Practical Cardiovascular Medicine E-Book

Elias B. Hanna

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 2880

Veröffentlichungsjahr: 2017

Beschreibung

Prepare yourself for success with this unique cardiology primer which distils the core information you require and presents it in an easily digestible format.  

• Provides cardiologists with a thorough and up-to-date review of cardiology, from pathophysiology to practical, evidence-based management
• Ably synthesizes pathophysiology fundamentals and evidence based approaches to prepare a physician for a subspecialty career in cardiology
• Clinical chapters cover coronary artery disease, heart failure, arrhythmias, valvular disorders, pericardial disorders, and peripheral arterial disease
• Practical chapters address ECG, coronary angiography, catheterization techniques, ecnocardiography, hemodynamics, and electrophysiological testing
• Includes over 650 figures, key notes boxes, references for further study, and coverage of clinical trials
• Review questions at the end of each chapter help clarify topics and can be used for Board preparation - over 375 questions in all!

Leseprobe

Table of Contents

Cover

Title Page

Preface

Abbreviations

Part 1: CORONARY ARTERY DISEASE

1 Non-ST-Segment Elevation Acute Coronary Syndrome

QUESTIONS AND ANSWERS

References

2 ST-Segment Elevation Myocardial Infarction

1. Definition, reperfusion, and general management

2. STEMI complications

QUESTIONS AND ANSWERS

References

3 Stable CAD and Approach to Chronic Chest Pain

QUESTIONS AND ANSWERS

References

Part 2: HEART FAILURE (CHRONIC AND ACUTE HEART FAILURE, SPECIFIC CARDIOMYOPATHIES, AND PATHOPHYSIOLOGY)

4 Heart Failure

DEFINITION, TYPES, CAUSES, AND DIAGNOSIS OF HEART FAILURE

1. DEFINITION AND TYPES OF HEART FAILURE

2. CAUSES OF HEART FAILURE

3. DIAGNOSTIC TESTS

CHRONIC TREATMENT OF HEART FAILURE

1. TREATMENT OF SYSTOLIC HEART FAILURE

2. TREATMENT OF HFPEF

ACUTE HEART FAILURE AND ACUTELY DECOMPENSATED HEART FAILURE

QUESTIONS AND ANSWERS

References

5 Additional Heart Failure Topics

1. SPECIFIC CARDIOMYOPATHIES

2. ADVANCED HEART FAILURE: HEART TRANSPLANT AND VENTRICULAR ASSIST DEVICES (VADS)

3. PATHOPHYSIOLOGY OF HEART FAILURE AND HEMODYNAMIC ASPECTS

References

Part 3: VALVULAR DISORDERS

6 Valvular Disorders

1. MITRAL REGURGITATION

2. MITRAL STENOSIS

3. AORTIC INSUFFICIENCY

4. AORTIC STENOSIS

5. TRICUSPID REGURGITATION AND STENOSIS

6. PULMONIC STENOSIS AND REGURGITATION

7. MIXED VALVULAR DISEASE; RADIATION HEART DISEASE

8. PROSTHETIC VALVES

9. AUSCULTATION AND SUMMARY IDEAS

QUESTIONS AND ANSWERS

References

Part 4: HYPERTROPHIC CARDIOMYOPATHY

7 Hypertrophic Cardiomyopathy

QUESTIONS AND ANSWERS

References

Part 5: ARRHYTHMIAS AND ELECTROPHYSIOLOGY

8 Approach to Narrow and Wide QRS Complex Tachyarrhythmias

QUESTIONS AND ANSWERS: Practice ECGs of wide complex tachycardias

Further reading

9 Ventricular Arrhythmias

QUESTIONS AND ANSWERS

Reference

Further reading

10 Atrial Fibrillation

QUESTIONS AND ANSWERS

Reference

Further reading

11 Atrial Flutter and Atrial Tachycardia

QUESTIONS AND ANSWERS

References

Further reading

12 Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia, Wolff–Parkinson–White Syndrome, and Junctional Rhythms

QUESTIONS AND ANSWERS

Further reading

13 Bradyarrhythmias

QUESTIONS AND ANSWERS

References

Chapter 14: Permanent Pacemaker and Implantable Cardioverter Defibrillator

QUESTIONS AND ANSWERS: Cases of PM troubleshooting

References

15 Basic Electrophysiologic Study

Further reading

16 Action Potential Features and Propagation

Further reading

Part 6: PERICARDIAL DISORDERS

17 Pericardial Disorders

1. ACUTE PERICARDITIS

2. TAMPONADE

3. PERICARDIAL EFFUSION

4. CONSTRICTIVE PERICARDITIS

QUESTIONS AND ANSWERS

References

Further reading

Part 7: CONGENITAL HEART DISEASE

18 Congenital Heart Disease

1. ACYANOTIC CONGENITAL HEART DISEASE

2. CYANOTIC CONGENITAL HEART DISEASE

3. MORE COMPLEX CYANOTIC CONGENITAL HEART DISEASE AND SHUNT PROCEDURES

QUESTIONS AND ANSWERS

References

Part 8: PERIPHERAL ARTERIAL DISEASE

19 Peripheral Arterial Disease

1. Lower extremity peripheral arterial disease

2. Carotid disease

3. Renal artery stenosis

QUESTIONS AND ANSWERS

References

20 Aortic Diseases

References

Part 9: OTHER CARDIOVASCULAR DISEASE STATES

21 Pulmonary Embolism and Deep Vein Thrombosis

1. PULMONARY EMBOLISM

2. DEEP VEIN THROMBOSIS

3. IMMUNE HEPARIN-INDUCED THROMBOCYTOPENIA

QUESTIONS AND ANSWERS

References

22 Shock and Fluid Responsiveness

1. SHOCK

2. FLUID RESPONSIVENESS

References

23 Hypertension

1. HYPERTENSION

2. HYPERTENSIVE URGENCIES AND EMERGENCIES

QUESTIONS AND ANSWERS

References

24 Dyslipidemia

QUESTIONS AND ANSWERS

References

25 Pulmonary Hypertension

QUESTIONS AND ANSWERS

References

26 Syncope

QUESTIONS AND ANSWERS

References

27 Chest Pain, Dyspnea, Palpitations

1. CHEST PAIN

2. ACUTE DYSPNEA

3. PALPITATIONS

References

28 Infective Endocarditis and Cardiac Rhythm Device Infections

1. INFECTIVE ENDOCARDITIS

2. CARDIAC RHYTHM DEVICE INFECTIONS

References

29 Preoperative Cardiac Evaluation

QUESTIONS AND ANSWERS

References

30 Miscellaneous Cardiac Topics

1. CARDIAC MASSES

2. PREGNANCY AND HEART DISEASE

3. HIV AND HEART DISEASE

4. COCAINE AND THE HEART

5. CHEMOTHERAPY AND HEART DISEASE

6. CHEST X-RAY

QUESTIONS AND ANSWERS

References

Part 10: CARDIAC TESTS

31 Electrocardiography

QUESTIONS AND ANSWERS

References

Further reading

32 Echocardiography

1. GENERAL ECHOCARDIOGRAPHY

2. TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) VIEWS

Further Reading

33 Stress Testing, Nuclear Imaging, Coronary CT Angiography

References

Further reading

Part 11: CARDIAC TESTS: INVASIVE CORONARY AND CARDIAC PROCEDURES

34 Angiographic Views

QUESTIONS AND ANSWERS

Further reading

35 Cardiac Catheterization Techniques, Tips, and Tricks

36 Hemodynamics

QUESTIONS AND ANSWERS: Additional hemodynamic cases

References

37 Intracoronary Imaging

1. INTRAVASCULAR ULTRASOUND (IVUS)

2. OPTICAL COHERENCE TOMOGRAPHY (OCT)

References

Further reading

38 Percutaneous Coronary Interventions and Complications, Intra-Aortic Balloon Pump, Ventricular Assist Devices, and Fractional Flow Reserve

QUESTIONS AND ANSWERS

Further reading

Index

End User License Agreement

List of Tables

Chapter 01

Table 1.1 ACS likelihood.

Table 1.2 Summary of antithrombotic therapy in ACS.

Table 1.3 Prognosis of NSTE-ACS.

Table 1.4 Angiographic findings in NSTE-ACS and rates of revascularization.

29–31

Table 1.5 Comparison of the three ADP receptor antagonists.

