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Parker- CV Path > Nichols- Hemodynamics 3 > Flashcards

Nichols- Hemodynamics 3 Flashcards

1
Q

Most common cause of RHF?

A

LHF

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2
Q

What is isolated RHF due to? What is this called?

A

Due to pulmonary vascular or parenchymal disease. Called cor pulmonale

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3
Q

What are some causes of cor pulmonale?

A
  1. Pulmonary emphysema
  2. Recurrent pulmonary thromboembolism
  3. Interstitial lung disease
  4. ARDS
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4
Q

Lower leg edema, hepatosplenomegaly, ascites, JVD, and weight gain from fluid retention are signs of?

A

RHF

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5
Q

Cardiac myocytes (except for SA and AV nodes) are dependent of what ion for their resting membrane potential?

A

K+

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6
Q

Ca2+ induced Ca2+ release is from Ca2+ binding to _________ receptors on the ______?

A

ryanodine receptors on the SR

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7
Q

A mutation in the gene for ryanodine receptors leads to a disease called?

A

Familial catecholeminergic polymorphic ventricular tachycardia. It would probably lead to reduced capacity for cardiac contraction

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8
Q

Abnormal depolarizations that interrupt phase 2, 3, or 4 and can lead to arrhythmias

A

Afterdepolarizations

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9
Q

These afterdepols occur during phase 2 or 3

A

Early afterdepols

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10
Q

A phase 2 early afterdepol is due to?

A

increased Ca2+ inflow

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11
Q

A phase 3 early afterdepol is due to?

A

increased Na+ inflow

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12
Q

Delayed afterdepols (DADs) occur during phase 4 due to?

A

increased intracellular Ca2+ probably from increased catecholamine stimulation

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13
Q

Describe a re-entrant tachycardia

A

An area of ischemia/infarction can slow down the conduction form the SA node. If the conduction can go around the infarction and reach it via a different pathway, you can get an ectopic pacemaker which can lead to ventricular tachyarrhythmia

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14
Q

Conduction thru SA node is?

A

Slow

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15
Q

Conduction thru atrial muscle fibers is?

A

Fast

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16
Q

Conduction thru AV node is?

A

Slow

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17
Q

Conduction thru His/Purkinje system is?

A

Fast as shit

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18
Q

Conduction thru ventricular muscle is?

A

Slow

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19
Q

A heart block in a young black patient suggests?

A

Sarcoidosis

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20
Q

PR interval represents?

A

Length of time for conduction signal to travel from SA node through the AV node and the His/Purkinje system

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21
Q

A lengthened PR interval >200ms suggests?

A

AV block

22
Q

QRS interval represents?

A

depolarization of ventricles

23
Q

Wide QRS implies?

A

Impulse form abnormal place (ectopic pacemaker)

24
Q

QT interval represents?

A

ventricular repolarization; shorter QT implies faster HR.. Longer QT implies myocardial ischemia, electrolyte abnormalities, or channelopathy.. its a bad thing!

25
Q

Lead V1-V4 abnormality implies?

A

ANTERIOR LV disease (LAD artery territory)

26
Q

Lead V5-V6 abnormality implies?

A

LATERAL LV disease (left circumflex artery)

27
Q

Lead II, III, VF abnormality implies?

A

INFERIOR LV disease (RCA)

28
Q

How can you decide whether a person has normal sinus tachycardia or whether their tachycardia is excessive?

A

Even during exercise, tachycardia should never breach 220-age

29
Q

This abnormal heart rhythm is irregular with increased HR and no P wave

A

Atrial fibrillation

30
Q

This abnormal heart rhythm has a HR of about 150 bpm and features 2 P waves for every QRS

A

Atrial flutter (usually from re-entrant circuit around tricuspid valve

31
Q

This abnormal heart rhythm is typically from a re-entrant circuit around the AV node. It can be cured by Valsalva, carotid sinus massage, or ice water to the face

A

Supraventricular tachycardia

32
Q

There are two types of ventricular tachyarrhythmias: tachycardia and fibrillation. Which one has a wide QRS complex and can be monomorphic or polymorphic?

A

Ventricular tachycardia

33
Q

Which ventricular tachyarrhythmia is fatal as dookie and must be defibrilated like freakin yesterday

A

Ventricular fibrillation

34
Q

Long QT syndrome known as Torsades de Pointes is a channelopathy affecting which cardiac ion channel?

A

Potassium channels

35
Q

What is the effect of the mutated K+ channel?

A

Decreased outward K+ current during repolarization –> prolonged repolarization –> long QT interval –> early afterdepolarizations

36
Q

Typical presentation of a channelopathy?

A

Baby that died in its sleep

37
Q

This channelopathy has a mutation in sodium channels

A

Brugada syndrome

38
Q

Brugada presents in what population?

A

Young Asian males

39
Q

Reduced Na+ channel functionality results in reduced Na+ inflow which leads to?

A

Shortened AP’s

40
Q

In Brugada syndrome, the presence of both normal & abnormal Na+ channels in the same tissue can lead to?

A

Ventricular arrhythmias –> vent fib

41
Q

Familial catecholemineric polymorphic ventricular tachycardia is a channelopathy with mutations in?

A

Ryanodine receptors in SR

42
Q

How do FCPVT patients present?

A

Life threatening vent tachy or vent fib during physical/emotional stress

43
Q

What is myocarditis?

A

Inflammation of heart muscle

44
Q

What usually causes myocarditis?

A

Parvovirus or HHV 6

45
Q

Myocarditis has 2 phases. Describe the early phase

A

Direct viral infection of myocytes

46
Q

Describe the late phase of myocarditis

A

Autoimmune attack on myocytes

47
Q

What does a heart with myocarditis look like?

A

Pale, mottled, flabby, dialated.. With inflammation

48
Q

This is a commonly underdiagnosed disease that presents in NORTHERN ITIALIANS!!!

A

Right ventricular cardiomyopahty

49
Q

What is RV cardiomyopathy?

A

Fatty replacement of myocytes in RV apex

50
Q

RV cardiomyopathy comes from a mutation in the gene that codes for?

A

Desmosomal proteins

Parker- CV Path (9 decks)

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