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Bedside Cardiology
Achyut Sarkar
1:
Bedside Cardiology: Is It Evidence-based?
Dyspnea
Jugular Venous Pressure
Pulse
Apical Impulse
Heart Sound
Murmur
Conclusion
References
2:
Functional Classification
NYHA1,2
Changes
Uncertain Diagnosis
No Heart Disease: Predisposing Etiologic Factor
No Heart Disease: Unexplained Manifestation
No Heart Disease
Criticism of NYHA Classification System
Canadian Cardiovascular Society Functional Classification of Angina Pectoris4
Specific Activity Scale5
Class I Activities
Class II Activities
Class III Activities
UCLA Congenital Heart Disease Functional Class6
WHO Classification of Functional Status in Pulmonary Arterial Hypertension7
The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation (SAF) Scale8
Duke Activity Status Index (DASI)9
Six-Minute Walking Test
3:
A Triad: Cardinal Symptoms in Cardiovascular System
Dyspnea
Definition
Physiologic Components of Dyspnea
Basic Mechanism
Length-Tension Inappropriateness/Neuromechanical/Efferent-Afferent Dissociation
Dyspnea in Heart Failure
Muscle Hypothesis
Lung Hypothesis
Assessment of Dyspnea
Severity
Formal Measurement of Dyspnea
Orthopnea
Paroxysmal Nocturnal Dyspnea
Trepopnea
Platypnea
Palpitation
Etiology
Cardiac Arrhythmias
Anxiety or Panic Disorder
Nonarrhythmic Cardiac Cause
Extracardiac Cause
Drugs
Approach
Symptoms
Circumstances
Chest Pain
Cardiac Chest Pain
Angina
Acute Myocardial Infarction (AMI)
Pericardial Pain
Pulmonary Embolism
Aortic Dissection
Chest Wall Pain
Gastrointestinal Diseases
Clinical Approach
4:
A Triad: Minor Symptoms in Cardiovascular System
Fatigue
Edema and Weight Gain
Hemoptysis and Cough
Hemoptysis: Assessment (Table 4-1)
Cough: Assessment
5:
A Triad: Cardinal Symptoms in Left-to-right Shunt
Pulmonary Problems in Left to Right (L-R) Shunt
6:
A Triad: Cardinal Symptoms in Congenital Cyanotic Heart Disease
Paroxysmal Hypoxic Spell
Mechanism
Associated Finding
Squatting
Hyperviscosity Syndrome
7:
Syndromes and Measurements
Syndromes
Marfan Syndrome (Figs 7-1 and 7-2)
Down Syndrome (Trisomy 21) (Fig. 7-3)
Turner Syndrome (Monosomy X) (Fig. 7-4)
Noonan Syndrome (Autosomal Dominant) (Fig. 7-5)
Holt-Oram Syndrome (autosomal dominant) (Fig. 7-6)
Williams Syndrome (Fig. 7-7)
Conotruncal Anomaly Face (Fig. 7-8)
Measurements
Hypertelorism
Low Set Ears (Figs 7-10 and 7-11)
Low Hairline (Fig. 7-12)
Short Neck
Upper-to-lower Segment Ratio
Span
High Arched Palate
8:
Clinical Instruments
Stethoscope
Bell vs Diaphragm
Tubing
Electronic (Digital) Stethoscope5
Ultrasound Stethoscope (Point-of-care echocardiography) (Fig. 8-1)
Sphygmomanometer
Manometer
Cuff Size (Table 8-1)
9:
A Triad: Cardinal Signs in Congenital Cyanotic Heart Disease
Cyanosis
Bluish Skin, No CCHD
Differential Cyanosis (Fig. 9-1)
Reverse Differential Cyanosis
Approach
Hyperoxia Test
Anemia
Clubbing
Mechanism
How to Detect Early Clubbing?