Table 1.6 Comparison of anticoagulants.

Chapter 02

Table 2.1 Limitations and contraindications of fibrinolysis.

Table 2.2 Revascularization timelines in STEMI.

Table 2.3 STEMI TIMI risk score.

Table 2.4 Differential diagnosis of a shock.

Chapter 03

Table 3.1 Indications for stress imaging, as opposed to plain treadmill stress ECG.

Table 3.2 Risk stratification with stress testing.

Table 3.3 Indications for revascularization and modality (PCI vs. CABG).

Table 3.4 Reasons for superiority of CABG vs. PCI.

Table 3.5 Variables analyzed in surgical risk scores (STS and EuroSCORE).

Table 3.6 CAD mortality.

Table 3.7 Causes and histology of SVG failure.

Chapter 04

Table 4.1 Reduction of ventricular volume improves cardiac output through four mechanisms.

Table 4.2 Acute HF therapy according to volume status and peripheral perfusion status.

Table 4.3 Diagnosis of the underlying mechanism of RV failure and tricuspid regurgitation: measurement of PA systolic pressure and PVR (pressure overload vs. volume overload vs. intrinsic RV disease).

Chapter 06

Table 6.1 Severity of MS.

Table 6.2 Classification of AS severity.

Table 6.3 Causes of low-gradient AS (AVA ≤ 1 cm

2

with a mean gradient < 40 mmHg).

Table 6.4 Causes of AVA > 1 cm

2

with a mean gradient > 40 mmHg.

Table 6.5 Auscultation features

Chapter 07

Table 7.1 Exam findings in HOCM versus AS.

Table 7.2 Differentiate LVOT obstruction of HOCM from hypertensive obstructive cardiomyopathy.

Table 7.3 Athlete’s heart vs. HOCM.

Chapter 08

Table 8.1 Summary of the approach to wide QRS complex tachycardia.

Table 8.2 Management of an acutely presenting, hemodynamically stable AF or atrial flutter.

Table 8.3 Management of focal atrial tachycardia.

Chapter 09

Table 9.1 Risk of sudden death and cardiac events in patients with long QT syndrome before the age of 40.

Chapter 10

Table 10.1 Factors predisposing to atrial fibrillation.

Table 10.2 Cases in which a rhythm-control strategy should be considered (first four are most important).

Table 10.3 Risk factors associated with failure of direct-current cardioversion, recurrence of AF after cardioversion, or progression of paroxysmal AF to persistent AF (first five are most important).

The best candidate for rhythm control is the patient having Table 10.2 criteria with none of Table 10.3 criteria

.

Table 10.4 Dosage of the drugs used for acute rate control.

Table 10.5 Stroke risk in patients with non-valvular atrial fibrillation not treated with anticoagulation.

Table 10.6 Major bleeding risk associated with HAS-BLED risk score in patients receiving warfarin.

Table 10.7 Rate control of AF with or without HF.

Table 10.8 New oral anticoagulants vs. warfarin.

Chapter 12

Table 12.1 Electrocardiographic localization of the AP.

Chapter 13

Table 13.1 Effect of atropine and exercise on AV block.

Table 13.2 Differential diagnosis of a regular, non-tachycardic (<100 bpm) narrow complex rhythm without P waves.

Table 13.3 Differential diagnosis of a regular, non-tachycardic wide complex rhythm without P waves.

Chapter 16

Table 16.1 Differentiation of various mechanisms of arrhythmias.

Chapter 17

Table 17.1 Comparison of hemodynamic findings in constrictive pericarditis, restrictive cardiomyopathy, and severe ventricular failure.

Table 17.2 The three most important recordings in the hemodynamic assessment of constriction.

Table 17.3 Echocardiographic differentiation between constrictive pericarditis and restrictive cardiomyopathy.

Chapter 19

Table 19.1 Differential diagnosis: arterial claudication, neurologic claudication (spinal stenosis), diabetic neuropathy, venous insufficiency.

Table 19.2 Acute limb ischemia vs. critical limb ischemia.

Table 19.3 Types of lower extremity ulcers.

Table 19.4 Classification of PAD severity based on ABI.

Table 19.5 Highlights of the TransAtlantic InterSociety Consensus (TASC) classification of angiographic extent and complexity.

Table 19.6 Management of lower extremity ulcers.

Table 19.7 High-risk features for CEA and carotid stenting.

Table 19.8 Signs of advanced renal parenchymal disease and signs of functional significance of a renal artery stenosis.

Chapter 20

Table 20.1 Types of endoleaks.

Chapter 21

Table 21.1 Risk factors for PE/DVT.

Table 21.2 Duration of long-term anticoagulation.

Chapter 22

Table 22.1 Hemodynamic findings in the four different types of shock.

Table 22.2 Causes of cardiogenic shock.

Table 22.3 General indications for transfusion in critically ill or ACS patients.

Chapter 23

Table 23.1 Situations that warrant workup for secondary HTN.

Table 23.2 Causes of secondary hypertension.

Table 23.3 Basic workup for any HTN.

Table 23.4 Specific workup when secondary HTN is suspected.

Table 23.5 Treatment in specific settings.

Chapter 25

Table 25.1 Classification of severity of pulmonary hypertension.

Chapter 26

Table 26.1 Features that suggest seizure rather than syncope.

Table 26.2 Clinical clues to the diagnosis of syncope.

2–5,8

Table 26.3 ECG or Holter findings suggestive of cardiac syncope.

Table 26.4 Types of response to tilt table testing.

Chapter 27

Table 27.1 Causes of chest pain.

Table 27.2 Causes of acute dyspnea.

Table 27.3 Diagnostic features of palpitations (duration, onset/offset, regularity, relation to exertion).

Table 27.4 Workup of palpitations.

Chapter 30

Table 30.1 Echocardiographic features allowing the differential diagnosis of a cardiac mass.

Table 30.2 Cardiovascular drugs and pregnancy.

Chapter 31

Table 31.1 Differential diagnosis of ST-segment depression and/or T-wave inversion.

Table 31.2 Differential diagnosis of ST-segment elevation.

Table 31.3 Localization of anterior MI.

Table 31.4 Differentiate RCA from LCx in inferior MI.

Chapter 32

Table 32.1 Severe valvular regurgitation.

Table 32.2 Severe valvular stenosis: severe AS, including low-gradient AS, and severe MS.

Table 32.3 Pitfalls of E/E’ in the evaluation of LA pressure.

Table 32.4 Beside the occluder profile, four causes of pressure gradient across a prosthetic valve.

Table 32.5 Echocardiographic differentiation between a physiologically high gradient and an intrinsic aortic prosthesis obstruction.

Table 32.6 Echocardiographic differentiation between a physiologically high gradient and an intrinsic mitral prosthesis obstruction.

Chapter 33

Table 33.1 Clinical probability of CAD.

Table 33.2 Standard Bruce treadmill protocol.

Table 33.3 High-risk stress ECG and Duke Treadmill Score (DTS).

Table 33.4 Sensitivity and specificity of various stress tests

Table 33.5 Risk stratification with stress testing.

Table 33.6 Indications to stop the stress test.

Table 33.7 Factors that reduce the sensitivity and specificity of any stress testing modality.

Chapter 36

Table 36.1 Correlation between LVEDP and mean PCWP.

Table 36.2 Fick equation.

Table 36.3 Normal exertional values of PCWP, PA pressure, and cardiac output, according to age.

Chapter 38

Table 38.1 Risk factors for stent thrombosis.

Table 38.2 Recurrent target vessel disease/angina after stenting.

Table 38.3 Peri-PCI antithrombotic therapy.

Table 38.4 Causes of lack of appropriate pressure augmentation.

List of Illustrations

Chapter 01

Figure 1.1 Platelet receptors and antiplatelet mechanisms of action.

Figure 1.2 Specific effects of the four anticoagulants.

Figure 1.3 Summary of anticoagulant use in NSTE-ACS, before catheterization and during PCI.

Figure 1.4 The concentric and eccentric lesions with smooth borders are predominantly seen in stable CAD, while the lesions with irregular or overhanging borders are predominantly seen in ACS.

Haziness

may be due to an unstable fissured plaque, with contrast faintly seeping through the fissures of the plaque beyond the true lumen; it may also be due to concentric calcium surrounding the lumen and does not necessarily imply instability.

Chapter 02

Figure 2.1 Phases of STEMI.

