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Cardio > Unit I week 2 > Flashcards

Unit I week 2 Flashcards

1
Q

Which Myosin Heavy Chain Isoforms are found in the heart?

A

α and β MHC isoforms are found in the heart:

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2
Q

Do the Myosin Heavy Chain Isoform heterodimers (αα, αβ and ββ) have differences?

A

Yes, heterodimers (αα, αβ and ββ) have distinct ATPase activity (and functional properties)

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3
Q

Are α and β Myosin Heavy Chain encoded by different genes or one gene with different splicing?

A

α and β MHC are encoded by different genes

and their expression is transcriptionally regulated

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4
Q

Myosin isoform and ATPase shifts are seen in phenotypically distinct models of cardiac hypertrophy. Physiological hypertrophy sees an increase in which isoform of myosin heavy chain? What happens to ATPase activity?

A

Increase in ATPase

and in αα isoform

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5
Q

Myosin isoform and ATPase shifts are seen in phenotypically distinct models of cardiac hypertrophy. pathological hypertrophy sees an increase in which isoform of myosin heavy chain? What happens to ATPase activity?

A

Decrease in ATPase

and increase ββ MHC

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6
Q

In response to stress, both the___ and the _____ of the contractile elements is altered

A

quantity, quality

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7
Q

The heart has ____ and ____ plasticity

A

phenotypic

genotypic

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8
Q

The phenotypic adaptions may involve what kind of “modifications”?

A

both transcriptional and post-translational modifications

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9
Q

Cellular mechanisms of LVH

A

-increase in Ca current via
L-type Ca channel

-Reduced SR pump fxn
(↑ PLB/SERCA2 ratio)

  • Impaired myofilament relaxation
  • Altered (increased) cytosolic calcium and new steady-state
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10
Q

Surprising example of gene transfer success in heart failure studies

A

SERCA2 Gene Transfer is Sufficient to Correct Mechanical

Defects in Cardiocytes From Patients with Heart Failure

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11
Q

What happens to LV function after a acute MI?

A

Immediate decreases seen at the time of an MI, but ejection fraction continues to decrease over time, suggesting a positive feedback mechanism that amplifies disease severity

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12
Q

How to calculate HR from boxes on an ECG

A

light lines 0.04 sec
heavy lines 0.2 sec
HR=300/# heavy lines between QRS’s
HR=1500/#mm between QRS’s

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13
Q

Ischemia due to sudden high oxygen demand in the presence of fixed coronary obstruction causes what ECG finding?

A

depression of the ST segment

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14
Q

Ischemia due to acute coronary artery obstruction during low O2 demand causes what ECG finding

A

T wave inversion

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15
Q

ST elevation is a sign of what?

A

transmural injury in acute coronary syndrome. TAKE ‘EM to CATH LAB

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16
Q

Development of sizable Q wave indicates

A

transmural necrosis from previous infarction

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17
Q

transmural acute myocardial infarct evolving over time

A

(early, hyperacute) peaked T wave
T wave inversion
ST elevation
Q wave/ST elevation/T inversion

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18
Q

Do sub endothelial infarcts have ST elevation or Q waves? What finding is characteristic of a sub endothelial infarct?

A

NO, only transmural infarcts cause these ECG findings. Persistent ST depression. Whereas ST depression may reflect transient ischemia without necrosis, ST depression lasting two or three days probably reflects a subendocardial infarct.

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19
Q

Common causes of prolonged QT

A

hypocalcemia, Class 1A or 3 anti-arrhythmic drugs, hypothermia

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20
Q

Hypercalcemia ____ the QT interval.

A

shortens

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21
Q

Most common cause of shortened QT interval

A

hyperparathyroidism.

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22
Q

Hypocalcemia _____ the QT interval, is more commonly encountered, has many causes, and may be associated with life threatening ventricular arrhythmias.

A

lengthens

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23
Q

Hypokalemia generally _____ QT interval. Other findings?

A

prolongs

-possible Uwaves and inverted T waves

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24
Q

At very high K+ levels a____ pattern appears without P or R waves. ___ ___ is the commonest cause.

A

sinusoidal

Renal failure

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25
Q

he normal sinus rate in adults is ___-___beats/min. A normal PR interval is __-__ seconds.

