10 common heart disease with changes on ECG

Reading File

Finding Sources

Reading File

Finding Sources

I now have excellent content from the medical library. Let me compile the comprehensive answer:

10 Common Heart Diseases and Their ECG Changes

1. Myocardial Infarction (STEMI)

The ECG is central to diagnosing acute MI. Three major phases occur:

Hyperacute (minutes): Tall, broad, "hyperacute" T waves over the ischemic zone - the earliest sign.

Acute (hours): ST segment elevation in leads overlying the infarcted territory (transmural ischemia shifts the ST vector toward the epicardium). Reciprocal ST depressions appear in opposite leads.

Evolving (hours-days): T-wave inversions develop in the same distribution. Pathological Q waves form as dead muscle becomes electrically silent.

Chronic (weeks-months): Persistent Q waves remain. The R wave fails to progress across precordial leads ("poor R-wave progression") in anterior infarcts.

Localisation by lead:

Territory	ST Elevation Leads
Anterior	V1-V4
Lateral	I, aVL, V5-V6
Inferior	II, III, aVF
Right ventricular	V1, right-sided leads (V3R-V4R)
Posterior	Reciprocal ST depression V1-V3

Harrison's Principles of Internal Medicine 22E; Ganong's Review of Medical Physiology, 26e

2. Non-ST Elevation Myocardial Infarction (NSTEMI) / Unstable Angina

With subendocardial ischemia, the ST vector shifts toward the subendocardium and ventricular cavity:

ST depression in anterior precordial leads (V1-V6, I, aVL)
ST elevation in aVR (a reciprocal finding indicating severe, diffuse subendocardial ischemia or left main/proximal LAD occlusion)
T-wave inversions (may be deep and symmetric - "Wellens' pattern" indicates critical LAD stenosis)
No pathological Q waves (non-Q wave infarction)

Absence of ST elevation does not exclude acute coronary thrombus; approximately one third of patients without ST elevation on post-arrest ECG still have acute coronary thrombus at catheterization.

Harrison's Principles of Internal Medicine 22E; Goldman-Cecil Medicine

3. Atrial Fibrillation (AF)

Classic ECG features:

Absent P waves - replaced by chaotic, irregular fibrillatory baseline (f waves at 350-600 bpm)
Irregularly irregular RR intervals (hallmark finding)
Variable ventricular rate (typically 100-160 bpm if uncontrolled)
QRS complexes are usually narrow (unless aberrant conduction or bundle branch block coexists)
With rapid ventricular response: may show rate-related ST depression

AF is the most common arrhythmia associated with acute ischemic stroke. New AF on ECG in cardiac metastases or structural disease carries significant prognostic weight.

Braunwald's Heart Disease; Harrison's Principles of Internal Medicine 22E

4. Atrioventricular (AV) Heart Block

Three degrees, each with distinct ECG patterns:

Degree	ECG Finding
First-degree	Prolonged PR interval (>200 ms); all P waves conduct
Second-degree (Mobitz I / Wenckebach)	Progressive PR lengthening until a P wave is blocked (dropped QRS); then cycle repeats
Second-degree (Mobitz II)	Constant PR interval with sudden non-conducted P waves; often progresses to complete block
Third-degree (Complete)	P waves and QRS complexes are independent (AV dissociation); ventricular rate determined by escape rhythm (junctional ~40-60 bpm; ventricular ~20-40 bpm, wide QRS)

In the setting of pulmonary embolism, new right bundle branch block suggests right ventricular strain and severe pulmonary hypertension; this can be a sign of AV conduction compromise.

Braunwald's Heart Disease; Goldman-Cecil Medicine

5. Pericarditis

Acute pericarditis produces a characteristic ECG pattern that evolves through four stages:

Stage 1 (acute): Diffuse saddle-shaped (concave up) ST elevation in almost all limb and precordial leads (except aVR and V1 which show ST depression). Importantly, PR segment depression (a hallmark - due to atrial myocarditis).
Stage 2: ST segments normalize; T waves flatten
Stage 3: Diffuse T-wave inversions
Stage 4: ECG normalizes

Key distinction from STEMI: Pericarditis ST elevation is diffuse (not territory-specific), concave up ("saddle-shaped"), and accompanied by PR depression. There are no reciprocal ST depressions (except aVR) and no Q waves.

