Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ICM > Cardio > Flashcards

Cardio Flashcards

1
Q

Valvular Heart Disease

A

because we didnt get enough in path…

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

What wave corresponds with an increase in atrial pressure?

A

A wave

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

What is the C wave?

A

Upward bulging of mitral valve into left atrium may produce a C wave early in systole

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

What is the V wave?

A

Atrial volume increases during ventricular systole due to passive filling from pulmonary veins

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

Normal mitral valve sounds?

A
  • Opening sound
    • Absent
  • Closing sound
    • production of S1 as a byproduct of mitral valve closure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Most common cause of valvular LV inflow obstruction?

A

Rheumatic mitral stenosis

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

What occurs to the Mitral valve in MV stenosis?

A
  • Diffuse fibrous thickening of leaflets
    • +/- calcification
  • Fusion of commissures
  • Thickened fused chordae
  • Greatest obstruction at apex
  • Aschoff nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What occurs to the left atrium and left ventricle in mitral stenosis?

A
  • Atrium
    • Enlarged, hypertrophied
    • Mural thrombi
      • especially if there is A. fib
  • Ventricle
    • normal or smaller sized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the normal size of mitral valve orfice? Mild MS? Severe MS?

A
  • Normal: 4-6cm
  • Mild MS: 2cm
  • Severe MS: 1cm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens to LV diastolic pressure in MS? LA?

A
  • LV diastolic pressure = normal
  • LA pressure = increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In MS what happens to the pulmonary artery pressure?

Cardiac output?

A
  • PAP
    • Normal
    • Later it increases because the LA pressure is pushing backwards on the pulmonary system
  • CO
    • Normal
    • Later decreases in decompensation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In the normal heart when there is an increase in flow what happens to the pressure gradient? What occurs in mitral stenosis

A
  • Normal heart
    • Large increase Q = little increase pressure gradient
  • MS
    • Small increase in Q = large increase in pressure gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs/Symptoms of MS?

A
  • Dyspnea/Orthopnea/PND
    • related to increased pulm. venous pressure
    • accentuated by increased BF across stenotic MV
  • Acute pulmonary edema
  • Hemoptysis
    • due to elevated pulm. venous pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens as a result of pulmonary HTN?

A
  • Cor pulmonale
  • Fatigue
  • Lower extremity edema, ascites
  • hepatic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Ortner’s syndrome?

A

In pulmonary hypertension when the pulmonary artery compresses the left recurrent laryngeal nerve resulting in hoarseness

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

What occurs to the point of maximal impulse in MS?

A

PMI is normal or decreased because the LV is smaller

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where/when would you have RV heave?

A

Occurs with pulmonary HTN along the parasternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Auscultation findings in mitral stenosis?

A
  • Loud S1
  • Onset of murmur after S2 (diastolic murmur)
    • HALLMARK**
  • Low pitched decrescendo murmur
  • Opening snap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nonrheumatic causes of mitral stenosis?

A
  • Congenital
    • single papillary muscle
  • Active infective endocarditis
  • Annular calcification
  • Cor triatriatum
    • congenital membrane sparating LA into 2 separate chambers
  • Neoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mitral regurgitation: What causes abnormalities of the valve leaflets?

A
  • Rheumatic heart disease
  • Floppy mitral valve
    • most common
  • IE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In mitral regurg. what obnomalities of the mitral anulus can occur?

A
  • Calcification
    • normal aging (degenerative)
    • associated with hypertension, aortic stenosis
    • chronic hypercalcemia
  • Dilation
    • LV (cardiomyopathy/ischemic disease)
    • Marfans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What can occur to the chordae tendinae to cause mitral regurg?

A
  • Elongation
    • marfans
  • Rupture
    • idopathic
    • trauma
    • IE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can occur to the papillary muscles in order to cause mitral regurg?

A
  • Malalignment
    • LV dilation
    • Hypertrophic obstructive cardiomyopathy
  • Dysfunction
    • ischemia
    • infiltrative - amyloid/sarcoid/neoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does the heart compensate for mitral regurgitation? What occurs to change the structure?

A
  • LV dilates to increase forward SV
    • Increased LVEDV
  • LA enlarged to to increased BV
  • Systolic LV function normal (until late)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In MR what happens to LA pressure? Pulm artery pressure? CO?