A

60-100

0.12-0.20

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26
Q

A regular, fast heart rate is called

A

sinus tachycardia. common during exercise or emotional stress

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27
Q

Regular slow heart rate is called

A

sinus bradycardia.

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28
Q

‘sick sinus syndrome’ happens in older people and can require the placement of a pacemaker. What irregular rhythm is this?

A

sinus bradycardia

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29
Q

common causes of 1st degree AV block

A

Drug-induced (beta blockers, some calcium blockers, digitalis)
Conduction system disease

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30
Q

Mobitz Type 1 AV block

A

Progressive prolongation of the PR interval until a ventricular beat is dropped

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31
Q

Mobitz type 2 AV block -Wenckebach

A

no change in PR length but not all P waves conduct

Intermittently dropped ventricular beats preceded by constant PR intervals.

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32
Q

When both Ps and QRSs show regular rhythm, but they are at different rates.With P rate>QRS rate, this is called what? Treatment?

A

3rd degree AV block.

May cause syncope or sudden death. Usually requires a pacemaker, rarely drugs

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33
Q

Main risk associated with atrial flutter

A

Atrial flutter has some risk of embolic stroke due to clot in the left atrium, and may result in rapid ventricular rates that are poorly tolerated.

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34
Q

Ttx atrial flutter

A

Anticoagulation, rate control with drugs, cardioversion, ablation

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35
Q

Almost all Afib patients are given what drug?

A

warfarin

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36
Q

Rate control drugs for A fib

A

beta blockers, some calcium channel blockers (diltiazem or verapamil) or digoxin

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37
Q

Because atrial fibrillation has a very high recurrence rate, most patients are managed with _____ and ___ ____.

A

anticoagulation

rate control

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38
Q

Atrial tachycardia is easily treated with….

A

easily terminated by adenosine infusion.

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39
Q

How to block reentry in atrial tachycardia

A

ablation

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40
Q

Rapis HR
Narrow QRS
Present but abnormal P waves

A

Atrial tachycardia

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41
Q

Regular rhythm , narrow QRS, no antecedent P waves

A

junctional rhythm

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42
Q

Premature ventricular complexes have:

A

no P waves and the QRS is widened and of abnormal shape.

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43
Q

V tachycardia

A

repeating wide QRS

No P

44
Q

Treatment for Ventricular tachycardia

A

emergency defibrillation.

45
Q

Where in the conduction system can Bradyarrhythmia problems develop?

A

Sinus node
AV node
Below the AV node

46
Q

Failure of sinus node discharge resulting in the absence of atrial depolarization and periods of ventricular asystole

A

sinus arrest

47
Q

Intermittent episodes of slow and fast rates from the SA node or atria

A

Bradycardia-Tachycardia (Brady-Tachy) Syndrome

48
Q

Chronotropic Incompetence

A

inability to

mount age-appropriate HR with exercise

49
Q

When should you be concerned about bradyarrhythmias?

A
  1. When the patient is symptomatic, no matter which part of the conduction system is affected.
    1. When the rhythm is infranodal (below the AV node).
50
Q

Acute treatment for unstable bradyarrhytmia patient .

Long term?

A

beta-agonists (dopamine or isoproterenol), transcutaneous pacing, temporary transvenous pacing.

Long term: Permanent pacemaker

51
Q

treatment of an irregular SVT

A

if unstable, shock, otherwise, all are treated with rate control,
antiarrhythmics or cardioversion

52
Q

treatment of a regular SVT

A

acute-shock

treat with adenosine for all types of regular sVT

53
Q

Tachyarrhythmias: Atrial Fibrillation- 5 C’s

A

Cause: Reverse

Control Rate

antiCoagulation

Control Rhythm

? Cure: Ablation

54
Q

Causes of Afib

A 
Hypertension 14%
IHD
Mitral valve Disease
Alcohol
Cardiomyopathies
Hyperthyroidism
Lone AF      14%
55
Q

Treatment for unstable afib

A

cardiovert

56
Q

Phamacological cardioversion for Afib rate control

A

Class III agents- ibutilide, amiodarone, dofetilide, sotalol

Class IC agents- flecainide, propafenone

57
Q

Rate Control drugs

A 
Betablockers 
Digoxin
Verapamil
Diltiazem
 Amiodarone can be used as a rate-controlling agent, especially in setting of decompensated heart failure
58
Q

If a patient is unstable in Vtach, what do you do? What do you give a stable patient?

