w3- SGL

Question 1

how would severe anemia or polycythemia impact cyanosis

Answer 1

May be less evident in cases of severe anemia

May be more notable in patients with polycythemia

Question 2

what are some compensatory changes that may occur as a result of hypoxia

Answer 2

Hyperventilation

Pulmonary Distribution of Blood Flow

Sympathetic Response

• Chemoreceptors* sense decreased partial pressure of oxygen. Central chemoreceptors depress oxidative metabolism in neural tissue, depressing respiration.
• Peripheral chemoreceptors* (in the aortic arch and carotid sinus) stimulate the cardiac and respiratory systems under hypoxic conditions.
• Increase in circulating catecholamines

Question 3

what is the cardiovascular response to hypoxia

Answer 3

Acutely –> increases cardiac output and redirects blood flow to all major organs, particularly the brain. Chronic hypoxia –> depressed cardiac output.

Question 4

what are the symptoms of pulmonary hypertension

Answer 4

Dyspnea, chest pain, fatigue, and lightheadedness

Later symptoms can include

o Syncope
o Abdominal distention

Ascites
o Peripheral edema

Among those with Eisenmenger physiology (left-to-right shunt), peripheral cyanosis is also seen

Question 5

what is the reason for the S1 and S2 sounds

Answer 5

S1 = vibrations coming from the closure of mitral valve (late diastole/early systole)

S2 = vibrations coming from the closure of aortic valve (late systole/early diastole)

Question 6

normal sounds are referenced to what side of the heart

Answer 6

left

Right heart sounds usually occur at lower pressure, and therefore are less audible than left heart

Question 7

what are S3 and S4 sounds indicative of

Answer 7

change in ventricular compliance

Question 8

describe the gradation of murmors

Answer 8

Question 9

what is the reason behind S2 splitting

Answer 9

S2 can be split due to inspiration → increased right heart filling time = delayed pulmonary valve

A2 = left-side aortic valve closure (usually louder)
oP2 = right-side pulmonary valve closure

Fixed splitting should not happen – consistent lagging pulmonary valve closure due to increased right ventricle stroke volume, which means it takes longer to fill/empty

Question 10

rationale behind a soft S1

Answer 10

mitral valve regurgitation

Question 11

differentiate the types of ASD

Answer 11

Primum ASD

Caused by the primum septum not fuzing

with the endocardial cushions, which leaves a defect at the base of the interatrial septum(typically large)

○ Typically not isolated, but instead endocardial cushion defects so they are accompanied by AV valve disorders

● Secundum ASD

70-75% of all ASD

○ Typically Isolated

○ A defect in the foramen ovale caused by

poor growth of the secundum septum or excessive absorption of the primum septum

● Sinus Venosus ASD

An abnormality of the insertion of the

superior or inferior vena cava which then

overrides the interatrial septum

○ Technically not ASD due to being caused

by defect in sinus venosus septum

Unroofing defect with absence of normal tissue between the right pulmonary veins and the right atrium

malposition of the insertion of the superior or inferior vena cava straddling the atrial septum

Question 12

risk factors for ASD

Answer 12

Maternal alcohol consumption during the

first trimester​ linked to double the risk of

ASD

○ Exposure to chemicals(vague) during the

first trimester increased risk

○ Increased incidence of ASD if a first

degree relative has ASD(some genetic

linkage)

○ Endocardial cushion defects are often

noted in patients with Trisomy 21

Question 13

what can JVP be used to measure

Answer 13

• The current status of right atrial pressure