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Cardiovascular > EXAM #1: REVIEW > Flashcards

EXAM #1: REVIEW Flashcards

1
Q

Draw and label the normal jugular venous pressure wave.

A

See ppt.

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2
Q

What is the “h” wave on the jugular venous pressure wave?

A

Continued filling of the RA during diastole

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3
Q

What condition will cause an absence of the “x” wave on the jugular venous pressure waveform?

A

Tricuspid regurgitation

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4
Q

What is and S3, and what causes it?

A
  • Rapid flow of blood from the atria to the ventricles
  • “Rapid ventricular filling”

*Volume overload (CHF) is a cause of S3

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5
Q

What causes a fixed splitting of S2?

A

Atrial Septal Defect

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6
Q

When does the opening snap of Mitral Valve Stenosis occur?

A

After the end of S2

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7
Q

What causes S3?

A
  • Rapid flow of blood from the atria to the ventricles

- “Rapid ventricular filling”

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8
Q

What is S4, and what causes it?

A

Atrial kick into non-compliant ventricles

*This can occur in LVH and MI

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9
Q

What are the three types of systolic murmurs?

A

1) Ejection
- Aortic and pulmonic stenosis
2) Pansystolic
3) Late systolic
- MVP

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10
Q

List the three pansystolic murmurs.

A

1) Mitral regurgitation
2) Tricuspid regurgitation
3) VSD

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11
Q

Where is aortic regurgitation best auscultated?

A

3rd of 4rd LEFT ICS

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12
Q

What are the two components of the EDV?

A

1) Ventricular filling

2) Atrial kick

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13
Q

Draw and label the ventricular pressure-volume loop.

A

See ppt.

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14
Q

What is the mechanism of the Frank-Starling principle of the heart?

A

Length of the sarcomere determines the sensitivity to Ca++

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15
Q

What is the mechanism of the ANREP effect?

A

Increased LV wall tension causes:

1) Increase cytosolic Na+
2) Increased cytosolic Ca++
3) Increased myocardial contraction

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16
Q

What is the normal conduction velocity and pacemaker rate of the SA node?

A
  • Less than 0.01 m/sec

- 60-100 bpm

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17
Q

What is the normal conduction velocity and pacemaker rate of the atrial myocardium?

A
  • 1.0 - 1.2

- None

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18
Q

What is the normal conduction velocity and pacemaker rate of the AV node?

A
  • 0.02 - 0.05 m/sec

- 40-55 bpm

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19
Q

What is the normal conduction velocity and pacemaker rate of the Bundle of His?

A
  • 1.2 - 2.0 m/sec

- 25-40 bpm

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20
Q

What is the normal conduction velocity and pacemaker rate of the Bundle Branches?

A
  • 2.0 - 4.0 m/sec

- 25-40 bpm

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21
Q

What is the normal conduction velocity and pacemaker rate of the Purkinje fibers?

A
  • 2.0 - 4.0 m/sec

- 25-40 bpm

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22
Q

What is the normal conduction velocity and pacemaker rate of the ventricular myocardium?

A
  • 0.3 - 1.0 m/sec

- none

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23
Q

What effect will a Na+ channel blocker have on the cardiac action potential?

A

Prolong the absolute refractory period

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24
Q

Outline the contraction phase of excitation-contraction coupling cardiac muscle.

A

1) Ca++ entry through voltage gated Ca++ channel
2) Ca++ binds RyR2
3) Ca++ release from the SR
4) Ca++ binds troponin

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25
Q

Outline the relaxation phase of excitation-contraction coupling in cardiac muscle.

A

Ca++ dissociates from troponin

  • Some is taken back up into the SR via SERCA, where it binds Calsequestrin
  • Some is pumped out of the cell via NCX and the plasma Ca-ATPase
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26
Q

What is the difference between a DAD and an EAD?

A

DAD= arrhythmia generated in phase 4

EAD= arrhythmia generated in phase 2 or 3

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27
Q

What causes DADs?