A 
SHOCK
Medications:
     Amiodarone
     Lidocaine 
     Procainamide
59
Q

Any unstable tachyarrhythmia….

A

SHOCK!

60
Q

Once thought a degenerative disease, the mechanism by which a healthy tricuspid aortic valve becomes stenotic is now believed to be similar to that of ________.

A

atherosclerosis

61
Q

The tricuspid aortic valves become stenotic in the sixth, seventh, and eighth decades of life, mainly caused by ______ deposits in the valve cusps and not by….

A

calcium

fusion of the commissures

62
Q

In developed countries, ____ ____ has become a very rare cause of aortic stenosis.

A

rheumatic fever

63
Q

When the aortic valve is affected by rheumatic heart disease the____ valve is almost always affected as well.

A

mitral

64
Q

What serves as the mainstay of diagnosis for aortic stenosis?

A

The echocardiogram with Doppler interrogation of the aortic valve

65
Q

What treatment is recommended for individuals with symptomatic severe aortic stenosis. Such patients have a dire outlook, with 75% dying within 3 years of symptom onset.

A

Valve replacement is recommended

66
Q

The cardinal symptoms of severe aortic stenosis are:

A

angina, syncope and shortness of breath

67
Q

What is the most common congenital cardiac malformation, occurring in 1% to 2% of the population?

A

Bicuspid Aortic Valve

68
Q

Will the majority of BAV patients eventually develop complications?

A

The majority of BAV patients develop complications eventually requiring treatment.

69
Q

Embryology of bicuspid Aortic Valve

A

abnormal aortic cusp formation during
valvulogenesis. Adjacent cusps fuse to form a single aberrant
cusp, larger than its counterpart yet smaller than 2 normal
cusps combined. BAVs are likely the result of a complex
developmental process, not simply the fusion of 2 normal
cusps.

70
Q

After development, BAV is associated with:

A

aortic dilation, aneurysms, and dissection . In light of this, the BAVs should be considered a disease of the entire aortic root.

71
Q

The status of elastic laminae of the aortic media

A

In patients with BAV deficient microfibrillar elements result in smooth muscle cell detachment, matrix metalloproteinases (MMPs) release, matrix disruption, cell death, and a loss of structural support and elasticity.

72
Q

Genetics of bicuspid aortic valve

A

Familial clustering: autosomal dominant inheritance with reduced penetrance
Males 4:1
Echocardiographic screening of first-degree relatives is warranted.

73
Q

Valvular complications of Bicuspid Aortic Valve

A

Aortic stenosis
***Most frequent valvulopathy

Aortic Insufficiency

Endocarditis

74
Q

Vascular complications of Bicuspid Aortic Valve

A

Aortic dilation
Aneurysm formation
Aortic dissection
Associations: Coarctaction, PDA, Coronary anomalies

75
Q

_____ is a valuable tool to evaluate the functional state of the valve as well as to measure the aortic diameter, chamber dimensions, and ventricular function

A

echocardiography

76
Q

Subvalvular disease

A 
thin membrane (the most common lesion), 
thick fibromuscular ridge, 
diffuse tunnel-like obstruction, 
Hypertrophic Obstructive Cardiomyopathy
abnormal mitral valve attachments, and
accessory endocardial cushion tissue
77
Q

Types of pulmonic stenosis

A

Acommissural
Unicommissural
Bicuspid
Dysplastic

78
Q

Stenosis of the ____ ____ is one of the more common forms of congenital heart disease.

A

pulmonic valve

79
Q

Typical timeline of diagnosis of pulmonic stenosis

A

Most are children however patients with congenital pulmonic stenosis may come to medical attention during adolescence or adulthood.

80
Q

Treatment of pulmonic stenosis

A

percutaneous balloon valvuloplasty has largely replaced surgical valvotomy except in patients with dysplastic valves.

