Clinical Medicine Interesting Facts

Clinical Approach to Central Chest Pain

2014-06-20T19:08:00.000+05:30

Clinical approach to “Central” Chest Pain

Differential diagnosis

Esophageal pain
- Esophageal spasm
- Esophageal reflux
Musculoskeletal pain
Anginal pain

History taking

Active process.
Direct questioning to check details and to confirm common understanding of the words.
Co-existing fundamentally different pain is also possible.

Characteristics of Angina “like” central chest pain

Site

Constant and characteristic for each patient (different for different patients).
Location is diffuse.
Not “inframammary”.

Character

Gripping/tight.
Not stabbing/sharp.

Severity

Unrelated to severity/duration of ischemia.
Silent ischemia: 50% of times.

Onset

Not abrupt.
Pain is either present or absent. It is not a background pain.

Duration and relief

Ischemia: 3-10 mins. Decreases with relaxation/rest/nitrates (Onset of action: 2-3 mins).
Infarction: pain > 30 mins. Any pain more than 30 mins without any subsequent evidence of myocardial infarction (Clinical, ECG, cardiac enzymes) - CARDIAC INVOLVEMENT UNLIKELY.

Initiation factor

Stable effort angina:
- Atherosclerotic plaque (leading to fixed coronary artery narrowing)
  - At rest and upto certain limit of effort: normal blood supply distally.
  - After certain limit: blood supply to distal region impaired, “angina” develops.
- Precipitated by: physical exertion, emotional stress, excessive meals, cold weather.
- Stereotype events: Rest (asymptomatic) –> Exertion (asymptomatic) –> more exertion (angina) –> Rest (asymptomatic)
Unstable angina/acute myocardial infarction:
- Plaque fissure
  - Thrombus –> intraluminal extension (Fixed component)
  - Chemical mediators –> VAsospasm (Dynamic component)
- Stereotype is lost
  - Angina: unexpected occurence, increased frequency and duration.
- Different cases have different proportion of:
  - THROMBUS ——— VASOSPASM (100% is called prinzmetal angina)
Symdrome X (Microvascular syndrome):
- Indistinguishable from Stable Effort Angina.

Confirmation of diagnosis

Stress Angina:
- Stress Testing: proves that chest pain is due to cardiac cause.
- Angiography: diagnosis of cause as coronary block.
Unstable Angina:
- Stress Testing: Potentially dangerous.
- Continuous ECG monitoring.
Syndrome X:
- Stress Testing: positive.
- Angiography: negative.

Cardiac vs esophageal pain

Chest pain > 30 min and ECG normal: Unlikely to be cardiac.
Chest pain decreasing with antacids: Esophageal.
Chest pain increased with deglutition of saliva: Esophageal.
Chest pain associated with dysphagia: Esophageal.

May be indistinguishable

Cardiac vs muscular pain

Chest pain induced by movement of part: Muscular pain.

Chest Radiograph: Cardiac Perspective

2014-06-20T19:04:00.000+05:30

Chest Radiograph

Congenital heart disease: Abnormal
Acquired heart disease: Usually Normal

PA view

Patient upright and breath held in full end inspiration.

Heart size

AP > PA view (as heart further from film in AP view).

Normal Chest Radiograph

Cardiac silhoutte (PA view)

Cardiac silhoutte (Lateral view)

Pulmonary vasculature

Heart size

Transverse cardiac diameter: \( \leq \) 16 cm in males and \( \leq \) 15 cm in females.
Cardiothoracic ratio: \( \leq \) 50%.