Rosen's Emergency Medicine; The Washington Manual of Medical Therapeutics

6. Hypertrophic Cardiomyopathy (HCM)

Left ventricular hypertrophy (LVH): Tall R waves in lateral leads (V5-V6, I, aVL), deep S waves in V1-V2. Voltage criteria: Sokolow-Lyon (SV1 + RV5 or V6 ≥35 mm)
Large septal Q waves: Deep, narrow Q waves in the lateral leads (I, aVL, V5-V6) and inferior leads - a distinctive feature of HCM reflecting septal hypertrophy
ST-T wave abnormalities: ST depression and T-wave inversions (strain pattern) in lateral leads
Left axis deviation
Arrhythmias: AF, ventricular tachycardia (a major cause of sudden cardiac death in young athletes)
Tintinalli's Emergency Medicine; Harrison's Principles of Internal Medicine 22E

7. Dilated Cardiomyopathy (DCM)

LVH pattern on ECG
Poor R-wave progression across precordial leads (V1-V4)
Nonspecific ST-T wave changes (diffuse, no territorial pattern)
Bundle branch block (left bundle branch block is common, causing wide QRS and secondary ST-T changes)
Atrial fibrillation (common due to atrial dilatation)
Ventricular ectopy and ventricular tachycardia (risk of sudden death)
Tintinalli's Emergency Medicine

8. Restrictive Cardiomyopathy (e.g., Cardiac Amyloidosis)

Low QRS voltage (characteristically low despite marked LV wall thickening on echo - a "voltage-mass discordance" that strongly suggests amyloidosis)
Pseudo-infarct pattern: Q waves or poor R-wave progression mimicking prior MI in the absence of coronary disease
Conduction disturbances: Bundle branch blocks, AV blocks
Atrial fibrillation (common)
Electrical alternans when pericardial effusion is present

Low voltage on ECG in the presence of echocardiographic LVH is a classic clue to cardiac amyloidosis.

Tintinalli's Emergency Medicine; Braunwald's Heart Disease

9. Pulmonary Embolism (PE)

PE produces right heart strain reflected on the ECG:

Sinus tachycardia - the most common finding
S1Q3T3 pattern: Deep S wave in lead I, Q wave and T-wave inversion in lead III (classic but neither sensitive nor specific)
Right bundle branch block (new RBBB indicates severe right ventricular strain - an adverse prognostic sign)
ST depression and T-wave inversions in right precordial leads (V1-V4)
P pulmonale: Tall, peaked P waves in II, III, aVF (right atrial enlargement)
Right axis deviation
Atrial fibrillation or flutter
QR pattern in V1 - associated with right ventricular strain and adverse outcome
Fuster and Hurst's The Heart, 15th Edition; Goldman-Cecil Medicine

10. Wolff-Parkinson-White (WPW) Syndrome

WPW results from an accessory pathway (Bundle of Kent) bypassing the AV node, causing ventricular pre-excitation:

Short PR interval (<120 ms) - AV node delay is bypassed
Delta wave - slurred upstroke at the beginning of the QRS (earliest ventricular activation through the slow-conducting accessory pathway)
Wide QRS (>120 ms) due to fusion of accessory pathway and normal conduction
Secondary ST-T wave changes in opposite direction to the delta wave/QRS
During tachycardia: orthodromic AVRT (narrow QRS, retrograde P waves after QRS); antidromic AVRT (very wide QRS, may mimic VT)
AF in WPW is dangerous: Can conduct very rapidly through the accessory pathway (bypassing AV nodal rate-limiting), potentially degenerating to VF
Goldman-Cecil Medicine; The Washington Manual of Medical Therapeutics; Fuster and Hurst's The Heart, 15th Edition

Quick Reference Summary Table

Condition	Key ECG Findings
STEMI	ST elevation (territory-specific) → T inversion → Q waves
NSTEMI/UA	ST depression, T inversions, ST elevation in aVR
Atrial Fibrillation	No P waves, irregularly irregular RR
AV Block	PR prolongation (1st), dropped beats (2nd), AV dissociation (3rd)
Pericarditis	Diffuse concave ST elevation, PR depression
HCM	LVH + large septal Q waves in lateral leads
Dilated Cardiomyopathy	LVH, poor R progression, nonspecific ST-T changes, LBBB
Restrictive/Amyloid	Low voltage + pseudo-infarct pattern
Pulmonary Embolism	Tachycardia, S1Q3T3, new RBBB, RV strain pattern
WPW	Short PR + delta wave + wide QRS

Note: ECG changes must always be interpreted alongside clinical presentation, history, and other investigations. No single ECG finding is pathognomonic, and many of these patterns can overlap.