A
  • LA pressure
    • Normal
    • Increases later (large V waves)
  • PAP/CO
    • Normal
    • Increase later
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complications of MR?

A
  • A. fib
    • chronic LA dilation
  • IE
  • Pulm htn and cor pulmonale
    • edema
    • hepatomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What occurs to the point of maximal impulse in MR?

A

Displaced and hyperdynamic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Auscultation findings in MR?

A
  • Diminished S1
  • Holosystolic murur
    • best heard at apex
  • S3
  • Variably present:
    • split S2
    • mid-diastolic murmur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Valvular causes of LV outflow obstruction? (were in the aortic valve now just FYIIII)

A
  • Congenital
    • most common
  • Rheumatic
  • Degenerative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Most common subvalvular causes of LV outflow obstruction?

A

Hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Congenital and acquired causes of aortic stenosis?

A
  • Congenital
    • unicuspid (severe)
    • Bicuspid: progressive fibrosis or calcification
  • Acquired
    • Rheumatic
      • MV involvement too
    • Hypercholesterolemia
    • Endocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Second most common congenital anomaly?

A

Bicuspid aortic valve: turbulent flow –> fibrosis and calcification over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What happens to the aorta in rheumatic fever?

A
  • Commisural fusion
  • Often regurgitation
  • MV must be affected as well
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is degenerative acquired aortic stenosis?

A
  • Senile wear and tear
  • Calcific deposition
  • Calcification of MV anulus, and coronaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Anatomical changes to LV in Aortic stenosis?

A
  • LV hypertrophy
    • Large LA-AA pressure gradient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Aortic stenosis:

Opening size? Pressure change? CO? Pulmonary arterial pressure?

A
  • Opening size <.75cm
  • Change in pressure >50mmhg
  • CO
    • normal
    • decreased later
  • PAP
    • increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Aortic stenosis:

LV systolic pressure?

LV diastolic pressure?

A
  • LV systolic pressure
    • extremely increased
  • LV diastolic pressure
    • increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Symptoms of aortic stenosis?

A
  • Angina
    • due to increased o2 demand (LVH)
  • Syncope
    • often orthostatic or exertional
    • decreased cerebral perfusion
    • arrhythmias
  • Dyspnea
    • orthopnea, PND, CHF
    • venous hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Aortic stenosis prognosis?

A

May be asymptomatic for many years but once symptoms develop –> poor prognosis with potential for sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Aortic stenosis:

What happens to the peripheral pulse?

Cardiac palpation?

A
  • Peripheral pulse
    • slow rise, low volume
  • Cardiac palpation
    • Palpable a-wave
    • systolic thriss in aortic area
    • sustained lift (LVH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Auscultation in aortic stenosis?

A
  • Prominent S4 gallop
  • Paradoxical splitting of S2
    • severe AS or decreased LV function
  • Aortic ejection sound
  • Systolic murmur
    • heard at the base of the heart
    • Radiation to the carotids
    • Decreases with LV failure
    • Rasping sound
    • Length of murmur is correlated with severity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Causes of cusp abnormality leading to aortic regurgitation?

A
  • Bacterial endocarditis
  • Rheumatic disease
  • Degenerative
  • Congenital
    • bicuspid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

causes of Aortic root dilation leading to aortic regurg?

A
  • Marfans
  • idiopathic
  • Ehlers-danlos
  • Pseudoxanthoma elasticum
  • Chronic systemic hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Tell me whatcha know about marfans?

A
  • AD
  • Musculoskeletal
    • long limbs, lax joints, high palate, pectus deformity
  • Lens deformity
  • ASCENDING AORTIC ANEURYSM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Causes of aortic root distortion leading to reurg?

A
  • Ankylosing spondylitis
  • Syphilis
  • Rheumatoid disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Causes of loss of commissureal support leading to aortic regurgitation?

A
  • Aortic dissection
  • Aortitis
    • inflammatory, syphilis
  • VSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is aortic dissection? What is it associated with?

A
  • Intimal tearing allowing propagation of blood between intima and media
  • Associations:
    • HTN
    • marfans
    • pregnancy
    • bicuspid aortic valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is Cor bovinum?

