Acute GE MANAGEMENT

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Acute Gastroenteritis (GE) — Management


1. Initial Assessment

History

Key features to elicit:
  • Duration of symptoms (diarrhea >14 days = persistent/chronic, not acute)
  • Stool character: watery vs. bloody, volume per episode
  • Associated symptoms: vomiting, fever, abdominal pain, tenesmus
  • Exposure history: foreign travel, raw seafood, undercooked meat, camping/untreated water, recent antibiotics, daycare, outbreaks
Bloody diarrhea + fever + tenesmus → dysentery pattern → suggests invasive organisms (Campylobacter, Shigella) Large volume watery diarrhea → small bowel involvement (viral, cholera) Vomiting predominating, little diarrhea → norovirus or preformed toxin (Staph aureus)

Physical Examination

Focus on:
  • Hydration status: dry mucous membranes, decreased skin turgor, sunken eyes (especially in children), reduced urine output
  • Vital signs: hypotension + tachycardia → significant dehydration; fever + altered mental status → possible sepsis
  • Abdominal exam: hyperactive bowel sounds are typical; focal tenderness, rebound, guarding, distension or rigidity → suspect surgical cause

Differential Diagnoses to Exclude

Small bowel obstruction, appendicitis, diverticulitis, IBD, ischemic bowel, pancreatitis, hepatobiliary pathology, celiac disease, irritable bowel syndrome.

2. Severity / Dehydration Assessment

Use the Clinical Dehydration Score (especially in children):
ScoreGeneral AppearanceEyesOral MucosaTears
0NormalNormalMoistNormal
1Thirsty, restless, or irritableMildly sunkenStickyDecreased
2Drowsy/non-responsive, limp, cold, diaphoreticVery sunkenDryNone
  • Score 0 = no dehydration
  • Score 1–4 = some dehydration
  • Score ≥5 = moderate–severe dehydration
Dehydration categories:
  • Mild (<5% body weight loss): thirsty, normal exam
  • Moderate (5–10%): tachycardia, dry mucosae, decreased skin turgor
  • Severe (>10%): hypotension, altered mental status, markedly decreased urine output, shock

3. Investigations

TestWhen
Serum glucoseAll infants/young children (hypoglycemia up to 9% prevalence)
Serum electrolytesModerate–severe dehydration, prolonged illness, very young infants, IV fluid therapy needed
CBCIll-appearing patient, bloody diarrhea (identify bacterial enterocolitis, HUS)
Stool cultureBloody diarrhea, fever, travel history, outbreaks, immunocompromised → send for Campylobacter, E. coli O157:H7, Salmonella, Shigella, Yersinia
Stool toxin assayNon-O157:H7 Shiga toxin-producing E. coli
C. difficile testingRecent antibiotics, community-acquired, hospitalised patients
Note: WBC and CRP are NOT reliable to distinguish viral vs. bacterial gastroenteritis. Stool cultures have a low yield in mild, uncomplicated cases.

4. Rehydration — The Cornerstone of Treatment

Oral Rehydration Therapy (ORT) — First-line for mild–moderate dehydration

ORT is equivalent to IV therapy in children with acute gastroenteritis for rehydration, reduction of subsequent diarrhea episodes, and prevention of complications. It is recommended by the AAP, WHO, and European Society of Pediatric Gastroenterology.
ORS options:
SolutionOsmolarity
Standard WHO ORS331 mOsm/kg
Reduced osmolarity WHO ORS245 mOsm/kg (preferred — less vomiting, less stool output)
Pedialyte (children)250 mOsm/kg
In children with mild gastroenteritis and minimal dehydration, dilute apple juice followed by preferred fluids is an acceptable alternative and results in fewer treatment failures than standard ORS.
Protocol:
  • Mild dehydration: 50 mL/kg ORS over 4 hours
  • Moderate dehydration: 100 mL/kg ORS over 4 hours
  • Supplement with 10 mL/kg per liquid stool and 2 mL/kg per vomiting episode
  • Give small, frequent sips if vomiting is present