Figure 2.2 The patient presents with chest discomfort that has lasted 3 hours and resolved 2 hours ago. Subtle ST elevation is seen in leads II and aVF, and in leads V

5

and V

6

, with subtle ST depression in V

1

–V

2

. Three features suggest that this mild ST elevation is actually STEMI: (i) Q waves; (ii) ST depression in reciprocal leads (V

1

–V

2

); (iii) wide T-wave morphology and fused ST-T segments in leads I, II, V

5

, and V

6

(

arrows

). This patient qualifies for emergent catheterization since his discomfort occurred in the last 24 hours. He is found to have an acutely occluded large obtuse marginal branch.

Figure 2.3 Fibrinolysis cascade and mechanism of action of fibrinolytics. Fibrinolytics activate plasminogen into plasmin, which degrades fibrin.

Figure 2.4 The timing of PCI in relation to thrombolysis in the pharmacoinvasive strategy, rescue PCI strategy, and facilitated PCI strategy, with the clinical trials that addressed and defined these strategies.

Figure 2.5 Stages of negative LV remodeling post-MI, also called infarct expansion.

Figure 2.6 Dynamic left ventricular outflow tract obstruction in apical infarction.

Figure 2.7 LV aneurysm and LV pseudoaneurysm.

Figure 2.8

Figure 2.9

Chapter 03

Figure 3.1 Clinical probability of CAD.

10

Figure 3.2 Diagnostic approach to chronic chest pain.

Chapter 04

Figure 4.1 Diagnosis of HFpEF by catheterization, echo, or BNP features, according to ESC criteria.

7

A normal or mildly dilated LV is defined as LV end-diastolic volume < 75 ml/m

2

or 96 ml/m

2

, respectively.

Figure 4.2 Change of LV filling pattern between compensated and decompensated HF.

Figure 4.3 Peri-infarct ischemia.

Figure 4.4 Fixed defect.

Figure 4.5 Proposed algorithm to guide revascularization in patients with ischemic LV dysfunction.

Figure 4.6 Case of chronic HF with LV dilatation and mild increase in PCWP.

Figure 4.7 Diuretic response in a normal individual and in HF. Note that no diuretic response occurs before achieving the threshold dose. The threshold is higher in HF and the diuresis achieved with the threshold dose is lower in HF than in normal individuals. Also, the difference between the threshold and the maximal effect is narrow in HF, suggesting the value of frequent dosing, rather than higher dosing, to increase the overall efficacy.

Figure inspired by reference 104.

Figure 4.8 Hemodynamic decompensation starts several weeks before clinical decompensation, even when the presentation seems abrupt and the weight gain is only mild, and even in HFpEF. Modified from Zile et al. (2008).

138

Figure 4.9 Mechanisms through which diuresis and inotropes initiate a benefit that is sustained over time.

Chapter 05

Figure 5.1 Simultaneous LA and LV pressure recordings in diastole.

Figure 5.2 Cardiac output–preload relationship (Frank–Starling curve).

Figure 5.3 The failing LV is exquisitely sensitive to changes in afterload.

Figure 5.4 Compliance curve, i.e., pressure–volume relationship in diastole.

Figure 5.5 Important HF figure, showing a

diastolic superimposition of the Frank–Starling curve (= cardiac output–end-diastolic volume curve) (lower curve) and the pressure–volume curve (upper curve) in three situations.

Figure 5.6 Pressure–volume loops.

Chapter 06

Figure 6.1

(a)

Illustration of a horizontal cut across the mitral plane on transthoracic echocardiography, showing the relationship of the cusps with the papillary muscles, aortic valve, and left atrial appendage (LAA). Also, illustration of how various TEE rotations cut the mitral valve. Note that the anterolateral and posteromedial papillary muscles (APM and PPM) are located between the two leaflets rather than underneath the corresponding leaflet (they are underneath the commissures). A

1

–A

3

are various anterior leaflet cusps, and P

1

–P

3

are various posterior leaflet cusps (A

3

and P

3

are the ones attached to the septum). The mitral annulus surrounding the anterior leaflet and separating the anterior leaflet from the aortic valve is fibrous and relatively straight, and forms the mitroaortic curtain or fibrous trigone. The posterior mitral annulus has a C shape and is muscular.

(b)

Illustration of how the mitral valve looks surgically when approached from inside the LA through the anterior heart. A

3

and P

3

are on the right (flipped view in comparison with TTE).

(c)

3D TEE view of the mitral valve (en face view). This view is similar to the surgical view. For orientation, identify the anterior leaflet (leaflet with the convex border) and the posterior annulus. The posterior annulus has a C shape, is muscular and contractile. It contracts in systole and contributes to the mitral valve competence. There are two commissures: anterolateral (AL

c

) and posteromedial (PM

c

).

Figure 6.2 Carpentier’s classification of the mechanisms of mitral regurgitation.

Figure 6.3 Mitral valve prolapse. The long-axis view defines prolapse, while the short-axis view defines which cups are involved (particularly when color Doppler is added).

Figure 6.4 Illustration of ischemic MR on longitudinal views.

(a)

Normal valvular anatomy. Both papillary muscles (PM) provide chordae to both mitral leaflets.

(b)

Inferior akinesis with posterolateral displacement of the posterior papillary muscle (PM). This leads to major restriction of the posterior leaflet and minor restriction of the anterior leaflet. The tethering force being more orthogonal to the posterior leaflet, the latter is more restricted than the anterior leaflet. In fact, the anterior leaflet overrides the posterior leaflet.

(c)

Anterior akinesis, by itself, does not lead to major restriction of any leaflet as it pulls the leaflets axially rather than sideways.

(d)

Anterior MI with global remodeling and global LV dilatation pulls both the anterior and posterior papillary muscles apically and posterolaterally. The more the LV is dilated and spherical, the more laterally the leaflets are pulled, the more severe the MR. Both leaflets are tethered, and the jet may be central or predominantly posterior (if the posterior leaflet is more tethered than the anterior leaflet). Note that ischemic MR cannot be anteriorly directed (it is either central or posterior).

Figure 6.5

(a)

Horizontal cut across the mitral valve. Normal ventricular, papillary muscle, and leaflet structures.

(b)

Inferior and inferolateral akinesis with posterior displacement of the posterior papillary muscle. As a result, the posterior leaflet is getting tethered with a posteriorly directed MR. The anterior leaflet is less affected.

(c)

Anterior akinesis with global spherical remodeling of the LV and posterolateral displacement of both the anterior papillary muscle (APM) and posterior papillary muscle (PPM). In addition, the apical remodeling leads to apical tethering of both papillary muscles. As a result, the posterior and anterior leaflets are getting tethered with a jet that is central (symmetric tethering of both leaflets) or posterior (predominant tethering of the posterior leaflet). Thus, posterior leaflet tethering may occur with anterior MI.

Figure 6.6 Difference in V wave and LV diastolic pressure between (1) chronic compensated MR and (2) acute or decompensated MR. In decompensated MR, V wave gets larger, Y descent gets deeper, while X descent gets shallower. LA pressure may switch from (1) to (2) with simple maneuvers: handgrip (↑ afterload), small volume loading, exercise. LA pressure may switch from (2) to (1) with sedation, acute hypertension control, or nitroprusside infusion (↓ preload and afterload). Reproduced with permission from Hanna EB. Mitral regurgitation. In: Hanna EB, Glancy DL.

Practical Cardiovascular Hemodynamics

. New York, NY: Demos Medical, 2012, p. 112.

Figure 6.7

(a)

Long-axis view in diastole. See the hockeystick shape of the anterior leaflet (

arrow

), the tip of which looks attached to the stiff posterior leaflet (

line

), with no diastolic opening. In fact,

both leaflets are tied together by the commissural fusion.

(b)

M-mode across the mitral valve. The E–F slope is flattened and the posterior leaflet is dragged towards the anterior leaflet (

arrowhead

).

(c)

Commissural fusion on the mitral short-axis view (

arrow

). Commissural calcium is seen (

arrowhead

). Rather than oval, the mitral opening has a “fish mouth” shape.

(d)

Apical four-chamber view shows severe chordal thickening extending to the papillary muscles (

arrows

). The mitral leaflets are thickened, and the thickening and immobility extend beyond the edges into the body of the leaflets. The Wilkins score is 10 (leaflet thickness = 2, calcium = 2, leaflet mobility = 2, chordal thickening = 4).