A

LV volume overload (happens in aortic regurg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Aortic regurgitation:

Pulse pressure?

Cardiac output?

LVEDP?

A
  • Increase pulse pressure
  • Normal CO until late
  • LVEDP normal, late increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Symptoms of aortic regurgitation?

A
  • Exertional dyspnea
  • orthopnea
  • PND
  • Angina
    • due to low BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Findings on physical exam of aortic regurgitation?

A
  • DeMusset’s sign
    • head bob in synchrony with beating heart
  • Corrigan’s pulse: bounding and forceful
  • Traube’s sign - s/d sounds over femoral artery
  • Muller’s sign - systolic pulsation of uvula
  • Quincke’s sign - capillary pulse in nailbed
  • Wide pulse pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Auscultation of aortic regurg?

A
  • S1 may be split
  • Systolic ejection sound murmur
    • blood flows backwards in diastole
  • S3 gallop may be present
  • High frequency diastolic murmur (“blow”)
    • Decrescendo pattern
    • Immediately after A2
  • Mid-late diastolic apical rumble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Most common cause of tricuspid stenosis?

Functional result?

A
  • Rheumatic disease
    • Always in association with concomitant MV
    • Minimal calcification
  • Functional result: inability of RA to empty leading to systemic venous congestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Triscuspid stenosis symptoms and signs?

A
  • Orthopnea, PND = UNUSUAL
  • RARE pulmonary edema
  • Fatigue
  • Weakness
  • Abdominal discomfort
    • due to congestion in the liver
    • ascites possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What occurs to the jugular venous pressure in tricuspid stenosis?

A
  • “giant” A waves
  • Slow Y descent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Auscultation findings in Tricuspid stenosis?

A
  • Opening snap
  • Diastolic murmur at the lower left stenal border
  • Both OS and murmur increase with inspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Causes of tricuspid regurgitation?

A
  • Rheumatic
  • IE
  • Ebsteins anomoly: congenital
    • septal and posterior leaflets displaced towards RV apex
  • Carcinoid valve disease
    • dilation of valve ring secondary to RVF or pulm HTN
  • Floppy (prolapse)
  • RV infarct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Most common cause of pure tricuspid regurg?

A
  • Anatomically normal
  • Dilation of RV and tricuspid anulus
    • PHTN
    • RV diastolic HTN
      • dilated cardiomyopathy
      • RVF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Tricuspid regurgitation:

RA pressure?

RV diastolic pressure?

Pulmonary artery systolic pressure?

A
  • RA pressure increases
    • Large V wave with prominent Y descent
  • RV dp increases
  • PAP
    • <40mmHg suggest primary valve etiology
    • <60mmHg suggests either 1 or 2ndary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Signs/Symptoms of Tricuspid valve regurg?

A
  • Progressive fatigue
  • anorexia
  • painful congestive hepatomegaly, ascites, edema
  • Throbbing pulsations in neck
  • A. fib is common
  • JVD
  • jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Triscuspid Regurgitation auscultation signs?

A
  • S3 gallop
    • increases with inspiration
  • Holosystolic murmur
    • lower left sternal border
    • increases with inspiration (carvallo’s sign)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Coronary Heart Disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Role of cytokines in atherosclerosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the coronary equivalents?

A
  • Diabetes
  • Framingham risk score >20%
    • takes into account smoking, lipids, cholesterold, physical activity etc..
  • Aortic atherosclerosis
  • Peripheral vascular disease with ABI (ankle brachial index) ratio of <0.9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Steps in the development of atherosclerosis?

A
  • LDL is oxidized and transported to the media
  • Breaks down the internal elastic lamina
  • Macrophages are activated
  • Smooth muscle cells migrate and proliferate in the media
  • Foam cells develop
  • Cellular apoptosis occurs
  • Neovascularization of the plaques via the vasa vasorum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is in the fatty streak? What occurs in advanced lesions?

A
  • Fatty streak
    • lipid laden monocytes, macrophages, and t-lymphocytes
  • Advanced lesions
    • There is fibrous cap development
    • Core easily becomes necrotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Atherosclerosis timeline

A

Just cool to look at

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What ratio determines the integrity of the lesion?