Analysis of Chest Radiograph

Cardiac shadow: ANATOMIC ASPECT.
Pulmonary vasculature: PHYSIOLOGIC ASPECT.
ORDER OF ANALYSIS
- Technical consideration
  - Overexposed: Pulmonary oligemia.
  - Underexposed: Increased pulmonary vasculature.
  - In expiration: Diffuse lung disease.
  - Rotated film: Abnormal heart size.
- Skeletal system
  - Pectus excavatum: Straightening of left heart border.
  - Straight back syndrome: Cardiomegaly.
  - Scoliosis.
  - Sternal depression & straight back syndrome: Associated with MVP.
  - Down syndrome: 11 pair of ribs & VSD.
  - Rib notching: Coarctation of aorta, pulmonary atresia, vena caval syndrome, Blalock Taussig Shunt.
- Upper abdomen
  - Gall stones, histus hernia in chest pain.
  - Situs.
- Lungs
- Cardiac shadow

Lungs

Look for co-existing lung diseases.
Pulmonary vasculature
- Increased
  - Pulmonary venous hypertension (PVH), PAH, pulmonary over-circulation.
- Decreased
  - Oligemia.
- Normal
  - DOESNOT EXCLUDE SIGNIFICANT MYOCARDIAL DISEASE, MILD VALVULAR DISEASE OR SMALL INTRA-CARDIAC SHUNT.
- Uneven

Abnormalities of Pulmonary circulation

Pulmonary venous hypertension (Close correlation exists between PCWP and extent of PVH in untreated patients)
- Stage 1 (< 12 mmHg)
  - Normal findings.
- Stage 2 (12 - 18 mmHg)
  - Pulmonary vein dilation. D/D: Basal emphysema.
    - Upper lobe diversion.
- Stage 3 (18 - 22 mmHg)
  - Interstitial edema. D/D: Non Cardiogenic Pulmonary Edema.
    - Perihilar haze.
    - Peribronchial cuffing.
    - Kerley B lines - Interlobular edema.
    - Kerley A lines - Thickened inter lobular septum.
- Stage 4 (> 22 mmHg)
  - Alveolar edema. D/D: Non Cardiogenic Pulmonary Edema.
    - Perihilar.
    - Can be patchy/asymmetrical.
    - Pleural effusion.
- Chronic PVH (Causes)
  - PAH.
  - Pulmonary hemosiderosis (bileteral, diffuse, granular).
  - Pulmonary ossicles (Calcified, basal, nodules upto 1 cm).
Pulmonary arterial hypertension (PAH)
- Definition: PAsysP > 30 mmHg.
- Features:
  - Central PA increased (D/D: Hilar lymphadenopathy - lymphadenopathy is more lobular).
  - Peripheral PA decreased.
  - Calcification of central PA.
Pulmonary over-circulation
- Pulmonary:systemic circulation < 2:1
  - No changes.
- Pulmonary:systemic circulation \( \geq \) 2:1
  - Central PA increased.
  - Peripheral PA increased (extending > lateral 1/3rd of lung field).
  - LOOK FOR CYANOSIS:
    - Present: Bidirectional shunt.
    - Absent: Left to right shunt.
Bronchial circulation
- Severe RV outflow obstruction.
Pulmonary oligemia
- TOF.
- Cardiac tamponade (Restricted filling of RV).
Uneven vascularity
- Pulmonary disease (Commonest cause).
- Cardiogenic causes
  - Pulmonary thrombo-embolism.
  - Shunt surgery.
  - Pulmonary arterial stenosis.
  - Pulmonary AV fistula.

