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MY 2016 RUSVM SAM 1 > Cardiac exam & Heart failure/Cardiovascular Conditions > Flashcards

Cardiac exam & Heart failure/Cardiovascular Conditions Flashcards

1
Q

What is the normal aortic BP

A

Systolic 120 Diastolic 80 written 120/80

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2
Q

What maintains aortic BP during diastole

A

Elastic muscle fibers stretch reflex

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3
Q

What creates the BP during systole

A

The contraction of the LV

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4
Q

What activates the SNS to maintain BP

A

baroreceptors

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5
Q

What is the Frank Starling relationship

A

increase in stretch (preload) = increase in force of contraction of muscle fibers

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6
Q

What is RAAS

A

Renin-angiotensin-aldosterone system

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7
Q

What is RAAS responsible for

A

Angiotensin II causes veno/arterioconstiction Aldosterone increases Na retention which leads to H2O retention which increases circulatory volume

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8
Q

What effect does the SNS have on CV system

A

veno/arterioconstriction +ve inotropy & chronotropy

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9
Q

How does the heart compensate for and increase in preload

A

hypertrophy

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10
Q

What is heart failure

A

Cardiac output is insufficient to meet body needs

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11
Q

When does heart failure occur

A

When heart disease is severe

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12
Q

What are the 2 major problems that are caused by heart disease

A

Volume overload Pressure overload

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13
Q

How does the heart compensate for a volume overload

A

eccentric hypertrophy enlargement of the ventricular volume (capacity)

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14
Q

Give an example of a condition that causes volume overload

A

myxomatous AV valve dz (endocardiosis)

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15
Q

What is the sequelae of eccentric hypertophy

A

there is a systolic emptying problem which leads to an increased afterload. Not all the blood leaves the ventricles after contraction

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16
Q

If an animal has an aortic/pulmonic (talking about the valves here) stenosis what type of overload would be caused

A

pressure overload

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17
Q

what type of hypertrophy would you see as a result of pressure overload in the ventricles

A

concentric hypertrophy

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18
Q

What are the sequelae of concentric hypertrophy

A

there is a diastolic filling problem which leads to an increased preload. Not enough space for the normal amount of blood that should fill the ventricles

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19
Q

In either case of hypertrophy how does the body try to maintain CO what changes in each type of hypertrophy

A

CO = SV * HR eccentric hypertrophy the stroke volume increases more concentric hypertrophy the heart rate increases more

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20
Q

What are the cardiac related CS of LCHF why

A

Left-sided congestive heart failure: hypotension pale mm incr. CRT incr. rate decr. pulses weakness syncope azotemia The left side pumps oxygenated blood to the body via the aorta. in failure (loss of effective pump) no blood is circulation which creates a relative hypovolemia that the body tries to compensate for.

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21
Q

Why is azotemia seen in LCHF

A

Because there is decr volume of blood flowing to kidneys therefore buildup of waste products

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22
Q

What are the pulmonary related CS of LCHF why

A

lung edema dyspnea coughing orthopnea tachypnea ex. intolerance cyanosis If there is a backup of blood in the LV there will be backup into the LA which will cause backup into lungs via pulmonary veins leading to fluid accumulation and decr in oxygen exchange

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23
Q

What are the CS of RCHF why

A

Ascites hepato-splenomegaly pleural effusion distension of veins hypotension If there is a backup of blood in the RV there will be backup into RA which will cause blood to remain in “great veins” beyond even their enormous reserve capability.

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24
Q

what is the hypotension in RCHF related to

A

The relative loss of circulating blood volume due to sequestration in extravascular compartment in addition to lack of an effective pump

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25
Q

which is more commonly seen in animals R or L CHF

A

Left

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26
Q

What are the clinical stages of heart failure

A

I - dz but NO CS II - CS w/normal to strenuous exercise III - CS w/ any activity IV - at rest

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27
Q

What stage of HF has dz but no CS

A

One

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28
Q

What stage of HF has CS with normal to strenuous exercise

A

Two

29
Q

What stage of HF has CS with any activity

A

Three

30
Q

What stage of HF has CS at rest

A

Four

31
Q

How do you do a CV system exam

A

TPR MM Thoracic palpation Auscultation

32
Q

what are the changes you might see in TPR if HF is present Why

A

decr. T incr. RR decr. P less circ bv will decr. T less oxygen in blood, body will try to get more pulses are difference between systolic & diastolic pressures if the pump is ineffective then less difference will be felt.

33
Q

why are MM pale

A

decr circ BV

34
Q

Why do you palpate the thorax

A

to locate the apical beat for good auscultation

35
Q

what are you listening to when you auscultate

A

you listen for normal or abnormal sounds

http: //multimedia.3m.com/mws/media/346089O/heart-and-lung-sounds-soundfile.wav?fn=Normal%20Split%20S1.wav
http: //multimedia.3m.com/mws/media/346098O/heart-and-lung-sounds-soundfile.wav?fn=Early%20Systolic%20Murmur.wav

36
Q

what happens if you hear abnormal heart sounds

A

you send for cardiac ultrasound!