Cyanosis without Clubbing in CCHD
Clubbing without Cyanosis
Unilateral Clubbing
10:
Jugular Venous Pulse
Veins
Jugular Venous Pressure (JVP)
Basic Hemodynamics
Reference Point
Body Position (Fig. 10-1)
Effect of Respiration
Method
Normal Pressure and Units
Normal Venous Pulse
Hemodynamic
Time Sequences (Fig. 10-5)
Abnormal Venous Pulse
Large and Giant ‘a’ Waves (Figs 10-7 and 10-8)
Cannon Wave
Absent ‘a’ Wave
Abnormal x Descent
Abnormal v Wave (Fig. 10-9)
Abnormal y Descent
Specific Situations
CHF: Hepatojugular Reflux (Abdominojugular Reflux)
Jugular Venous Pulse in Arrhythmia
Jugular Venous Pulse in Pericardial Disease
Jugular Venous Pulse in Congenital Cyanotic Heart Disease
Other Venous Pulses
Hepatic Pulse
Upper Arm Veins
11:
Arterial Pulse
Origin of Pulse
Proximal Aortic Pulse (Fig. 11-1)
Carotid Pulse
Changes during Peripheral Transmission (Fig. 11-2)
Basic Method (Table 11-1)
Rate and Rhythm
Rate of Rise
Volume
Character: Double-peaked/Double-beating Pulse (Fig. 11-3)
Bisferiens (Double-peaked) Pulse
Dicrotic (Double-peaked) Pulse
Anacrotic (Double-peaked) Pulse/Pulsus Parvus et Tardus
Character: Rapidly Rising, High Volume, Rapidly Collapsing Pulse (Fig. 11-4)
Character: Pulsus Alternans (Mechanical Alternans)
Character: Pulsus Paradoxus (Table 11-7)
Condition of Arterial Wall
Synchrony
Pulse in Hypertension
Pulse in AR
Pulse in HOCM
Pulse in Coarctation of Aorta (Fig. 11-5)
Arterial Bruit (Murmur) and Thrill
12:
Blood Pressure
Definition
Determinants
Pulse Pressure
Mean Pressure
Proportional Pulse Pressure
Korotkoff Sound
Korotkoff Sound: Five Phases
Diastolic Pressure
Auscultatory Gap
BP in Two Arms
Arm vs Leg Pressure
How to Measure Leg Pressure (Figs 12-1 and 12-2)
Hill's Sign
Coarctation of Aorta
Checkpoints during BP Measurement
Blood Pressure in Thigh
BP Measurement in Children
Flush Method
Doppler Method
Oscillometric Techniques
BP Measurement in Arrhythmia
BP Measurement in Shock
Exercise and BP
Pseudohypertension
White Coat Hypertension
Masked Hypertension
Orthostatic Hypertension
Vascular Stiffness
13:
Palpation
Apical Impulse (Fig. 13-1)
Right Ventricular Impulse
Biventricular Hypertrophy/Impulse (Fig. 13-7)
Arterial Pulsation
Heart Sound
Atrial Impulse
Inward Retractions (Fig. 13-9)
Thrill
Special Clinical Conditions
14:
First Heart Sound (S1)
Mechanism
Timing
Splitting
Physiological
Pathological
Intensity (Table 14-1)
Increased Intensity (Table 14-2)
Decreased Intensity (Table 14-3)
Varying Intensity
Sound Surrounding S1 (Fig. 14-1)
15:
Second Heart Sound (S2)
Mechanism
Splitting
Physiological Splitting (Fig. 15-1)
Pathological Splitting (Table 15-1)
Wide Splitting (Persistent Nonfixed Splitting) (Table 15-2)
Wide Fixed Splitting (Fig. 15-3)
Splitting in Pulmonary Hypertension
Reverse Splitting (Fig. 15-4)
Persistently Single (Table 15-4)
Intensity
16:
Third Heart Sound (S3)
Physiology (Fig. 16-1)
How to Detect it
Left Sided vs Right Sided S3
Physiologic S3 vs Gallop Sound
Gallop Sound
Physiologic S3
How to Differentiate Physiologic S3 vs Pathologic S3
S3 due to High Flow
S3 in Ventricular Dysfunction
17:
Fourth Heart Sound (S4)
Physiology (Fig. 17-1)
How to Detect it
Pressure Over Load
Raised End Diastolic Pressure (Fig. 17-2)
Right-sided S4
AV Block
Others
18:
Ejection Sound
Pulmonary Valvular Click (Fig. 18-1)
Pulmonary Stenosis vs ASD
Pulmonary Vascular Click
Aortic Valvular Click (Fig. 18-2)
Bicuspid Aortic Valve
Aortic Vascular Click
Clinical Importance of Click
19:
Nonejection Sound
Midsystolic Click (Fig. 19-1)
Other Causes of Nonejection Click (Table 19-1)
Pseudoejection Sound
Mitral Opening Snap (OS)
Tricuspid Opening Snap
Pericardial Sound
Pericardial Knock
Pericardial Rub
