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Clinical pathways
Dr Saeed Ahmad Chaudhary
Medical Officer ER
Recep Tayyip Erdogan Hospital
(Indus Hospital ) Muzaffargarh
Objectives
 UNDERSTAND THE CAUSES OF CHEST PAIN
 UNDERSTAND THE IMPORTANCE OF HISTORY
TAKING
 REALIZE THE LIFE THREATENING CAUSES OF
CHEST PAIN
 INVESTIGATIONS
 LEARN COMMON ECG CHANGES
Chest Pain ( Don’t Panic)
 5 Million emergency department visits
 2 million hospitalizations annually with cost of more
than $8 billion
 Cardiac etiology found in less than one third
 2% of patients with acute MI are unrecognized and
discharged from the ED
Accurate Diagnosis Remains A
Challenge
CHEST PAIN ASSESSMENT
A
• History
• Examination
B
• ECG
• CARDIAC EZYMES
C
• CXR
• OTHERS
INITIAL APPROACH
 Assume the worst!
Before any Diagnostic studies
 100% Oxygen
 IV access
 Monitoring
 ECG quickly
 History taking
Chest Pain: Physical Examination
 _ Vital signs and general appearance
 _ Carotids and JVP
 _ Lungs
 _ Cardiac examination
 _ Thoracic cage
 _ Abdominal examination
 _ Periphery (pulses)
 _ Skin
Chest Pain? Origin?
• HEART
• LUNGS
• OESOPHAGUS
• MUSCULOSKELETAL STRUCTURES OF
THORAX NECK,OR SHOULDER
• ABDOMEN
• ANXIETY MANIFESTATION
WHAT LIES IN THE CHEST
SKIN
MUSCLES
BONES
JOINTS
HEART AND VESSELS
LUNGS AND AIRWAYS
OESOPHAGUS
NERVES
IS THE KEY TO THE
DIAGNOSIS OF ETIOLOGY
OF CHEST PAIN
HISTORY
PAIN HOW DESCRIBED?
 STABBING
 BURNING
 TWISTING
 TEARING
 SQUEEZING
 TERRIFYING
 NAUSEATING
 SICKENING
Penetrating or Tissue
Destructive Process
Bodily Or Emotional
Reaction
H/O CHEST PAIN IN THE
EMERGENCY DEPARTMENT
HEART ATTACK
 ANSWER IS NO……
RELAX
 IS IT ENOUGH TO RULE OUT
HEART ATTACK?
Life Threatening Chest Pain in
the Emergency Department
• Myocardial Infarction
• USA
• Aortic Dissection
• Tension Pneumothorax
• Pulmonary Embolus
• Ruptured
Esophagus/Perforated
Life Threatening Chest Pain in
the Emergency Department
COMMON CAUSES OF CHEST PAIN
 ANXIETY
 CARDIAC
 AORTIC
 OESOPHAGEAL
 LUNGS/PLEURA
 MUSCULOSKELETAL
 NEUROLOGICAL
MYOCARDIAL
ISCHEMIA(ANGINA)
MI
MYOCARDITIS
PERICARDITIS
MVP
ESOPHAGITIS
ESOPH SPASM
MW SYNDROME
AORTIC DISSECTION
AORTIC ANEURYSM
BRONCHOSPASM:::PE:::PI
PNEUMONIA:::::TB:::::CTDs
TRACHEITIS PLEURITIS
PNEUMOTHORAX
MALIGNANCY
OA ,RIB #
I/C MUSCLE INJURY
TEITZE`S SYND
BORNHOLM`S DISEASE
PROLAPSED I/V DISC
HERPES ZOSTER
THORACIC OUTLET
SYNDROME
CARDIAC
OR
NON-CARDIAC PAIN?
LIFE THREATENING CAUSES OF CHEST PAIN
ISCHEMIC CARDIAC PAIN
Site Of Origin of Chest Pain Central
Character Of
Chest Pain
•TYPICALLY DULL
•CONSTRICTING IN NECK
•CHOKING
•HEAVY
•DESCRIBED BY PATIENTS AS
---SQUEEZING
-------CRUSHING
-----------BURNING
---------------ACHING
•BUT NOT SHARP STABBING
•BUT NOT PRICKING, KNIFE-
LIKE
•SENSATION CAN BE DESCRIBED
AS BREATHLESSNESS
SEVERE
PROLONGED
ASSOCIATED WITH
CLINICAL
EVIDENCE OF
ACUTE SERIOUS
ILLNESS
RADIATION
 Because of common/overlapping neural pathways, many
conditions, both cardiac and extra-cardiac can result in chest pain.