Cardiac shadow

Systemic veins
- SVC
  - Increased flow: Supra-cardiac anomalous pulmonary vein return.
  - Increased pressure: Rt HF, Tricuspid valvular disease, Cardiac tamponade, Constrictive pericarditis.
  - Obstruction: Mediastinitis, Mediastinal tumor.
- Azygous vein
  - IVC obstruction.
- IVC
  - Rt HF.
  - TR/TS.
Right atrium dilation
- Increased prominence of lower half of right heart border.
Right ventricle dilation
- PA view
  - Apex outwards and upwards.
  - Gross dilation: forms Lt heart border and bump just below pulmonary trunk.
- Lateral view
  - Decreased retro-sternal space.
- Pulmonary trunk
  - Increased
    - PAH: associated peripheral pruning.
    - Pulmonary over-circulation: associated pulmonary plethora.
    - Post stenotic/idiopathic: associated normal pulmonary vasculature.
  - Decreased
    - TOF.
    - Pulmonary atresia.
  - Absent
    - Corrected transposition of Great Vessels.
Left atrium dilation
- Increased carinal angle.
- Right sided double density (marked dilation: can form right border).
- Denting of esophagus (Lateral view, Barium swallow).
- Straightening/convexity of left atrial appendage.
Left ventricle
- Hypertrophy
  - Increased Lt heart border convexity.
- Dilatation
  - PA: Apex outwards and downwards, increased cardio-thoracic ratio.
Aorta
- Increased Ascending Aorta
  - Post-stenotic dilation.
  - Aneurysm.
- Increased Aortic Knuckle
  - Aneurysm.
  - PDA.
  - Pulmonary atresia.
- Increased Descending Aorta
  - Aneurysm.
- Increased Thoracic Aorta
  - Systemic hypertension.
  - Aortic regurgitation.
Pericardium
- Pericardial effusion
  - Non-specific globular enlargement.
  - Normal pulmonary vasculature.
- Congenital absence of pericardium
  - Left displacement of cardiac shadow.
Cardiac calcification
- Fluoroscopy better than Plain Films.
- VALVE CALCIFICATION
  - Aortic valve
    - PA view: over spine (may be obscured)
    - Lateral view: (see figure)
  - Mitral valve
    - PA view: Lt side of spine
    - Lateral: (see figure)

Relationship between vertebral bodies and spinal cord levels

2013-11-26T17:14:00.001+05:30

Relationship between vertebral bodies, spinal cord and spinal radicles

Introduction

Recently, while taking a bedside clinic on neurology, I along with my students realised that we knew so little about the vertical relationship between vertebral bodies, spinal cord and radicles which are coming out of the cord. We got confused for the lowest part of spinal cord (conus) and cauda medullaris.

I thought of writing my know how on the subject and try to see that if doubt solves.

Assumption of the model

We know that in adult the spinal cord ends at lower end of LV1 (1st lumbar vertebral body). We also know that for the neonate (new born), this level is at LV4.

So we can assume that at the start spinal cord ended at SV4, meaning both spinal cord and its protective cover (vertebral bodies) were at the same level. With the growing fetus, vertebral body grows (lengthens) caudally while spinal cord (being composed of neurons with very limited growth potential) does not grow to the same length leading to the confusion about the levels of vertebral body, spinal cord and radicles.

Naming the radicles, vertebral bodies

1st nerve root arises out between occiput and 1st vertebral body, it is known as 1st cervical nerve root

So for the cervical nerve roots, a particular numbered nerve root comes out above that particular numbered vertebral body. Example, 3rd cervical radicle comes out of the vertebral body above CV3 (between CV2 and CV3).

Nerve root coming out between CV7 and TV1 is known as 8th cervical nerve root (not 1st thoracic nerve root as expected). And 1st thoracic nerve root arises out between TV1 and TV2. So, for thoracic vertebra downwards a particular numbered nerve root comes out below that particular numbered vertebral body.

Also, the final nerve root (4th sacral nerve root) arises between SV4 and coccyx.

Situation in fetus

Following figure depicts the situation in fetus where vertebral bodies are being developed around the spinal cord. Length of vertebral bodies is same as that of the spinal cord.

In the above figure, it can be seen that the nerve roots are arising from the respective spinal levels and are coming out of the vertebral foramina. So, spinal levels correspond to the respective vertebral bodies level.

Situation in adult

As described earlier in assumption section, with growth of fetus, vertebral bodies grow more than the spinal cord leading to the discrepancy in the respective levels.

The following figure depicts the situation in adult.