A

Ratio between synthesis and breakdown. Increased breakdown leads to a weaker, more unstable, plaque

69
Q

What can cause plaque rupture?

A
  • Decreased collagen synthesis
  • Increased collagen breakdown
  • Smooth muscle apoptosis
70
Q

What leads to plaque erosion?

A
  • Increased endothelial cell apoptosis
  • Basement membrane breakdown
71
Q

Erosion is likely to cause? What populations are most affected?

A
  • Sudden cardiac death > acute coronary syndrome
  • Older women > younger women
  • Younger men > older men
72
Q

Increased expression of what leads to thrombosis?

A
  • Tissue factor
  • Fibrinogen
  • Plasminogen activator inhibitor
73
Q

Relationship between amount of stenosis and likelihood of MI?

A

None. The quality of the plaque plays the most important role

74
Q

Healthy vs. dysfunctional vascular endothelium?

A
  • Healthy
    • dilation, growth inhibition, antithrombic, antiinflammatory, anti-oxidation
  • Dysfunctional
    • constriction, growth promotion, prothrombic, proinflammatory, and pro-oxidation
75
Q

Endothelial dependence on Adenosine? NO?

A
  • Coronary response to increased demand
  • Adenosine
    • not endothelium dependent
    • potent vasodilator
  • NO
    • endothelium dependence
76
Q

Characteristics of plaques prone to rupture?

Initial response of the vessel?

A
  • Characteristics
    • thin fibrous cap
    • lipid, macrophage rich
    • smooth muscle poor/apoptosis
    • remodeling of the artery
    • adventitial inflammation
    • neovascularization
  • Initial response
    • stretching and growth to preserve the lumen
77
Q

What is the fractional flow reserve?

A
  • FFR = Flow Dilated / Flow Initial
  • FFR = Pressure Dilated / Pressure Initial
78
Q

Consequence/complication of coronary artery disease?

A
  • Angina
    • Stable/unstable
  • MI
    • NSTEMI/STEMI
  • LV dysfunction
    • ischemica causes diastolic dysfunction first
  • HF
  • Myocardial stunning, hibernation, and necrosis
79
Q

What is myocardial stunning?

A

Brief period of myocardial ischemia resulting in prolonged myocardial dysfunction with gradual return

80
Q

What is myocardial hibernation?

A

Impaired LV function secondary to reduced coronary BF that can be resored toward normal by revascularization

81
Q

Ways to evaluate Angina Pectoris?

A
  • ECG
  • TM with nuclear imaging
  • Catheterization
  • Intravascular ultrasound
  • Fractional flow reserve
82
Q

In angina, what is prognosis dependent upon?

A

Prognosis is dependent upon left ventricular function and amount of myocardium at risk from ischemia

83
Q

In unstable angina and an NSTEMI MI how does micronecrosis occur?

A

Surface of thrombus associated with plaque rupture is covered with activated platelets which are sheared off by blood flow and occlude distal beds causing regions of micronecrosis

84
Q

What are the three “A”s of platelet function?

A
  • Adhesion: platelet GP1B receptor
  • Activation: TXA2, serotonin, ADP, fibrinogen etc
  • Aggregation: crosslinking of platelets by fibrinogen or VWF
85
Q

Diagnosis of a STEMI?

A
  • Ischemic chest pain
  • Characteristic ECG changes
  • Elevated cardiac markers
  • ST Elevation in 2+ contiguous leads
86
Q

Peripheral Arterial Disease

A

this was the easiest lecture. he better ask super easy questions!

87
Q

What is Peripheral arterial Disease (PAD) the most common cause of?

A

Atherosclerosis of the peripheral arteries is the most common cause of symptomatic obstruction in the peripheral arterial tree

88
Q

What is the difference between incidence and prevalence?

A
  • Prevalence
    • # with the disease/ # of people in the population
  • Incidence
    • measure of the probability of occurrence of a given medical condition in a population within a specified period of time
89
Q

Two main risk factors to peripheral artery disease?

A
  • Diabetes
  • Smoking
  • ***Definitely know
90
Q

What is PAD tell you about what is happening with the rest of the body?

