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Cardiology and Cardiac Surgery > Diagnostic Tests and Approach to ECG > Flashcards

Diagnostic Tests and Approach to ECG Flashcards

1
Q

What are the lateral leads in an ECG

A

I, aVL, V5, V6

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2
Q

What are the inferior leads in an ECG

A

II, III, aVF

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3
Q

What are the anterior leads in an ECG

A

V1-V4

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4
Q

Take some time to go over tutorials and practice on http://www.ecgmadesimple.com/

A

yay!

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5
Q

Normal heart rate

A

60-100 bpm

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6
Q

Atrial rate in paroxysmal tachycardia

A

150-250 bpm

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7
Q

Atrial rate in atrial flutter

A

250-350 bpm

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8
Q

Atrial rate in atrial fibrillation

A

> 350 bpm

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9
Q

How do you calculate rate on an ECG with regular rhythm

A

to calculate the rate, divide 300 by number of large squares between 2 QRS complexes (there are 300
large squares in 1 min: 300 x 200 msec = 60 sec)

or remember 300-150-100-75-60-50-43

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10
Q

How do you calculate rate on an ECG with irregular rhythm

A

6 x number of R-R intervals in 10 s (the “rhythm strips” are 10 sec recordings)

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11
Q

Rate for atrial escape rhythm

A

60-80 bpm

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12
Q

Rate for junctional escape rhythm

A

40-60 bpm

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13
Q

Rate for ventricular escape rhythm

A

20-40 bpm

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14
Q

What is an example of a regularly irregular pattern

A

Atrial flutter

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15
Q

What are examples of an irregularly irregular pattern

A

Atrial fibrillation, ventricular fibrillation

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16
Q

What are 3 things that must be satisfied to have normal sinus rhythm

A
  1. P wave precedes each QRS; QRS follows each P wave
  2. P wave axis is normal (positive in 2 out of the 3 following leads I, II, aVF)
  3. Rate between 60-100 bpm
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17
Q

What is considered normal axis, LAD, RAD?

A

normal axis: -30º to 90º (i.e. positive QRS in leads I and II)

Left axis deviation (LAD): axis 90º

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18
Q

Differential diagnosis for LAD

A
  • Left anterior hemiblock
  • Inferior MI
  • WPW
  • RV pacing
  • Normal variant
  • Elevated diaphragm
  • Lead misplacement
  • Endocardial cushion defect
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19
Q

Differential diagnosis for RAD

A
  • RVH
  • Left posterior hemiblock
  • Pulmonary embolism
  • COPD
  • Lateral MI
  • WPW
  • Dextrocardia
  • Septal defects
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20
Q

What are signs of complete LBBB on ECG

A

QRS duration >120 msec

Broad notched R waves in leads V4, and V5, and usually I, aVL

Deep broad S waves in leads V1-2

Secondary ST-T changes (-ve in leads with broad notched R waves, +ve in V1-2) are usually present

LBBB can mask ECG signs of MI

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21
Q

What are signs of complete RBBB on ECG

A

QRS duration >120 msec

Positive QRS in lead V1 (rSR’ or occasionally broad R wave)

Broad S waves in leads I, V5-6 (>40 msec)

Usually secondary T wave inversion in leads V1-2

Frontal axis determination using only the first 60 msec

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22
Q

What are signs on ECG of Left Anterior Fascicular Block (LAFB) (aka Left Anterior Hemiblock)

A

Left Axis Deviation (-30º to -90º)

  • Small q and prominent R in leads I
    and aVL
  • Small r and prominent S in leads II,
    III, and aVF
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23
Q

What are signs on ECG of Left Posterior Fascicular Block (LPFB) (aka Left Posterior Hemiblock)

A

Right Axis Deviation (110º to 180º)

  • Small r and prominent S in leads I and
    aVL
  • Small q and prominent R in leads II, III,
    and aVF
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24
Q

What are signs on ECG of bifascicular block

A

RBBB Pattern

  • Small q and prominent R
  • The first 60 msec (1.5 small squares) of the QRS shows the pattern of LAFB or LPFB
  • Bifascicular block refers to impaired conduction in two of the three fascicles, most commonly a RBBB and left anterior hemiblock; the appearance on an ECG meets the criteria for both types of blocks
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25
Q