Implications

The above sketch shows following implications:

Spinal cord ends at lower end of LV1, meaning that we cannot have myelopathy below LV1 level. The area is known as cauda equina region. Any lesion at levels below LV1 will lead to confusing picutre of patchy LMN/neuropathic dificit depending on vertical level (LV1 - LV5, SV1 - SV5) and horizontal level (medial vs lateral). There will not be any evidence of myelopathy.

a. Medially situated lesions. As sacral nerve roots exit out of the vertebral canal the last, they are situated most medially. Medially situated lesions will lead to involvement of sacral roots at all levels (from LV2 to SV4).

b. Laterally situated lesions. Depending on the vertical site of the lesion, nerve roots will get involved. A lesion at LV4 will lead to involvement of L4 onwards nerve roots (as nerve roots till L3 have already exited out of the spinal canal).

The relationship between vertebral body number and spinal level can be found at this site. Excerpt for the same is given below.

In summary, spinal vertebral and spinal cord segmental levels are not necessarily the same. In the upper spinal cord, the  first two cervical cord segments roughly match the first two cervical vertebral levels. However, the C3 through C8 segments of the spinal cords are situated between C3 through C7 bony vertebral levels. Likewise, in the thoracic spinal cord, the first two thoracic cord segments roughly match first two thoracic vertebral levels. However, T3 through T12 cord segments are situated between T3 to T8. The lumbar cord segments are situated at the T9 through T11 levels while the sacral segments are situated from T12 to L1. The tip of the spinal cord or conus is situated at L2 vertebral level. Below L2, there is only spinal roots, called the cauda equina.

Lesion at a particular vertebral body will lead to involvement of respective (same numbered) exiting nerve root, involvement of spinal segment (level depends on the level of vertebral body involvement) and UMN involvement below the spinal segment involvement. Example, a lesion at TV1 will lead to involvement of C8/T1 nerve roots (which are exiting out from intervertebral foramina), T4 spinal segment involvement (LMN lesion) and UMN involvement below T4 level.

You are requested to comment and put up your suggestions. I will be grateful.

Suman

Jugular Venous Waves analysis in tachyarrhythmia diagnosis

2013-11-19T17:37:00.000+05:30

JUGULAR VENOUS WAVEFORMS AND CAROTID PULSATIONS IN TACHYARRHYTHMIA DIAGNOSIS: A READILY AVAILABLE BUT OFTEN FORGOTTEN TOOL

Background

The content of this post was written by me few years ago. It builds conceptual framework on JVP and carotid wave analysis for tachyarrhythmia diagnosis. Many concepts written in this post are practical with a bit of practice and spending time with patients. The techniques written here can be used as important adjunct to 12 lead surface ECG tracing in diagnosing tachyarrythmia.

You are requested to read and understand the content and give your frank comments.

Introduction

Tachyarrhythmia diagnosis is a challenge that all of us face as daily routine. Usually it requires a good and fast analysis of surface ECG. This article discusses different aspects of using clinical examination especially jugular venous waveforms (JVW) and carotid pulsations (CP) in diagnosis of arrhythmias. Many of the techniques seem to be impractical and be of academic interest only but a lot of them fare better chances in accurate and rapid diagnoses of arrhythmias than using a 12 lead surface ECG.

JVWs and ECG correlation in sinus rhythm

ECG gives us the electrical activity of whole heart during cardiac cycle and JVWs and CPs give us mechanical activity during cardiac cycle.

Usually the mechanical activity follows the electrical activity (depolarization) by a few milliseconds. The following are the correlation of phase of cardiac cycle and the ECG waveforms:

Cardiac cycle	ECG waveforms	Electrical cycle
Ventricular systole (0.3 secs)	Q – T interval (start of QRS to end of T), only approximately	Vent depolarization + vent repolarization (Stage 1, 2, 3)
Ventricular diastole (0.5 secs)	T – Q interval	Stage of resting membrane potential (Stage 4)
Atrial systole	P wave or PR interval (approximately)	Atrial depolarization

JVWs are formed due to mechanical activities inside the atria and they may or may not be dependent on mechanical activities of ventricles. CPs are solely due to ventricular systole.