IV Rehydration — for moderate–severe dehydration or ORT failure

  • Normal saline (0.9% NaCl) or Lactated Ringer's bolus 20 mL/kg IV, repeat as needed
  • Transition to oral rehydration as soon as tolerated
  • Reassess hydration status after each bolus

5. Antiemetics

DrugNotes
Ondansetron (0.15 mg/kg IV/PO; max 4–8 mg)First-line; reduces vomiting, decreases IV fluid need, improves ORT success; systematic review supports use in pediatric gastroenteritis
MetoclopramideAlternative in adults
PromethazineAvoid in children <2 years (respiratory depression risk)

6. Antidiarrheals

DrugNotes
LoperamideUseful in adults with non-dysenteric traveler's diarrhea; avoid in children, bloody diarrhea, or suspected invasive infection
Bismuth subsalicylateCan reduce stool frequency; caution in children (Reye's syndrome risk)
Do not use antidiarrheals in dysenteric illness (bloody diarrhea, high fever) — risk of toxic megacolon, worsened HUS.

7. Antibiotics

Most acute gastroenteritis is viral — antibiotics are NOT routinely indicated.
Empiric antibiotics are considered when:
  • Severe dysenteric illness (high fever, bloody diarrhea)
  • Immunocompromised patient
  • Traveler's diarrhea (moderate–severe)
  • Suspected cholera
OrganismAntibiotic of Choice
CampylobacterAzithromycin 500 mg OD × 3 days (or ciprofloxacin, but resistance rising)
ShigellaAzithromycin or ciprofloxacin × 3–5 days
Salmonella (non-typhoidal)Usually self-limiting; treat if severe, elderly, immunocompromised → fluoroquinolone or azithromycin
Typhoid (Salmonella typhi)Azithromycin or ceftriaxone
C. difficileOral vancomycin 125 mg QID × 10 days (preferred); metronidazole if mild
Traveler's diarrheaAzithromycin or rifaximin × 3 days
CholeraDoxycycline 300 mg single dose; azithromycin in children/pregnant
E. coli O157:H7 (STEC)Avoid antibiotics — increases risk of HUS
GiardiaMetronidazole 250 mg TID × 7–10 days or tinidazole single dose
CryptosporidiumNitazoxanide (especially in immunocompromised)

8. Diet and Feeding

  • Early refeeding is encouraged once rehydration is underway — fasting worsens bowel absorptive capacity
  • Resume age-appropriate diet as soon as tolerated
  • In children, breastfeeding should continue throughout illness
  • Avoid: sugary drinks, apple juice (full strength), carbonated beverages (hyperosmolar — worsen diarrhea)
  • Lactose restriction is generally not necessary unless clear lactose intolerance

9. Zinc Supplementation (Children)

  • WHO recommends zinc 10–20 mg/day × 10–14 days in children <5 years in developing settings
  • Reduces severity and duration of diarrhea, decreases risk of future episodes

10. Probiotics

  • Some evidence for Lactobacillus rhamnosus GG and Saccharomyces boulardii reducing duration of diarrhea by ~1 day in children
  • Not universally recommended in all guidelines but reasonable adjunct

11. Disposition

CriteriaDisposition
Well-appearing, minimal/no dehydration, tolerating ORTDischarge with return precautions
Moderate dehydration responding to IV/ORTObserve; discharge when tolerating fluids
Severe dehydration, persistent vomiting, unable to tolerate ORTAdmit
Bloody diarrhea with severe illness, sepsis signsAdmit + urgent investigation
Very young infants, elderly, immunocompromised, comorbiditiesLower threshold for admission
Return precautions — advise to return if:
  • No improvement in 48 hours
  • Worsening symptoms, inability to keep fluids down
  • Bloody stools, high fever
  • Signs of worsening dehydration (markedly reduced urine output, extreme lethargy)