Also with ECG interpretation

Finding Sources

Reading File

Finding Sources

Reading File

I now have rich, textbook-sourced content on ECG interpretation. Let me deliver the comprehensive expanded response.

10 Common Heart Diseases: ECG Changes + Full ECG Interpretation Guide

PART 1 - SYSTEMATIC ECG INTERPRETATION (14-Step Approach)

Before diagnosing any condition, every ECG should be analysed in this order. Skipping steps is the most common source of missed diagnoses.

"Many mistakes in ECG interpretation are errors of omission. Therefore, a systematic approach is essential." - Harrison's Principles of Internal Medicine 22E

Step 1 - Standardisation & Technical Quality

Standard calibration: 10 mm = 1 mV (check the calibration marker at the start of the strip)
Paper speed: 25 mm/sec (standard); each small box = 0.04 s; each large box = 0.2 s
Check for: lead reversal, poor contact, patient movement artifact, correct lead placement
Low-amplitude calibration (5 mm = 1 mV) halves all voltages - can mimic low-voltage states

Step 2 - Heart Rate

Quick method: Count large boxes between R-R interval → divide 300 by that number

Large boxes (R-R)	Rate (bpm)
1	300
2	150
3	100
4	75
5	60
6	50

Normal: 60-100 bpm
Tachycardia: >100 bpm
Bradycardia: <60 bpm
For irregular rhythms: count QRS complexes in a 10-second strip × 6

Step 3 - Rhythm

Ask three questions:

Where is the pacemaker? - Is there a P wave before every QRS? Is it positive in II and negative in aVR? (= sinus origin)
Is conduction normal? - Does every P wave conduct through to the QRS?
Is the rhythm regular? - Are RR intervals constant?

Finding	Interpretation
P wave (+) in II, (–) in aVR, before every QRS	Normal sinus rhythm
No P waves, irregular RR	Atrial fibrillation
Saw-tooth flutter waves at ~300 bpm	Atrial flutter
P waves present but no relation to QRS	Complete (3rd degree) AV block
Narrow QRS tachycardia, no visible P waves	AVNRT / junctional tachycardia
Wide QRS tachycardia, AV dissociation	Ventricular tachycardia

Step 4 - PR Interval

Normal: 120-200 ms (3-5 small boxes)
Short PR (<120 ms): pre-excitation (WPW), junctional rhythm
Long PR (>200 ms): 1st degree AV block
Progressively lengthening PR: Mobitz I (Wenckebach)
PR depression (below isoelectric line): pericarditis (atrial injury current)

Step 5 - QRS Duration

Normal: 80-120 ms (2-3 small boxes)
120 ms = bundle branch block or ventricular conduction delay

LBBB: Wide QRS, broad monophasic R in I/V5/V6, QS in V1, no septal Q waves RBBB: Wide QRS, RSR' ("rabbit ears") in V1, wide S in I/V5/V6

Step 6 - QT / QTc Interval

Measured from start of QRS to end of T wave
Normal QTc: <440 ms (men), <460 ms (women) - corrected by Bazett formula: QTc = QT / √RR
Prolonged QTc: Risk of Torsades de Pointes (polymorphic VT)
Causes: drugs (quinidine, amiodarone, antipsychotics), hypokalemia, hypocalcemia, congenital LQTS

Step 7 - Mean QRS Electrical Axis

Normal axis lies between -30° and +90° in the frontal plane.

Axis	Leads I & aVF	Causes
Normal (0° to +90°)	Both positive	Normal
Left axis deviation (<-30°)	I positive, aVF negative	LAFB, LVH, inferior MI, HCM
Right axis deviation (>+90°)	I negative, aVF positive	RVH, PE, RBBB, lateral MI, WPW
Extreme axis ("northwest")	Both negative	VT, severe hyperkalemia

Step 8 - P Waves

Normal: <0.12 s duration, <2.5 mm amplitude, upright in II, inverted in aVR
P mitrale (broad, notched P in II, biphasic in V1 with wide terminal negative deflection): Left atrial enlargement (mitral stenosis, LVF)
P pulmonale (tall, peaked P >2.5 mm in II): Right atrial enlargement (COPD, pulmonary hypertension, PE)
Absent P waves: AF, junctional rhythm, hyperkalemia