A

Increased Ca++

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28
Q

What causes EADs?

A

Prolonged action potential duration/ changes in ion flux

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29
Q

List four mechanisms that will prolong the action potential duration.

A

1) Reduced K+ current
2) Reduced Ca++ current
3) Increased Na+/Ca++ exchange activity
4) Increase late Na+ current

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30
Q

List four examples of re-entrant circuits.

A

1) WPW
2) AVNRT
3) A-flutter
4) PSVT

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31
Q

List two examples of functional re-entry.

A

1) Monomorphic VT

2) Polymorphic VT or VF

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32
Q

What types of SDs may lead to cardiac compromise?

A

Cranial
Cervical
Thoracic

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33
Q

What happens when there is a decrease in left vagal tone?

A

Ectopic foci

V-fib

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34
Q

What happens when there is an increase in left vagal tone?

A

AV Block

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35
Q

Overactivation of the SNS can result in what cardiac abnormality?

A

SVT

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36
Q

What does an increase in right vagal tone result in?

A

Sinus Brady

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37
Q

What is the effect of increase right vagal tone on the coronary arteries?

A

Vasoconstriction

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38
Q

List six SDs that can cause cardiac dysfunction.

A

1) OA
2) Lower cervical
3) Thoracic inlet
4) Rib dysfunction
5) Flattened thoracic kyphosis
6) Abnormal gait

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39
Q

List four tissue changes that will result in a passive arrhythmia.

A

1) Gap junction changes
2) Fat deposition
3) Fibrosis
4) Changes in cell size

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40
Q

List four passive mechanisms that regulate pulmonary blood flow.

A

1) Gravity
2) Body position
3) Extravascular pressure
4) Intravascular pressure

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41
Q

What is extravascular compression in the heart?

A

Compression of the coronary arteries with increased chamber pressure during systole

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42
Q

What does the PR interval correspond to?

A

Depolarization in the:

  • AV node
  • His Bundle
  • Bundle Branches
  • Purkinje fibers
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43
Q

Where are q-waves normal?

A 
aVR 
II 
III 
aVF 
aVL 
V4-V6
44
Q

What is the normal amplitude of T-waves?

A
  • Limb leads= less than 5mm

- Chest= less than 10mm

45
Q

What causes u-waves?

A

1) Hypokalemia

2) Quinidine

46
Q

List the three etiologies of atrial enlargement.

A

1) Mitral or tricuspid valve disease
2) Ischemia
3) HTN

47
Q

What are the ECG criteria for RVH?

A

1) RAE
2) RAD
3) R-wave in V1 greater than or equal to 7mm

48
Q

List four etiologies of a 2nd degree AV block.

A

1) Vagotonia
2) Acute inferior MI
3) Drugs
4) Aortic valve disease

49
Q

List three etiologies of AV dissociation.

A

1) Acceleration of a subsidiary pacemaker
2) Decreased sinus automaticity
3) Re-entrant ventricular tachycardia

50
Q

List the four things that will cause a tall r-wave in V1.

A

1) RVH
2) RBBB
3) WPW
4) Dextrocardia

51
Q

What are the three general features of premature beats

A

1) Occur early in the cycle
2) Prevent occurrence of the next normal beat
3) Generate a pause of varying length

52
Q

What is the definition of Grade 1 PVC?

A

Less than 30 PVCs an hour

53
Q

What are the clinical implications of a left premature ventricular beat?

A

More likely to be caused by IHD and to degenerate to V-fib

Remember, Left= upright in V1

54
Q

What are the two common types of re-entrant junctional tachyarrhythmias?

A

1) AV junctional tachycardia

2) AV bypass tachycardia

55
Q

What are the two subtypes of AV junctional tachycardia?

A

1) Slow-fast

2) Fast-slow

56
Q

What are the two subtypes of AV bypass tachycardia?

A

1) Orthodromic

2) Antidromic

57
Q

What is the definition of a re-entry ventricular tachyarrhythmia?