A

Peripheral artery disease is a surrogate marker for vascular disease elsewhere: stroke/heart disease.

PAD likely wont kill you, the stroke or MI may

91
Q

When does the 5 year risk of limb loss go up?

A

SIGNIFICANTLY goes up for a diabetic patient

Nondiabetic risk: 5%

Diabetic risk: 25%

92
Q

What is claudication?

A

“Angina” of the lower legs. Can walk. Cramps. Pain. Patient does better with rest. This is all exertional related. Highly unlikely that you will lose your legs (again, unless diabetic)

93
Q

Claudication is commonly misdiagnosed as what?

A

Arthritis

94
Q

What are some obvious and unique signs of PAD?

A
  • Shiny skin
  • Hair loss
95
Q

What are you checking for in the physical exam for PAD?

A
  • Hair loss on distal limbs
  • Edema/tenderness
  • Pulses
  • Check both pressures in the upper extremity
  • Check for bruits
    • abdominal
      • renal art. stenosis/mesenteric stenosis/ iliac disease/aneurysm
    • Remoral
96
Q

Non-invasive tests for PAD?

A
  • ABI
  • Exercise test
  • Segmental pressures
  • MRA
  • CTA
97
Q

What is Amaurosis fugax?

A

Sudden loss of vision in the eye that does come back. This is usually a sign of artery disease

98
Q

Ankle-Brachial Index:

Normal?

Moderate?

Severe?

A
  • Normal
    • 0.95-1.05
  • Moderate
    • .55-.9
  • Severe
    • <0.4 with critical limb ischemia
99
Q

Change in the doppler waveform in PAD?

A

Normal is triphasic but can be –> biphasic –> monophasic –> flat flow (or even reversal) in severe PAD

100
Q

What is Leriche syndrome?

A

Atheroma of distal aorta and eventually occlusion; however, due to slow nature of the occlusion the body has generated collaterals to compensate. Doesnt lead to bone loss

101
Q

Risks of CTA?

A

Radiation

Renal necrotozicity

Less technology dependency

102
Q

Main thing to keep in mind when treating PAD?

A

MUST treat the underlying cause

(stop smoking, control diabetes, exercise etc)

103
Q

Medical treatment options for PAD?

A
  • Risk factor modification
  • Exercise therapy
  • Drug therapy
104
Q

Physical Diagnosis

A
105
Q

Difference between central and peripheral cyanosis?

A
  • Central
    • entire circulation involved: face/lips/exposed tissue
  • Peripheral
    • environmental exposure/stasis to extremities
    • more local
106
Q

What is pulse pressure? Difference between narrow and wide?

A
  • PP = SBP-DBP
    • reflects compliance of the cardiovascular system
  • Narrow: <20mmHg
    • low C.O
  • Wide: >100mmHg
    • high C.O.
    • Decreased TPR and increased arterial stiffness
107
Q

What is paradoxical pulse? What does it indicate if it is high?

A
  • Paradoxical pulse is the decrease in SBP with inspiration
  • >15mmHg is an important sign of pericardial disease and cardiac tamponade
108
Q

What is Pulses alternans?

A

Beat to beat variation in intensity or amplitude of the arterial pulse: indicative of CHF

109
Q

Where is venous pulse reflected?

What are the pulse waves?

A
  • Venous pulse is reflected in the jugular veins
    • distended in recumbant position
    • Normal <7cmH2O
  • Pulse waves
    • A wave - atrial contraction
    • X descent - atrial relaxation
    • V wave - peak of atrial filling
    • Y descent - atrial emptying
110
Q

What is SI?

A
  • Onset of systole/QRS complex
  • Closure of the mitral/tricuspid valves
  • Heard near the apex of the heart
111
Q

What is SII?

A
  • End of systole
  • Closure of aortic and pulmonary valves
  • Normally split on inspiration and single on expiration
112
Q

What is wide splitting in SII?

A
  • Right bundle branch block
    • reversed splitting; wider on expiration
  • Left bundle branch block
    • severe aortic stenosis and htn
113
Q

In what situation would you ALWAYS hear a split SII?

Length of systole versus diastole?

A
  • Persistant splitting in ASD
    • RV pumps 3x as LV
  • Systole is shorter than diastole
    • SAME as diastole with increased HR (exercise)
114
Q

What is SIII? Difference between children and adults?

