Cv Path Lecture 01 Part 1

Front 1

Describe a summation gallop

Back 1

-Occurs in a patient with S1, S2, S3, and S4
-If the patient develops tachycardia, diastole becomes shorter and S3 and S4 can coalesce
-S3+S4 is a long middiastolic, low pitched sound and is louder than S1 or S2

Front 2

Describe S4

Back 2

-Occurs in late diastole and coincides with contraction of the atria
-Generated by the left (or right) atrium vigorously contracting against a stiffened ventricle
-Usually indicated the presence of cardiac disease (specifically, a decrease in ventricular compliance typically resulting from ventricular hypertrophy or myocardial ischemia)
-A dull, low-pitched sound best heard with the bell
-Left sided S4 loudest at apex with the patient lying in the left lateral decubitus position
-Referred to as an atrial gallop

Front 3

What is another name for a pathologic S3?

Back 3

Ventricular gallop

Front 4

What does an S3 imply in a middle-aged or older adult?

Back 4

Volume overload owing to congestive heart failure or the increased transvalvular flow that accompanies advanced mitral or tricuspid regurgitation

Front 5

What does an S3 imply in a child/young adult?

Back 5

The presence of a supple ventricle capable of normal rapid expansion in early diastole

Front 6

Describe S3 (What it sounds like, where to heart it, what causes it, what it means)

Back 6

-When present occurs in early diastole, following the opening of the atriventricular valves, during the ventricular rapid filling phase
-Dull, low pitched sound best heard with the bell of the stethoscope
-Left sided S3 loudest over the cardiac apex while patients lie in the left lateral decubitis position
-Right sided S3 loudest at the lower-left sterna border
-Result from tensing of the chordate tendinae during rapid filling and expansion of the ventricule
-Normal finding in children and young adults
-Abnormal in middle-aged or older adults

Front 7

Describe approximation of the severity of mitral stenosis. Why is this the case?

Back 7

-Can be approximated by the time interval between A2 and the opening snap: the more advanced the stenosis, the shorter the interval.
-The degree of left atrial pressure elevation corresponds to the severity of mitral stenosis
-When the ventricle relaxes in diastole, the greater the left atrial pressure, the earlier the mitral valve opens
-Mild stenosis is marked by less elevated left atrial pressure than severe stenosis

Front 8

Describe how to distinguish the A2-OS sequence from a widely split S2

Back 8

Careful auscultation at the pulmonic area during inspiration reveals three sounds occurring in rapid succession, which corresponds to aortic closure (A2), pulmonic closure(P2), and then the opening snap (OS). The three sounds become two on expiration

Front 9

Describe the opening snap

Back 9

-Mitral or tricuspid valvular stenosis produce a sound when the affected valve opens
-It is a sharp, high-pitched sound
-Timing does not vary significantly with respiration
-With mitral stenosis, it is best heard between the apex and left sterna border, just after the aortic closure sound (A2), when the left ventricular pressure falls fellow that of the left atrium

Front 10

Describe mid- or late-systolic clicks

Back 10

-Typically caused by systolic prolapsed of the mitral or tricuspid valves, in which the leaflets bulge abnormally from the ventricular side of the atrioventricular junction into the atrium during ventricular contraction,
-This is often accompanied by valvular regurgitation
-Loudest over the mitral or tricuspid auscultatory regions

Front 11

Contrast the aortic and pulmonic ejection clicks

Back 11

-Aortic ejection click is heart both at the base and the apex of the heart and does not vary with respiration.
-Pulmonic ejection click is heard only at the base and its intensity diminished during inspiration

Front 12

Describe the generation of ejection clicks from dilatation of the root of the aorta or pulmonary artery

Back 12

-Sound is associated with sudden tensing of the aortic or pulmonic root with the onset of blood flow into the vessel.