Figure 6.8 Two examples of mitral stenosis with a diastolic pressure gradient between PCWP and LV at a heart rate of 60 bpm (

dark filled areas)

.

Figure 6.9 False impression of MS resulting from the use of PCWP as a surrogate for LA pressure in a patient with severe MR. When LA–LV pressures are simultaneously recorded, an early diastolic gradient is seen between LA and LV and is quickly followed by diastasis. However, when PCWP–LV pressure recording is performed, the damped and prolonged Y descent creates the impression of a large pressure gradient and a lack of diastasis, even when PCWP is appropriately shifted to the left, thus creating the impression of MS. Also, in comparison to patients without concomitant MR, patients with combined MS and MR are more likely to have their transmitral gradient overestimated with the use of PCWP.

Figure 6.10 β-blockers slow the heart rate and allow more LA emptying, which ultimately reduces LA pressure, V and A waves.

Figure 6.11 Aortic leaflets and their relation to the ascending aorta. A normal valve apparatus consists of aortic tissue that extends from the

sinotubular junction

, forms local aortic dilatations called

aortic root or sinuses of Valsalva (S)

, then touches the ventricle and suspends the aortic

leaflets

(

L

) (also called semilunar

cusps

). The sinuses of Valsalva are an extension of the aortic wall tissue. The sinotubular junction, rich in elastic tissue, provides the main support for the sinuses. The coronary arteries originate from the sinuses of Valsalva or just above them. Two-thirds of the circumference of the aortic valve is connected to the muscular ventricular septum, while the remaining one-third is in fibrous continuity with the anterior mitral leaflet (fibrous trigone, close to the non-coronary posterior cusp) (see Figure 6.1). At one point posteriorly, the aortic valve is in continuity with the interatrial septum. The

annulus

is a ring formed by the junction of the basal valvular hinges (leaflets’ insertion on the ventricle).

Figure 6.12

Figure 6.13

(a)

Difference in aortic orifice shape between the tricuspid and bicuspid aortic valves (short-axis view). Bicuspid valves are in fact “bicommissural” valves, while unicuspid valves are “unicommissural” or “acommissural” valves. The commmissures of a bicuspid valve (

arc

) may be partially fused, leading to AS at an early age; otherwise, AS develops later in life. Note that aortic opening/closure becomes eccentric in bicuspid valves; this is seen on M-mode analysis of the aortic valve. On echo, instead of analyzing how many cusps are seen when the valve is closed, it is best to analyze how the aortic valve opens: an elliptical rather than a triangular opening is a hint to a bicuspid valve. RCC and LCC are often fused, NCC being the cusp looking towards the IAS.

(b)

Doming of the bicuspid aortic valve on a long-axis view.

Figure 6.14 Peak-to-peak gradient is the difference between the two peaks (

horizontal bars

). Peak instantaneous gradient is the largest difference between the two curves (

white vertical line

). Mean gradient is the integration of all gradients (g

ray area

). LV pressure peaks early and the aortic pressure peaks late, which is the opposite of what is found in HOCM.

Figure 6.15 Pressure recovery phenomenon.

Figure 6.16 Prosthetic valves. Surgical bioprostheses typically have a metallic stent frame that extends from the sewing ring to each strut. Stentless bioprostheses have very thin rings and struts without any metal.

Figure 6.17 Bioprosthetic valve as seen on fluoroscopy. The ring and the three struts (

arrowheads

) are mounted over a metallic stent frame, which explains their visualization on fluoroscopy. The leaflets, per se, do not contain any metal and are not visualized.

Figure 6.18

Figure 6.19

Figure 6.20

Figure 6.21

Chapter 07

Figure 7.1

(a)

Asymmetric septal hypertrophy with increased velocity across the LVOT (

3 arrows

). This increased systolic velocity creates a Venturi effect that pulls the anterior mitral leaflet (SAM) and creates LVOT obstruction as well as a posteriorly directed MR (

blue arrow

). Note the anatomic contiguity of the mitral and aortic valves. Pulsed-wave Doppler should be used to sequentially interrogate the LV from apex up to the LVOT in order to confirm the anatomical level of obstruction. Note the normal velocity across the LV body, LVOT proximal to the obstruction and distal to it, and aorta (

single arrows

).

(b)

Pressure is increased throughout LV inflow, LV body, LVOT (

+++

), and drops beyond the LVOT obstruction (

+

). Even pressure at the mitral valve level (inflow tract pressure) is elevated.

Figure 7.2 Parasternal long-axis view of a patient with HOCM, showing SAM of the anterior leaflet tip. Not just the leaflet gets drawn to the septum, but also the chordae (chordal SAM).

Figure 7.3 M-mode of SAM. The

star

corresponds to the gap between the anterior and posterior leaflets in systole, leading to severe MR in this patient.

Figure 7.4 HOCM hemodynamics.

Figure 7.5 Brockenbrough phenomenon after a premature beat in HOCM. Note the increase in pressure gradient (

interrupted lines

) but the reduction in aortic pulse pressure (

double arrows

) after a pause in HOCM, vs. the increase in pressure gradient with an increase in aortic pulse pressure in AS. Note the “spike and dome” appearance of the aortic pressure in HOCM, which becomes more pronounced with worsening obstruction (after the pause).

Figure 7.6 LVOT velocity in HOCM: late-peaking dagger-shape LVOT velocity (

arrows

). This is opposed to the parabolic, symmetrical AS Doppler. Occasionally, an older patient may have both AS and HOCM. The continuous-wave Doppler will show two superimposed but distinct ejection envelopes (e.g., AS envelope within the HOCM envelope).

Figure 7.7 In the elderly, elongation of the aorta sharpens the angle between the aorta and the septum (

arrow

) and leads to a sigmoid “stocky” septum. A mild septal hypertrophy is transformed into a more severe, discrete septal thickening (DUST: discrete upper septal thickening).

Chapter 08

Figure 8.1 Approach to narrow QRS complex tachycardias.

Figure 8.2 Narrow complex tachycardia, regular, rate ~200 bpm. Differential diagnosis: AVNRT, AVRT, atrial tachycardia with 1:1 conduction, or atrial flutter with 2:1 conduction.

Figure 8.3 Explanation of how a wide QRS complex (aberrancy) may occur with SVT. RBBB, LBBB, or RBBB + LAFB may be seen. RBBB + LPFB is rare.

Figure 8.4 There are two types of SVT with pre-excitation, i.e., SVT with antegrade conduction over an accessory pathway (WPW syndrome):

Figure 8.5 Difference in QRS morphology between bundle branch block and VT. The QRS description is in reference to lead V

1

.

Figure 8.6 QRS morphology when VT originates in the posterior wall or the apical wall.

Figure 8.7 Differences in morphology between SVT with aberrancy and VT. SVT with aberrancy has a typical LBBB or RBBB morphology. Conversely, VT is suggested by:

Figure 8.8 Run of wide complex tachycardia on a telemetry strip: is it VT or SVT?

Figure 8.9 Wide complex tachycardia: VT or SVT?

Figure 8.10 Two short tachycardia runs. The tachycardia starts after a regularly occurring sinus P wave (

bar

) at a shorter PR interval (the

bar

marches out with the

arrows

). This is typical of a PVC, which occurs without disrupting the timing of the underlying sinus P waves. PAC would have started with a premature P wave. Thus, the tachycardia starts with a PVC and has the same morphology as the PVC. This is VT.

Figure 8.11 Wide complex, regular tachycardia, at a rate of ~135 bpm. QRS looks narrow in some leads; this is due to the fact that part of the QRS is isoelectric in those leads. That is why QRS should be measured in the lead where it is widest. QRS is wide (~140 ms) in lead V

3

in particular.

Figure 8.12 The baseline rhythm is sinus, consisting of QRS complexes (R) preceded by sinus P waves. Outside these complexes, there are premature complexes occurring in a bigeminal pattern (R1, R2, R3, R4). These could be PVCs or PACs with aberrancy. Look for P waves preceding these complexes: there is a P wave before each complex, marked #. It is an inverted, non-sinus P wave and occurs prematurely. This means that R1–R4 are PACs with aberrancy rather than PVCs. These PACs have aberrant conduction because they occur very prematurely, while the right bundle is still in its refractory period, which leads to RBBB morphology. Note that the aberrancy (QRS widening) is less pronounced when PAC is less premature. This is a form of

Ashman’s phenomenon

. R–R1 interval <R–R3 interval <R–R4 interval; hence, R4 is not aberrant.