37
Q

What are normal heart sounds

A

Lub-Dub

38
Q

What are some types of abnormal heart sounds

A

gallops

clicks

murmurs

39
Q

what are gallops sounds

A

S3 & S4

which are normal in LA but abn in SA

40
Q

what are clicks

A

when the valves are slow to close due to chordae tendinae being stretched so you hear it as a separate sound

Lub-click-Dub

41
Q

What causes murmurs

A

murmurs are the sounds of turbulent blood flow due to narrowing of a vessel, valvular insufficiency, incr. blood flow or decr. blood viscosity

42
Q

What are things you’d use to describe a murmur

A

where is occurs in cardiac cycle: systolic or diastolic

where it is loudest: apex or base

intensity on a scale of 1 to 6 with 6 being most severe grade of murmur

43
Q

what use are radiographs with HF

A

Really good at seeing lung status in CHF

Size & shape of pulmonary vessels

evidence of pleural edema

somewhat good at determining whether heart is enlarged esp for DCM and where

44
Q

What is the best modality to evaluate HF

A

Echocardiogram!

45
Q

Where does blood flowing into left atrium (LA) come from?

A

the lungs

specifically the pulmonary veins

46
Q

Blood flows into atria during _________ which is the _______ phase of cardiac cycle?

A

diastole, resting

47
Q

Blood flows from LA to left ventricle (LV) through the ______ or ____ ________________ _____ during which phase?

A

mitral (human term), left atrioventricular valve
diastolye

48
Q

What is the mechanical means to cause the blood flow into the heart during diastole?

A

negative pressure created during inspiration

49
Q

At end of passive filling phase the atria contract which results in?

A

last little bit of blood squeezed into LV to ↑ volume to allow for ↑ contraction due to Frank-Starling relationship

50
Q

Why doesn’t blood flow backwards into LA when LV contracts?

A

Due to closure of LAV valve

51
Q

Why doesn’t LAV valve prolapse back into atrium during ventricular contraction?

A

Chordae tendinae holding it in place.

52
Q

what is another name for myxomatous AV valve dz?

A

endocardiosis

53
Q

what type of overload does endocardiosis lead to?

what part of cardiac cycle problem? afterload or preload?

what type of hypertrophy?

A

volume overload
systolic emptying problem (↑ afterload)
eccentric hypertrophy

54
Q

what type of overload does aortic/pulmonic stenosis lead to?
what part of cardiac cycle problem? afterload or preload?
what type of hypertrophy?

A

pressure overload
diastolic filling problem (↑ preload)
concentric hypertrophy

55
Q

CS of LCHF
Front side vs back side

A

Front side = signs as a direct result of heart failure
hypotension
syncope
ex intolerance
mm: pale, cyanotic
CRT ↑
↑ HR
↓ pulses
weakness
azotemia
Back side = signs due to consequences of direct CS of heart failure
lung edema
dyspnea
coughing
orthophnea
tachypnea
ex intolerance
cyanosis

56
Q

CS of RCHF

A

Front side vs back side much less common than LCHF
Front side:
Syncope
weakness
ex. intolerance
azotemia
Back side:
ascites
hepato-plenomegaly
pleural effusion
distension of veins
hypotension

57
Q

Which spp coughs more with CHF dogs or cats?

A

dogs

58
Q

Clinical stages of heart failure

A

1: dz but no CS 2: CS w/ normal or strenuous exercise 3: CS w/ any activity 4: CS at rest

59
Q

What changes in TPR may be seen w/ pt w/ CHF

A

T: may be ↓ d/t ↓perfusion R: RR may be ↑ d/t hypoxia P: rate ↑, rhythym reg or irreg, quality ±↓

60
Q

what are MM supposed to be?

A

pink, moist

61
Q

ddx of pale MM

A

anemia shock heart failure

62
Q

ddx of cyanotic mm

A

heart failure R→L shunts

63
Q

ddx of bright red mm

A

sepsis R→L shunts erythrocytosis

64
Q

ddx of yellow mm

A

liver problem pernicious anemia

65
Q

what is felt on thoracic palpation

A

apical beat -mitral valve if displaced caudally from right behind elbow think ddx of what can displace heart caudally

66
Q

what is normally heard on thoracic auscultation?
What do the sounds represent?

A

normal heart sounds -LubDub Lub=closure of AV valves, start of systole Dub=closure of aortic/pulmonic valves, start of diastole

67
Q

What are the abnormal sounds that can be heard on auscultation

A

gallops = S3 +S4 sounds (normal in LA abn in SA) -S3= filling of ventricles (lubdubdub) -S4= contraction of atria (dublubdub) clicks= mitral valve dz (lubclickdub) murmurs= turbulance of blood flow, ↑ blood flow (hyperthyroidism), ↓viscosity (anemia)

68
Q

How to describe murmurs

A

functional (physiological) vs pathological

timing in cardiac cycle -systolic vs diastolic pansystolic vs holosystolic -lubwooshdub = holosystolic -wooshwooshwoosh = pansystolic continuous aka washing machine Location & radiation of murmur -base vs apex Intensity of murmur -grade 1-6
what dz has characteristic washing machine murmur PDA

69
Q

grades of murmur intensity

A

Grade 1: very soft, over sm area Grade 2: Grade 3: Grade 6: very loud, off the chest wall, over the entire thorax, palpable thrill

MY 2016 RUSVM SAM 1 (12 decks)

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