Key Pathogens Summary

PathogenIncubationDurationKey Feature
Norovirus12–48 h1–3 daysExplosive vomiting, mild diarrhea, outbreaks
Rotavirus1–3 days3–8 daysChildren <5, watery diarrhea
Campylobacter2–5 days5–14 daysMost common bacterial; dysentery, raw poultry
Salmonella (NTS)12–24 h2–7 daysEggs/poultry; fever + watery diarrhea
Shigella1–2 days2–7 daysDysentery, toxigenic; person-to-person
E. coli O157:H73–8 days5–10 daysBloody diarrhea, HUS risk; avoid antibiotics
Staph aureus1–6 h<24 hPreformed toxin, rapid onset vomiting
C. difficileVariableVariableRecent antibiotics, hospital-acquired
Giardia1–3 weeksWeeksCamping/water, bloating, fatty stools

Sources:
  • Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th ed., Ch. 131
  • Rosen's Emergency Medicine: Concepts and Clinical Practice, Ch. 80
  • Yamada's Textbook of Gastroenterology, 7th ed., Ch. Syndromic Management of Gastroenteritis

CVS examination

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cardiovascular examination JVP jugular venous pulse waveform

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Cardiovascular System (CVS) Examination


SEQUENCE OF EXAMINATION

General approach: Inspection → Pulse → Blood Pressure → JVP → Precordium (Inspection → Palpation → Auscultation) → Peripheral signs

1. GENERAL INSPECTION

Look for signs from the end of the bed:
Facies & habitus:
  • Malar flush (mitral stenosis)
  • Pallor (anaemia, low output states)
  • Central cyanosis (check tongue and lips — congenital heart disease, Eisenmenger's)
  • Peripheral cyanosis (fingers/toes — low output, cold)
  • Marfan's syndrome (tall, arachnodactyly, high-arched palate — aortic root disease)
  • Turner's syndrome (coarctation of aorta)
  • Down's syndrome (ASD, VSD, AV canal defects)
Signs of distress: dyspnoea at rest, orthopnoea (pillows), cachexia (chronic heart failure)

2. HANDS

SignAssociation
ClubbingCyanotic congenital heart disease, infective endocarditis
Splinter haemorrhagesInfective endocarditis (also trauma)
Osler's nodesPainful, tender nodules on fingertips — infective endocarditis
Janeway lesionsPainless haemorrhagic macules on palms — infective endocarditis
KoilonychiaIron deficiency → high-output cardiac failure
Peripheral cyanosis / pallorPoor perfusion
Tendon xanthomataHypercholesterolaemia → IHD
Capillary refill time: Normal <2 seconds.

3. RADIAL PULSE

Assess simultaneously at both wrists (radio-radial delay → coarctation of aorta, aortic dissection, subclavian stenosis).

Rate

  • Normal: 60–100 bpm
  • Bradycardia <60, tachycardia >100

Rhythm

  • Regular — sinus rhythm
  • Irregularly irregular — atrial fibrillation
  • Regularly irregular — ectopics, 2nd degree AV block

Character (best assessed at carotid)

PulseDescriptionCause
NormalSmooth upstroke, sustained peak
Slow-rising (pulsus parvus et tardus)Weak, delayed upstrokeAortic stenosis
Collapsing / water-hammerRapid upstroke, quick collapseAortic regurgitation
BisferiensDouble-peaked in systoleSevere AR + AS combined
Pulsus alternansAlternating strong and weak beatsSevere LV dysfunction
Pulsus paradoxusExaggerated fall in systolic BP (>10 mmHg) during inspirationCardiac tamponade, severe asthma
Pulsus bigeminusAlternating normal + ectopic beatsBigeminy

Volume: Full, normal, or low (reduced → poor output, dehydration, AS)


4. BLOOD PRESSURE

  • Measure in both arms (difference >20 mmHg → aortic dissection, subclavian stenosis, coarctation)
  • Pulse pressure = systolic − diastolic
    • Wide (>60 mmHg): AR, PDA, hyperthyroidism, anaemia, fever
    • Narrow (<25 mmHg): AS, cardiac tamponade, severe heart failure
Postural BP: Drop >20 mmHg systolic or >10 mmHg diastolic on standing = orthostatic hypotension