Step 9 - QRS Voltages

LVH criteria:

Sokolow-Lyon: SV1 + RV5 or RV6 ≥ 35 mm
Cornell: RaVL + SV3 >28 mm (men), >20 mm (women)

Low voltage (<5 mm in limb leads, <10 mm in precordial leads):

Causes: pericardial effusion, cardiac tamponade, restrictive/infiltrative cardiomyopathy (amyloidosis), hypothyroidism, obesity, COPD

Step 10 - Precordial R-Wave Progression

Normal: R waves increase from V1 to V5/V6 (R/S ratio >1 by V3-V4)
Poor R-wave progression (R waves fail to grow or remain small V1-V4):
- Anterior MI, dilated cardiomyopathy, LBBB, RVH, obesity, COPD

Step 11 - Abnormal Q Waves

Septal q waves (small, narrow, <0.04 s, <25% of R height) in I, aVL, V5-V6 = normal
Pathological Q waves (≥0.04 s duration OR ≥25% of R height) = transmural infarction or scar
Q waves in aVR are always normal

Step 12 - ST Segments

Normal: isoelectric (at baseline between J-point and T wave)
ST elevation: STEMI, pericarditis, Brugada, early repolarization, LV aneurysm, vasospasm
ST depression: Subendocardial ischemia, NSTEMI, digoxin effect (sagging "reverse tick"), LBBB strain, RVH strain
J-point: The junction between QRS and ST segment; elevation at the J-point with rapid upstroke = early repolarization (benign variant)

Step 13 - T Waves

Normal: Upright in I, II, V2-V6; inverted in aVR; may be inverted in III, V1
Hyperacute T waves (tall, broad, peaked): Early STEMI, hyperkalemia
Symmetrical deep T-wave inversions: Ischemia, Wellens' pattern (critical LAD stenosis), PE (V1-V4), HCM, RVH
Flat/inverted T waves: LVH with strain, digoxin, electrolyte disturbance

Step 14 - U Waves

Small deflection after T wave, best seen in V2-V3
Prominent U waves (U > T): Hypokalemia (classic), bradycardia, class IA antiarrhythmics
Negative U waves: Ischemia, LVH

PART 2 - ECG INTERPRETATION IN EACH OF THE 10 HEART DISEASES

1. STEMI - Systematic Interpretation

Parameter	Finding
Rate	Often normal or tachycardia (pain/sympathetic activation)
Rhythm	Sinus; watch for ventricular ectopy
PR interval	Normal (unless inferior MI involves AV node branch)
QRS duration	Normal initially; LBBB may develop
QRS axis	May shift depending on territory
P waves	Normal
QRS voltages	May decrease as myocardium dies
R-wave progression	Lost in anterior MI ("poor R-wave progression")
Q waves	Develop hours-days after onset (pathological Q waves in territory)
ST segments	ST elevation ≥1 mm in ≥2 contiguous leads (key diagnostic criterion)
T waves	Hyperacute (peaked, broad) early → later deep inversions
U waves	Normally not relevant

Reading it: First confirm ST elevation in a territory. Then look for reciprocal ST depressions in opposite leads (confirms true elevation, not artifact). Then trace the evolution - hyperacute T → ST elevation → Q wave formation → T-wave inversion.

2. NSTEMI / Unstable Angina - Systematic Interpretation

Parameter	Finding
Rate	Tachycardia possible
Rhythm	Sinus; AF may be precipitant
PR interval	Normal
QRS duration	Normal (unless prior LBBB/RBBB)
ST segments	ST depression ≥0.5 mm in ischemic territory; ST elevation in aVR ≥1 mm
T waves	Symmetrical deep T-wave inversions (Wellens' pattern in V1-V4 = critical LAD)
Q waves	Absent (no full thickness necrosis)

Reading it: The absence of ST elevation does not exclude ACS. Deep, symmetric T-wave inversions in V1-V4 (Wellens' sign) indicate the LAD is critically narrowed and is a pre-infarction warning requiring urgent catheterisation.