Figure 8.13 Very wide QRS complex tachycardia (particularly wide in lead I, ~200 ms), very fast (rate ~240 bpm), and grossly irregular. Because it is so fast, it may initially seem regular; but on careful assessment one sees that R–R intervals are grossly irregular, with some R–R intervals being half the size of other R–R intervals, without any particular pattern (irregularly irregular) (

double arrows

).

Figure 8.14 Short RP narrow complex tachycardia, initially suggestive of AVNRT or AVRT (

arrows

indicate P waves). After adenosine, the P waves keep marching out at the same rate unaffected by adenosine, while AV conduction is blocked and ventricular escape beats are seen. Thus, this is atrial tachycardia. Adenosine was helpful in establishing the diagnosis. Soon afterwards, the 1:1 AV conduction will resume.

Figure 8.15 Two types of QRS complexes are seen: (1) narrow complexes preceded by sinus P waves; (2) wide complexes that seem to be preceded by sinus P waves (

arrows

) but are, in reality, coming too close to the P waves and dissociated from them, with a variable PR interval (ventricular complexes).

Figure 8.16 Again, two types of QRS complexes are seen: (1) narrow complexes preceded by a sinus P wave; (2) wide complexes preceded by the same sinus P wave (best seen in V

2

–V

6

). These wide complexes are not premature, hence they are not PVCs.

Figure 8.17 Alternation between wide and narrow QRS complexes. Both QRS complexes are occurring regularly after the regular sinus P waves (

arrows

), with a constant P–QRS relationship. The P–P interval and PR intervals are constant. The morphology suggests intermittent LBBB. Diagnosis: sinus rhythm with alternating LBBB.

Figure 8.18 A run of wide complex tachycardia. It is irregular, but this does not necessarily imply AF. In a short run of VT or at the onset of VT, VT may be irregular.

Figure 8.19 Regular wide complex tachycardia, QRS width ~180 ms (lead II).

Figure 8.20 Wide complex tachycardia, regular, at a rate of ~155 bpm. The QRS is widest in lead aVF (~140 ms).

Figure 8.21 This is the baseline ECG of the patient in Figure 8.20. It shows an anterior MI pattern; however, the QS pattern does not extend all the way to V

6

and the axis is normal. Note the morphology of QRS in lead II, and see how the three different-looking complexes in Figure 8.20 are fusion between this narrow QRS and the VT’s QRS.

Figure 8.22 Wide complex tachycardia on telemetry or Holter monitoring. Is it SVT or VT?

Figure 8.23 Run of wide complex tachycardia. Is it VT or SVT?

Figure 8.24 The baseline rhythm is AF and the baseline QRS is marked by

lines

. Runs of wide complexes are seen.

In a patient with baseline AF, are the wide complex runs VT or aberrant runs of AF?

Figure 8.25 Baseline sinus rhythm with LBBB morphology. Two runs of wide complex tachycardia are seen (

horizontal lines

). Are these runs VT or SVT with aberrancy?

Chapter 09

Figure 9.1 Wide premature complexes with a different morphology than the baseline QRS, and with prominent ST–T changes opposite to QRS, occurring in a trigeminal pattern. These are typically PVCs, but could be PACs with bundle branch block (aberrancy). They fall after normally occurring, non-premature P waves with a

shorter PR interval than the sinus beats, which is typical of PVCs

. Sinus P waves keep marching out through the PVCs.

Figure 9.2 Tachycardia that seems narrow but has a different morphology than the native QRS and is associated with secondary ST/T abnormalities → VT or SVT with aberrancy. To differentiate, see how the tachycardia starts. It does not start after a premature P wave, but rather starts after a regularly occurring sinus P wave (

third arrow

) with a shorter PR interval than regularly: this means it starts with a PVC. It has the same morphology as this PVC → the tachycardia is VT. Also, one can regularly march out sinus P waves scattered within the tachycardia and dissociated from the QRS complexes, which is diagnostic of VT. These P waves are marked by

arrows

. One P wave falls within a QRS (marked by an

interrupted line

).

Figure 9.3 Wide complex rhythm at a rate of 70 bpm. P waves are initially seen after every QRS (

blue arrows

). This could be consistent with a ventricular rhythm with 1:1 VA conduction. However, further down the strip, those P waves start coming sooner and fall onto the QRS complexes (

two complexes under the bar

), then appear before the QRS complexes and get conducted (

black arrows

). Thus, these P waves are actually sinus P waves dissociated from the ventricular rhythm. This dissociation is an isorhythmic AV dissociation, wherein the ventricular and sinus rhythms have close rates: when the sinus rhythm speeds up, it takes over and P waves get conducted. When it slightly slows down, the ventricular rhythm takes over. This is AIVR in a patient with anterolateral STEMI. While classically seen after reperfusion, it may very well be seen in non-reperfused infarcts such as this one. ST elevation is seen on both the ventricular and sinus-originating complexes. ST elevation that is concordant to QRS is indicative of STEMI, even in ventricular complexes.

Figure 9.4 Torsades de pointes initiation.

Figure 9.5 QT interval is markedly prolonged (QTc = 730 ms). T wave is wide and ample in lead V

3

, is deeply inverted in the inferior leads, and demonstrates beat-to-beat alternation in morphology and amplitude, the so-called macroscopic T wave alternans. In addition, alternation in T-wave polarity is seen in lead V

5.

T wave alternans may be seen with any cause of prolonged QT and implies severe heterogeneity of ventricular repolarization and an

imminent risk of TdP

; it is more characteristically seen in the congenital long QT syndromes. While this patient has hypokalemia, the wide and ample T-wave morphology without ST depression is not consistent with hypokalemia. The shape is consistent with long QT syndrome or ischemia.

Arrows

of two different lengths point to the two different T-wave morphologies.

Figure 9.6 Torsades de pointes that degenerates into

Figure 9.7 Typical ST–T morphologies in hypokalemia, hypocalcemia, and congenital long QT syndromes (LQT). In hypokalemia, ST segment is depressed and U wave is large while T wave is flattened. In hypocalcemia and LQT3, QT interval is prolonged as a result of ST-segment prolongation and, as opposed to other congenital LQT or QT prolongation secondary to drugs, there is no significant widening of the T wave. In LQT1, T wave is wide and ample without ST-segment depression, similar to Figure 9.5. In LQT2, T wave is wide and notched (double hump). LQT1 may have a morphology similar to LQT3 and is actually the most common LQT with this morphology.

In all long QT cases, particularly congenital LQT, the T wave may become notched after a pause, the notch representing the early afterdepolarization (EAD) wave that triggers TdP.

Figure 9.8 Brugada syndrome.

Figure 9.9

Chapter 10

Figure 10.1 LV diastolic filling pattern in compensated HF, decompensated HF, decompensated HF secondary to AF, and effects of DCCV.

Figure 10.2 Chronic antiarrhythmic drug therapy for the prevention of recurrent paroxysmal or persistent atrial fibrillation. Note that β-blockers are often the first-line antiarrhythmic agents because of their safety in comparison to other anti-arrhythmic drugs. This figure mainly applies to patients who have symptomatic AF recurrences despite rate control. Reproduced with permission of Elsevier from Wann LS, Curtis AB, January CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation. J Am Coll Cardiol 2011; 57: 223–42.

Figure 10.3 Yearly risk of stroke and intracranial hemorrhage with warfarin according to INR. The yearly intracranial hemorrhage risk is reduced from 0.5% per year to ~0.25% with the new anticoagulants. Data from Flaker et al. 2006.

50

Chapter 11

Figure 11.1 Flutter circuit with illustration of the net atrial vectors of depolarization (

gray arrows

) seen by the specific lead and the subsequent morphology of the flutter waves. The

gray star

indicates the starting point of the depolarization vector for illustration purposes. In typical counterclockwise flutter, the negative flutter wave is close to the QRS. Lead V

1

overlies the RA and mainly sees the local current in the RA, hence the positive deflection in V

1

, with possible return to isoelectric baseline between deflections.

Figure 11.2 Aflutter with flutter waves rate (F wave) ~300 per minute and 2:1 conduction. It is a typical counterclockwise Aflutter, with negative flutter waves in lead II. At first glance, it seems there is ST elevation where the asterisks (*) are placed. This is, in fact, the upslope of the flutter waves.