What are signs of ECG for a nonspecific intraventricular block

A
  • QRS duration >120 msec

* absence of definitive criteria for LBBB or RBBB

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26
Q

What are signs on ECG for LVH

A

(S in V1) + (R in V5 or V6)
>35 mm above for age 40
>40 mm for age 31-40
>45 mm for age 21-30

R in aVL >11 mm

(R in I) + (S in III) >25 mm

Additional criteria
LV strain pattern (asymmetric ST depression and T wave
inversion in leads I, aVL, V4-V6)
Left atrial enlargement

N.B. The more criteria present, the more likely LVH is present.
If only one voltage criteria present, it is called minimal voltage criteria for LVH which could be a normal variant

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27
Q

What are signs on ECG for RVH

A

Right axis deviation

R/S ratio >1 or qR in lead V1

RV strain pattern: ST segment depression and T wave inversion in leads V1-2

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28
Q

What are signs on ECG for left atrial enlargement

A

Biphasic P wave with the negative terminal component of the P wave in lead V1 ≥1 mm wide and ≥1 mm deep

P wave >100 msec, could be notched in lead II (“P mitrale”)

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29
Q

What are signs on ECG for right atrial enlargement

A

P wave >2.5 mm in height in leads II, III, or aVF (“P pulmonale”)

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30
Q

What are signs on ECG for ischemia

A

■ ST segment depression

■ T wave inversion (most commonly in V1-V6)

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31
Q

What are signs on ECG for injury/infarct

A

■ transmural (involving the epicardium) - ST elevation in the leads facing the area injured/infarcted
■ subendocardial - marked ST depression in the leads facing the affected area
■ may be accompanied by enzyme changes and other signs of MI

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32
Q

STEMI ST elevation pattern

A

At least 1 mm in 2 adjacent limb leads or at least 1-2 mm in adjacent precordial leads (signifies complete occlusion and transmural ischemic injury)

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33
Q

Early pericarditis ST elevation pattern

A

Diffuse pattern in early pericarditis

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34
Q

Coronary artery spasm (ex. Prinzmetal angina) ST elevation pattern

A

Transient ST elevation in patients with coronary artery spasm (e.g. Prinzmetal angina) which can be slight or prominent (>10 mm)

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35
Q

What are the typical sequential changes of an evolving MI

A
  1. hyperacute T waves (tall, symmetric T waves) in the leads facing the infarcted area, with or without
    ST elevation
  2. ST elevation (injury pattern) in the leads facing the infarcted area
    ◆ usually in the first hours post infarct
    ◆ in acute posterior MI, there is ST depression in V1-V3 (reciprocal to ST elevation in the posterior leads, that are not recorded in the standard 12-lead ECG) - get a 15-lead ECG

3.significant Q waves: >40 msec or >1/3 of the total QRS and present in at least 2 consecutive leads in
the same territory (hours to days post-infarct)
◆ Q waves of infarction may appear in the very early stages, with or without ST changes
◆ non-Q wave infarction: there may be only ST or T changes despite clinical evidence of infarction

  1. inverted T waves (one day to weeks after infarction)
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36
Q

What are ECG signs of a completed infarction

A

■ abnormal Q waves (Q waves may be present in leads III and aVL in normal individuals due to initial septal depolarization)

■ duration >40 msec (>30 msec in aVF for inferior infarction)

■ Q/QRS voltage ratio is >33%

■ present in at least 2 consecutive leads in the same territory

■ abnormal R waves (R/S ratio >1, duration >40 msec) in V1 and occasionally in V2 are found in
posterior infarction (usually in association with signs of inferior and/or lateral infarction)
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37
Q

What areas of the heart does the LAD supply

A

Anteroseptal
Anterior
Anterolateral
Extensive anterior

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38
Q

What areas of the heart does the Right coronary artery supply

A

Inferior
Posterior MI (assoc. with inf. MI)
Right ventricle

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39
Q

What areas of the heart does the left circumflex artery supply

A

Lateral

Isolated posterior MI

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40
Q

What leads are affected by an LAD infarct

A

V1, V2
V3, V4
I, aVL, V3-6
I, aVL, V1-6

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41
Q

What leads are affected by a right coronary artery infarct

A

II, III, aVF
V3R, V4R (right sided chest leads)
V1, V2 (prominent R waves)