A

3x consecutive QRS complexes

58
Q

What are the common mechanisms of most ventricular tachyarrhythmias?

A

Re-entry

1) Mirco or macro re-entry
2) Common with ischemia/ post-MI

59
Q

List four things that V-Tac is associated with.

A

1) IHD
2) Cardiomyopathy
3) Valvular disease
4) Drugs

60
Q

List the three class IA antiarrhythmatics.

A
  • Quinidine
  • Procainamide
  • Disopyramide
61
Q

What are the specific adverse effects associated with Class IA antiarrhythmatics that have limited their clinical use?

A

1) Increase mortality in atrial arrhythmias
2) QT prolongation and Torsdades
3) G6PD hemolytic anemia induction

62
Q

What adverse effect is associated with the Class IC antiarrhythmatics?

A

QT prolongation and Torsades

63
Q

What are the major adverse effects associated with Sotalol?

A

1) Torsades

2) Excessive beta-blockade

64
Q

What drugs are used for rhythm control in a-fib?

A

No IHD= Flecainide or Propafenone

IHD= Sotalol or Amiodarone

65
Q

What drugs are used for rate control in a-fib?

A

1) Beta blockers
2) Diltiazem
3) Digoxin

66
Q

What total serum cholesterol increases the risk for atherosclerosis?

A

160 mg/dL

67
Q

What are the two “unusual” risk factors for atherosclerosis?

A

1) Homocystine

2) Chlamidya pneumonia

68
Q

What chemotaxant molecule recruits macrophages to sites of endothelial injury/ accumulated lipids?

A

Monocyte chemoattractant protein 1 (MCP-1)

69
Q

What are the three morphologic stages of atherosclerosis?

A

1) Fatty streak
2) Proliferative lesion
3) Atherosclerotic plaque or “atheroma”

70
Q

What does ABPI stand for?

A

Anke Brachial Pressure Index

71
Q

What is the equation for blood pressure?

A

Blood pressure= CO x SVR

72
Q

List six etiologies of cardiogenic shock in children.

A
  • Rheumatic fever
  • Cardiomyopathy
  • Pneumothorax
  • Hyperkalemia
  • Hypocalcemia
  • Congenital heart disease
73
Q

What are the symptoms of cardiogenic shock in children?

A

VAGUE!

  • Poor feeding
  • Decreased activity

Syncope and AMS if severe

74
Q

List six lab tests that should be ordered for a child in suspected cardiogenic shock.

A

1) Glucose
2) Electrolytes
3) Ca++
4) Blood gas
5) Cardiac enzymes
6) Viral titers

75
Q

Once an airway has been established and IV access (or IO) has been attained, how do you manage a child in cardiogenic shock?

A

1) Boluses of 5-10 mL/kg of isotonic fluid
2) Glucose
3) Maintain temperature
4) Drugs

76
Q

List the drugs that you would consider for a child in cardiogenic shock.

A 
Dopamine 
Dobutamine 
Epinephrine 
Milrinone 
Nitroprusside 
Nitrous Oxide
77
Q

What drugs are CONTRAINDICATED in the setting of cardiogenic shock?

A

Phenylephrine

Norepinephrine

78
Q

What is the definition of a positive family history for CAD in men vs. women?

A

Men= 1st degree relative under 55

Women= same but under 65

79
Q

How much does DM increase the risk of a “hard CVD event?”

A

20%

80
Q

List the markers for metabolic syndrome.

A

1) Diabetic dyslipidemia
2) PAH
3) Central abdominal obesity
4) Insulin resistance

81
Q

List six mechanisms that explain how smoking enhances atherosclerosis.

A

1) Hemodynamic stress
2) Endothelial injury
3) Lipid changes
4) Enhanced coagulation
5) Arrhythmogenesis
6) Hypoxia

82
Q

What are four complications of CAD?