Front 13

Describe the generation of ejection clicks from aortic or pulmonary valves stenosis

Back 13

-The sound occurs as the valve leaflets reach their maximal level of ascent into the great artery, just prior to blood ejection
-At that moment, the rapidly ascending valve reaches its elastic limit and decelerates abruptly, an action thought to result in sound generation

Front 14

Describe ejection clicks

Back 14

-Abnormal early systolic sounds
-Occur shortly after S1 and coincide with the opening of the aortic or pulmonic valves.
-Have a sharp, high pitched quality
-Best heart with the diaphragm of the stethoscope placed over the aortic and pulmonic areas.
-Indicate the presence of aortic or pulmonic valve stenosis or dilatation of the pulmonic artery or aorta.

Front 15

Describe Left bundle branch block (LBBB)

Back 15

The spread of electrical activity through the left ventricle is impaired, resulting in late ventricular contraction and delayed closure of the aortic valve such that it follows P2. During inspiration, as in the normal case, the pulmonic valve closure sound is delayed and the aortic valve closure sound moves earlier. This results in narrowing and often superimposition of the two sounds, thus, there is no apparent split at the height of inspiration.

Front 16

What is paradoxical splitting of S2? What is the most common cause in adults?

Back 16

Also called reverse splitting. It refers to an audible separation of A2 and P2 during expiration that disappears on inspiration, the opposite of the normal situation. It reflects an abnormal delay in the closure of the aortic valve such that P2 precedes A2. The most common cause in adults if Left bundle branch block (LBBB). It may also be seen in situations where left ventricular ejection is greatly prolonged, such as in aortic stenosis.

Front 17

Why doesn’t the pattern of fixed splitting of S2 change during the respiratory cycle with atrial septal defects?

Back 17

1) Inspiration does not substantially increase further the already elevated pulmonary capacitance
2) Augmented filling of the atrium from the systemic veins during inspiration is counterbalanced by a reciprocal decrease in the left to right transatrial shunt, eliminating respiratory variations in right ventricular filling

Front 18

Describe the fixed splitting of S2 from atrial septal defects

Back 18

-Chronic volume overload of the right-sided circulation results in a high capacitance, low resistance pulmonary vascular system.
-The alteration in pulmonary hemodynamics delays the back pressure responsible for the closure of the pulmonic valve.
-Thus, P2 occurs later than normal, even during expiration, such that there is a wider than normal separation of A2 and P2.

Front 19

What is fixed splitting of S2? When does it occur?

Back 19

An abnormally widened interval between A2 and P2 that persists unchanged through the respiratory cycle. Most commonly from atrial septal defect

Front 20

What is widened splitting of S2? When does it occur?

Back 20

An increase in the time interval between A2 and P2, such that the two components are audibly separated even during expiration and become more widely separated in inspiration.
This pattern is usually the result of delayed closure of the pulmonic valve, which occurs in right bundle branch block and pulmonic valve stenosis.

Front 21

How is A2 affected by inspiration?

Back 21

-Capacitance of intrathoracic pulmonary veins is increased by negative pressure generated by inspiration
-Venous return to the left atrium and ventricle temporarily decreases
-Reduced filling of the LV causes a reduced stroke volume during the next systolic contraction and therefore shortens the time required for LV emptying
-Therefore, A2 occurs slightly earlier in inspiration than during expiration

Front 22

Where is S2 best heard?

Back 22

Second left intercostals space next to the sternum (pulmonic area)

Front 23

What does S2 intensity depend on?

Back 23

The velocity of blood coursing back toward the valves from the aorta and pulmonary artery after the completion of ventricular contraction and the suddenness with which that motion is arrested by the closing valves

Front 24

When is S2 accentuated?

Back 24

In systemic hypertension or pulmonary arterial hypertension
The diastolic pressure in the respective great artery is higher than normal, such that the velocity of the blood surging toward the valve is elevated and S2 is accentuated.

Front 25

When is S2 diminished?

Back 25

Severe aortic stenosis or pulmonic valve stenosis the valve commissures are nearly in a fixed position, such that the contribution of the stenotic valve to S2 is diminished

Front 26

Why is S1 diminished in patients with mitral regurgitation?

Back 26

The mitral leaflets may not come into full contact with one another as they close.

Front 27

Why is S1 diminished in severe mitral stenosis?

Back 27

The leaflets are nearly fixed in position throughout the cardiac cycle and therefore there is reduced movement of the valves

Front 28

Why is S1 diminished in patients with “stiffened” left ventricles?

