Pt w/ Chest Pain Flashcards
Initial differential diagnoses
CARDIAC
- ACS
- Stable angina
- Aortic Dissection
- Tamponade/pericardial effusion
- Pericarditis
RESP
- Pneumothorax
- PE
- Pneumonia
MSK
-Chosdrochondritis
Psych
-Anxiety
GI
- reflux
- pancreatitis
- Osphageal rupture
- AAA
ACS
- characteristic presentation
- signs of ACS (2)
- Crushing central chest pain that might radiate to arm, neck, jaw (commonly on LHS) - can radiate through to back
- This pain is not taken away (or not permanently) by sub-lingual GTN
- Exertional pattern of onset
- Associated:
- N + V
- sweating
- pallor
- anxiety
- palpitations
Signs: Tachycardic, low BP
-PMH of angina, IHD / other thrombotic events
What is the difference in pathophysiology between stable angina and ACS?
Stable angina
-excertional ischemia (controlled by rest/GTN)
Unstable angina
- ischemia at rest (plaque rupture-partial occlusion)
- not controlled by rest/GTN
NSTEMI
- ischemia AND infarction (plaque rupture-partial occlusion)
- raised cardiac markers
STEMI
- ischemia AND infarction (plaque rupture-complete occlusion)
- raised cardiac markers
Silent MIs
- who gets them
- how do they present
Silent MIs
- diabetic and elderly get them
- N and V
- SOB (acute pulmonary oedema)
- Indigestion
- Can present with syncope
Most common vessel affected?
Aetiology and RFx for ACS
Usually due to thrombosis formation in coronary artery - most commonly the Left Anterior descending Artery
RFx
Non-modifiable
-male/caucasian/FH/age
Modifiable
-Obesity/high blood pressure/smoking/high cholesterol, diabetes/diet/sedentary lifestyle
Investigations for potential MI
Bedside
-ECG
Bloods
- FBC
- Cardiac marker (Troponin and CK)
- unstable angina wont have raised trop
- Us and Es
- Glucose
- Lipid profile
Imaging
- Consider chest X ray- to look for other causes (dont delay treatment)
- Echo (look at wall movement deformities
When does troponin start to rise?
- And what about another biochemical marker (when does it rise, why isn’t it as good)
Troponin start to rise by 3 hours (no point taking before) and peaks at 12 hours (if troponin isn’t raised by 6 hours ACS is unlikely)
- Creatinine Kinase is another marker. Peak levels occur at 24 hours but rise might come sooner. Not very specific (high false positives - approx 15%)
ECG for stable/unstable/NSTEMI/STEMI (in order)
STABLE ANGINA
-normal ECG
UNSTABLE ANGINA
- May get ST segment depression during pain (resolves after pain)
- May get T wave inversion
NSTEMI
- ST depression
- T wave inversion at place of infarction (with time they may resolve, or may stay)
STEMI (in order)
ST elevation or NEW left bundle branch block
Initial managment for unstable angina and NSTEMI? (ACS without ST elevation)
MONAT
- Morphine (5-10mg IV) and metoclopramide
- Oxygen (low flow) if sats <94% or breathless
- Nitrates (GTN spray 2 puffs)
- Aspirin (300mg PO, then 75mg OD)
- Ticagrelor if 6 month mortality >1.5% (180mg PO, then 90mg OD)
Then measure troponin and determine GRACE score (6month mortality risk) (determine whether they should have angiogram)
GRACE SCORE
- Clinically unstable: immediate angiogram and PCI
- Intermediate or high risk of cardiovascular event >3%: coronary angiogram and PCI within 96 hours of admission
- Low risk of cardiovascular event <3%: exclusively medical management
High risk patients go on to have:
- another antiplatelet (tigagrelor) if 6month mortality is >1.5% and no CI (bleeding)
- anticoagulation (Fondaparinux. However must be UFH if angiography planned within 24 hours)
- Glycoprotein 2b/3a (Tirofiban) if planned angiography within 96 hours of hospital admission.
- IV nitrate
- Beta blocker
How many leads do you need to see ST elevation on to be classed as a STEMI?
STEMI (either new LBBB or ST elevation)
-ST elevation
*>1mm in at least 2 contiguous LIMB leads
OR
*>2mm in at least 2 contiguous CHEST lead
Initial managment for ACS (with ST elevation)
When would you do PCI
include what drugs you would take with PCI or alternatively thrombolysis
ABCDEG assessment and MONAT
- Morphine (5-10mg IV) and metoclopramide
- Oxygen (low flow) if sats <90% or breathless
- Nitrates (GTN spray)
- Aspirin (300mg PO, then 75mg OD)
- Ticagrelor (180mg PO, then 90mg OD)
If <12 hours since onset and PCI available within 2 hours
-Do PCI with with anticoagulant (unfractionated heparin as shorter half-life)
If <12 hrs since onset + PCI NOT available within 2 hours
- Thrombolysis (alteplase/streptokinase)
- Anticoagulation (LMWH heparin-enoxaparin or fondaparinux)
- THEN transferred to PCI centre (either rescue PCI or angiography)
if they cant have either reperfussion treatments, give heparin
What long term management should these post MI patients be on?