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42
Q

What leads are affected by a left circumflex artery infarct

A

I, aVL, V5-6

V1, V2 (prominent R waves)

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43
Q

What ECG changes can be seen with hyperkalemia

A

■ mild to moderate (K+ 5-7 mmol/L):
tall peaked T waves
■ severe (K+>7 mmol/L):
progressive changes whereby P waves flatten and disappear, QRS widens and may show bizarre patterns, axis shifts left or right, ST shift with tall T waves, eventually becomes a “sine wave” pattern

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44
Q

What ECG changes can be seen with hypokalemia

A

■ ST segment depression, prolonged QT interval, low T waves, prominent U waves (U>T)
■ enhances the toxic effects of digitalis

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45
Q

What ECG changes can be seen with hypercalcemia

A

■ shortened QT interval (more extracellular Ca2+ means shorter plateau in cardiac action potential)

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46
Q

What ECG changes can be seen with hypocalcemia

A

■ prolonged QT interval (less extracellular Ca2+ means longer plateau in cardiac action potential)

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47
Q

What ECG changes can be seen with hypothermia

A
  • sinus bradycardia
  • when severe, prolonged QRS and QT intervals
  • AFib with slow ventricular response and other atrial/ventricular dysrhythmias
  • Osborne J waves: “hump-like” waves at the junction of the J point and the ST segment
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48
Q

What ECG changes can be seen in pericarditis

A
  • early: diffuse ST segment elevation ± PR segment depression, upright T waves
  • later: isoelectric ST segment, flat or inverted T waves
  • ± tachycardia
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49
Q

When do different pacemakers discharge

A

• Demand pacemaker has discharge (narrow
vertical spike on ECG strip) prior to widened
QRS
• Atrial pacemaker has discharge prior to P
wave
• Triggered pacemaker has discharge
following the P wave but prior to the
widened QRS
• Atrial and ventricular pacing have discharge
before the P wave and widened QRS wave

50
Q

What are side effects of digitalis

A

Palpitations, fatigue, visual changes (yellow
vision), decreased appetite, hallucinations,
confusion, and depression

51
Q

What are ECG changes that can be seen with digitalis

A

■ therapeutic levels may be associated with “digitalis effect”
◆ ST downsloping or “scooping”
◆ T wave depression or inversion
◆ QT shortening ± U waves
◆ slowing of ventricular rate in AFib
◆ toxic levels associated with:
– arrhythmias: paroxysmal atrial tachycardia (PAT) with conduction block, severe bradycardia in AFib, accelerated junctional rhythms, PVCs, ventricular tachycardia (see Arrhythmias, C16)
– “regularization” of ventricular rate in AFib due to a junctional rhythm and AV dissociation

52
Q

What are ECG changes that can be seen with Cor Pulmonale

A

■low voltage, right axis deviation (RAD), poor R wave progression in precordial leads
■ RAE and RVH with strain
■ multifocal atrial tachycardia (MAT)

53
Q

What are ECG changes that can be seen with massive pulmonary embolism

A

■ sinus tachycardia and AFib/atrial flutter are the most common arrhythmias
■ RAD, RVH with strain
■ most specific sign is S1Q3T3 (S in I, Q and inverted T wave in III) but rather uncommon

54
Q

Describe a normal P wave on ECG

A

• the P wave represents atrial contraction; best leads: II, VI
■ lead II: the P wave should be rounded, <120 msec and <2.5 mm in height
■ lead VI: the P wave is biphasic with a negative phase slightly greater than the positive phase

55
Q

Describe a P wave in atrial flutter

A

sawtooth P wave (Hint: flip the ECG upside-down to see it better if unclear)

56
Q

Describe a P wave in atrial fibrillation

A

absent P wave, may have fibrillatory wave, irregular rhythm

57
Q

Describe a P wave in Right atrial enlargement

A

tall P wave (>2.5 mm) in II or V1 (P pulmonale)

58
Q

Describe a P wave in left atrial enlargement

A

negative deflection >1 mm deep or >1 mm wide in V1, wide (>100 msec)

notched P wave in II may be present (P mitrale)