'a' wave

It is solely due to atrial contraction, irrespective the mechanical state of the ventricle. It corresponds to atrial depolarization and P wave in ECG. If atrial contraction takes place against closed AV valves, usually when the ventricle is also in systole, ‘a’ wave’s amplitude increases and is known as cannon wave. In sinus rhythm, it is recognized as positive wave appearing just before carotid pulse. In tachyarrhythmias, it is usually the only positive wave seen in the jugular veins, as v wave is submerged being the smaller wave and due to shortened ventricular systole.

'x' descent

It corresponds to the start of ventricular systole and corresponds to ventricular depolarization and QRS complex in ECG. It is not a good indicator of ventricular systole as it may get modified depending on the mechanical state of atrium, e.g. in very early atrial premature beat, when ventricle is still in systole, it may be superimposed with a very premature a wave (cannon wave).

'v' wave

It occurs in late ventricular systole and is a slow rising positive wave. It is the only positive wave seen in atrial fibrillation. In tachyarrhythmias, it is usually not appreciated because of reasons cited above.

Carotid pulsation

CP is caused solely due to ventricular contraction and therefore represents ventricular systole and QRS complex in ECG.

To summarize, ‘a’ wave can be considered to be representative of P wave and carotid pulsation of QRS complex. Other waveforms do not serve much purpose in tachyarrhythmia diagnosis as they depend on combined synchronized activity of atrium and ventricle, which usually do not take place in cases of arrhythmias.

Recognition of ‘a’ wave during tachyarrhythmia

JVWs are always appreciated in supine position with patient’s neck in neutral position. In thick, short necked individuals it becomes prominent after extending the neck. Sometimes, it is better appreciated during inspiration. It is usually differentiated from CP by the fact that JVWs are better seen then felt, unlike CPs. Other characters do not hold good (like two positive waves in a cardiac cycle) or are difficult to appreciate (like changes with respiration and posture) in cases of arrhythmias.

Presence of two positive waves in jugular vein per cardiac cycle with regular CPs suggests sinus rhythm and recognition of the waveforms are as already described. In tachyarrhythmias (fast CPs), the only positive waves seen are a waves, v waves being submerged.

Clinical classification of arrhythmias

The following are the common clinical types of tachyarrhythmias:

Premature beats in midst of regular CPs (Aim: to differentiate between atrial, nodal and ventricular premature beats)
Irregularly irregular CPs of varying volumes (Aim: to differentiate between atrial fibrillation, multiple premature beats, atrial flutter with variable conduction and multifocal tachycardia)
Regular fast CPs [Aim: to differentiate between supranodal, nodal and infranodal (AV dissociation present) tachycardia]

Clinical recognition of AV dissociation (AVD)

AVD signifies regular and independent electrical, so mechanical, activity of atrium and ventricle. It usually occurs due to physiological or pathological blockage of conduction through AV node. Atrial systole can occur during any of the phases of ventricular cycle. Each ventricular systole is preceded by ventricular diastole with variable filling due to variable state of atrium resulting in a beat to beat variability of carotid volume and systolic blood pressure. Although ‘a’ waves are regularly placed, their volume also vary and when atrial and ventricular systole occur simultaneously, cannon waves are produced which occur irregularly by chance.

Clinical recognition of retrograde conduction (RC)

Retrograde conduction denotes electrical activation of atrium retrogradely following activation of AV node (nodal rhythm) or ventricle (infranodal rhythm). It usually occur in conditions where (infra) nodal rate is faster than the sinus rate, due to which the retrograde impulse has got a receptive AV node more often. Once the distal impulse gets conducted retrogradely through AV node discharging sinus node, sinus node does not get chances to take over resulting in regular occurrence of retrograde conduction. If the (infra) nodal rate is slower than the sinus rate, chances that the distal impulse will get receptive AV node is much less and even if it finds one, it is not sustained as sinus impulse takes over eventually. In conditions involving the first mechanism, atrial systole occurs during ventricular systole (after a few milliseconds) regularly, generating regular cannon waves, whose rate is same as that of CPs. In conditions involving second mechanism, ‘a’ waves are irregular (due to occasional premature discharge of sinus node) with irregular cannon waves (c.f. AVD where irregular cannon waves are associated with regular ‘a’ waves).