81
Q

Shape of mitral valve annulus

A

not planar, hyperbolic paraboloid

82
Q

Mitral valve stenosis is normally from

A

rheumatic fever

83
Q

Mitral valve myxomatous

A

Associated with

  • Connective tissue disease -Hereditary
  • Results in prolaspe, redundancy and Incompetence of the valve
84
Q

Mitral valve prolapse sequelea

A
  1. Long asymptomatic course
  2. Left atrial enlargement
    – Atrial arrhythmias – fibrillation
  3. Left ventricle volume overload
    dilatation
    dysfunction
  4. Heart Failure symptoms
  5. Risk for endocarditis
    
85
Q

aortic stenosis + symptoms =

A

surgery (Valve replacement)

86
Q

Mitral valve prolapse, on exam

A 
– Mid systolic click
– Late diastolic or holosystolic murmur
(Classically in the apex)
–  Decrease LV size intensify: Valsalva, dehydration
– Increase LV size decrease murmur:
Squatting, Hydration
87
Q

Myxomatous mitral valve Treatment

A

a. Surgical Treatment: repair or replacement

b. Medical treatment: reduce after load (Decrease BP), Treat HF with diuretics

88
Q

Mitral valve regurgitation is usually a _______ disease, meaning that the problem lies with the _____ ____. What causes the problems?

A

functional

Left ventricle: restriction of leaflets, feathering of chord, dilation and flattening of annulus

89
Q

On exam, functional mitral regurgitation shows:

A

Holosystolic murmur @ apex (quiet S1)

Signs of LV dysfunction including S3, S4, Loud P2 (plum HTN), Lateral displacement of apical impulse, edema, crackles, JVD

90
Q

Functional mitral regurgitation treatment

A

a. Medical: Treat underlying cardiomyopathy: ACEIs, BBs, spirolactone, revascularization, Bi-ventricular pacing, transplant

B. all of this generally comes before primary mitral valve surgery, which is very controversial

91
Q

about 90% of all mitral stenosis can be attributed to what?

A

Rheumatic heart disease

92
Q

When does valvulopathy appear in relation to initial strep infection

A

While rheumatic fever occurs 2-4 weeks after strep, valvulopathy can present years later

93
Q

Does mitral stenosis present right away?

A

No, it generally has a long asymptomatic period

94
Q

Characteristics of mitral stenosis

A 
1. Left atrial enlargement (can be massive)
     – Atrial arrhythmias
      – Clots, strokes
2. Heart failure symptoms
3. Pulmonary Hypertension
    Right ventricular dysfunction
    Tricuspid regurgitation
95
Q

On exam, mitral stenosis would present with:

A
  • Loud S2
  • Opening snap
  • Diastolic rumble at apex
  • Signs of plum HTN: Loud P2, RV lift or thrill, JVD, tricuspid regurgitation murmur
96
Q

Treatment for mitral stenosis

A
  1. Valvuloplasty
  2. Surgical replacement
  3. Medical treatment: BBs, diuretics, anticoag, antibiotics
97
Q

Prophylactic treatment with Penicillin for rheumatic fever

A

used until age 18-21 or risk of strep throat is low, longer for those with valvulopathy (at least age 40).

98
Q

The tricuspid valve has _ leaflets and _ papillary muscles

A

3,3

99
Q

Tricuspid regurgitation is usually attributable to what?

A

secondary to right heart failure or plum HTN

100
Q

How frequent is primary tricuspid valve disease?

A

RARE! Congenital (epstien’s abnormality), endocarditis, carcinoid, rheumatic (much less than mitral valve)

101
Q

Can rheumatic fever affect the tricuspid valve?

A

Yes, but much less frequently than mitral valve disease

102
Q

Since tricuspid regurgitation is associated with underlying ___ ___ and ___ ____, common symptoms are:

A

RV disease and plum HTN

  • Edema
  • JVD
  • Hepatic congestion
103
Q

On exam, tricuspid regurgitation would show

A

Holosystolic murmur at left lower sternal border

  • increases with inspiration
  • Loud P2 (pulm HTN)
104
Q

Tricuspid stenosis is common/rare. It can occur as a result of ______ ______

A

rare

Carcinoid syndrome

105
Q

Tricuspid stenosis will present with symptoms associated with dysfunction of the ___ ____, including:

A

right heart

JVD, edema, hepatic congestion

106
Q

On exam, tricuspid stenosis would show:

A

diastolic murmur at left lower sternal border that increases with inspiration

Cardio (3 decks)

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