3. Atrial Fibrillation - Systematic Interpretation

Parameter	Finding
Rate	Ventricular rate variable: 100-160 (uncontrolled), <80 (rate-controlled)
Rhythm	Irregularly irregular - the hallmark
P waves	Absent - replaced by irregular fibrillatory baseline (f waves, >350 bpm)
PR interval	Not measurable (no P waves)
QRS duration	Usually narrow; wide if aberrant conduction or pre-existing BBB
ST/T	May show rate-related depression at fast ventricular rates

Reading it: Confirm (1) no organised P waves, (2) irregular baseline between QRS complexes, (3) irregularly irregular QRS complexes. If QRS is wide and very fast (>200 bpm) in AF, suspect WPW with conduction via accessory pathway - a life-threatening emergency.

4. AV Heart Block - Systematic Interpretation

Work through the PR interval and P:QRS ratio methodically:

Degree	Rate	Rhythm	PR	P:QRS	QRS
1st degree	Normal	Regular	>200 ms, constant	1:1	Normal
2nd degree Mobitz I	Normal/slow	Irregular (grouped beats)	Progressively ↑ then dropped beat	Some P waves not conducted	Normal (usually)
2nd degree Mobitz II	Normal/slow	Regular with pauses	Constant PR, sudden dropped QRS	Some P waves not conducted	Often wide (RBBB/LBBB)
3rd degree (complete)	Slow (20-60 bpm)	Regular (escape rhythm)	No relationship between P and QRS	AV dissociation	Wide (ventricular escape) or narrow (junctional)

Reading it: Count the P waves and QRS complexes separately. If there are more P waves than QRS complexes, there is AV block. In complete block, the PP interval and RR interval are each regular but independent of each other.

5. Acute Pericarditis - Systematic Interpretation

Parameter	Finding
Rate	Sinus tachycardia (pain/fever)
Rhythm	Sinus; AF possible
PR segment	PR depression in most leads (II, V4-V6); PR elevation in aVR - pathognomonic of atrial injury
ST segments	Diffuse, concave-up ("saddle-shaped") ST elevation in almost all leads except aVR/V1 (ST depression there)
T waves	Initially upright; later diffuse T-wave inversions after ST normalises
Q waves	Absent (no myocardial necrosis)

Reading it: The "saddle-shape" of ST elevation (concave upward, like a smile) differs from the convex/tombstone ST elevation of STEMI. PR depression in II is the most specific sign. Involvement of nearly all leads without a clear vascular territory distinguishes it from MI. The 4 stages:

Stage 1: PR depression + diffuse ST elevation
Stage 2: ST normalises, T waves flatten
Stage 3: Diffuse T-wave inversions
Stage 4: Full normalisation

6. Hypertrophic Cardiomyopathy (HCM) - Systematic Interpretation

Parameter	Finding
Rate	Normal; paroxysmal AF or VT possible
Rhythm	Sinus; atrial or ventricular ectopy
QRS axis	Left axis deviation common
QRS voltages	Markedly increased (LVH voltage criteria met)
Q waves	Abnormally deep, narrow Q waves in lateral leads (I, aVL, V5-V6) and inferior leads - from massive septal depolarisation, not infarction. Key distinguishing feature
ST/T	ST depression and T-wave inversions in lateral leads (strain pattern)
R-wave progression	Normal or exaggerated

Reading it: Young patient with LVH + large septal Q waves in lateral leads without history of MI = HCM until proven otherwise. These Q waves are narrow (<40 ms) unlike the broad Q waves of infarction. Apical HCM (Yamaguchi type) produces giant T-wave inversions (>10 mm deep) in V3-V5 - a dramatic pattern.

7. Dilated Cardiomyopathy (DCM) - Systematic Interpretation

Parameter	Finding
Rate	Tachycardia; AF very common
Rhythm	AF, ventricular ectopy (PVCs, NSVT)
PR interval	May be prolonged
QRS duration	Often widened - LBBB common (>120 ms with broad R in lateral leads, QS in V1)
QRS axis	Left axis deviation with LBBB
QRS voltages	May show LVH or, paradoxically, low voltage as myocardium is replaced by fibrosis
R-wave progression	Poor (flat or absent R waves V1-V4)
Q waves	Pseudo-infarct Q waves possible (from fibrosis) despite no coronary disease
ST/T	Diffuse nonspecific ST-T changes; secondary changes in leads with LBBB

Reading it: DCM is a diagnosis of exclusion on ECG - the changes are non-specific. LBBB in a patient with heart failure symptoms is a red flag for DCM and may indicate need for cardiac resynchronisation therapy (CRT).