59
Q

What is the PR interval

A

the P-R interval shows the delay between atrial and ventricular contraction that is mediated by the AV
node; the magnitude of the delay is referred to as “dromotropy”

positive dromotropy increases conduction velocity (e.g. epinephrine stimulation), negative dromotropy
decreases velocity (e.g vagal stimulation)
60
Q

Normal PR interval

A

120-200 ms

61
Q

Long PR interval differential diagnosis

A

■heart block
◆ first degree: fixed, prolonged P-R interval
◆ second degree Mobitz I/Wenckebach: steadily prolonging P-R interval to eventual dropped beat
◆ second degree Mobitz II/Hay: fixed P-R interval with ratio of beat to dropped beat (e.g. for every
3 beats, there is one dropped beat [3:1])
◆ third degree/complete: variable P-R intervals, P-P and R-R intervals individually constant but not in sync

■ atrial flutter

■ sinus bradycardia (normal to have long P-R if heart rate slow)

■ hypokalemia

■ “trifascicular” block -1st degree AV block with LAHF and complete RBBB

62
Q

Short PR interval differential diagnosis

A

■ pre-excitation syndrome (delta wave: upswooping of the P-R segment into the QRS complex indicating pre-excitation)
◆ accessory pathways
◆ WPW

■ low atrial rhythm

63
Q

When is a Q wave pathological

A

if Q wave ≥1 small square (≥40 msec) or >33% of the total

QRS

64
Q

What does the QRS represent

A

Where ventricular contraction is visualized

65
Q

What is considered an insignificant Q wave

A
  • Septal depolarization by the left bundle
  • Seen in leads I II, III, aVL, V5, V6
  • <40 msec
66
Q

Components of the QRS to check for

A

• rate
- check the R-R interval to see if it matches the P-P interval

  • amplitude: check for hypertrophy
  • narrow width (<120 msec) QRS means that the His-Purkinje system is being used
  • wide width (>120 msec) QRS means that the His-Purkinje system is being bypassed or is diseased
67
Q

What is the differential for a wide QRS

A

BBB

VT

ventricular hypertrophy

cardiomyopathy

WPW

ectopic ventricular beat

hyperkalemia

drugs (e.g. TCAs, antiarrhythmics)

68
Q

What does the ST segment represent

A

corresponds to the completion of ventricular depolarization

69
Q

What is a situation where you can have a STEMI without ST elevation

A

lateral ST depression (leads I, aVL, V5, V6) may actually indicate a STEMI in the right heart

70
Q

What does the T wave represent

A

this is the repolarization phase of the ventricles (repolarization of the atria are obscured by the QRS
complex)

71
Q

What are different T wave pathologies and the differential diagnosis for each

A

• pathology when T wave variation occur in consecutive leads

■ inversion: BBB, ischemia, hypertrophy, drugs (e.g. digitalis), pulmonary embolism (lead III as part
of S1Q3T3 sign)

■ elevation: infarction (STEMI, Prinzmetal, hyperacute), hyperkalemia (wider, peaked)

■ flattened: hypokalemia, pericarditis, drugs (e.g. digitalis), pericardial effusion

■ variations: T wave alterans; beat-to-beat variations due to PVC overlap (R on T phenomenon which
may precipitate VT or VFib)

• appropriate T wave discordance: in BBB, T wave deflection should be opposite to that of the terminal
QRS deflection (i.e. T wave negative if ends with R or R’; positive if ends with S)

■ inappropriate T wave concordance suggests ischemia or infarction

72
Q

What does the QT interval represent

A

this represents the duration of ventricular depolarization and repolarization and is often difficult to
interpret

73
Q

How to calculate QTc and what is the normal range

A

• corrected QT (QTc) is often used instead in practice to correct for the repolarization duration; QTc =
QT ÷ √RR

• normal QTc is 360-450 msec for males and 360-460 msec for females

74
Q

What is the consequence of increased QTc

A

■ increased (>450 msec for males and >460 msec for females): risk of Torsades de Pointes (a lethal tachyarrhythmia)

75
Q

What causes increased QTc

A

◆ genetic Long QT Syndrome (often a channelopathy)
◆ drugs: antibiotics, SSRIs, antipsychotics, antiarrhythmics
◆ electrolytes: low Ca2+, low Mg2+, low K+
◆ others: hypothyroidism, hypothermia, cardiomyopathy

