricuspid valve

H - mitral valve

What is the pacemaker of the heart?

SA node

What structure slows the depolarization wave going from the atria to the ventricles?

AV node

What carries the impulse to the apex of the ventricles?

• the bundle of his

• the right and left bundle branches

What does the P wave represent?

atrial depolarization

What does the QRS complex respresent?

ventricular depolarization and atrial repolarization

What does the T wave represent?

ventricular re-polarization

What part of the ECG represents the depolarization wave as it passes through the AV node?

PR segment

Why is there not a wave representing atrial repolarization?

Occurs at the same time as the QRS complex

Sino Atrial (SA) node =

• pacemaker

• sets pace of heart because it depolarizes spontaneously (has automaticity) more frequently than any other spontaneously depolarizing cell in the heart

Only way depolarization wave can get to ventricles is through the

AV node

What is the function of the AV node?

• It delays depolarization wave long enough for blood to be physically moved from the atria (by atrial contraction) into the ventricles

• Without this delay, the whole heart would contract at once

AV node delay shows up on ECG as the —-

flat PR segment

AV nodes passes depolarization wave to ventricles producing—-

large QRS complex

Sodium (Na+) is usually at higher concentrations —- the cell

outside

Potassium (K+) is at higher concentrations —- the cell

inside

Some ions (Na+ and K+) sneak through - but are put into their correct spot by the

Sodium-Potassium-adenosine triphosphatase (ATPase) pump

Membrane remains in polarized state until the membrane is stimulated by?

• a neurotransmitter

• an adjacent part of cell membrane depolarizing

• other stimulus

Depolarization occurs when…

There is a sudden influx of sodium into the cell, makes the inside of the cell more positive, and the separate “poles” of Na+ and K+ no longer exist

Wave of depolarization

The influx of sodium causing adjacent sodium channels to also open up creating a depolarization wave along the cell

When the inside of the cell becomes positively charged what happens?

the sodium channel snaps shut - no more sodium can pass through the membrane

Repolarization occurs when…

• the strong positive charge inside the cell (from Na+ influx) plus the concentration gradient of K+ forces the postassium molecules out of the cell

• Positive charge inside cell opens postassium channel

What happens when the ions are on the wrong side of the membrane?

• The Na+/K+/ATPase pump gets to work and switches the ions so they are back to their original positions (sodium out, potassium in)

• The cell is now repolarized and ready to fire (depolarize) again

Phase 0 - Cardiac muscle cell

Cardiac muscle cells depolarize with sodium influx

Phase 1 - Cardiac muscle cell

K+ channels open

Phase 2

an influx of calcium (Ca++) that keeps the inside of the cell positive in spite of K+ leaving the cell - charge remains same

Phase 3

Once Ca++ channels close, K+ continues to efflux and completes repolarization similar to what was seen with the neuron

What makes special conducting cells like the SA node, AV node, bundles, and Purkinje cells, special?

They are capable of depolarizing on their own without any stimulus - they possess automaticity and fire at their own inherent rate

What allows special conducting cells to have automaticity?

They have membranes that are leaky to Na+ influx in Phase 4 (the baseline) → Phase 4 creeps upwards to threshold and the cell depolarizes

Phase 4

resting baseline

List conducting cells from most leaky to least leaky

SA node (most) → AV nodes → Bundle branches (slowest)

SA node inherent rate (leakiest so they reach threshold quickest) of automaticity determines —-

the heart rate for the whole heart - why SA node is the pacemaker

Refractory period

Period of time in which a cell CANNOT be restimulated to depolarize

Absolute refractory period (ARP)

The time during which the cardiac cell cannot depolarize REGARDLESS of the strength of the stimulus

Relative refractory period (RRP)

The time during which the cardiac cell may depolarize IF a sufficient stimulus is provided

Fibrillation

Heart is not contracting in a coordinated manner

What does the sympathetic NS do for the cardiovascular system?

• Norepinephrine epinephrine on adrenergic receptors

• Stimulates SA node = increased HR

• Stimulates AV node = quicker conduction of depolarization wave from atria to ventricles

• Stimulates cardiac muscle = greater force of contraction

• Vasoconstriction of peripheral vasculature = harder for heart to inject blood into the arterial system

What does the parasympathetic NS do for the cardiovascular system?

• Acetylcholine on cholinergic receptors

• SA node effect = slows automaticity = slows HR

• AV node effect = slows conduction of depolarization wave from atria to ventricles

• Cardiac muscle = NO EFFECT

• Vasculature = NO EFFECT

BETA 1 (B1) receptors

• Sympathetic NS receptor

• located on SA node, AV node, cardiac muscle

• Increase HR and force of contraction

• “B for beat” - B1 receptor stimulation increases the heartbeat

BETA (B2) receptors

• Sympathetic NS receptor

• located on bronchioles and skeletal muscle vessels

• Dilates the bronchioles by relaxing the smooth muscle

• “B for bronchioles” - B2 receptor stimulation causes bronchodilation

• Causes blood vessels (arterioles) in the skeletal muscle to relax → produces vasodilation of arterioles and greater blood flow to the skeletal muscles (for fighting or fleeing)

Alpha 1 receptors

• located on peripheral vasculature (skin, SQ tissue, MMs), GI tract, kidneys, etc

• Stimulation causes smooth muscle surrounding small arterioles (part of the arterial system located just prior to the capillaries) to constrict

• A1 receptors cause arteriolar vasoconstriction

• Increases resistance to flow and increases workload on the heart

Alpha 2 receptrors

• located on the presynaptic terminal of the neuron that releases norepinephrine

• When activated alpha 2 receptors inhibit neurotransmitter release from presynaptic neurons

• when stimulated by norepinephrine (or any drug that mimics norepinephrine) will shut down further release of norepinephrine

arrhythmia

any abnormal pattern of electrical activity of the heart

Ectopic focus

• can be a damaged myocardial cell that becomes leaky to sodium and fires on its own before the normal depolarization wave arrives

• the ectopic focus becomes the new pacemaker of the heart if it depolarizes more frequently than the SA node

Premature ventricular contractions (PVCs)

A singular ectopic focus beat can cause the ventricles to contract prematurely out of sequence with the rest of the heart

Paroxysm

A short series of PVCs

Flutter

A longer series of PVCs that continues

Fibrillation

When the organization of the contractions completely breaks down so that no recognizable pattern can be recognized on the ECG

A rapid regular HR caused by a problem with the SA node would be called what?

supraventricular tachycardia