Figure 11.3 Typical counterclockwise Aflutter with variable conduction: 5:1, 4:1, 3:1, 2:1. The rhythm is overall irregular, but there is some repetition of the same R–R intervals. The interval between the 1st and 2nd, the 3rd and 4th, and the 7th and 8th R–R are equal. Typical sawtooth Aflutter waves are seen in lead II. In V

1

, there are upright P waves with an isoelectric baseline.

Figure 11.4 Another typical counterclockwise 2:1 Aflutter. See how F is negative in lead II, and positive in lead V

1

, without return to baseline.

Figure 11.5 Rhythm in lead V

1

(

above

) and lead II (

below

) with a ladder diagram showing how variable AV block occurs. Two levels of second-degree block are present in the AV junction: 2:1 block high in the AV junction and 3:2 type I block low in the AV junction. Flutter waves are indicated by vertical lines in the atrial (A) portion of the diagram. Every other flutter wave is blocked high, at level 1. Of those impulses making it through level 1, one-third are blocked at level 2, and two-thirds are conducted to the ventricles (V). Overall, this translates into an alternation of 2:1 and 4:1 conduction. The QRS complexes following the short R–R intervals are wide because of a functional block in the right bundle branch (Ashman type of aberrancy).

Figure 11.6 Coarse fibrillatory AF waves that simulate Aflutter in lead V1. Note their lack of consistent morphology and timing, and the lack of flutter waves in lead II.

Figure 11.7 2:1 atrial tachycardia, with an atrial rate of ~140 per minute. P wave is negative in the inferior leads, implying a low atrial origin; it is negative in lead V

1

and upright in aVL, implying a right atrial origin. A premature P occurs and breaks the atrial tachycardia at the end of the recording. The change in the T morphology before the premature complex suggests the occurrence of a P wave different from the previous P waves (premature P). The fact that AT breaks with a PAC implies reentrant AT.

Figure 11.8 Atrial escape rhythm (rate ~50 bpm) that developed in a patient who had sudden slowing of the sinus rate (e.g., hypervagal situation). The arrows point to the ectopic P waves (morphology different from the sinus P waves).

Chapter 12

Figure 12.1 AVNRT usually starts with a PAC that has a long PR interval as it goes through the slow pathway.

The slow pathway is slower but has a shorter refractory period than the fast pathway

, allowing conduction of the PAC. If, at the time the impulse reaches the distal slow pathway, the fast pathway is still in its refractory period, the reentrant circuit of AVNRT will not launch. A few subsequent sinus P waves may keep conducting over the slow pathway (Figure 12.5).

Figure 12.2

(a)

Arrows point to the retrograde P wave that is superimposed on the ST segment, appearing as a notch on the ST segment.

(b)

An ECG of the same patient in sinus rhythm after adenosine therapy: note the difference in V

1

–V

2

and in the inferior leads (no “pseudo-r’” or “pseudo S”).

Figure 12.3 Narrow complex tachycardia with retrograde P waves (

arrows

) seen in leads III and V

1

. RP is short, < 1/2 RR interval; hence, atrial tachycardia is unlikely. In AVNRT, P wave typically falls within or immediately after QRS (RP interval < 90 ms), giving a pseudo-S shape in the inferior leads and pseudo-r’ shape in V

1

. In this case, P wave falls a bit further away and RP is > 90 ms; thus, the arrhythmia could be either AVNRT or AVRT.

Figure 12.4 P waves are seen just before the QRS, with a PR interval < 110 ms. In a narrow complex tachycardia, this suggests AVNRT, although it is only seen in 4% of AVNRTs.

Figure 12.5 Sinus rhythm is present throughout the tracing. Vertical lines indicate P waves. Initially, the PR interval is normal (0.20 s), but after a couplet of PVCs (4th and 5th QRS complexes), the PR interval lengthens markedly. The AV conduction shifts from the fast pathway to the slow pathway. With the 7th sinus P wave after the couplet, the PR returns to normal.

Figure 12.6 Anatomy of the slow pathway, fast pathway, and compact AV node. Note their potential relationship with a His catheter and coronary sinus catheter. The Koch triangle, where the slow pathway lies, is bordered by the His, the coronary sinus, and the tricuspid annulus. The crista terminalis is behind the Koch triangle. A slow potential recorded across the slow pathway is shown. CS, coronary sinus.

Figure 12.7 An appropriately timed PAC conducts down the slow pathway but cannot go deep enough as the distal parts of this pathway (1) or the fast pathway (2) are in the refractory period. Eventually, the reentrant cycle is broken and the next P wave is a sinus P wave. Depending on where the block occurs:

Figure 12.8 Electrocardiographic features of pre-excitation. Arrows point to the positive and negative delta waves.

Figure 12.9 Amount of myocardium depolarized by the accessory pathway (gray circle) vs. the AV node (blue circle) depends on the speed of AV conduction, how far laterally the AP originates, and the refractory period of the AP. A PAC is slowly conducted through the AV node, which allows more ventricular mass to be depolarized through the AP. However, a very premature PAC may get blocked across the AP which, although faster than the AV node, has a longer refractory period and is more likely to block its conduction.

Figure 12.10 A slur is seen on the upslope of the QRS complex (e.g., leads II, III, aVF, V

2

–V

6

, as marked by the

arrows

). Also, note how the P wave is very close to the QRS complex (almost abuts it). The QRS seems negative in V

1

but the initial deflection, i.e., delta wave, is positive. The accessory pathway is left-sided, as delta is positive in V

1

–V

2

; it is left lateral, as delta wave is negative (pseudo-Q wave) in aVL.

Figure 12.11 Concealed accessory pathway (AP).

Figure 12.12 Manifest accessory pathway.

Figure 12.13 Irregular tachycardia with wide, polymorphic, bizarre-looking QRS, with VT rather than SVT features (positive QRS concordance in V1–V6, QRS morphology not consistent with RBBB or LBBB). This is a pre-excited AF in a patient with WPW. Note that, as opposed to aberrancy, QRS becomes wider after a longer R–R interval (

arrows

). AP is likely left posteroseptal (delta wave is negative in the inferior leads).

Figure 12.14 In AVNRT, the occurrence of a PAC or PVC (

gray bar

) either blocks the tachycardia, or, as in this case, gets conducted to the atria or ventricles but does not change the reentry, which keeps looping at its own rate. The interval between the QRS preceding the premature beat and that following it is double the R–R interval of the tachycardia.

Figure 12.15 Bundle branch block during orthodromic AVRT.

Figure 12.16 When the wide complex tachycardia becomes narrow, the R–R interval becomes shorter (the rate becomes faster). This implies orthodromic AVRT with transient block of the bundle branch ipsilateral to the AP (the bundle branch involved in the reentry).

Figure 12.17 A 22-year-old woman with no prior cardiac history presents with runs of SVT interspersed with sinus beats. The SVT rate is ~105 bpm. Two types of P waves are seen: sinus P waves (

arrowheads

) and P waves related to SVT (

arrows

). RP interval is long (long RP tachycardia). The differential diagnosis of this SVT includes:

Figure 12.18 Two types of QRS complex are seen. This intermittent widening of the QRS may represent intermittent bundle branch block (BBB) or intermittent pre-excitation. Intermittent BBB usually occurs with an increase in rate, but that is not the case here. Moreover, the morphology of the wide QRS favors pre-excitation. A positive delta wave with a short PR interval is seen on the wide complexes in leads I and V

5

, while a negative delta wave (pseudo-Q wave) is seen in the inferior lead. This intermittent conduction across the accessory pathway implies a long refractory period and an inability to consistently conduct even at a normal rate (good prognosis). The AP is likely posteroseptal.

Figure 12.19 Another WPW pattern on a baseline ECG. Note the short PR, with P almost attached to R. There is a positive delta slur on the upslope of R wave in lead I, and a negative delta slur manifested as Q wave in leads III and aVF (delta marked by arrows). Delta wave is negative in the inferior leads, implying that the AP is posteroseptal, with the electrical depolarization going away from the inferior wall. The delta wave is positive in lead I, meaning that the impulse propagates towards the left lateral wall. Delta wave is negative in lead V

1

, implying that the AP is right-sided, and thus the AP is right posteroseptal. The sharp delta transition in lead V

2

is consistent with a posteroseptal pathway.