76
Q

What causes decreased QTc

A

■ decreased (<360 msec)
◆ electrolytes: high Ca++
◆ drugs: digoxin
◆ others: hyperthyroidism

77
Q

What is a potential consequence of decreased QTc

A

Risk of VFib

78
Q

What is the meaning of a U wave

A

origin unclear but may be repolarization of Purkinje fibres or delayed/prolonged repolarization of the
myocardium
• more visible at slower heart rates
• deflection follows T wave with <25% of the amplitude

79
Q

What can an abnormal U wave be caused by

A

• variations from norm could indicate pathologic conditions:
■ prominent (>25% of T wave): electrolyte (low K+), drugs (digoxin, antiarrhythmics)
■ inverted (from T wave): ischemia, volume overload

80
Q

Differential diagnosis of ST elevation

A

ST Elevation I HELP A PAL

Ischemia with reciprocal changes

Hypothermia (Osborne waves)
Early repolarization (normal variant, need old
ECGs to confirm)
LBBB
Post-MI

Acute STEMI

Prinzmetal’s (Vasospastic) angina
Acute pericarditis (diffuse changes)
Left/right ventricular aneurysm

81
Q

Differential diagnosis of ST depression

A

ST Depression WAR SHIP

WPW syndrome
Acute NSTEMI
RBBB/LBBB

STEMI with reciprocal changes
Hypertrophy (LVH or RVH) with strain
Ischemia
Post-MI

82
Q

Troponin I, Troponin T peak and duration of elevation

A

1-2 days

Up to 2 weeks

83
Q

CK-MB peak and duration of elevation

A

1 day

3 days

84
Q

What are cardiac biomarkers outside of Troponin and CK

A

■ AST and LDH also increased in MI (low specificity)

■ BNP and NT-proBNP: secreted by ventricles in response to increased end-diastolic pressure and volume
◆ DDx of elevated BNP: CHF, AFib, PE, COPD exacerbation, pulmonary HTN

85
Q

What is the protocol for ordering cardiac biomarkers

A

check troponin I at presentation and 8 h later ± creatine kinase-MB

86
Q

What is the role of ordering B-Type Natriuretic Peptide in the Evaluation and Management of Acute Dyspnea (BASEL study)?

A

In patients with acute dyspnea, measurement of B-type natriuretic peptide improves clinical outcomes (need for hospitalization or intensive care) and reduces time to discharge and total cost of treatment.

87
Q

What is ambulatory ECG

A

■ extended ambulatory ECG of 24 or 48 h or 14 or 28 d duration
■ provides a view of only two or three leads of electrocardiographic data over an extended period of time
■ permits evaluation of changing dynamic cardiac electrical phenomena that are often transient and of
brief duration

88
Q

What is continuous loop ECG monitoring

A

◆ a small, lightweight, battery operated recorder that records two or three channels of ECG data
◆ patient activated event markers
◆ minimum of 24-48 h

89
Q

What is implantable device ECG monitoring

A

◆ subcutaneous monitoring device for the detection of cardiac arrhythmias
◆ typically implanted in the left pectoral region and stores events when the device is activated automatically according to programmed criteria or manually with magnet application
◆ can be used for months to years

90
Q

Contraindications to ambulatory ECG monitoring

A

None other than patient refusal and adhesive allergy

91
Q

Indications for transesophageal echocardiography

A

■ should be performed as the initial test in certain life-threatening situations, (e.g. aortic dissection)
when other tests contraindicated (e.g. CT angiography in patient with renal failure)
■ intracardiac thrombi, tumours, valvular vegetations (infective endocarditis), aortic dissection, aortic
atheromas, prosthetic valve function, shunt, technically inadequate transthoracic study
■ evaluation for left atrial/left atrial appendage thrombus in a patient with atrial fibrillation/atrial
flutter to facilitate clinical decision making regarding electrical cardioversion or ablation

92
Q

TEE risks

A

■ serious complications are extremely rare (<1 in 5,000)
■ esophageal perforation
■ gastrointestinal bleeding
■ pharyngeal hematoma

93
Q

Indications for stress echocardiography

A

■ useful alternative to other stress imaging modalities

■ when ECG cannot be interpreted appropriately

■ intermediate pre-test probability with normal/equivocal exercise ECG

■ post-ACS when used to decide on potential efficacy of revascularization

■ To evaluate the clinical significance of valvular heart disease

■ evaluation of myocardial viability, dyspnea of possible cardiac origin, mitral valve disease, aortic stenosis, mitral regurgitation, pulmonary hypertension, and patients with hypertrophic cardiomyopathy (for LVOT obstruction