8. Restrictive Cardiomyopathy / Cardiac Amyloidosis - Systematic Interpretation

Parameter	Finding
Rate	Normal or AF
Rhythm	AF; conduction disturbances
PR interval	May be prolonged (AV block)
QRS duration	Conduction delays; BBB
QRS voltages	Characteristically LOW (<5 mm in limb leads) - the most striking feature despite thick walls on echo
R-wave progression	Poor; pseudo-infarct pattern (QS complexes mimicking prior MI in V1-V4)
Q waves	Pseudo-infarct Q waves in multiple territories
ST/T	Non-specific changes

Reading it: The "voltage-mass discordance" is the diagnostic clue - the echo shows thick walls (increased mass) but the ECG shows low voltage. In all other conditions that cause thick walls (hypertension, HCM), the ECG shows HIGH voltage. Low voltage + pseudo-infarct pattern + thick walls on echo = amyloidosis until proven otherwise.

9. Pulmonary Embolism (PE) - Systematic Interpretation

Parameter	Finding
Rate	Sinus tachycardia (most common finding, ~40%)
Rhythm	AF possible; sinus tachycardia typical
QRS axis	Right axis deviation
P waves	P pulmonale - tall, peaked P in II (right atrial enlargement)
QRS duration	New RBBB - a sign of severe right ventricular strain, adverse prognosis
Q waves	Q wave in lead III (part of S1Q3T3)
ST/T	T-wave inversions in V1-V4 (right precordial leads, right ventricular strain pattern); T inversion in lead III
"S1Q3T3"	Deep S wave in lead I + Q wave in III + T-wave inversion in III = classic but only ~20% sensitivity

Reading it: No single ECG finding confirms PE. The full picture matters: sinus tachycardia + new RBBB + right precordial T inversions + right axis deviation in a hypoxic patient = high suspicion for massive PE. The QR pattern in V1 (QS with no R, or small R) is associated with right ventricular strain and poor prognosis. Normal ECG does NOT exclude PE.

10. Wolff-Parkinson-White (WPW) Syndrome - Systematic Interpretation

Parameter	Finding
Rate	Normal in sinus rhythm; very fast during tachycardia
Rhythm	Sinus; paroxysmal SVT (AVRT), AF
PR interval	Short (<120 ms) - AV nodal delay bypassed
QRS duration	Widened (>120 ms) - fusion of accessory pathway and normal conduction
Delta wave	Slurred, slow upstroke at the beginning of the QRS in multiple leads - pathognomonic
QRS axis	Variable (right or left axis depending on accessory pathway location)
ST/T	Secondary ST-T changes (discordant to QRS/delta direction)
Pseudo-MI	Delta waves may produce pseudo-Q waves mimicking infarction

Reading it: Short PR + delta wave + wide QRS = the WPW triad. During orthodromic AVRT (most common), the tachycardia is narrow-complex (conducts down the AV node, retrogradely up the accessory pathway) with retrograde P waves visible after the QRS. During AF with WPW: very rapid, irregular, wide-complex - can degenerate to VF. Never give AV nodal blocking agents (adenosine, verapamil) in AF with WPW - this can precipitate VF.

Master ECG Interpretation Checklist

1.  Calibration & lead placement OK?
2.  Heart rate: bradycardia / normal / tachycardia?
3.  Rhythm: regular / irregular? P before every QRS?
4.  PR interval: short / normal / prolonged?
5.  QRS duration: narrow / wide?
6.  QTc: normal / prolonged?
7.  Axis: normal / LAD / RAD?
8.  P waves: size, shape, morphology?
9.  QRS voltages: LVH / low voltage?
10. R-wave progression: normal / poor?
11. Q waves: septal (normal) / pathological?
12. ST segments: isoelectric / elevated / depressed?
13. T waves: upright / inverted / hyperacute?
14. U waves: absent / prominent?
    → Compare with previous ECG
    → Correlate with clinical context

Sources: Harrison's Principles of Internal Medicine 22E; Ganong's Review of Medical Physiology 26e; Tintinalli's Emergency Medicine; Braunwald's Heart Disease; Goldman-Cecil Medicine; Fuster and Hurst's The Heart 15e; Medical Physiology (Boron & Boulpaep)

This is a shared conversation. Sign in to Orris to start your own chat.