Back 28

Atrial contraction results in higher-than-normal pressure at the end of diastole. This greater pressure causes the mitral leaflets to drift together more rapidly, so they are forced closed from a smaller-than-normal distance when ventricular contraction begins, thus reducing the intensity of S1.

Front 29

Which varies with the respiratory cycle: S1 or S2?

Back 29

S2. The sounds are fused as one sound during expiration but become audibly separated during inspiration, a situation termed physiologic splitting

Front 30

Describe the mechanism of physiologic splitting

Back 30

-Expansion of the chest during inspiration causes the intrathoracic pressure to become more negative
-The negative pressure transiently increases the capacitance (and reduces the impedance) of the intrathoracic pulmonary vessels
-As a result, there is a temporary delay in the diastolic “back pressure” of the pulmonary artery responsible for closure of the pulmonic valve.
-Thus P2 is delayed

Front 31

What forces the tricuspid and mitral valve leaflets apart?

Back 31

Atrial contraction at the end of diastole

Front 32

Why does a shortened PR interval result in accentuated S1?

Back 32

The valve leaflets do not have sufficient time to drift back together and are therefore forced shut from a relatively wide distance

Front 33

Why does mild mitral stenosis result in an accentuated S1?

Back 33

A prolonged diastolic pressure gradient exists between the left atrium and ventricle, which keeps the mobile portions of the mitral leaflets farther apart than normal during diastole. Because the leaflets are wide apart at the onset of systole, they are forced shut loudly when the ventricle contracts

Front 34

Why is S1 accentuated when the heart rate is more rapid than normal?

Back 34

Diastole is shortened and the leaflets have insufficient time to drift back together before the ventricles contract.

Front 35

Why is S1 diminished in first-degree AV block?

Back 35

There is an abnormally prolonged PR interval, which delays the onset of ventricular contraction. Following atrial contraction the mitral and tricuspid valves have additional time to float back together so that the leaflets are forced closed only from a small distance

Front 36

Right bundle branch block

Back 36

S1 is split due to delayed closure of the tricuspid valve

Front 37

Factors determining intensity of S1

Back 37

1) Distance separating the leaflets of open valves at the onset of ventricular contraction
2) Mobility of the leaflets (normal, or rigid because of stenosis)
3) The rate of rise of ventricular pressure

Front 38

What are the causes of an accentuated S1 sound?

Back 38

1. Shortened PR interval
2. Mild mitral stenosis
3. High cardiac output states or tachycardia (e.g. exercise or anemia)

Front 39

What are the causes of diminished S1 sound?

Back 39

1. Lengthened PR interval: first-degree AV nodal block
2. Mitral regurgitation
3. Severe mitral stenosis
4. “Stiff” left ventricle (e.g., systemic hypertension)

Front 40

What is the PR interval related to?

Back 40

The distance between the open valve leaflets at the onset of ventricular contraction – the period between the onset of atrial and ventricular activation

Front 41

a wave

Back 41

In late diastole the atrial contraction propels a final bolus of blood into each ventricle. This produces a brief further rise in atrial and ventricular pressures

Front 42

S1

Back 42

– First heart sound created as ventricular pressure exceeds atrial pressure and the tricuspid and mitral valves close in early systole. The mitral valve closes slightly before the tricuspid valve (0.01sec), but heard as a single sound. Loudest near apex of heart. High frequency sound.

Front 43

S2

Back 43

Second heart sound created at the conclusion of ventricular ejection. Ventricular pressure falls below that of the aorta and pulmonary artery thus closing the aortic and pulmonic valves. The aortic component precedes the pulmonary component.

Front 44

c wave

Back 44

A small rise in atrial pressure as the mitral and tricuspid valves close and bulge into their respective atria.

Front 45

v wave

Back 45

The result of passive filling of the atria from the systemic and pulmonary veins during systole, a period during which blood accumulates in the atria because the mitral and tricuspid valves are closed.

Front 46

Systole

Back 46

Ventricular contraction. From S1 to S2. Length constant.

Front 47

Diastole

Back 47

Ventricular relaxation and filling. From S2 to S1. Length varies with heart rate.