94
Q

Contraindications for stress echocardiography

A

■ contraindications to exercise testing

■ contraindications to dobutamine stress echocardiography: tachyarrhythmias and systemic hypertension

■ AAA has been considered as a relative contraindication to exercise testing or dobutamine stress echocardiography

95
Q

What is a contrast echo with agitated saline contrast

A

■ improves resolution and provides real-time assessment of intracardiac blood flow

■ conventional agent is agitated saline (contains microbubbles of air)

■ allows visualization of right heart and intracardiac shunts, most commonly patent foramen ovale (PFO) and intrapulmonary shunt

96
Q

What is contrast echo with transpulmonary contrast agents

A

description: newer contrast agents are capable of crossing the pulmonary bed and achieving left heart opacification following intravenous injection

these contrast agents improve visualization of endocardial borders and enhance evaluation of LV ejection fraction and wall motion abnormalities (in patients with technically inadequate echocardiograms), and intracardiac mass

97
Q

Risks of contrast echo with transpulmonary contrast agents

A

■ risk of non fatal MI and death are rare

■ ultrasound contrast agents may cause back pain, headache, urticaria, and anaphylaxis

98
Q

Indications for exercise stress testing

A

■ patients with intermediate (10-90%) pretest probability of CAD based on age, gender, and symptoms

■ ST depression <1 mm at rest, no left bundle branch block, no digoxin or estrogen use

■ exercise test results stratify patients into risk groups

  1. low risk patients can be treated medically without invasive testing
  2. intermediate risk patients may need additional testing in the form of exercise imaging studies or cardiac catheterization
  3. high risk patients should be referred for cardiac catheterization
99
Q

Contraindications for exercise stress testing

A

■ acute myocardial infarction (within 2 days)
■ unstable angina pectoris
■ uncontrolled arrhythmias causing symptoms of hemodynamic compromise
■ symptomatic severe valvular stenosis
■ uncontrolled symptomatic heart failure
■ active endocarditis or acute myocarditis or pericarditis
■ acute aortic dissection
■ acute pulmonary or systemic embolism
■ acute non-cardiac disorders that may affect exercise performance or may be aggravated by exercise

100
Q

When should you terminate exercise stress testing

A

◆ patient’s desire to stop
◆ drop in systolic blood pressure of >10 mmHg from baseline despite an increase in workload, when accompanied by other evidence of ischemia
◆ moderate to severe angina
◆ ST elevation (>1 mm) in leads without diagnostic Q-waves (other than V1 or aVR)
◆ increasing nervous system symptoms (e.g. ataxia, dizziness, or near syncope)
◆ signs of poor perfusion (cyanosis or pallor)
◆ technical difficulties in monitoring ECG or systolic blood pressure
◆ sustained ventricular tachycardia

101
Q

What is the cardiac index

A

CI = CO/body surface area
◆ cardiac index is a measure of cardiac function
◆ <1.8 L/min/m2 usually means cardiogenic shock
◆ 2.6-4.2 L/min/m2 is considered normal

102
Q

What is the pulmonary capillary wedge pressure and what does it measure

A

◆ obtained by advancing the catheter to wedge in the distal pulmonary artery
◆ records pressure measured from the pulmonary venous system
◆ in the absence of pulmonary venous disease reflects left atrial pressure

103
Q

What information can be obtained from right heart catheterization (Swan-Ganz catheter)

A

■ obtain direct measurements of central venous, right-sided intracardiac, pulmonary artery, and pulmonary artery occlusion pressures
■ can estimate cardiac output, systemic and pulmonary vascular resistance as well as mixed venous oxyhemoglobin saturation, oxygen delivery, and oxygen uptake

104
Q

Indications for Swan Ganz catheter

A

■ unexplained or unknown volume status in shock

■ severe cardiogenic shock (e.g. acute valvular disease, suspected pericardial tamponade)

■ suspected or known pulmonary artery hypertension

■ severe underlying cardiopulmonary disease (e.g. congenital heart disease, left-to-right shunt severe valvular disease, pulmonary hypertension) and undergoing corrective or other surgery