Approach to diagnosis of tachyarrhythmias

The first step is to analyze CPs for regularity and amplitude. Next step is to sub-classify rhythm as under mentioned and proceed:

Premature beats in midst of regular CPs

Conditions to be differentiated are atrial, nodal or ventricular premature beats. Usually differentiating between all these conditions are difficult as premature beats are occasional (resulting in failure to anticipate it and the findings) and in between we have got both ‘a’ and ‘v’ waves. Atrial premature beat (APB) is characterized by premature ‘a’ wave, which if very premature can occur while ventricle is still in systole (P’ occurring on preceding T wave) resulting in premature cannon wave. The corresponding CP is low in volume or absent (if APB finds AVN in state of refractoriness). The same findings will also be there in nodal or ventricular premature beats if there is retrograde conduction to atrium (except that in these cases the premature ‘a’ wave will always be a cannon wave). But in classic nodal and ventricular premature beats, the premature impulse finds a refractory AVN. This results in regularly placed ‘a’ wave, which usually is a cannon wave as atrial systole occurs at the time when ventricle is in systole.

Irregularly irregular CPs

The diseases can be further subdivided into two categories depending on the CP rate:

CP rate < 100/min: Main differentials are atrial fibrillation, atrial flutter with variable conduction and multiple premature beats. Since the CP rate is less than 100/min, we can distinguish the JVWs with relative ease. If there is only one positive wave per cardiac cycle (between two CPs), the diagnosis is atrial fibrillation. If we appreciate two positive waves in a cardiac cycle, the diagnosis is premature beats. If there is occasional cannon wave, the diagnosis is nodal/ventricular premature beat. In atrial flutter, we can appreciate multiple regular, positive waves (multiple ‘a’ waves rate of which will be same as atrial rate in ECG), some of which will be cannon waves. 2:1 conduction, where there will be only two positive waves per cardiac cycle, will not be considered in this subgroup as CP rate is more than 100/min.
CP rate >= 100/min: Main differentials are atrial fibrillation, multifocal atrial tachycardia and atrial flutter with fast conduction. Differentiating conditions in this group is difficult because of fast ventricular as well as atrial rate, which results in difficulty in appreciating number of positive waves per CP cycle. Otherwise, the logic behind differentiating the abovementioned conditions are same as for conditions where CP rate is less than 100/min.

Regular fast CPs

This group consists of diseases that are life threatening, and for those proper diagnosis is required before initiating treatment. Proper clinical examination, in this sub group, can sometimes yield more information than ECG analysis.

Main differentials in this subgroup are:

Without AVD (supraventricular tachycardia)

a. Sinus/atrial tachycardia, atrial flutter with regular fast conduction

b. AVNRT/AVRT

c. Ventricular tachycardia with RC
With AVD (ventricular tachycardia)

a. Typical ventricular tachycardia

The main differentiating feature between ventricular versus supraventricular tachycardia is the presence of AVD in former and absence in later conditions. When wide QRS complex tachycardia is analyzed to differentiate between two sub groups using ECG, AVD is not usually appreciated as P waves get merged within rapidly occurring widened QRS complexes or T waves. So, we concentrate on the morphological characteristics of QRS complex, which are less accurate. In clinical method, AVD can easily be appreciated and so emphasis is placed on detection of the same.

As was earlier noted, AVD is characterized by regular ‘a’ waves, rate of which is different from rate of CP, whose amplitude keeps on varying depending on the state in which the ventricle is in and sometimes (irregularly) as cannon waves when ventricle is in systole. In ventricular tachycardia, for one atrial cycle (time period between two consequent atrial systoles or ‘a’ waves) ventricle undergoes more than one cycles (usually 2 – 3). Each ventricular cycle will produce separate ‘x’, ‘v’ and ‘y’ descent whose amplitude will differ depending on the atrial state. The JVP is characterized by multiple positive waves of variable amplitudes per atrial cycle (ventricular cycle is too fast to be appreciated). Only waves that can be easily appreciated are the cannon waves, which are irregular. CP amplitudes are appreciated as equal as their rate is fast and atrial state is more or less same for each ventricular filling phase. So, in the presence of rapid CPs, the only easily discernable clinical evidence of AVD and thus, ventricular tachycardia is presence of irregular cannon waves.