A
  • SIII = Filling sound in early diastole due to rapid filling of the ventricle
    • Occurs immediately after SII
    • Listen at the apex
  • Normal in children
  • Pathological in adults
    • CHF
    • Increased LVEDV
    • Ventricular gallop
115
Q

What is SIV? Cause?

A
  • Ventricular filling sound in late diastole due to atrial contraction
    • Heard right before SI at the apex
  • Due to cardiomyopathy or hypertension
  • Poor ventricular compliance with hypertrophy
    • not necessarily increased volume
  • Either ventricle is involved
  • “atrial sound or gallop” (although it originates in the ventricle)
116
Q

What is the ejection click? Cause?

A
  • Ejection click is created during early systole in the aortic or pulmonic valves
    • Heard at the left sternal border right after SI
      • almost sounds like “double SI”
  • This is due to either of these valves being stenotic
117
Q

What is a systolic click? vs Opening snap?

A
  • Both occur at the apex
  • Systolic click
    • mitral/tricuspid valve prolapse
    • often accompanied by late systolic murmur
  • Opening snap
    • Mitral/tricuspid valve stenosis
      • Same as SIII timing
118
Q

What is a holosystolic murmur and what causes it?

A
  • Extends from SI to SII
  • Caused my mitral/tricuspid regurgitation of VSD
119
Q

What is a midsystolic murmur? Causes?

A
  • Ejection murmur that begins after SI and ends before SII
  • Pulmonic or aortic stenosis
    • Pulmonic: common in kids and in high output states
    • Aortic: sclerosis at the base of the valve and hypertension
120
Q

What is an early diastolic murmur caused by?

A
  • High pressure gradient right after SII
  • Aortic or pulmonic regurgitation
  • “blowing or soft”
121
Q

Characteristics of mid-diastolic murmurs? Causes?

A
  • Low frequency due to turburlent flow over mitral or tricuspid valves; lower pressure gradients
  • Due to mitral or tricuspid stenosis/regurg, VSD, or ASD
122
Q

What is a continuous murmur? Two main types?

A
  • Extend directly from systole into diastole although not necessarily continuously present
  • A-V shunt
    • PDA, coronary artery fistula, Pulmonary A-V fistula
  • Narrowed artery
    • coarctation of aorta and pulmonary artery stenosis
123
Q

Components of a pericardial friction rub? (i typed rum initially - liquor on my mind?)

A
  • Pre systole
  • Systolic
  • Early diastole
124
Q

Features of a functional systolic murmur?

A
  • short duration
  • early to mid systole
  • Left sternal border sound with normal SII
  • Decreased intensity on standing
  • Remainder of exam is normal
125
Q

How is aortic stenosis categorized?

A
  • Delayed/weak carotid pulse = 5
  • Decreased/absent A2 = 3
  • Late murmur at R upper sternal border = 2
  • Calcification on chest film = 4
  • 0-6 = Not significant
  • 7-9 = intermediate
  • 10+ = moderate to severe
126
Q

Diagnostic Methods

A

I HATEEE TESTING CRIZZAP

127
Q

Five finger approache includes?

A
  1. History
  2. Physical
  3. ECG
  4. Lab tests
  5. Imaging
128
Q

Role of the CK enzymes?

Basic blood panels taken?

A
  • Makes ADP
  • Basic blood panel
    • CBC
    • BMP
    • Liver panel
129
Q

Targeted blood panels?

A
  • Cardiac enzymes
    • Old: CPK, MB; myoglobin
    • New: troponin
  • BNP
  • Lipids
130
Q

Significance of elevated troponin?

A
  • Evidence of tissue injury
  • Demand - ischemia
    • mismatch of supply and demand
131
Q

What is BNP? Sensitivity versus specificity?

A
  • Brain Natriuretic peptide secreted by myocytes secondary to stretching
    • increases natriuresis
  • Very sensitive - rules out HF but does not diagnose it
  • NOT specific: elevated in pulmonary disease, RF, shock, cirrhosis… etc
132
Q

Relationship between troponin level and possible causes

A
  • Below 1 - multiple causes, mild effects
    • .001 = normal
  • 10 = medium sized MI or severe myocarditis
  • 100mg/L - large MI
133
Q

5 major lipoproteins? (this is REVIEW)

ApoA1 and ApoB = ?