105
Q

Contraindications for Swan Ganz catheter

A

■ lack of consent
■ infection at the insertion site
■ the presence of a right ventricular assist device
■ insertion during cardiopulmonary bypass

106
Q

How do you introduce a left heart catheter

A

accomplished by introducing a catheter into the brachial or femoral artery and advancing it through the aorta, across the aortic valve, and into the left venricle

107
Q

What does left heart catheter evaluate

A

evaluates mitral and aortic valvular defects and myocardial disease

systolic and end-diastolic pressure tracings recorded

LV size, wall motion and ejection fraction can be assessed by injecting contrast into the LV (left ventriculography) via femoral/radial artery catheterization

cardiac output

108
Q

Left heart catheterization indications

A

■ identification of the extent and severity of CAD and evaluation of left ventricular function

■ assessment of the severity of valvular or myocardial disorders (e.g. aortic stenosis or insufficiency, mitral stenosis or insufficiency, and various cardiomyopathies) to determine the need for surgical correction

■ collection of data to confirm and complement noninvasive studies

■ determination of the presence of CAD in patients with confusing clinical presentations or chest pain of uncertain origin

109
Q

Right atrium/central venous pressure

A

1-8 mm Hg

110
Q

Right ventricle pressure (systolic)

A

1-8 (15-30) mm Hg

111
Q

Pulmonary artery pressure (systolic)

A

4-12 mm Hg (15-30)

112
Q

Left atrium/pulmonary capillary wedge pressure

A

4-12 mm Hg

113
Q

Left ventricle end diastolic pressure

A

4-12 mm Hg

114
Q

Left heart catheterization contraindications

A

■ severe uncontrolled hypertension
■ ventricular arrhythmias
■ acute stroke
■ severe anemia
■ active gastrointestinal bleeding
■ allergy to radiographic contrast
■ acute renal failure
■ uncompensated congestive failure (so that the patient cannot lie flat)
■ unexplained febrile illness or untreated active infection
■ electrolyte abnormalities (e.g. hypokalemia)
■ severe coagulopathy

115
Q

Indications for coronary angiography

A

Informally:
■ to define the coronary anatomy and the degree of luminal obstruction of the coronary arteries
■ to determine the presence and extent of obstructive CAD
■ to assess the feasibility and appropriateness of various forms of therapy, such as revascularization by percutaneous or surgical interventions
■ can also be used when the diagnosis of CAD is uncertain and CAD cannot be reasonably excluded by noninvasive technique

ACC/AHA:
• Disabling (CCS classes III and IV) chronic stable angina despite medical therapy

  • High-risk criteria on clinical assessment or non-invasive testing
  • Serious ventricular arrhythmia or CHF
  • Uncertain diagnosis or prognosis after non-invasive testing
  • Inability to undergo non-invasive testing
116
Q

What is the Gold standard for localizing and quantifying CAD

A

Coronary angiography

117
Q

What is coronary angiography

A

■ radiographic visualization of the coronary vessels after injection of radiopaque contrast media

■ coronary vasculature accessed via the coronary ostia

118
Q

Coronary angiography contraindications

A

severe renal failure (due to contrast agent toxicity – must check patient’s renal status)

119
Q

What is considered hemodynamically significant stenosis of the coronary arteries

A

defined as 70% or more narrowing of the luminal diameter

120
Q

What provocative pharmacological agents can be used to unmask pathology with coronary angiography

A

■ fluid loading may unmask latent pericardial constriction
■ afterload reduction or inotropic stimulation may be used to increase the outflow tract gradient in HCM
■ coronary vasoreactive agents (e.g. methylergonovine, acetylcholine)
■ a variety of pulmonary vasoreactive agents in primary pulmonary HTN (e.g. oxygen, calcium channel blockers, adenosine, nitric oxide, or prostacyclin)

121
Q

Contrast enhanced CT coronary angiography indications

A

often used to assess coronary artery and previous graft stenosis/viability that could not be seen during coronary angiography

122
Q

Cardiac MRI indications

A

Valuable in assessment of congenital cardiac anomalies, abnormalities of the aorta, assessment of viable myocardium, and assessment of cardiomyopathies

Cardiology and Cardiac Surgery (11 decks)

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