Figure 12.20 Alternation of a narrow and an equidistant wide QRS (

vertical arrows

). Ventricular bigeminy is unlikely, since QRSs are equidistant. PR interval shortens and a delta wave is seen on the wider beats (

oblique arrows

). This is intermittent pre-excitation. Every other QRS conducts antegradely over an accessory pathway with a delta wave and a short PR interval (WPW). The next beat proceeds down the AV node rather than the accessory pathway, the accessory pathway being in a refractory period. This is 2:1 conduction over the accessory pathway at a high sinus rate. This alternation in pre-excitation on the same ECG is likely secondary to a long AP refractory period, which blocks every other beat. Intermittent pre-excitation on separate ECGs is less reassuring, as it may be due to increased AV nodal conduction, rather than AP block. Intermittent pre-excitation during exercise is also less reassuring. The pathway is likely a left lateral pathway (QRS is negative but delta is positive in V

1

).

Figure 12.21 At first glance, this ECG shows a wide and tall R wave in V

1

, Q wave in leads I and aVL, and ST-segment depression localized to leads V

1

–V

3

. This may suggest posterior and lateral Q-wave MI, and the ST depression suggests this MI is acute. On further ECG analysis:

Chapter 13

Figure 13.1 Wenckebach 3:2 AV block. P–P intervals are typically regular. P–, non-conducted P wave.

Figure 13.2 Wenckebach 5:4 AV block. P–P intervals are regular.

PR progressively lengthens, whereas R–R progressively shortens.

This is due to the fact that the absolute PR interval increases less with each cycle, not compensating for the larger reduction of the preceding RP interval, P–P interval being stable (e.g., PR 200 → 280 → 300).

Figure 13.3 High-grade AV block.

Figure 13.4 Wenckebach AV block. Two groups of beats are seen, which raises the suspicion of a second-degree AV block. P2 is not conducted: this could be AV block or a block of a very premature PAC. Since P2 is not premature, the diagnosis is AV block. The clue to Wenckebach is the progressive PR prolongation, especially manifest when comparing P3R to P1R (P3R <P1R) and the progressive R–R shortening before the block.

Figure 13.5 ECG of a patient presenting with palpitations. Looking at parts 1 and 2 of this ECG, no P wave is seen and one might think the patient has a junctional rhythm.

Sinus rhythm with a very long PR interval should be considered in any case of presumed junctional rhythm

. The pause between 1 and 2 unveils the diagnosis. P waves are seen: P1 is a blocked P wave, P2 and P3 are conducted with a progressively longer PR interval. Thus, the patient has a Mobitz type 1 AV block with a very long cycle. Outside P2 and P3, PR interval is very long with P waves falling onto T waves (fusion of P and T). Palpitations are due to simultaneous atrial and ventricular contractions.

Figure 13.6 Third-degree AV block with regular P rate and regular QRS rate, unrelated to each other. Many P waves fall onto the QRS–T complexes and appear as notches over QRS or T.

PR interval is variable but R–R interval is regular, which implies AV dissociation and, in this case, complete AV block.

Figure 13.7 Regular, slow QRS rate of ~33 bpm. P rate is mainly regular at ~75 bpm. There is AV dissociation, with no evidence of any P-wave conduction (as also evidenced by the regular QRS escape rhythm). This is complete AV block. P’ could be a PAC or a retrogradely conducted P wave (patients with abnormal AV conduction may have a preserved VA retrograde conduction).

Figure 13.8 At first glance, the rhythm seems to be sinus bradycardia, ~40 bpm, and the waves that follow QRS complexes seem to be U waves. However,

in any sinus bradycardia of 40–50 bpm, one must verify whether the true rhythm is, in fact, a sinus rhythm of 80–100 bpm with 2:1 AV block.

The presumed U waves are actually P waves as they march out with P waves preceding the QRS complexes (

arrows

).Thus, the rhythm is a sinus rhythm with 2:1 AV block. In 2:1 AV block, one cannot tell if the dropped QRS is preceded by progressive PR prolongation or not, i.e., Mobitz I or II. In order to say Mobitz I or II in 2:1 AV block, analyze the following:

Figure 13.9 Outside the PVC, the rhythm seems regular. But on further analysis, there is some R–R irregularity.

Figure 13.10 P blocks (

arrow

) without being premature and without progressive PR prolongation before the dropped beat, or PR shortening after the dropped beat. This implies Mobitz II AV block,

further suggested by the wide QRS

. The rate is ~60 bpm and the patient is asymptomatic, which may falsely suggest that the block is innocuous. In fact, this block is ominous because it is likely Mobitz II not Mobitz I, with a class I indication for pacemaker placement.

That is why it is important to carefully analyze every small pause. A benign Mobitz I or a blocked PAC may simulate the malignant Mobitz II block.

Figure 13.11 Note the block of a P wave (

vertical arrow

). This blocked P wave is not premature, and therefore the diagnosis is AV block. This blocked P wave is not preceded by any change in PR interval, even when PR intervals before and after the blocked P wave are compared (

bars

), which is concerning for a Mobitz II AV block. However, note that the P–P interval preceding the pause is lengthening progressively, a hint to an increase in vagal tone causing the AV block (

line of arrows

). Therefore, this is an AV nodal block, an equivalent of Mobitz I AV block. Also, the narrow QRS argues against Mobitz II AV block. Note that a junctional escape complex is seen after the pause (

horizontal arrow

), and coincides with the subsequent sinus P wave (

arrowhead

), preventing it from getting conducted: this is isorhythmic AV dissociation over one beat.

Figure 13.12 Mobitz I vs. Mobitz II AV block. (1) is the right bundle, (2) is the left bundle, (3) is the left anterior fascicle, (4) is the left posterior fascicle.

Figure 13.13 Complete AV block, with underlying sinus tachycardia (

arrows

point to sinus P waves), and a wide QRS escape of ~25 bpm. The escape has the morphology of pseudo-RBBB + LAFB. It may be a junctional escape with RBBB + LAFB; however, short of a baseline ECG showing RBBB + LAFB, the escape should be considered ventricular. The RBBB morphology suggests a left ventricular origin, while the LAFB morphology suggests a posterior origin. Overall, the block is infranodal and the escape originates from the LV posterior wall close to the posterior fascicle. The underlying sinus tachycardia indicates that the complete AV block is due to an intrinsic conduction disease, rather than a high vagal tone or drugs.

Figure 13.14 Second-degree Mobitz II AV block, with 3:2 block alternating with 2:1 block (

arrows

point to P waves). In lead V

1

, one can see that on the conducted beats, RBBB alternates with LBBB. Beside Mobitz II, the alternation of RBBB and LBBB is indicative of infranodal AV block. In fact, QRS is dropped when both bundles simultaneously block in a patient with underlying RBBB, LBBB, or alternating RBBB and LBBB.

Figure 13.15 P waves and QRS complexes are dissociated on most beats, with most P waves not conducted to the ventricles (

blue arrows, solid and dashed

). One knows that these P waves are not conducted by the fact that: (1) they fall too close to the QRS complexes or there are ≥2 P waves for every QRS; (2)

the R–R interval is steady despite varying PR distance

; if some P waves were to conduct at various PR intervals, the R–R interval would vary as well. Two P waves are conducted (

gray arrows

), and this is indicated by the fact that their R–R interval (

gray double-arrows

) is shorter than the remaining, dominant, R–R interval (

blue double-arrows

); and by the fact that QRS following these P waves is narrow (ventricular capture from a sinus-originating stimulation).

Figure 13.16 Another example of a high-grade AV block. Most P waves are not conducted (

blue arrows

) and a wide ventricular escape rhythm is seen. Occasionally, P wave conducts (

gray arrows

), and this manifests as a shorter R–R interval (

double-arrows

) and a narrow QRS complex. Note that the P–P interval containing a QRS is shorter than the P–P interval that does not contain a QRS (ventriculophasic sinus arrhythmia). The PR interval of the conducted P waves is ~200 ms (not significantly prolonged), which, along with the wide escape, indicates an infranodal block.

Figure 13.17 AF with a ventricular rate that is slow and mostly regular. This is AF with an almost complete AV block and a wide, regular escape rhythm that is ventricular in origin. Two narrower QRS complexes occur at a shorter R–R distance and signify occasional AV conduction. This is AF with a high-grade rather than a complete AV block.