 Cardiac pain is mediated through upper 5 thoracic ganglia and
spinal roots, but ramifications from adjoining spinal roots
always exist.
 Therefore pain in the chest may originate from any structure in
thorax and upper abdomen innervated through lower cervical to
D6/D7 spinal roots
•NECK
•JAW
•UPPER OR LOWER ARM
•BACK
ASSOCIATED FEATURES
SINGS
SYMPATHATIC
STIMULATION
PALLOR
SWEATING
TACHYCARDIA
VAGAL
STIMULATION
NAUSEA
BRADYCARDIA
SIGNS OF IMPAIRED MYOCARDIAL FUNCTION
HYPOTENSION
OLIGURIA
COLD PERIPHERIES
NARROW PULSE PRESSURE
RAISED JVP
S3
QUIET S1
DIFFUSE APICAL IMPULSE
LUNG CREPTS
SIGNS OF TISSUE DAMAGE-------FEVER
SIGNS OF COMPLICATIONS----MR,,,,,,,PERICARDITIS
Painless ACS
GRACE Study
– 8.4% (1763/20,881) patients
with ACS presented WITHOUT
chest pain
• Not initially recognised as ACS in
23.8%
– Dyspnoea 49.3%
– Diaphoresis 26.2%
– N&V 24.3%
– Syncope 19.1%
Diabetic
Females
Elderly
Risk
Factors
Cardiac Risk Factors
•Smoking
•Diabetes
•HTN
•Hyperlipidaemia
•Family History
•Known Ischemic Heart Disease
•Male ,
•Age >40
•Chronic cocaine use in the
younger pts.
Lesser known cardiac risk factors
•SLE
•Rheumatoid Disease
•Asian
•Prothrombotic Disease
•Cocaine
INVESTIGATIONS
ECG Provides documentary evidence of cardiac
ischemia/infarction when positive.
Normal in ~ 50% initially who are later Dx as having an AMI.
A normal ECG does not exclude an AMI
ST-Segment Elevation MI
ST Depression or Dynamic T wave Inversions
New LBBB
Myoglobin CK-MB
Isoenzyme
Troponin
( T, I)
Specific/Sensitive high sensitivity
but poor
specificity
Less Sensitivity
and specificity
Most Specific &
Most Sensitive
Raises in 1 hour 4-6 Hours 4-8 Hours
Peaks in 4-12 Hours 24 Hours 18-24 Hours
Remains
Elevated
24-36 hours 36-48 Hours 10-14 Days
Remarks 100% within 3 hrs
of AMI
predictive of
mortality
prognostic
information
False Positive Skeletal muscle
injury, Heavy
alcohol, Renal
failure , Shock
states
exercise, trauma,
muscle dz, DM,
PE
renal dz,
poly/dermatomyo
sitis
PLASMA BIOCHEMICAL MARKERS
CBC -----------LEUKOCYTOSIS ON 1st DAY—PEAKS 2-4
DAYS
ESR------------RAISED WITHIN 3 DAYS
CRP------------ELEVATED
CXR------------PUMONARY EDEMA,,,CARDIOMEGALY
ECHO--------WMA?
Chest Pain
Duration
ECG
a) ST
b) T wave
Cardiac
Enzymes
Troponin
(T,I)
Angina Less than 10 min a) Normal
b) Normal
-ve -ve
Un-stable
Angina
> 10 mins a) Slight
Depression/
Elevation
b) Poor/
Inversion
-ve /slightly
raised
-ve
NSTMI > 20 mins ST Depression +ve +ve
STEMI > 20 mins ST Elevation +ve +ve
Aortic Dissection
Clinical Presentation
 History:
 >90% with abrupt and severe pain in the chest or
between the scapulae
 “tearing” or “ripping”
 Can be dull or pressure-like
 Anterior chest ~ ascending aorta -Type A; Back ~
descending aorta –Type B
 Nausea, vomiting, diaphoresis common
 Definition:
 Intimal tear with entry of blood into the media
 “dissects” between the intima and adventitia
 #1 site: ascending aorta at the ligamentum arteriosum
 Stanford Classification:
 A: involves Ascending aorta (w/ or w/o descending)
 80% of dissections
 B: descending aorta only
Associated signs & symptoms based on
progression of dissection:
Carotid arteries: stroke
Spinal arteries: paraplegia
Abdominal aorta/renal arteries/iliacs: Abdominal/flank
pain
Coronary arteries: pericardial effusion/tamponade
Laryngeal nerve compression: hoarseness
Tracheal compression: dyspnea/stridor/wheezing
Esophageal compression: dysphagia
Physical Examination:
•BP differential?