Mediastinal Crunch (Hamman Sign)
Prosthetic Sound (Fig. 19-5)
Mechanical Prosthesis
Ball-and-cage Valve
Tilting-disk Valve
Bioprosthesis
20:
Murmur
Systolic Murmur (Table 20-2) (Fig. 20-3)
Ejection Systolic Murmur (Midsystolic Murmur) (Table 20-3)
Physiology (Fig. 20-4)
Aortic Stenosis (Fig. 20-5)
Hypertrophic Cardiomyopathy (HCM)
ESM in Presence of Severe AR
Aortic Sclerosis
Pulmonary Stenosis (Fig. 20-6)
PS with VSD (Fig. 20-7)
Peripheral Pulmonary Artery Stenosis
Pansystolic Murmur
Physiology
Mitral Regurgitation (Fig. 20-8)
Tricuspid Regurgitation
VSD (Fig. 20-9)
Early Systolic Murmur
Acute MR (Fig. 20-10)
Primary TR (Table 20-5)
Other Causes
Late Systolic Murmur
MVP
Papillary Muscle Dysfunction
Diastolic Murmur (Table 20-6 and Fig. 20-11)
Aortic Regurgitation
Acute Aortic Regurgitation
Pulmonary Regurgitation (Fig. 20-13)
Hypertensive
Normotensive
Dock Murmur
Mitral Stenosis
Other Causes of LV Inflow Obstruction
Tricuspid Stenosis
Austin Flint Murmur
Carey-Coombs Murmur
Chronic Renal Failure
Other Causes
Continuous Murmur (Table 20-7)
Systolodiastolic Murmur (Mimicking Continuous Murmur)
PDA (Fig. 20-16)
ALCAPA
Coronary Arteriovenous Fistula (CAVF) (Fig. 20-17)
RSOV (Fig. 20-18)
Pulmonary Arteriovenous Fistula
Venous Hum (Fig. 20-18)
Mammary Soufflé
21:
Innocent Murmur and Sound
Prevalence
How to Establish the Innocence (Table 21-2)
Still's Murmur
Functional Murmur in Adult
Innocent Pulmonary Murmur
Supraclavicular Murmur/Bruit (Figs 21-1A and B)
Pulmonary Branch Murmur
Diastolic Murmur
22:
Dynamic Auscultation
Prompt Sauatting
Hemodynamics
Effect
AR
HOCM
AS, PS
MR, VSD
Procedure (Figs 22-1A and B)
Standing
Hemodynamic
Effect
HOCM
AR, PS, MR, TR
S4-S1 vs S1-Ejection Sound
Physiological S3 vs Pathological S3
MVP
Continuous Murmur of Patent Ductus Arteriosus (PDA) vs Venous Hum
Procedure
Valsalva
Hemodynamic
Effect (Fig. 22-2)
Procedure (Fig. 22-3)
Muller Maneuver
Isometric Handgrip
Hemodynamic
Effect
Procedure
Transient Arterial Occlusion
Hemodynamic
Effect
Procedure
Passive Leg Raising
Premature Beat
Respiration
Pharmacologic Agent
Vasodilator
Vasoconstrictor
23:
Is your Patient in Heart Failure?
Bedside Assessment of Heart Failure (Table 23-2)
Dyspnea on Exertion
Orthopnea
Pulmonary rales/wheeze
Increased JVP
Edema
Fatigue
Clinical Aids
Proportional Pulse Pressure
Orthostasis
Valsalva Maneuever
Instrumental Aids
Different Criteria for Heart Failure
Framingham Criteria for Heart Failure10(Table 23-3)
Boston Criteria for Heart Failure (Table 23-4)
Ross Criteria of Heart Failure12(Table 23-5)
New York University Pediatric Heart Failure Index (PHFI) (Table 23-6)
24:
Clinical Assessment: Pulmonary Hypertension
Definition
Clinical Classification of PH (Table 24-1)
Clinical Features
Clinical Impression
S2
Splitting in Pulmonary Hypertension
Intensity
Pulmonary Regurgitation Murmur
Hemodynamics of PH
Clinical (Table 24-3)
Right Heart Catheterization (Table 24-4)
Echocardiogram (Table 24-5)
25:
Segmental Approach in Congenital Heart Disease
Connection and Relation
Segmental Approach
Cardiac Position
Cardiac Malposition
Dextrocardia
Right Sided Heart
Intracardiac Abnormalities in Right Sided Heart
Situs
Abdominothoracic Situs
Abdominovisceral Situs
Situs: Great Vessels
Thoracovisceral Situs
Thoracovisceral Situs
Atrial Situs
Right and Left Atrium
Morphological Identification of Ventricles
Right and Left Ventricles
Angiographic Identification of Ventricles
Angiographic Identification
Situs Solitus (SS)
Situs Inversus (SI)
Sinus Ambiguous
Heterotaxy
Atrioventricular Connection
Connection
A-V Alignment
Double-inlet Ventricle
Van Praagh
Single-inlet
Common-inlet Ventricle
A-V Connection: Concordance
A-V Connection: Discordance
A-V Alignment: Overriding