A
  • Chylomicrons, VLDL, LDL, HDL, IDL
  • Apo A1 = component of HDL
  • Apo B = component of non-HDL

All merkers for atherosclerosis/plaques/calcifications

134
Q

Uses of ECG? Normal heart vector?

A
  • Ecg
    • Screening, diagnosis, monitoring
  • Normal heart vector = +60
135
Q

EKG of premature atrial contraction?

A
136
Q

EKG of premature ventricular contraction?

A
137
Q

EKG of atrial flutter?

Atrial fibrillation?

Ventricular tachycardia?

A
138
Q

EKG of v. fib, left bundle branch block? right bundle branch block?

A
139
Q

Different types of ECG monitors?

A
  • Ambulatory
    • portable and worn for varied lengths of time
    • three leads
  • Holter
    • 24hr/48hr/2wk monitors
    • Continuously records and when returned the data is downloaded
  • Event monitor
    • longer term with daily auto transmission
    • will also detect tachy/brady episodes
  • Loop recorders
    • subcutaneously over the heart
    • auto detects arrhythmias
140
Q

What is baye’s theorem?

A
  • When prevalence is low - higher risk of false +
  • When prevalence is high - higher risk of false -
  • Predictive power is best in patients with intermediate prevalence
    • higher the workload the better the prognosis
    • lower workload predicts poor prognosis
141
Q

Treadmill testing:

Goal?

Double product?

Best predictor of ischemia?

A
  • Goal
    • Goal: Maximum exercise capacity to increase sensitivity
  • Double product – peak BP x peak HR - indication of the energy demand of the heart and energy consumption of the heart. >20,000 is good
  • The best predictor of ischemia is horizontal to downsloping ST depression of ≥1 mm (80 milliseconds past J-point).
142
Q

Indications for pharmacologic stress testing?

Types of testing?

A
  • Indication: cant exercise, pacemaker, aortic aneurysm, abnormal EKG, poorly controlled HTN, COPD
  • Coronary vasodilators (adenosine)
    • Perfusion worsens when you dilate non-stenosed coronaries versus stenosed
  • Inotropes (dobutamine)
    • Increases stress and myocardial O2 demand –> ischemia in stenosed patient
143
Q

Three types of nuclear imaging and uses?

A
  • Thallium - 201
    • Na/K pump to enter myocytes for viability testing
  • Technetium
    • Stress testing and eval of LV function
  • PET scan with Rubidium
    • Used for viability

View the PET images for normal/inferior ischemia/anterior ischemia in ppt?

144
Q

What does ultrasound use for imaging?

A
  • High frequency sound wave to discern images, function, and direction of BF
  • Audible sound = 20kHz; US = 2-5 MHz
  • Use of doppler
145
Q

Different ultrasound views?

A

Transthoracic
•Apical (A) 4 chamber
•Parasternal
•Short axis
•A – 2 Chamber

Can also be done transesophageally to visualize

146
Q

Use of contrast echo?

A
  • To evaluate for shunts – agitated saline
  • To enhance endocardial borders – echogenic microspheres
147
Q

Use of intracardiac ultrasound?

What is a stress echo?

A

•Used during structural heart disease procedures.

ASD closure
•A.fib ablations

Stress echo = standard stress test then imaging

148
Q

CT cardiac applications?

A
  • Coronary arteries anatomy and morphology
  • Coronary artery calcium score
  • Cardiac anatomy – Pericardial disease; Masses
  • Coronary plaque characterization
  • Congenital Heart disease
  • Postop. Evaluation (CABG)
  • Electrophysiology
  • Newer – Perfusion and Fractional flow reserve.
  • Aortic evaluation – aneurysms, dissections
149
Q

Signs/Symptoms of cardiac disease

A
150
Q

Causes of dyspnea?

A
  • cardiac/pulmonry disease
  • anemia
  • metabolic acidosis
  • obesity
  • poor physical condition
  • neuromuscular disease
  • psychogenic disorders
151
Q

Different mechanisms for dyspnea?