Second subgroup of tachycardia, which include AVNRT/AVRT and ventricular tachycardia with retrograde conduction is characterized by almost simultaneous, rapid atrial and ventricular systole. This is appreciated in jugular veins as regular, rapid cannon waves (frog sign). All other waveforms are not appreciated.

Third subgroup, which include atrial and sinus tachycardia, do not produce any cannon waves. These conditions are difficult to differentiate from atrial flutter with fast conduction (2:1), which will also have two positive waves per cardiac cycle. In atrial flutter, however, few of ‘a’ waves will be cannon waves (regularly occurring).

The clinical methods described above are quite effective in differentiating different tachycardias, especially between supraventricular and ventricular tachycardia. It however cannot differentiate between ventricular tachycardia with retrograde conduction and AV (N) RT which obviously have different treatment strategies.

Conclusion

This article describe in brief the approach to differentiate different tachyarrhythmias by observing patient’s JVWs and CPs without aid of surface 12 lead ECG. The methods described above can lead to pretty accurate and rapid diagnoses and can sometimes supplement ECG tracing in reaching accurate diagnosis. The advantage with clinical method is that we observe JVWs (atrial activity) and CPs (ventricular activity) as two separate tracings (more like tracings during electrophysiological study) unlike in surface ECG, where both atrial and ventricular activity is merged in a single tracing leading to some important information getting missed.

ECG: A Primer

2013-11-19T17:34:00.000+05:30

Electrocardiography: the basics

The content in this post was written by me a few years ago. It will act as an introductory ECG for Undergraduates and Postgraduates.

Lead placement

Bipolar leads

Unipolar Augmented Limb Leads

Voltage increased by 50%
aVR: all waves are negative
aVL: Lateral wall
aVF: Inferior wall

Unipolar Precordial Leads (Chest Leads)

V1: 4th intercostal space (right sternal level) (right ventricle)
V2: 4th intercostal space (left sternal level) (Septum)
V3: between V2 and V4 (Septum)
V4: 5th intercostal space in mid clavicular line (Septum)
V5: 5th intercostal space in anterior axillary line (Apical)
V6: 5th intercostal space in mid axillary line (Apical)
V7: 5th intercostal space in posterior axillary line (Posterior)
V8: 5th intercostal space below lower angle of scapula (Posterior)

Right sided chest leads (for right ventricle)

V3R and V4R: same as V3 and V4, on right side of chest

Always get it done in case of inferior wall myocardial infarction to detect right ventricular myocardial infarction

Orientation of limb leads

ECG paper

1mm (1 small square) = 0.04 sec on horizontal axis (Duration)
1mm (1 small square) = 0.1 mV on vertical axis (Amplitude)
5mm = 0.2 sec on horizontal axis
In 1 minute, ECG paper moves by 300 thick lines (1500mm), if speed of paper is 25mm/sec

Calibration of machine

1mV produces deflection of 10mm vertically
Patient and machine properly grounded
25mm/sec speed

Normal wave form

Criteria for normal P wave

Duration < 0.12 sec (3mm)
Amplitude < 0.25mV(2.5mm)
Upright in all leads except aVR
Smooth and rounded
May be upright or biphasic in leads V1 and V2, if biphasic terminal negative deflection (width x depth) < 0.03mmsec.