A-V Alignment: Straddling
A-V Alignment: Both Overriding and Straddling
Loop
Loop: CC-TGA
Loop: TGA
Bulboventricular Loop
SI, AV Dicordance (d-loop), Transposition (corrected transposition) with D-malposition of Aorta
SI, AV Concordance (I-loop), Transposition with L-malposition of Aorta
Ventriculoarterial Connection
Tal Geva Classification
PS Rao Classification
Anderson Classification
Ventriculoarterial Connection
Normal Ventriculoarterial Connection
Transposition
Double Outlet
Single Trunk
Conus
Great Artery Spatial Relations
Spatial Relation: Anatomically Corrected Malposition (S, D, L)
Anatomically Corrected Malposition
Spatial Relation: Aorta in CC-TGA
Spatial Relation: Aorta
26:
Clinical Approach: Congenital Cyanotic Heart Disease
Pathophysiological Classification
Tetralogy Physiology
Transposition Physiology
Parallel Circulation
Eisenmenger Physiology (EP)
Systemic PAH with Shunt Reversal
Common Mixing Physiology
Mixed Physiology (Effectively Two Physiologies)
History-onset of Cyanosis
Natural History Suggestive of Increased Flow
Cyanosis with Increased Flow
History
Gradual Cool Down of Symptoms of Increased Flow/CHF
General Examination
Differential Cyanosis
Pulse
Absent Lower Limb Pulsations
JVP
Palpation
Thrill
Apical Impulse (Commonest is Rv Type Apex)
Heart Sound
S1
S2
S3/S4
Ejection Click
Murmur
Systolic Murmur
Diastolic Murmur
Continuous Murmur
Thus, from Clinical Examination, Initial Impression—CCHD with
Next Step: To Look at X-ray Chest for Vascularity
X-Ray Chest with Increased Flow
Increased flow: TGA
Increased flow: TAPVC
Increased flow: Truncus Arteriosus
ASD, Eisenmenger Physiology
Thus, X-Ray chest may identify the individual entities amongst the group.
X-Ray Chest with Decreased Flow
Then, Probabilities are Shortlisted to
Then, to look at ECG:
ECG: Right, occasionally left axis, counterclockwise depolarization
Otherwise, ECG may show right axis; vectorcardiogram showing clockwise depolarization in frontal plane.
27:
Clinical Approach: Tetralogy Physiology
Tetralogy Physiology
Tetralogy Physiology: Hemodynamics
Tetralogy Physiology: How to Grade Severity*
Mild
Moderate
Severe
Extremely Severe
Under Umbrella of Tetralogy Physiology
Group I (Pure)
Group II (Mixed physiology)
Tetralogy Physiology: Fallot's Tetralogy
Tetralogy Physiology: VSD, Pulmonary Atresia
X-Ray Chest: VSD, Pulmonary Atresia
Tetralogy Physiology: DORV, PS
Tetralogy Physiology: CC-TGA, VSD, PS
Tetralogy Physiology: Univentricular Connection, PS
Tetralogy Physiology: Univentricular Connection, PS
Noninverted Outlet Chamber
Inverted Outlet Chamber
Tetralogy Physiology: TGA, VSD, PS
Tetralogy Physiology: Tricuspid Atresia, VSD, PS
28:
Clinical Approach: Eisenmenger Physiology
Syndrome/Complex
Incidence
Who are Clinically Susceptible
Incidence in Large Shunt
Congenital, Systemic-to-Pulmonary Shunts Associated with Pulmonary Arterial Hypertension (PAH)
Diseases Leading to Eisenmenger Syndrome
Great Artery Level
Ventricular Level
Atrial Level
Both Atrial and Ventricular Level
Diseases Leading to Eisenmenger Syndrome
Mixing Physiology with Unobstructed Pulmonary Flow
Transposition Physiology
Onset of Eisenmenger Syndrome
Sex Distribution
Presenting Symptoms
Dyspnea
Hemoptysis
Squatting
Triad
Eisenmenger: Cardiac Findings
Eisenmenger: Palpation
Eisenmenger: Auscultation
S2
Graham Steell Murmur
Eisenmenger Syndrome: ASD
Eisenmenger Syndrome: VSD
Eisenmennger Syndrome: PDA
Eisenmenger Complex
Eisenmenger Syndrome: Survival
Eisenmenger Syndrome: Poor Prognostic Markers
Eisenmenger Syndrome: Cause of Death
How to Assess that PAH is Hyperkinetic (Reversible) or Obstructive (Irreversible)
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