5. JUGULAR VENOUS PRESSURE (JVP)

JVP waveform diagram showing normal and tricuspid regurgitation patterns
Bedside JVP assessment positioning

Technique

  • Patient at 30–45° with head slightly rotated to the left
  • Use the internal jugular vein (preferred; not valved, directly in line with RA)
  • Measure vertical height of pulsation above the sternal angle (angle of Louis)
  • Normal: <4.5 cm above sternal angle at 45°
  • Pulsations above the clavicle in the sitting position are clearly abnormal (clavicle-to-RA distance ≥10 cm)

JVP vs Carotid Pulse — How to Distinguish

FeatureJVPCarotid
WaveformBiphasic (two peaks in sinus rhythm)Monophasic
PalpableNot easily palpableEasily palpable
ObliterableObliterated by gentle pressureNot obliterated
Changes with postureYes — falls with sitting upNo
Changes with inspirationFalls in inspiration (normally)No change

The JVP Waveform

ComponentTimingRepresents
a waveJust after P wave, before S1Right atrial presystolic contraction
c waveAfter a waveTricuspid valve pushed into RA during early ventricular systole
x descentAfter a/c wavesFall in RA pressure after tricuspid opening
v waveDuring ventricular systoleAtrial filling (venous return against closed tricuspid)
y descentAfter v waveFall in RA pressure as tricuspid opens and RV fills

Abnormal JVP Waveforms

AbnormalityCause
Elevated JVP (raised all components)Right heart failure, tricuspid stenosis, cardiac tamponade, SVC obstruction, fluid overload
Giant a waveTricuspid stenosis, pulmonary hypertension, RV hypertrophy (reduced RV compliance)
Cannon a waveAV dissociation (RA contracts against closed tricuspid) — confirms ventricular tachycardia
Absent a waveAtrial fibrillation
Giant v waveTricuspid regurgitation (ventricularnised waveform, steep y descent)
Prominent x descentCardiac tamponade, constrictive pericarditis
Prominent y descentConstrictive pericarditis, severe TR
Kussmaul's signJVP rises with inspiration (opposite of normal) — constrictive pericarditis, RV infarct
Abdominojugular refluxSustained JVP rise >3 cm with abdominal pressure × 10 sec — right heart failure, volume overload

6. FACE & NECK

  • Eyes: corneal arcus (hypercholesterolaemia), xanthelasma (hyperlipidaemia), conjunctival pallor (anaemia)
  • Mouth: central cyanosis (tongue), high-arched palate (Marfan's)
  • Carotid pulse: character and volume (slow-rising = AS; collapsing = AR)
  • Carotid bruits: auscultate over carotids (atherosclerosis, radiation of AS)

7. PRECORDIUM

Inspection

  • Chest shape: pectus excavatum, pectus carinatum, kyphoscoliosis (may displace heart, cause murmurs)
  • Visible apex beat: normally in 5th ICS, mid-clavicular line
  • Scars: midline sternotomy (CABG, valve replacement), left lateral thoracotomy (mitral valvotomy, PDA ligation), pacemaker/ICD pocket (left infraclavicular)
  • Prominent pulsations: left parasternal heave, visible apex

Palpation

Apex beat:
  • Normally: 5th ICS, mid-clavicular line
  • Assess: position, character, and area
Apex CharacterDescriptionCause
Heaving / sustained / pressure-loadedForceful, sustained, not displacedAortic stenosis, hypertension (LVH)
Thrusting / hyperdynamic / volume-loadedForceful, may be displacedAortic or mitral regurgitation
Displaced laterally ± inferiorlyBeyond MCLLV dilatation (DCM, severe MR, AR)
TappingPalpable S1Mitral stenosis
Double impulseTwo pulsationsHOCM, LV aneurysm
ImpalpableObesity, COPD, effusion, dextrocardia
Parasternal heave (left hand over left sternal edge):
  • Sustained left parasternal lift → RV hypertrophy / dilatation (pulmonary hypertension, pulmonary stenosis, ASD)
Thrills (palpable murmurs — indicate grade ≥4/6):
  • Systolic thrill at aortic area → AS
  • Systolic thrill at LSE → VSD, HOCM
  • Diastolic thrill at apex → MS
P2 palpability: Palpable P2 at left upper sternal edge → pulmonary hypertension

8. AUSCULTATION

Technique

  • Diaphragm: high-frequency sounds (S1, S2, AR murmur, pericardial rub)
  • Bell: low-frequency sounds (S3, S4, MS rumble) — use with light pressure

Auscultatory Areas

AreaLocationBest Hears
Aortic2nd ICS, right sternal edgeAS, AR
Pulmonary2nd ICS, left sternal edgePS, pulmonary regurgitation, P2
TricuspidLower left sternal edge (4th/5th ICS)TR, TS, VSD
Mitral (Apex)5th ICS, mid-clavicular lineMS, MR, S3, S4
Manoeuvres:
  • Left lateral decubitus position + bell at apex → best for MS rumble and S3/S4
  • Sitting forward, expiration → best for AR early diastolic murmur
  • Standing → suppresses most murmurs; HOCM louder, MVP click moves earlier
  • Squatting → most murmurs louder; HOCM softer, MVP click moves later
  • Valsalva → HOCM louder (decreased preload)

Heart Sounds

S1 (Mitral + Tricuspid Closure)

S1 AbnormalityCause
Loud S1Mitral stenosis (if mobile valve), short PR interval, tachycardia
Soft S1Long PR interval (1st degree AV block), MR, calcified/immobile mitral valve, poor LV function
Variable S1AF, complete heart block (cannon a wave), ectopics

S2 (Aortic + Pulmonary Closure)

  • Physiological splitting of S2: heard in inspiration (A2 before P2); splitting widens in inspiration, narrows in expiration
  • Wide fixed splitting: ASD (equalization of RA/LA pressures)
  • Wide splitting with respiratory variation: RBBB, pulmonary stenosis (delayed P2), pulmonary hypertension with RV failure
  • Reversed/paradoxical splitting: LBBB, AS, HOCM (delayed A2; splits on expiration, closes on inspiration)
  • Loud A2: systemic hypertension
  • Loud P2 (palpable): pulmonary hypertension
  • Soft A2: severe AS

S3 (Ventricular Gallop)

  • Low-pitched, heard at apex with bell, in early diastole (Ken-tuck-y)
  • Physiological in children and young adults (<40 years)
  • Pathological in adults → indicates LV failure, dilated cardiomyopathy, severe MR

S4 (Atrial Gallop)

  • Low-pitched, heard just before S1 (Ten-nes-see)
  • Due to atrial contraction into a stiff, non-compliant ventricle
  • Causes: LVH (hypertension, AS, HOCM), acute MI, hypertrophic cardiomyopathy
  • Never heard in AF (no atrial contraction)

Opening Snap (OS)

  • High-pitched, early diastolic sound after S2
  • Mitral stenosis (mobile, non-calcified valve)
  • Short S2–OS interval → more severe MS (high LA pressure)

Ejection Click

  • High-pitched early systolic click
  • Aortic or pulmonary valve stenosis (bicuspid aortic valve, valvular PS)
  • Pulmonary ejection click softens with inspiration (unique among right-sided sounds)

Mid-Systolic Click

  • Mitral valve prolapse (MVP)
  • Moves earlier with standing/Valsalva (reduced preload)
  • Moves later with squatting/leg raising (increased preload)

Pericardial Friction Rub

  • High-pitched, scratchy, three-component sound (systolic + early diastolic + presystolic)
  • Heard best with patient sitting forward, in expiration
  • Acute pericarditis, post-MI (Dressler's syndrome), uraemia

Murmurs

Grading (Levine Scale)

GradeDescription
1/6Very faint; heard only with concentration
2/6Faint but immediately audible
3/6Moderately loud; no thrill
4/6Loud; thrill present
5/6Very loud; thrill; heard with stethoscope edge
6/6Audible without stethoscope

Systolic Murmurs

MurmurTimingLocationRadiationQualityKey Features
Aortic StenosisEjection systolic (ESM)Aortic areaCarotidsHarsh, crescendo-decrescendoSlow-rising pulse, soft A2, S4; radiates to carotids
Mitral RegurgitationPansystolicApexAxillaSoft, blowingDisplaced apex, soft S1, S3
Tricuspid RegurgitationPansystolicLower LSENo radiationBlowingLouder in inspiration (Carvallo's sign), elevated JVP with giant v wave
VSDPansystolicLower LSEAcross precordiumHarshThrill common
HOCMEjection systolicLSE/ApexHarshLouder with Valsalva/standing; softer with squatting/leg raise
Pulmonary StenosisEjection systolicPulmonary areaHarshEjection click, wide P2 splitting
MVPLate systolicApexPreceded by mid-systolic click

Diastolic Murmurs (always pathological)

MurmurTimingLocationQualityKey Features
Aortic RegurgitationEarly diastolic (decrescendo)LSE (sitting forward, expiration)Soft, high-pitched, blowingCollapsing pulse, wide pulse pressure
Mitral StenosisMid-diastolic rumbleApex (LLD, bell)Low-pitched, rumblingLoud S1, opening snap; presystolic accentuation in sinus rhythm
Pulmonary RegurgitationEarly diastolicPulmonary areaBlowingGraham Steell murmur in pulmonary HTN
Tricuspid StenosisMid-diastolicLower LSELow-pitchedRare; louder in inspiration

Continuous Murmurs

  • PDA: continuous "machinery" murmur, upper LSE
  • AV fistula, coarctation collaterals

9. PERIPHERAL EXAMINATION

  • Sacral oedema: pitting, in bedridden patients (right heart failure)
  • Ankle/leg oedema: bilateral pitting → right heart failure, hypoalbuminaemia; unilateral → DVT, lymphoedema
  • Hepatomegaly: tender, pulsatile in TR; congestive hepatomegaly in RHF
  • Splenomegaly: infective endocarditis
  • Ascites: severe right heart failure, constrictive pericarditis
  • Lung bases: fine end-inspiratory crepitations → pulmonary oedema (LHF)

10. CLOSING THE EXAMINATION

State you would like to:
  • Check temperature chart, urine output
  • Review ECG, chest X-ray, echocardiogram
  • Measure oxygen saturation
  • Fundoscopy (hypertensive/diabetic changes, Roth spots in endocarditis)

Sources:
  • Harrison's Principles of Internal Medicine, 22nd ed., Ch. 246 — Cardiovascular Examination
  • Fuster & Hurst's The Heart, 15th ed. — Clinical Cardiovascular Examination
  • Goldman-Cecil Medicine — Physical Examination for Detection of Cardiovascular Disease

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CVS Examination — Illustrated Guide


1. GENERAL INSPECTION & HANDS

Start from the end of the bed — look for dyspnoea, cyanosis, cachexia, abnormal habitus (Marfan's, Down's).
Hands — key signs:
Clubbing with peripheral cyanosis
Digital clubbing with peripheral cyanosis — seen in cyanotic congenital heart disease and infective endocarditis
Bilateral clubbing — drumstick appearance
Severe bilateral digital clubbing — loss of Schamroth window, increased Lovibond angle
Splinter haemorrhages
Splinter haemorrhages (linear dark streaks under nail bed) — classic sign of infective endocarditis or vasculitis
SignSignificance
ClubbingCyanotic CHD, IE
Splinter haemorrhagesInfective endocarditis
Osler's nodesPainful fingertip nodules — IE
Janeway lesionsPainless palmar macules — IE
XanthomataHypercholesterolaemia → IHD
Peripheral cyanosisLow output, poor perfusion

2. PULSE — Rate, Rhythm, Character

Assess radial pulse for rate and rhythm. Assess character at the carotid (best site).
Pulse TypeFeelCause
NormalSmooth upstroke, sustained peak
Slow-rising (pulsus parvus et tardus)Weak, delayed, plateauAortic stenosis
Collapsing (water-hammer)Rapid upstroke, sudden collapseAortic regurgitation
Pulsus alternansAlternating strong/weak beatsSevere LV dysfunction
Pulsus paradoxusSystolic BP falls >10 mmHg on inspirationCardiac tamponade
BisferiensDouble peak in systoleSevere AR ± AS, HOCM
Radio-radial delay (different pulses in each wrist) → coarctation of aorta / aortic dissection Radio-femoral delay → coarctation of aorta

3. BLOOD PRESSURE

  • Measure both arms — difference >20 mmHg → aortic dissection, subclavian stenosis
  • Wide pulse pressure (>60 mmHg): AR, PDA, thyrotoxicosis, anaemia
  • Narrow pulse pressure (<25 mmHg): severe AS, tamponade, heart failure

4. JUGULAR VENOUS PRESSURE (JVP)

Technique — Patient positioning

JVP assessment — patient at 45°, head turned left, IJV course marked
Patient positioned at 45°. Blue dotted line marks the course of the internal jugular vein (IJV), running deep to the sternocleidomastoid. The vertical height of pulsation above the sternal angle is measured.
  • Normal: <4.5 cm above sternal angle at 45°
  • Pulsation above the clavicle in sitting = always elevated (clavicle–RA distance ≥10 cm)
  • Use internal jugular vein (preferred — not valved, directly communicates with RA)

The JVP Waveform

JVP waveform — normal, mild and severe TR, with ECG correlation
Panel A: Normal JVP waveform showing a, c, x, v, y components. Panel B: Progressive changes in tricuspid regurgitation — giant v wave increasingly dominates and merges with c wave. Panel C: Timing of JVP waveform relative to the ECG — a wave follows the P wave; v wave occurs during ventricular systole.
ComponentTimingRepresents
a waveAfter P wave, before S1RA presystolic contraction
c waveEarly systoleTricuspid pushed into RA
x descentAfter a/cRA pressure fall
v waveDuring ventricular systolePassive atrial filling
y descentAfter vTricuspid opens, RV fills

Abnormal JVP — Clinical Correlations

AbnormalityCause
Elevated JVP (all components raised)RHF, fluid overload, tamponade, SVC obstruction
Giant a waveTS, pulmonary HTN, RVH
Cannon a waveAV dissociation → confirms VT
Absent a waveAtrial fibrillation
Giant v waveTricuspid regurgitation
Prominent x descentCardiac tamponade
Prominent y descentConstrictive pericarditis, severe TR
Kussmaul's signJVP ↑ on inspiration — constrictive pericarditis, RV infarct
Abdominojugular refluxJVP rises >3 cm with sustained abdominal pressure — RHF

5. PRECORDIUM

Auscultation Areas

Cardiac auscultation areas on the precordium
Standard stethoscope placement landmarks on the anterior chest wall
AreaLocationBest hears
Aortic2nd ICS, right sternal edgeAS, AR
Pulmonary2nd ICS, left sternal edgePS, P2, PR
Tricuspid4th–5th ICS, left sternal edgeTR, TS, VSD
Mitral (Apex)5th ICS, mid-clavicular lineMS, MR, S3, S4

Apex Beat Character

CharacterFeelCause
Heaving / pressure-loadedSustained, not displacedAS, hypertension (LVH)
Thrusting / volume-loadedHyperdynamic, may be displacedAR, MR
Displaced laterallyBeyond MCLLV dilatation (DCM, severe MR/AR)
TappingPalpable S1Mitral stenosis
Double impulseTwo pulsationsHOCM, LV aneurysm
Left parasternal heave → RV hypertrophy (pulmonary hypertension, ASD, PS)

6. HEART SOUNDS

S1 & S2 — Normal and Abnormal

SoundNormalAbnormalCause
S1Closure of mitral + tricuspidLoud S1MS (mobile valve), short PR, tachycardia
Soft S1Long PR (1° HB), calcified MV, poor LV function
Variable S1AF, complete heart block
S2Closure of aortic (A2) + pulmonary (P2)Wide fixed splitASD
Wide variable splitRBBB, pulmonary stenosis
Physiological split widens in inspirationParadoxical split (widens in expiration)LBBB, severe AS
Loud P2 (palpable)Pulmonary hypertension

S3 and S4

Extra SoundTimingMnemonicSignificance
S3 (ventricular gallop)Early diastole (after S2)Ken-tuck-YPathological in adults → LV failure, DCM, severe MR
S4 (atrial gallop)Late diastole (before S1)TEN-nes-seeLVH (HTN, AS, HOCM), acute MI; absent in AF
Use the bell with light pressure at the apex for S3 and S4. Position patient in left lateral decubitus.

Opening Snap, Clicks, Rub

SoundTimingCause
Opening snap (high-pitched)Early diastole after S2MS (mobile valve); shorter S2–OS interval = more severe
Ejection click (early systolic)Immediately after S1AS (bicuspid valve), PS
Mid-systolic clickMid-systoleMVP — moves earlier with standing/Valsalva
Pericardial rubScratchy, 3-componentAcute pericarditis, Dressler's, uraemia

7. MURMURS

Radiation Patterns — AS and MR

Murmur distribution patterns for AS and MR by severity
AS murmur: begins isolated at the base, spreads to apical-base distribution as severity increases (radiates to carotids). MR murmur: begins isolated at apex, spreads broadly toward the axilla and base as severity increases.

Systolic Murmurs

MurmurTypeLocationRadiationKey Clues
Aortic StenosisEjection systolic (ESM)Aortic areaCarotidsSlow-rising pulse, soft A2, S4; loudest in expiration
Mitral RegurgitationPansystolicApexAxillaDisplaced apex, soft S1, S3; loudest in expiration/left lateral
Tricuspid RegurgitationPansystolicLower LSELouder in inspiration (Carvallo's sign); giant v wave in JVP
VSDPansystolicLower LSEAll over precordiumLoud, thrill common
HOCMESMLSE/ApexLouder with Valsalva/standing; softer with squatting
Pulmonary StenosisESMPulmonary areaEjection click; wide split S2
MVPLate systolicApexPreceded by mid-systolic click

Diastolic Murmurs (always pathological)

MurmurTimingLocationKey Clues
Aortic RegurgitationEarly diastolic decrescendoLSE (sitting forward, expiration)Collapsing pulse, wide PP, displaced apex
Mitral StenosisMid-diastolic rumbleApex (bell, LLD, expiration)Loud S1, OS, tapping apex; presystolic accentuation in SR
Pulmonary RegurgitationEarly diastolicPulmonary areaGraham Steell murmur in pulmonary HTN

Dynamic Manoeuvres

ManoeuvreEffect on PreloadHOCMAS/MR/ARMVP Click
Valsalva / StandingDecreasesLouderSofterMoves earlier
Squatting / Leg raiseIncreasesSofterLouderMoves later
InspirationIncreases RV fillingRight-sided murmurs louder

8. PERIPHERAL SIGNS (Complete the Exam)

FindingSignificance
Bilateral ankle/sacral pitting oedemaRight heart failure
Tender hepatomegalyCongestive hepatomegaly (RHF)
Pulsatile liverTricuspid regurgitation
Fine basal crepitationsPulmonary oedema (LHF)
SplenomegalyInfective endocarditis
Xanthelasma / corneal arcusHypercholesterolaemia
Roth spots (fundoscopy)Infective endocarditis

Summary — "What to Say at the End"

"To complete my examination I would like to:
  • Check the blood pressure in both arms and lying/standing
  • Review the ECG, chest X-ray, and echocardiogram
  • Measure oxygen saturation
  • Perform fundoscopy (HTN, diabetic, Roth spots)
  • Check urine dipstick (haematuria in IE, proteinuria in HTN)"

Sources: Harrison's Principles of Internal Medicine 22nd ed. — Cardiovascular Examination | Fuster & Hurst's The Heart, 15th ed.
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