bilateral arm BPs – significant if >20mmHg difference
Most commonly: normal heart and lung
•Aortic insufficiency murmur in 16-20%
•Unequal, decreased, or absent peripheral pulses only found in 50%
 ECG
– AMI (new Q or STE) – 3.2%
– Ischaemia – 15%
– No abnormalities – 31.3%
– Non specific T wave changes – 41.4%
– LVH – 26.1%
Investigations
Risk Factors – Atherosclerosis, HTN (uncontrolled),
Coarctation of Aorta, Bicuspid Aortic Valve, Aortic
Stenosis, Marfan Syn, Ehlers-Danlos Syn, Pregnancy
CXR
CXR
a)-Mediastinal widening (61.6%) , b)- Widening of aortic contour (49.9%),
c)-Pleural effusion (L>R) (19.2%), d)-Apical pleural cap, e)-Calcium sign
(14%), f)– Depressed left main bronchus , g)-Tracheal or oesophageal
displacement, h)-No abnormalities noted 12.4%
TEE ( High Sensitivity and Specificity )
Aortic Angiography
CT or MR
Pulmonary Embolism
“Classic Triad”:
Sharp Pleuritic CP, Dyspnea, hemoptysis in only 20% of pts.
Pain is often pleural
Reproduciable with breathing, palpation
•Dyspnea (79%)
•Dyspnea at rest (61%)
•Dyspnea exertion (16%)
•Orthopnea (36%)
•Pleuritic chest pain (49%)
•Non pleuritic chest pain (17%)
•Cough (43%)
•Calf or thigh swelling (39%)
•Calf or thigh pain (41%)
SIGNS
•RR > 20/min (57%)
•Tachycardia (26%)
•Increased P2 (15%)
•JVP distension (13%)
•Rales (21%)
•Wheeze (3%)
•Decreased breath sounds (21%)
•Signs of calf or thigh DVT (47%)
Hypercoagulability
Pregnancy; malignancy; estrogen
therapy; deficiencies of protein C,
protein S, AT III
Endothelial
damage
Recent surgery, trauma
Venous stasis
Prolonged travel;
bed Ridden
#1 Risk Factor = Prior DVT/PE
Risk Factors;
Virchow’s triad:
 10-15% of patients will have no
identifiable risk factor at the time of
presentation
Pre-test Probability
Investigations;
 ECG
– Tachycardia most common • approx. 1/3 patients
– T wave inversion • V1-3 (inferior leads)
– S1Q3T3 Pattern • 20% patients
CXR; Specific signs in massive/submassive PE
Fleisher’s sign – distended central pulmonary artery
Fleisher Lines – long bands of focal atelectasis
Hampton Hump – pleural wedge shaped consolidation
Biomarkers
– Markers of right heart strain
– Troponin
– BNP
• Takes time for rise
• RV smaller muscle mass therefore threshold lower
• >90
D Dimer
–ve – discharge False –ve <1%
D Dimer +ve
– Many false positives
Malignancy– Recent surgery– Infection– DIC– Trauma– ACS– CVA– AF
Vacuities-Superficial phlebitis
ECHO
– RV dilatation
– RV hypokinesis
– Pardoxical septal wall movement
– Tricuspid regurgitation
Imaging
•COLLOR DOPPLER
•VENTILATION–PERFUSION (VQ) SCAN
if normal CXR
•CT PULMONARY ANGIOGRAPHY (CTPA)
if definitive diagnosis urgent
•MRI
Tension Pneumothorax
Clinical Presentation;
 SUDDEN-ONSET UNILAT. CHEST PAIN,PLEURITIC SHARP
 BREATHLESSNESS
 ASYMPTOMATIC (NOT TENSION PNEUMOTHORAX)
 DEC OR ABSENT BREATH SOUNDS (IF PNEUMOTHORAX MORE THAN15%).
 RESONANT ON PERCUSSION
 MEDIASTINAL DISPLACEMENT TO OPPOSITE SIDE
 TACHYCARDIA
 HYPOTENSION
 CYANOSIS
 TRACHEAL DISPLACEMENT
 ASYMMETRIC LUNG EXPANSION.
Risks Factors:
Sudden Change in barometric pressure
Smokers, COPD, Idiopathic Bleb DZ
Especially tall, thin male smokers
Only 10 – 20% occur with exertion
Tension Pneumothorax
when a pneumothorax (primary spontaneous, secondary
spontaneous, or traumatic) leads to significant impairment
of Respiration and/or Blood Circulation
Diagnosis;
CLINICAL
CXR
Diagnosis can be
difficult in patients of
COPD
Esophageal Rupture: Boerhaave
Syndrome
 Substernal, sharp CP
 Sudden onset after forceful vomiting
 Dyspneic, diaphoretic, and ill-appearing
 Shock
 Sub-cutaneous Emphysema
Causes?
 Most Common Iatrogenic (Endoscopic Perforation)
 Malignancy
 Corrosive Strictures Perforation
 Post Radiotherapy Strictures
CXR;
SQ air, Pleural Effusions, Pneumothorax, pneumoperitoneum, pneumomediastinum
Water Soluble Contrast Study
Pericarditis
 Chest pain , Severe Pleuritic localized
 Aggravated by lying supine, coughing swallowing and
deep inspiration.
 Relieved by sitting up and leaning forward.
 It might be preceded by viral illness.
Inflammation Of Pericardial Sac
Causes;
Idiopathic
Infection
Acute MI
Uremia
Neoplasm
(Hodgkin
Lymphoma,
breast and Ca
lung )
PERICARDIAL FRICTION RUB
FEVER
LEUCOCYTOSIS
ECG
wide spread ST elevation with PR depression
CXR
• MAY SHOWS FLUID
COLLECTION
•MAY BE DRY
ECHO
Pericardial effusion
INFECTIOUS ACUTE MYOCARDITIS
OFTEN FOLLOWS
URTI
 CHEST PAIN
S/O HEART
FAILURE
ECG
•NON-SPECIFIC
ST-T CHANGES
•CONDUCTION
•DISTURBANCES
•VENTRICULAR
ECTOPICS
CXR
CARDIOMEGALY
MITRAL VALVE PROLAPSE
 SHARP LEFT SIDED
CHEST PAIN AT APEX
 DYSPNEA
 FATIGUE
 PALPITATION
 REDUCE BY LYING
DOWN
 FEMALES
 THIN
 CHEST WALL
DEFORMITIES
 MID-SYSTOLIC CLICKS
AT APEX
 ECHO
 CARDIAC CATH
Gastroesophageal Pain
 •BURNING
 •PROLONGED
 •SUBSTERNAL/EPIGASTRIC , CAN RADIATE TO BACK
 •REGURGITATION OF LIQUIDS OR FOOD
 •INCREASED BY CHOCOLATE,COFFEE
 •RELATION WITH SUPINE POSITION, EATING,
DRINKING, & GET PRECIPITATED BY EXERCISE
 •AFTER LARGE MEAL
 •LYING AFTER MEAL
 •OVERWEIGHT
 •MAY BE RELIEVED BY NITRATES
CAN MIMIC
ANGINAL PAIN
MUSCULOSKELETAL CHEST PAIN
 •RAPID ONSET
 •CONSTANT
 •INCREASES WITH DEEP
BREATHING AND CHANGE IN
POSTURE
 •REPRODUCED/TENDER BY
PALPATION
 •HISTORY OF RECENT
EXERCISE/EXERTION
 •VITALS ARE STABLE
 •ANXIETY/ATTENTION
DEMANDING/MOTIVES
•ARTHRITIS
•COSTOCONDRITIS
•INTERCOSTAL MUSCLE
INJURY
•COXSACKIE VIRAL
INFECTION
•MINOR SOFT TISSUE
INJURIES
TEITZE`S SYNDROME
IDIOPATHIC COSTOCONDRITIS
•LOCALIZED PAIN/TENDERNESS AT
COSTOCONDRAL JUNCTION
•ENHANCED BY
EMOTION,COUGHING,SNEEZING
•2nd.RIB MOST AFFECTED
Herpes Zoster (Shingles)
 Chest pain ,Unilateral
 Burning, tickling, tingling,
and/or numbness occurs in the
left parasternal area, following
the dermatomes.
 Flu-like symptoms (without a
fever), such as chills
 Swelling and tenderness of the
lymph nodes
Chest pain from Shingles can
occur before the onset of vesicles
thus making a reliable diagnosis
difficult.
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Approach to a patient with chest pain

  • 1. Clinical pathways Dr Saeed Ahmad Chaudhary Medical Officer ER Recep Tayyip Erdogan Hospital (Indus Hospital ) Muzaffargarh
  • 2. Objectives  UNDERSTAND THE CAUSES OF CHEST PAIN  UNDERSTAND THE IMPORTANCE OF HISTORY TAKING  REALIZE THE LIFE THREATENING CAUSES OF CHEST PAIN  INVESTIGATIONS  LEARN COMMON ECG CHANGES
  • 3. Chest Pain ( Don’t Panic)  5 Million emergency department visits  2 million hospitalizations annually with cost of more than $8 billion  Cardiac etiology found in less than one third  2% of patients with acute MI are unrecognized and discharged from the ED Accurate Diagnosis Remains A Challenge
  • 4. CHEST PAIN ASSESSMENT A • History • Examination B • ECG • CARDIAC EZYMES C • CXR • OTHERS
  • 5. INITIAL APPROACH  Assume the worst! Before any Diagnostic studies  100% Oxygen  IV access  Monitoring  ECG quickly  History taking
  • 6. Chest Pain: Physical Examination  _ Vital signs and general appearance  _ Carotids and JVP  _ Lungs  _ Cardiac examination  _ Thoracic cage  _ Abdominal examination  _ Periphery (pulses)  _ Skin
  • 7. Chest Pain? Origin? • HEART • LUNGS • OESOPHAGUS • MUSCULOSKELETAL STRUCTURES OF THORAX NECK,OR SHOULDER • ABDOMEN • ANXIETY MANIFESTATION WHAT LIES IN THE CHEST SKIN MUSCLES BONES JOINTS HEART AND VESSELS LUNGS AND AIRWAYS OESOPHAGUS NERVES
  • 8. IS THE KEY TO THE DIAGNOSIS OF ETIOLOGY OF CHEST PAIN HISTORY
  • 9.
  • 10. PAIN HOW DESCRIBED?  STABBING  BURNING  TWISTING  TEARING  SQUEEZING  TERRIFYING  NAUSEATING  SICKENING Penetrating or Tissue Destructive Process Bodily Or Emotional Reaction
  • 11. H/O CHEST PAIN IN THE EMERGENCY DEPARTMENT HEART ATTACK  ANSWER IS NO…… RELAX  IS IT ENOUGH TO RULE OUT HEART ATTACK?
  • 12. Life Threatening Chest Pain in the Emergency Department • Myocardial Infarction • USA • Aortic Dissection • Tension Pneumothorax • Pulmonary Embolus • Ruptured Esophagus/Perforated Life Threatening Chest Pain in the Emergency Department
  • 13. COMMON CAUSES OF CHEST PAIN  ANXIETY  CARDIAC  AORTIC  OESOPHAGEAL  LUNGS/PLEURA  MUSCULOSKELETAL  NEUROLOGICAL MYOCARDIAL ISCHEMIA(ANGINA) MI MYOCARDITIS PERICARDITIS MVP ESOPHAGITIS ESOPH SPASM MW SYNDROME AORTIC DISSECTION AORTIC ANEURYSM BRONCHOSPASM:::PE:::PI PNEUMONIA:::::TB:::::CTDs TRACHEITIS PLEURITIS PNEUMOTHORAX MALIGNANCY OA ,RIB # I/C MUSCLE INJURY TEITZE`S SYND BORNHOLM`S DISEASE PROLAPSED I/V DISC HERPES ZOSTER THORACIC OUTLET SYNDROME
  • 15. LIFE THREATENING CAUSES OF CHEST PAIN
  • 16.
  • 17. ISCHEMIC CARDIAC PAIN Site Of Origin of Chest Pain Central Character Of Chest Pain •TYPICALLY DULL •CONSTRICTING IN NECK •CHOKING •HEAVY •DESCRIBED BY PATIENTS AS ---SQUEEZING -------CRUSHING -----------BURNING ---------------ACHING •BUT NOT SHARP STABBING •BUT NOT PRICKING, KNIFE- LIKE •SENSATION CAN BE DESCRIBED AS BREATHLESSNESS SEVERE PROLONGED ASSOCIATED WITH CLINICAL EVIDENCE OF ACUTE SERIOUS ILLNESS
  • 18. RADIATION  Because of common/overlapping neural pathways, many conditions, both cardiac and extra-cardiac can result in chest pain.  Cardiac pain is mediated through upper 5 thoracic ganglia and spinal roots, but ramifications from adjoining spinal roots always exist.  Therefore pain in the chest may originate from any structure in thorax and upper abdomen innervated through lower cervical to D6/D7 spinal roots •NECK •JAW •UPPER OR LOWER ARM •BACK
  • 19. ASSOCIATED FEATURES SINGS SYMPATHATIC STIMULATION PALLOR SWEATING TACHYCARDIA VAGAL STIMULATION NAUSEA BRADYCARDIA SIGNS OF IMPAIRED MYOCARDIAL FUNCTION HYPOTENSION OLIGURIA COLD PERIPHERIES NARROW PULSE PRESSURE RAISED JVP S3 QUIET S1 DIFFUSE APICAL IMPULSE LUNG CREPTS SIGNS OF TISSUE DAMAGE-------FEVER SIGNS OF COMPLICATIONS----MR,,,,,,,PERICARDITIS
  • 20. Painless ACS GRACE Study – 8.4% (1763/20,881) patients with ACS presented WITHOUT chest pain • Not initially recognised as ACS in 23.8% – Dyspnoea 49.3% – Diaphoresis 26.2% – N&V 24.3% – Syncope 19.1% Diabetic Females Elderly
  • 21. Risk Factors Cardiac Risk Factors •Smoking •Diabetes •HTN •Hyperlipidaemia •Family History •Known Ischemic Heart Disease •Male , •Age >40 •Chronic cocaine use in the younger pts. Lesser known cardiac risk factors •SLE •Rheumatoid Disease •Asian •Prothrombotic Disease •Cocaine
  • 22. INVESTIGATIONS ECG Provides documentary evidence of cardiac ischemia/infarction when positive. Normal in ~ 50% initially who are later Dx as having an AMI. A normal ECG does not exclude an AMI
  • 24. ST Depression or Dynamic T wave Inversions
  • 26. Myoglobin CK-MB Isoenzyme Troponin ( T, I) Specific/Sensitive high sensitivity but poor specificity Less Sensitivity and specificity Most Specific & Most Sensitive Raises in 1 hour 4-6 Hours 4-8 Hours Peaks in 4-12 Hours 24 Hours 18-24 Hours Remains Elevated 24-36 hours 36-48 Hours 10-14 Days Remarks 100% within 3 hrs of AMI predictive of mortality prognostic information False Positive Skeletal muscle injury, Heavy alcohol, Renal failure , Shock states exercise, trauma, muscle dz, DM, PE renal dz, poly/dermatomyo sitis PLASMA BIOCHEMICAL MARKERS
  • 27. CBC -----------LEUKOCYTOSIS ON 1st DAY—PEAKS 2-4 DAYS ESR------------RAISED WITHIN 3 DAYS CRP------------ELEVATED CXR------------PUMONARY EDEMA,,,CARDIOMEGALY ECHO--------WMA?
  • 28.
  • 29. Chest Pain Duration ECG a) ST b) T wave Cardiac Enzymes Troponin (T,I) Angina Less than 10 min a) Normal b) Normal -ve -ve Un-stable Angina > 10 mins a) Slight Depression/ Elevation b) Poor/ Inversion -ve /slightly raised -ve NSTMI > 20 mins ST Depression +ve +ve STEMI > 20 mins ST Elevation +ve +ve
  • 30. Aortic Dissection Clinical Presentation  History:  >90% with abrupt and severe pain in the chest or between the scapulae  “tearing” or “ripping”  Can be dull or pressure-like  Anterior chest ~ ascending aorta -Type A; Back ~ descending aorta –Type B  Nausea, vomiting, diaphoresis common  Definition:  Intimal tear with entry of blood into the media  “dissects” between the intima and adventitia  #1 site: ascending aorta at the ligamentum arteriosum  Stanford Classification:  A: involves Ascending aorta (w/ or w/o descending)  80% of dissections  B: descending aorta only
  • 31. Associated signs & symptoms based on progression of dissection: Carotid arteries: stroke Spinal arteries: paraplegia Abdominal aorta/renal arteries/iliacs: Abdominal/flank pain Coronary arteries: pericardial effusion/tamponade Laryngeal nerve compression: hoarseness Tracheal compression: dyspnea/stridor/wheezing Esophageal compression: dysphagia Physical Examination: •BP differential? bilateral arm BPs – significant if >20mmHg difference Most commonly: normal heart and lung •Aortic insufficiency murmur in 16-20% •Unequal, decreased, or absent peripheral pulses only found in 50%
  • 32.  ECG – AMI (new Q or STE) – 3.2% – Ischaemia – 15% – No abnormalities – 31.3% – Non specific T wave changes – 41.4% – LVH – 26.1% Investigations Risk Factors – Atherosclerosis, HTN (uncontrolled), Coarctation of Aorta, Bicuspid Aortic Valve, Aortic Stenosis, Marfan Syn, Ehlers-Danlos Syn, Pregnancy
  • 34. CXR a)-Mediastinal widening (61.6%) , b)- Widening of aortic contour (49.9%), c)-Pleural effusion (L>R) (19.2%), d)-Apical pleural cap, e)-Calcium sign (14%), f)– Depressed left main bronchus , g)-Tracheal or oesophageal displacement, h)-No abnormalities noted 12.4% TEE ( High Sensitivity and Specificity ) Aortic Angiography CT or MR
  • 35. Pulmonary Embolism “Classic Triad”: Sharp Pleuritic CP, Dyspnea, hemoptysis in only 20% of pts. Pain is often pleural Reproduciable with breathing, palpation •Dyspnea (79%) •Dyspnea at rest (61%) •Dyspnea exertion (16%) •Orthopnea (36%) •Pleuritic chest pain (49%) •Non pleuritic chest pain (17%) •Cough (43%) •Calf or thigh swelling (39%) •Calf or thigh pain (41%) SIGNS •RR > 20/min (57%) •Tachycardia (26%) •Increased P2 (15%) •JVP distension (13%) •Rales (21%) •Wheeze (3%) •Decreased breath sounds (21%) •Signs of calf or thigh DVT (47%)
  • 36. Hypercoagulability Pregnancy; malignancy; estrogen therapy; deficiencies of protein C, protein S, AT III Endothelial damage Recent surgery, trauma Venous stasis Prolonged travel; bed Ridden #1 Risk Factor = Prior DVT/PE Risk Factors; Virchow’s triad:  10-15% of patients will have no identifiable risk factor at the time of presentation Pre-test Probability
  • 37. Investigations;  ECG – Tachycardia most common • approx. 1/3 patients – T wave inversion • V1-3 (inferior leads) – S1Q3T3 Pattern • 20% patients
  • 38. CXR; Specific signs in massive/submassive PE Fleisher’s sign – distended central pulmonary artery
  • 39. Fleisher Lines – long bands of focal atelectasis
  • 40. Hampton Hump – pleural wedge shaped consolidation
  • 41. Biomarkers – Markers of right heart strain – Troponin – BNP • Takes time for rise • RV smaller muscle mass therefore threshold lower • >90 D Dimer –ve – discharge False –ve <1% D Dimer +ve – Many false positives Malignancy– Recent surgery– Infection– DIC– Trauma– ACS– CVA– AF Vacuities-Superficial phlebitis
  • 42. ECHO – RV dilatation – RV hypokinesis – Pardoxical septal wall movement – Tricuspid regurgitation Imaging •COLLOR DOPPLER •VENTILATION–PERFUSION (VQ) SCAN if normal CXR •CT PULMONARY ANGIOGRAPHY (CTPA) if definitive diagnosis urgent •MRI
  • 43. Tension Pneumothorax Clinical Presentation;  SUDDEN-ONSET UNILAT. CHEST PAIN,PLEURITIC SHARP  BREATHLESSNESS  ASYMPTOMATIC (NOT TENSION PNEUMOTHORAX)  DEC OR ABSENT BREATH SOUNDS (IF PNEUMOTHORAX MORE THAN15%).  RESONANT ON PERCUSSION  MEDIASTINAL DISPLACEMENT TO OPPOSITE SIDE  TACHYCARDIA  HYPOTENSION  CYANOSIS  TRACHEAL DISPLACEMENT  ASYMMETRIC LUNG EXPANSION. Risks Factors: Sudden Change in barometric pressure Smokers, COPD, Idiopathic Bleb DZ Especially tall, thin male smokers Only 10 – 20% occur with exertion
  • 44. Tension Pneumothorax when a pneumothorax (primary spontaneous, secondary spontaneous, or traumatic) leads to significant impairment of Respiration and/or Blood Circulation
  • 46. Esophageal Rupture: Boerhaave Syndrome  Substernal, sharp CP  Sudden onset after forceful vomiting  Dyspneic, diaphoretic, and ill-appearing  Shock  Sub-cutaneous Emphysema Causes?  Most Common Iatrogenic (Endoscopic Perforation)  Malignancy  Corrosive Strictures Perforation  Post Radiotherapy Strictures
  • 47. CXR; SQ air, Pleural Effusions, Pneumothorax, pneumoperitoneum, pneumomediastinum Water Soluble Contrast Study
  • 48. Pericarditis  Chest pain , Severe Pleuritic localized  Aggravated by lying supine, coughing swallowing and deep inspiration.  Relieved by sitting up and leaning forward.  It might be preceded by viral illness. Inflammation Of Pericardial Sac Causes; Idiopathic Infection Acute MI Uremia Neoplasm (Hodgkin Lymphoma, breast and Ca lung ) PERICARDIAL FRICTION RUB FEVER LEUCOCYTOSIS
  • 49. ECG wide spread ST elevation with PR depression
  • 50. CXR • MAY SHOWS FLUID COLLECTION •MAY BE DRY ECHO Pericardial effusion
  • 51. INFECTIOUS ACUTE MYOCARDITIS OFTEN FOLLOWS URTI  CHEST PAIN S/O HEART FAILURE ECG •NON-SPECIFIC ST-T CHANGES •CONDUCTION •DISTURBANCES •VENTRICULAR ECTOPICS CXR CARDIOMEGALY
  • 52. MITRAL VALVE PROLAPSE  SHARP LEFT SIDED CHEST PAIN AT APEX  DYSPNEA  FATIGUE  PALPITATION  REDUCE BY LYING DOWN  FEMALES  THIN  CHEST WALL DEFORMITIES  MID-SYSTOLIC CLICKS AT APEX  ECHO  CARDIAC CATH
  • 53. Gastroesophageal Pain  •BURNING  •PROLONGED  •SUBSTERNAL/EPIGASTRIC , CAN RADIATE TO BACK  •REGURGITATION OF LIQUIDS OR FOOD  •INCREASED BY CHOCOLATE,COFFEE  •RELATION WITH SUPINE POSITION, EATING, DRINKING, & GET PRECIPITATED BY EXERCISE  •AFTER LARGE MEAL  •LYING AFTER MEAL  •OVERWEIGHT  •MAY BE RELIEVED BY NITRATES CAN MIMIC ANGINAL PAIN
  • 54. MUSCULOSKELETAL CHEST PAIN  •RAPID ONSET  •CONSTANT  •INCREASES WITH DEEP BREATHING AND CHANGE IN POSTURE  •REPRODUCED/TENDER BY PALPATION  •HISTORY OF RECENT EXERCISE/EXERTION  •VITALS ARE STABLE  •ANXIETY/ATTENTION DEMANDING/MOTIVES •ARTHRITIS •COSTOCONDRITIS •INTERCOSTAL MUSCLE INJURY •COXSACKIE VIRAL INFECTION •MINOR SOFT TISSUE INJURIES TEITZE`S SYNDROME IDIOPATHIC COSTOCONDRITIS •LOCALIZED PAIN/TENDERNESS AT COSTOCONDRAL JUNCTION •ENHANCED BY EMOTION,COUGHING,SNEEZING •2nd.RIB MOST AFFECTED
  • 55. Herpes Zoster (Shingles)  Chest pain ,Unilateral  Burning, tickling, tingling, and/or numbness occurs in the left parasternal area, following the dermatomes.  Flu-like symptoms (without a fever), such as chills  Swelling and tenderness of the lymph nodes Chest pain from Shingles can occur before the onset of vesicles thus making a reliable diagnosis difficult.

Hinweis der Redaktion

  1. Positive if CK/MB > 5% of total CK and 2 times normal