A

1) ACS
2) Sudden cardiac death
3) Dilated cardiomyopathy
4) A-fib/flutter

83
Q

What are the three major determinants of myocardial oxygen demand?

A

1) HR
2) Contractility
3) Wall tension

84
Q

List the labs that are part of the work-up for chest pain.

A

1) Lipid panel
2) CBC
3) Blood chemistry w/
- Electrolytes
- BUN
- Creatinine
4) UA for:
- Protein
- Glucose

85
Q

List the five etiologies of non-idiopathic dilated cardiomyopathy.

A

1) IHD
2) HTN
3) Alcoholism
4) Infectious (Chagas and coxsackie)
5) Metabolic

86
Q

List three complication of dilated cardiomyopathy.

A

1) Biventricular CHF
2) Arrhythmia
3) Mitral/tricuspid valve regurgitation

87
Q

List the signs of LV failure.

A
  • Tachycardia
  • Cardiac apex displaced left and down
  • Apical lift/thrill
  • Murmur
  • S3
88
Q

What heart sound is universal in heart failure?

A

S3

89
Q

What lab tests should you order in a patient with alcoholic dilated cardiomyopathy?

A

1) Blood alcohol
2) Liver transaminases/chem.
3) Vitamin tests. e.g. Thamine

90
Q

What are the different gross manifestations of hypertropic cardiomyopathy?

A

1) Increased mass
2) Asymmetric septal hypertrophy
3) Concentric hypertrophy
4) Apical hypertrophy

91
Q

What are the signs of hypertrophic cardiomyopathy?

A

1) Displaced/bifid LV
2) Bisferiens carotid pulse
3) Systolic murmur
4) S4

92
Q

What are the ECG changes that are associated with hypertrophic cardiomyopathy?

A

1) Increased voltage in anterior leads
2) ST and T-wave changes
3) Q-waves in inferior and lateral leads
4) Ventricular arrhythmia

93
Q

List the causes of restrictive cardiomyopathy.

A

1) Amlyoidosis
2) Sarcoidosis
3) Edocardial fibroelastosis
4) Loeffler Syndrome
5) Hemochromatosis

94
Q

What ECG changes are associated with restrictive cardiomyopathy?

A

Low voltage and diminished QRS amplitude

95
Q

What are the two general etiologies of aortic regurgitation?

A

1) Aortic root dilation

2) Valve damage

96
Q

What are the different valve defects that are associated with aortic regurgitation?

A

1) Bicupsid aortic valve
2) Degeneration with age
3) Rheumatic fever
4) Endocarditis
5) Degeneration of a prosthetic valve

97
Q

What can cause dilation of the aortic root?

A

1) Trauma
2) Marfan’s Syndrome
3) Syphlitic aneurysm (tertiary syphilis)
4) Aortic dissection

98
Q

What are the physical exam manifestations of aortic regurgitation?

A
  • Bounding pulse
  • Pulsating nail bed
  • Head bobbing
  • S3
  • Ejection click
99
Q

How is the murmur of aortic regurgitation described?

A
  • Diastolic
  • Decrescendo
  • “Blowing”
100
Q

What is commonly associated with aortic regurgitation?

A

Aortic stenosis

101
Q

What is the mainstay of treatment for aortic regurgitation?

A

ACE inhibitors

102
Q

What are the symptoms aortic stenosis?

A

1) Angina
2) Syncope with exertion
3) HF

103
Q

How is the murmur of aortic stenosis described?

A
  • Crescendo/decresendo
  • Loud
  • Late
104
Q

What two drugs are specifically indicated for Familial Hyperlipidemia?

A

1) Mipomersen

2) Lomitapide

105
Q

What is the MOA of Mipomersen?

A

Blocks the production of apoB mRNA

*Cannot make VLDL or LDL

106
Q

What is the MOA of Lomitapide?

A

Oral MTB inhibitor, which is necessary for ApoB lipoproteins

107
Q

What is the function of PCSK9?

A

Expression of LDL receptors

Cardiovascular (38 decks)

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