A
  • diastolic abnormality
    • increased pulmonary venous pressure
  • Systolic abnormality
    • metabolic acidosis from anaerobic metabolism
  • exertional dyspnea
  • orthopnea, PND
152
Q

Causes of chest pain?

A
  • cardiac
    • MI/angina
    • pulm htn
    • pericarditis
  • aortic dissection
  • pulmonary: embolus, pneumonia, pleuritis, pneumothorax
  • musculoskeletal
  • neurological
  • gastrointestinal
  • psychogenic: hyperventilation
153
Q

Mechanisms of chest pain?

A
  • Angina
  • MI/dissection/PE/pericarditis
154
Q

Symptoms of cardiac disease?

A
  • dyspnea
  • chest pain
  • edema
  • fatigue (low CO)
  • palpitation
  • syncope (due to decrease in global cerebral perfusion)
155
Q

Risk factors for coronary heart disease?

A
  • Age
  • Gender
  • Hyperlipidemia
  • Hypertension
  • Family history
  • Diabetes
  • Smoking
156
Q

Leading cause of mortality in women?

Difference between women and men in this disease?

A

Leading cause is coronary artery disease

  • Presenting symptom is most commonly angina in women
    • Often atypical angina
  • Presenting symptom in men is most commonly MI
  • Sudden death is more common in men
157
Q

What is metabolic syndrome?

A
  • Obesity: men and women BMI >30
  • Diabetes: men and women fasting blood sugar >110
  • Hypertension: men and women BP >135/85
  • Hyperlipidemia
    • both men and women triglycerides >150
    • HDL cholesterol
      • men <40
      • women <50
158
Q

continuation of peripheral arterial disease I because i thought i was done but apppppppparently i was NAHT!

A

<3 choo! :D

159
Q

What is thromboangiitis obliterans? Treatment?

A
  • Also known as buerger’s disease
  • digital necrosis and can lead to loss of an extremity
  • starts with digital arteries and progresses
  • unsure of mechanism
  • ONLY treatment is to stop smoking
160
Q

Causes of limb ischemia? How long to restore flow?

A
  • A. fib
  • AAA with mural thrombus
    • AAA?
  • Trauma
  • SBE
  • Popliteal aneurysm thrombosis
  • dissection
  • Only a 4-6 hour window to prevent death or irreversible damage to the limb
161
Q

Six “P”s of acute limb ischemia presentation?

A
  1. Pain
  2. Pallor
  3. Pulselessness
  4. Poikilothermia
  5. Paresthesias
  6. Paralysis
162
Q

What is subclavian steal syndrome?

A
  • Classically from LS stenosis or occlusion
  • Arm activity –> vasodilation in arm –> sets up a negative pressure gradient –> causes vertebral flow to reverse –> brainstem ischemia and syncope
163
Q

How do you detect subclavian steal syndrome?

A
  • Symptoms
  • Pressure differential in arms
  • Ultrasound
  • Angiography
164
Q

Signs/Symptoms of acute mesenteric ischemia?

A
  • Severe abdominal pain out of proportion to findings
  • Bloody stool
  • Dilated bowel with thickened walls
  • Progression to shock, sepsis, and death
165
Q

Risk factors for acute mesenteric ischemia?

A
  • Being old
  • A. fib
  • Hypercoaguable states
166
Q

Abdominal aortic aneurysm:

Association?

Diagnosis?

A
  • Association
    • smoking
    • family hx
  • Diagnosis
    • intense abdominal pain, pulsatile mass, hypotension, and shock
    • Follow with ultrasounds until size >5.5 cm
167
Q

What is aortic dissection? Propagation?

A
  • Intimal damage that causes blood to go into the media and form a hematoma
  • Can dissect retrograde into pericardial space causing a tamponade
  • Can propagate anywhere:
    • CNS, viscera, pleural space
168
Q

Aortic dissection signs/symptoms?

A
  • Sudden onset tearing pain
    • Pain radiates to the back
  • Associated with shock, stroke, acute aortic insufficiency, and ischemic gut
169
Q

Diagnosis of aortic dissection?

A
  • Widened mediastinum on CXR
  • Pressure differential
  • Acute upper or lower extremity ischemia

ICM (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions