The heart Flashcards

1
Q

Mention the parts of the heart.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 types of cardiac muscle that compose the heart and what type of muscle is the cardiac muscle?

A

Cardiac muscle is striated. The 3 major typer of cardiac muscle are: atrial muscle, ventricular muscle, and specialized excitatory and conductive muscle fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Whta type of myofibrils are found in the cardiac muscle?

A

Actin and myosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is the heart considered a synccytium and what are the 2 syncytiums it is composed of?

A

It is a syncytium because the many cardiac cells are so interconnected that when one cell becomes excited, the action potential rapidly spreads to all of them.

The heart is composed of two syncytiums: the atrial syncytium, and the ventricular syncytium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the phases of the action potetial in the heart?

A

Phase 0 (depolarization). Membrane potential becomes more positive. Voltage-gated sodium channels (fast sodium channels) open and permit sodium to rapidly flow into the cell and depolarize it.

Phase 1 (initial repolarization). The fast sodium channels close, the cell begins to repolarize, and potassium ions leave the cell through open potassium channels.

Phase 2 (plateau). L-type calcium channels (slow calcium channels, or calcium -sodium channels) open and fast potassium channels close. A brief initial repolarization occurs and the action potential plateaus due to (1) increased Ca permeability and (2) decreased K permeability. The voltage-gated Ca channels open slowly on phases 1 and 0, and Ca enters the cell, K channels then close. Combination of low K efflux and high Ca influx maintains a prolonged depolarization period, causing the action potential to plateau.

Phase 3 (rapid repolarization), Ca channels close and slow K channels open. This permits K ions to rapidly exit the cell, ending the plateau and returning the cell membrane potential to its resting level.

Phase 4 (resting membrane potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define systole and diastole.

A

Diastole is the period of relaxation, during which the heart fills with blood.

Systole is the period of contraction.

Diastole - deja - release - relax / Systole - sigue - continue - contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are P, Q, R, S and T waves on the ECG ?

Mention their relationship with the heart cycle.

A

P wave - caused by spread of depolarization through the atria. It is followed by atrial contraction causing a slight rise in the atrial pressure curve.

QRS waves - are a result of electrical depolarization of the ventricles. This initiates contraction of the ventricles and causes the ventricular pressure to rise. QRS complex begins slightly before ventricular systole.

T wave - represents repolarization of the ventricles when the ventricular muscle fibers begin to relax. Occurs slightly before the end of ventricular contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does a, c, and v mean in the atrial pressure wave??

A

a wave - caused by atrial contraction.

c wave - the ventricles begin to contract; caused partly by slight backflow of blood into the atria, but mainly by bulging of the A-V valves backward toward the atria (due to increasing pressure in the ventricles).

v wave - occurs toward the end of ventricular contraction. It results from slow flow of blood into the atria from the veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the period of isovoluic contraction?

A

It is the period when contraction is occurring in the ventricles, but no emptying occurs (period of isovolumic or isometric contraction).

Ocurrs after ventricular contraction begins, the ventricular pressure rises abruptly, causing the A-V valves to close. Time is required for the ventricle to build up sufficient pressure to push the semilunar valves open against the pressures in the aorta and pulmonary artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mention 3 important aspects of the period of ventricular ejection.

A
  • When ventricular pressure rises pushing the semilunar valves open, 60% of the blood in the ventricle is ejected during systole
  • The first third is called the period of rapid ejection (about 70% of this portion flows out during theses period).
  • The last two thirds are called the period of slow ejection (the remaining 30% empties during these period).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mention the relationship of the heart sound with the heart cycle.

A

First heart sound (S1) - Contraction of the ventricles. First a sound caused by closure of the A-V valves is heard (vibration pitch is low and relatively long-lasting)

Second heart sound (S2) - When aortic and pulmonary valves close at the end of systole. A a rapid snap (valves close rapidly), and the surroundings vibrate for a short period.

Third heart sound (S3) - Occurs at the beginning of the middle 3rd of diastole. It is believed that is caused by the oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria.

Fourth heart sound (S4) - Atrial contraction sound. Presumably, it is caused by the inrush of blood into the ventricles, which initiates vibrations similar to those of the third heart sound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mention the 4 phases during the cardiac cycle.

A
  • Phase I: Period of filling. The amount of blood that remains in the ventricle after the previous heartbeat, is called end-systolic volume
  • Phase II: Period of isovolumic contraction. Volume of the ventricle does not change (all valves are closed), however, the pressure inside the ventricle increases.
  • Phase III: Period of ejection. Systolic pressure rises and volume of the ventricle decreases.
  • Phase IV: Period of isovolumic relaxation. At the end of the period of ejection the aortic valve closes and the ventricular pressure falls back to the diastolic pressure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the Frank-Starling mechanism?

A

It is the ability of the heart to adapt to increasing volumes of inflowing blood. It means that the greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta.

In addition to the important effect of lengthening the heart muscle, the stretch of the right atrial wall directly increases the heart rate by 10 to 20%, which also helps increase the amount of blood pumped each minute, (this contribution is less than the Frank-Starling mechanism).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the effect of sympathetic and parasympathetic stimulation of the heart?

A

Strong sympathetic stimulation can increase the heart rate. It can also increase the force of heart contraction to as much as double the normal rate, increasing the volume of blood pumped and increasing the ejection pressure.

Parasympathetic (Vagal) stimulation reduces HR and strength of contraction. Strong stimulation of the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a lower rate as long as the parasympathetic stimulation continues. Vagal stimulation can also decrease the strength of heart muscle contraction by 20 - 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of K and Ca ions in the heart?

A

Excess K causes the heart to become dilated and flaccid and also slows the heart rate. It can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle.

This results because high K concentration decreases the resting membrane potential and partially depolarizes the cell membrane, causing the membrane potential to be less negative. This decreases the intensity of the action potential, making contraction of the heart progressively weaker.

Excess Ca effect is almost exactly opposite to K, Ca ions initiate the cardiac contractile process, causing the heart to move toward spastic contraction. Conversely, deficiency of calcium ions causes cardiac weakness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What effect does temperature has on heart function?

A

Heat increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self-excitation process.

Prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes weakness.

17
Q

Mention the conduction of the heart.

A

Sinus node (sinoatrial or S-A node) - normal rhythmical impulses are generated

Internodal pathways - conduct impulses from the sinus node to the atrioventricular (A-V) node

A-V node - the impulses from the atria are delayed before passing into the ventricles

A-V bundle - impulses are conducted from the atria into the ventricles

Left and right bundle branches of Purkinje fibers - conduct the cardiac impulses to all parts of the ventricles

18
Q

What 3 structures form or terminate in the A-V node?

A

Three small bands (anterior, middle, and posterior internodal pathways) that curve through the anterior, lateral, and posterior atrial walls and terminate in the A-V node.

19
Q

If the A-V node and Purkinje fibers have self-stimulated intrinsic rythmical rate, why is the sinus node, the one controlling the heart rythm?

A

The discharge rate of the sinus node is considerably faster than the natural self-excitatory discharge rate of either the A-V node or the Purkinje fibers.

20
Q

What is an ectopic pacemaker and why does it occur?

A

Is a pacemaker elsewhere than the sinus node.

It causes an abnormal sequence of contraction, it can be caused because other part of the heart develops a rhyth­mical discharge rate that is more rapid than the sinus node, shifting the pacemaker from the sinus node to the A-V node or to the excited Purkinje fibers.

Another cause can be a blockage of transmission of the cardiac impulse from the sinus node to the other parts of the heart.

21
Q

How are the sympathetic and parasympathetic nerves distrubuted in the heart?

A

The parasympathetic nerves (the vagi) are distributed mainly to the S-A and A-V nodes, to a lesser extent to the muscle of the two atria, and very little directly to the ventricular muscle.

The sympathetic nerves, conversely, are distributed to all parts of the heart, with strong representation to the ventricular muscle, as well as to all the other areas.

22
Q

What are the effects of acetylcholine in the heart and how is it released?

A

Parasympathetic nerves causes the hormone acetylcholine to be released at the vagal endings.

It decreases the rate of rhythm of the sinus node, and it decreases the excitability of the A-V junctional fibers between the atrial musculature and the A-V node.

It also increases the permeability of the fiber membranes to K ions, which allows rapid leakage out of the conductive fibers. This causes increased negativity inside the fibers, hyperpolarization, making this excitable tissue much less excitable.

23
Q

What causes release of norepinephrine and what is its effect on the heart?

A

Stimulation of the sympathetic nerves releases norepinephrine at the sympathetic nerve endings.

It stimulates beta-1 adrenergic receptors, which mediate the effects on heart rate. This increases the permeability of the fiber membrane to sodium and calcium ions, causing a more positive resting potential, this accelerates self-excitation and, increases the heart rate.

The increase in permeability to calcium ions is partially responsible for the increase in contractile strength of the cardiac muscle due to the powerful role in exciting the contractile process of the myofibrils.

24
Q

What causes sinus arrythmia?

A

Can result from any circulatory condition that alter the strengths of the sympathetic and parasympathetic nerve signals to the heart sinus node. The “respiratory” type, results from “spillover” of signals from the medullary respiratory center into the adjacent vasomotor center during inspiratory and expiratory cycles. This causes an alternate increase and decrease in the number of impulses transmitted through the sympathetic and vagus nerves to the heart.

25
Q

Mention 3 conditions that can cause an A-V block.

A
  1. Ischemia of the A-V node. - This often delays or blocks conduction from the atria to the ventricles.
  2. Compression of the A-V bundle. - By scar tissue or calcified portions of the heart.
  3. Inflammation of the A-V node. - It depresses the conduction and results frequently from different types of myocarditis.
  4. Extreme stimulation of the heart by the vagus nerves. - Increased or strong vagal tone / athletic or well conditioned horses.
26
Q

What is the diference between 1st, 2nd, and 3rd degree block?

A

1st degree - Is a prolonged P-R (or P-Q) interval due to a delay of conduction from the atria to the ventricles without an actual blockage of conduction.

2nd degree - conduction through the A-V bundle is slowed enough to increase the P-R interval enough to pass through the bundle into the ventricles and sometimes not strong enough. When this happens, there is an atrial P wave with no QRS-T (dropped beats).

3rd degree - There is a complete block of the impulse from the atria into the ventricles. Ventricles spontaneously establish their own signal, so P waves become dissociated from the QRS-T complexes.

27
Q

What are the 2 types of second degree A-V block?

A
  • Type I block is a progressive prolongation of the PR interval until a ventricular beat is dropped, it is then followed by resetting of the PR and repeating of the abnormal cycle.
  • Type II block is usually a fixed number of nonconducted P waves for every QRS complex. It is generally caused by an abnormality of the bundle of His-Purkinje system
28
Q

What can cause a premature contraction?

A

Most premature contractions result from ectopic foci in the heart.

Possible causes of ectopic foci are local areas of ischemia; small calcified plaques pressing against the adjacent cardiac muscle; and toxic irritation of the A-V node, Purkinje system, or myocardium caused by infection, or drugs.

29
Q

Describe an APC.

Waht can cause them?

A

The P wave of the beat occurres too soon in the heart cycle, the interval between the premature contraction and the next succeeding contraction is slightly prolonged (a compensatory pause). Premature atrial contractions occur frequently in otherwise healthy individuals like athletes or secondary to toxic conditions like lack of sleep or certain drugs.

30
Q

What can a VPC cause on the ECG?

A

The QRS complex can be considerably prolonged - The impulse is conducted mainly through slowly conducting muscle

The QRS complex can have a high voltage - the normal impulse usually passes through both ventricles nearly simultaneously, when PVC occurs, the impulse travels in only one direction, so one entire side or end of the ventricles is depolarized.

After almost all PVCs, the T wave has an electrical potential polarity exactly opposite to that of the QRS complex.

Many other PVCs result from stray impulses or re-entrant signals that originate around the borders of infarcted or ischemic areas of the heart

31
Q

What does P-Q or P-R interval represent?

A

Beginning of the electrical excitation of the atria and electrical excitation of the ventricles

32
Q

What does Q-T interval represents?

A

The contraction of the ventricle

33
Q

What does each lead represent on the ECG?

A

Lead I.

Lead II.

Lead III.

34
Q

What defines a sinus tachycardia and what can cause it?

A

Normal ECG with an increased rate.

35
Q

What is an electrical alternans and what can be the cause?

A

Is a partial intraventricular block every other heartbeat. ECG could also show tachycardia, probably a reason the block has occurred (when HR is rapid, it may be impossible for some portions of the Purkinje system to recover from the previous refractory period). Many other conditions that depress the heart, such as ischemia, myocarditis, or digitalis toxicity, can also cause incomplete intraventricular block, resulting in electrical alternans.