Normal QRS complex

Limb leads

Size of Q wave a. in lead aVL or aVF must have depth < ¼th of the height of ensuing R wave b. must be < 0.04 sec (1mm wide)
Any Q wave in lead III or aVR should be ignored
R wave in aVL must be < 13mm

Precordial leads

Steady progression from V1 (rS) to V6 (qR, qRs)
Transition zone usually between V2 and V4
Minimum voltage: atleast one R wave should be > 8mm
Maximum voltage: tallest R wave should be < 27mm and deepest S wave < 30mm
q wave should be < 0.04 sec

Normal T wave

Limb leads

upright if QRS complex is positive & inverted if QRS complex is negative
always upright in Lead I & II
always negative in aVR

Precordial leads

V1 and V2: normally upright, may be inverted
must be upright in lead V3 to V6

Heart rate

Heart rate = 1500 / No of small squares between adjacent R-R interval

PR interval

Normal PR interval ranges from 0.12 to 0.20 sec
Start of P wave to start of QRS complex

Abnormal ST segment

Inverted tick mark sign: Digitalis effect
Depressed or horizontal: ischemia
Raised with convexity upwards: Myocardial infarction
Raised with concavity upwards: Pericarditis

QRS width

Upper limit: 0.10 sec
> 0.12 sec: BBB or intraventriclar conduction defect
VAT (Ventricular Activation Time): Max 0.03 sec in V1 and V2, 0.05 sec in V5 and V6

ST segment

Must not deviate > 1mm above or below isoelectric line in any lead

QRS axis

If QRS complexes reach for each other in leads I and aVF, it is right axis deviation
If QRS complexes leave each other in leads I and aVF, it is left axis deviation
If QRS complexes are positive in leads I and aVF, it is normal axis
RAD is seen in normal individual, right ventricular hypertrophy, isolated RBBB and left posterior hemiblock
LAD is seen in obese individuals, left ventricular hypertrophy and left anterior hemiblock

Myocardial Infarction: ECG changes

Regions of myocardial damage & corresponding ECG changes

Conventional electrodes cover wide area and hence record all the three regions

Abnormal Q waves should be

> 0.04sec duration
≥ 25% deeper than height of ensuing R wave (which must exceed 5mm)
> 4mm deep
Present in leads V5 and V6 when associated with LBBB. In LBBB the normal septal Q wave disappears in lead V5 and V6, hence even a small Q wave in these leads suggest infarction of the interventricular septum.
Poor progression of R wave in chest leads also suggest abnormality in QRS complex suggestive of anterior wall myocardial necrosis

Regression of changes

ST segment is the first to return to the isoelectric line
An abnormal inverted T wave develops after a few days and lasts for a week
Abnormal Q wave persists

Site of infarction

Thickness of wall involved

Subendocardial injury: ST depression
Transmural injury: ST elevation

Region of ventricle invovled

Area	ST elevation
Anteroseptal	V1-V4
Anterolateral	I, aVL
Apical	V5, V6
Inferior	II, III, aVF
Posterior	V8, V9
	Tall R wave, ST depression, tall T wave in V1
Right ventricle	V1 (not in V2, V3)
	V3R, V4R

Conditions simulating inferior wall MI

In normal persons, Q wave may be present and T wave may be inverted in lead III. But, they revert to normal in deep inspiration. Hence, they must be present in II, III and aVF, and persist even after deep inspiration to be significant.

Criteria to diagnose MI in presence of RBBB

ST segment is displaced in the same direction as the terminal QRS deflection in right precordial leads
ST segment becomes coved convex upwards
T wave becomes symmetrical, inverted and arrow headed
In septal infarction, Q wave may appear in leads V1-V3

Criteria to diagnose MI in presence of LBBB

Q wave present in lead I, aVL, V5 and V6 with ↓ R wave in V5 and V6
ST elevation > 1mm in leads with positive terminal QRS complex
ST segment elevation > 5mm in leads with negative terminal QRS complex
ST segment depression or elevation < 1mm in V1, V2
Initial slurring of QRS complex in V1

Conclusion

I finish with the above post. There are many new aspects about ECG analysis which have been developed in last few years. I have not touched upon arrhythmia diagnosis. You are welcome to suggest corrections, modifications and additions.