Figure 13.18 4:3 Mobitz I SA block. Progressive lenghtening of the sinus impulse-to-P-wave interval, with shortening of the P–P interval, before the drop of one full P–QRS complex. It mimics a sinus pause.

Figure 13.19 A whole P–QRS drops, which may be consistent with a sinus pause. On looking more carefully, group beating is seen. In addition, the P–P as well as the R–R intervals progressively shorten before the P–QRS drops. This is a 5:4 SA Wenckebach block; it is not AV Wenckebach, as PR interval is constant and the whole P–QRS drops. This is not sinus arrhythmia, as in the latter, P–P interval progressively, rather than abruptly, lengthens (not an abrupt jump from the shortest P–P to the longest P–P).

Figure 13.20 3:2 type II SA block. Both P and QRS intermittently drop (stars).

Figure 13.21 Sinus arrest or third-degree SA block with a ventricular escape rhythm. The fact that the escape is ventricular (wide and slow, originating from below the AV node), proves that there is AV infranodal disease in addition to the SA nodal block.

Figure 13.22 No P wave is seen → complete SA block vs. AF with small fibrillatory waves. The rhythm is a slow, wide complex rhythm at a rate of 30 bpm, suggesting a ventricular escape rhythm (slow and wide). This means that, in addition to the SA block, there is an infranodal, high-grade AV block. In fact, in the absence of AV infranodal disease, SA block should lead to a junctional rather than ventricular escape rhythm.

Figure 13.23 Outside PVCs, the rhythm seems regular, but, on further analysis, there is some R–R irregularity. Analyze the P–QRS relationship: some QRS complexes seem to be preceded by P waves with a consistent PR relationship (conducted P waves, called P’ and marked by

blue arrows

). On the other hand, some QRS complexes are not preceded by any P wave (junctional QRS). This suggests a sinus rhythm and a junctional rhythm competing at a rate of ~60 bpm. When the sinus rhythm slows a bit, the junctional rhythm takes over. Note that during the junctional rhythm, sinus P waves occur regularly, dissociated from the QRS complexes and falling around them, marked by the

gray arrows

. There is no AV block, as P wave gets conducted whenever it occurs long enough after the QRS and whenever the junctional rhythm does not kick in close to it.

Figure 13.24 1, right bundle; 2, left bundle; 3, left anterior fascicle; 4, left posterior fascicle.

Figure 13.25 Suppose that a tachycardia-mediated LBBB has developed at a rate of 100 bpm (R–R interval = 600 ms). When the heart rate slows back down to 100 bpm, the LBBB persists. For a 600 ms interval between impulses reaching the AV node, it takes the left bundle that is now blocked an extra 75 ms to be depolarized, so that the interval between the left bundle depolarization and the next impulse is 600 – 75 = 525 ms. This perpetuates the LBBB even at a rate <100 bpm. The left bundle may recover once the cycle length is 675 ms (HR = 88).

Chapter 14

Figure 14.1

The paced QRS morphology varies according to the vector of depolarization. Analyze the QRS morphology in lead I, the inferior leads, and the precordial leads V

1

–V

6

.

In RV apical pacing, the QRS is characterized by a left axis and by being negative in the inferior leads II, III, and aVF. It has an LBBB morphology, and similarly to LBBB, QRS may be negative in V

1

–V

3

and upright in V

4

–V

6

, I, and aVL. However, the vector of depolarization may also be looking away from all precordial leads, leading to a deep negative QS in V

1

–V

6

, and may be looking away to the right, leading to a negative QRS in lead I. If the vector is looking to the right, the QRS may paradoxically be upright in leads V

1

and V

2

, simulating LV or BiV pacing (especially if V

1

is high in relation to the heart).

Figure 14.2 Ventricular pacing regularly tracking the sinus P activity (DDD PM, VAT action). The paced ventricular complexes have an LBBB morphology with QS or rS pattern that extends further to the left (V

1

–V

6

) than in a typical LBBB (in which QRS often transitions to positive in lead V

4

). The large Q wave in lead I is not typical of RV apical pacing but may be seen if the vector of depolarization is turned a bit rightward. BiV pacing is unlikely, because of the negative QRS in V

1

–V

2

. This is not RVOT pacing, because in RVOT pacing the depolarization vector is directed up to down, and the QRS is consequently [+] in the inferior leads.

Figure 14.3 VVI pacing in a patient with no P wave (sinus arrest or subtle AF). RV lead is in the RVOT (QRS is positive in the inferior leads). Off/on failure to capture is noted (

arrow

, failure to capture). This is actually a temporary pacemaker.

RVOT is an unstable position for a temporary pacemaker.

Figure 14.4 Ventricular pacing that consistently tracks a preceding sinus P wave. This is AV sequential pacing (probable DDD mode). Note that QRS is negative in lead I and starts with a Q wave, and QRS is positive in V

1

: this is typical of BiV pacing. Also, PR is very short to ensure ~100% pacing, which is characteristic of BiV programming. Q or qR in lead I is rare in RV pacing, but is often present with BiV pacing (90%). If initially present with BiV pacing, the loss of Q wave in lead I is 100% predictive of loss of LV capture.

Figure 14.5 Atrial flutter with variable conduction. Note that when the R–R interval increases to >1200 ms (which corresponds to 6 large boxes, or a rate of 50 bpm), V pacing kicks in at an interval of 1000 ms (60 bpm). This is called

hysteresis

, wherein V pacing is initiated only when the heart rate drops well below the programmed pacing rate, allowing a reduction of V pacing.

Figure 14.6 Prominent R wave in V

1

–V

2

may suggest BiV pacing. However, there is no Q wave in lead I, which suggests that RV pacing is more likely (RV apical pacing by the fact that QRS is negative in the inferior leads and in V

4

–V

6

).

V

1

may be placed one intercostal space lower and the ECG repeated; QRS of V

1

should become negative in RV apical pacing.

Figure 14.7 DDD pacemaker timing intervals.

Figure 14.8 Sinus/atrial tachycardia with atrial rate > upper rate. Case where TARP (total atrial refractory period) = URI (upper rate interval), which leads to 2:1 ventricular pacing pattern. Other abbreviations as in Figure 14.7.

Figure 14.9 Sinus tachycardia with pseudo-Wenckebach ventricular pacing pattern. In contrast to Figure 14.8, PVARP is short with TARP <URI. This shortened PVARP allows AS to fall outside PVARP and get tracked. AVI extends after every cycle, until one beat drops. It is a pseudo-Wenckebach rather than a true Wenckebach pattern, as the R–R interval remains steady rather than shortens.

Figure 14.10 Difference between maximal tracking rate, mode-switch rate, and maximal sensor rate.

Figure 14.11 Various lead configurations for pacemakers (first two images) and ICD (third image).

Figure 14.12 Example of a “quick look” or “summary” screen of pacemaker/ICD interrogation.

Figure 14.13 Insulation break and lead fracture.

Figure 14.14 Triggers and mechanisms of PMT.

Figure 14.15 Fusion, pseudofusion, and ventricular safety pacing.

Figure 14.16 In fusion beats, the native conduction reaches the ventricle around the same time as the expected pacemaker spike, leading to a fusion between the native and paced QRS complex. In pseudofusion, the QRS seen is purely the result of the native conduction, the pacemaker spike does not result in any ventricular stimulation; the resulting QRS is similar in morphology to the intrinsic QRS.

Figure 14.17 Various patterns of LV activation in LBBB.

Black arrows

indicate the spread of electrical activation across the conduction system,

dashed arrows

indicate the spread of activation across the LV.

(A)

In most LBBB patterns, on the longitudinal axis, the LV is slowly depolarized from mid-level or apex to base. This is also the case in RV apical pacing, including RV pacing that is performed as part of BiV pacing.

(B)

In LBBB, on the short-axis view, the LV is depolarized from the septum to the lateral wall. The depolarization starts at the anterior, mid, or posterior septum, and spreads towards the anterior wall and then the lateral wall. Combining both longitudinal and short-axis views, the

posterolateral basal

site is seen as the site of latest activation, but any

basal

site, including

anterior basal

, is relatively late.

(C)

The pattern of activation of the papillary muscles is shown on a short-axis view. The posteromedial papillary muscle is activated sooner than the anterolateral papillary muscle; this is less prominent in the case of a more anterior trans-septal breakthrough of activation.