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PCM 3 exam 1- MARIYA > CV integration lab > Flashcards

CV integration lab Flashcards

1
Q

Venous return to the RV _____ during normal inspiration and a ____ in venous return to the LV.

A

Venous return to the RV increases during normal inspiration (increases in vol) and decreases in venous return to the left ventricle (reduction of vol)

These changes in venous return can alter intensity of murmurs and heart sounds, primarily those that

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2
Q

During inspiration, there is an increase in the splitting of:

A

S2 as A2 and P2 are separated (due to longer RV ejection time compared to LV ejection time during inspo)

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3
Q

Describe S3 and S4 heart sounds of RV origin w/ inspo and expo:

A

decrease with expo

increase with inspo

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4
Q

Describe S3 and S4 from left side of heart with inspo and expo:

A

increase with expo

decrease with inspo

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5
Q

Describe tricuspid stenosis with inspo and expo:

A

opening snap decreases with expo

opening snap increases with inspo

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6
Q

Describe mitral stenosis with inspo and expo:

A

opposite of tricuspid

opening snap increase wit expo

opening snap decreases with inspo

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7
Q

Pulmonary ejection sounds with inspo and expo:

A

decrease in inspo

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8
Q

Inspiration increases the intensity of murmurs originating from the ___ of the heart.

What are they also?

A

R side of the heart

Murmurs= tricuspid stenosis, pulmonary regurg, systolic murmur of tricuspid regurg (cavallo’s sign) and presystolic murmur of ebsteins anomaly)

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9
Q

What happens in MVP?

A

inspiratory decrease in venous return to the left side of heart reduces LV volume

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10
Q

In what pathological heart issue does murmur and click occur earlier and may diminish?

A

Mitral valve prolapse

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11
Q

When might a loud first heart sound be heard?

A

fever or exercise (hyperdynamic)

mitral stenosis

atrial myxoma

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12
Q

When might a soft first heart sound be heard?

A

low CO @ rest, HF

tachy

severe mitral reflux (caused by destruction of valve)

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13
Q

What would produce a variable intensity in the first heart sound?

A

atrial fibrillation

complete heart block

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14
Q

What is a second heart sound?

A

audible expiratory spitting means >30 msec difference in timing of the aortic (A2) and pulmonic (P2) components of the second heart sound

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15
Q

Where is splitting of S2 best heard over?

A

over 2nd left ICS

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16
Q

normal P2 is often softer than which sound? where is it rarely audible

A

normal P2 is often softer than A2

rarely audible at apex

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17
Q

If P2 is audible over apex what is the diff dx?

A

significant pulmonary HTN

Atrial septal defect

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18
Q

Second heart sound findings should always be present in what positions?

A

upright and supine

normal subjects may have expiratory splitting when recumbant that disappears when upright

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19
Q

When can you hear a loud aortic component of second second?

A

systemic HTN

dilated aortic root

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20
Q

When can you hear a soft aortic component of second second?

A

calcific aortic stenosis

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21
Q

What kind of second heart sound would you hear with pulmonary htn?

A

loud pulmonary component of second sound

22
Q

What shock is caused by failure of the heart as a pump to deliver adequate perfusion to peripheral tissues

A

cardiogenic shock

23
Q

What shock is caused by failure of arterial circulatory bed to maintain adequate perfusing pressure to peripheral tissues?

A

distributive shock

24
Q

What shock is caused by significant reduction in cicrculating vascular volume, resulting in reduced perfusing pressure to peripheral tissues

A

hypovolemic shock

25
Q

What regulates HR?

A

autonomic NS

26
Q

what influences stroke volume?

A

LV preload, afterload, and myocardial contractility

27
Q

Systemic Vascular resistance is governed by:

A

arterial tone, arterial volume, and structural integrity of vessels themselves

28
Q

Example of someone running up hill and CV performance of what happens:

A

runner experiences ruge in serum catecholamines–> increased SNS output–> increased HR–> increased myocardial contractility–> increased CO; arteriolar tone will increase as result of VC effects of catecholamines–> increase in perfusion pressure–> adequate blood flow to joggers LE and diaphragm

29
Q

When does shock typically occur?

A

when there is a massive perturbation of one or more of the processes (HR/ stroke vol/SVR, etc.) that cannot be compensated for by adoptions in other areas

30
Q

What components are the main ones that go into tissue perfusion pressure?

A

CO (HRx SV)

SVR (arterial tone/volume/integrity)

31
Q

A patient presents with unexplained sinus tachy and a BP of 90/75 (hypotensive BP), what would the main differential that you would think about be?

A

shock

could also consider cardiac tamponade..

32
Q

If you see a pt with shock who has bradychardia (or lower than expected HR), what should you consider doing next?

A

ways to increase HR

33
Q

In a patient with suspected shock, it is critical to check what early?

A

arterial blood gases and lactate levels

34
Q

What is associated with better outcome in a patient with cardiogenic shock and what should you exclude immediately?

A

exclude acute MI immediately

EARLY revascularization is assoc with better outcomes!

35
Q

What would be a cause of a wide, fixed splitting S2

A

atrial septal defect

36
Q

What would be a cause of wide split S2, varying with inspo

A

pulmonary stenosis, RBBB

37
Q

What would be the cause of paradoxical splitting of S2

A

hypertrophic cardiomyopathy

38
Q

If you see diffuse ST elevations on all leads(and/or sometimes PR depression), what should you suspect?

A

acute pericarditis

39
Q

How would you describe a pericardial friction rub?

A

a three component scratchy rub that is loudest over the left sternal border

40
Q

The dx of acute pericarditis requres presence of at least 2 of the following criteria:

A

typical chest pain

pericardial friction rub

widespread ST segment elevation

new or worsening pericardial effusion

41
Q

Common clinical features of cardiac tamponade include:

A 
Dyspnea
Hypotension
Tachy
Jugular venous distention
Pulsus pardoxus of >10 mmHg
42
Q

Constrictive pericarditis can complicate any pericardial dz (acute pericarditis or cardiac surgery). How do these pts typically present?

A

progressive dyspnea
edema
ascites
cachexia

elevated JVP, pulsus paradoxus, Kussmauls sign, and/or pericardial knock

43
Q

In a pt with acute pericarditis, the sharp pleuritic chest pain typically IMPROVES when the pt:

A

sits up and leans fwd

44
Q

Where is pericardial friction rub heard best upon auscultation?

A

scratchy sound best heard with diaphragm and loudest over left sternal border

45
Q

Pts with suspected pericardial dz should undergo initial evaluation with:

A

ECG, CXR, and Echo

46
Q

Pericardial effusion and cardiac tamponade on ECG:

A

low QRS voltage (bc fluid in bw heart and ECG leads) and sometimes electrical alternans (QRS reflecting swinging in heart in pericardial fluid)

47
Q

What ECG findings would you find in constrictive pericarditis?

A

no specific findings

nonspecific ST and T waves changes are common

48
Q

What is the CXR in acute pericarditis?

Pericardial effusion ?

constrictive pericarditis?

A

acute pericarditis= typically NORMAL

Pericardial effusion (with or w/out tamponade) = cardiomegaly with clear lung fields

Constrictive pericarditis= pericardial calcification (uncommon)

49
Q

What test should you perform rapidly if you suspect tamponade?

A

echocardiography

normal in acute pericarditis unless assoc. with pericardial effusion

50
Q

What test has a major role in IDENTIFICATION of a pericardial effusion and in assessing its hemodynamic significance?

A

Echocardiography

51
Q

What is the treatment for cardiac tamponade?

A

immediate removal of pericardial fluid

PCM 3 exam 1- MARIYA (6 decks)

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