MANAGMENT OF RISK FACTORS
- Diet (low salt, high fibre, reduced fats)
- Alcohol
- Exercise
- Weight
- Diabetes control
- Hypertension control
- Smoking stoping
CARDIOPREOTECTIVE MEDICATION (ABAS)
- DUAL ANTIPLATLET- aspirin 75mg plus ticagrelor 90mg for 12 months (then aspirin forever)
- BETA BLOCKER reduces myocardial demand (Short-acting (metoprolol) → long (atenolol) (verapamil/diltiazam if contraindicated)
- ACE inhibitor if LV dysfunction, diabetes or HTN
- high dose STATIN 80mg (secondary prevention)
MANAGE COMPLICATOINS
MANAGE COMORBIDITIES
MANAGE MENTAL HEALTH
SAFTEY NET and FOLLOW UP
What is aortic dissection?
How does it present? (history/exam)
What criteria should you use?
AORTIC DISSECTION
- injury to innermost layer of aorta
- resulting in separation of the aortic wall
Presentation
- Sudden, tearing pain that radiates to back (inter scapular)
- Most severe at its onset
- SOB and anxiety
- Syncope
- Heart/renal failure
Symptoms depend on what level
- carotid-stroke symptoms or altered mental state
- coeliac plexus-mesenteric ischemia (abdo pain)
- coronary-MI
- lower limb-acute limb ischemia (pale feet)
- horners syndrome (ie, ptosis, miosis, anhidrosis)
Examination
- May be hypertensive or hypotensive (hypotension can occur in ascending aortic dissection)
- unequal pulses/BP in arms or legs
- acute limb weakness
- widening of mediastinum
- DE BAKEYS CRITERIA
What risk factors should you ask about in your history? (aortic dissection)
Caused by tear in aortic endothelium (not necessarily all the way through might just bleed between layers of endothelium) - DeBakey classification of where the bleeding is
PC
-have you had any trauma?
…unilateral tongue weakness after car crash with whiplash injury = carotid artery dissection
PMH
- chest pain, palpitations, SOB
- strokes/heart attacks/HTN/diabetes/High cholesterol
- Marfaans and Ehlers Danlos?
SH
- smoke?
- IV drugs?
FH
-family members having aneurysm?
Investigations for aortic dissection
What i the gold standard for diagnosis?
Bloods
- FBC
- Us and Es (look for affect on kidneys)
- Troponin
- CROSS MATCH FOR 10 UNITS
ECG (normal, might have LVH abnormalities
CT angiogram definitive test in most patients)
MRI ANGIOGRAPHY - gold standard of diagnosis
CXR (widening of mediastinum)
Echo/TOE (trans oesophageal echo)
Initial management for aortic dissection
Aortic dissection
- Manage in resus
- Large bore cannulas (get bloods) cross match 10U
- ICU input - insert arterial line
- Analgesia - Diamorphine 2.5-10mg IV slow (5min infusion)
Type A(ascending aorta/arch)
• Emergency surgical repair refer to cardiothorasics
Type B(not ascending aorta)
• Conservative management
• Bed rest
• Reduce BP with IV labetalol to prevent rupture (aim for systolic 100-120mmHg)
Presentation of PE
PE Sudden onset chest pain breathlessness haemoptysis dizziness SYNCOPE Prev. red, swollen, hot leg
Examination findings in PE
PE Tachycardia Tachypnoeic Hypotension Raised JVP Plural rub Swollen tender legs Massive PE presents as hypotension and cardiac arrest
Questions to ask in suspected PE?
PC
swollen/painful legs?
coughing up blood?
PMH have you ever had cancer? or cancer treatment? (6months) have you recently been travelling? have you recently had surgery? have you been immobile more than usual? are you pregnant? have you ever had PE/DVT?
DH
are you on the pill?
are you on any hormone replacement tablets
Investigations for suspected PE
What imaging do you do? (how long do you have)
What do you do if there is a delay for CTPA?
- A to E assessment
Airway
Breathing
-Do an ABG, oxygen sats, RR, chest x ray
Circulation
-Bloods (FBC, clotting-cause, Us and Es-contrast, CRP, DDimer)
-ECG - Chest x ray to exclude other pathology
- Calculate Wells score (<4 Dimer, 4+ CTPA or V/Q if pregnant)
Explain a d-dimer blood test
What should you do depending on the WELLS score?
D Dimer
- Highly sensitive but not specific meaning it’s good at RULING OUT but not ruling people in
- if it’s low it means they definitely don’t have one but even if its high doesn’t mean they necessarily have it (just a clot break down product- trauma, MI, surgery, infection, bleed, pregnancy, LD, KD)
WELLS SCORE
- If Wells 4+ (PE likely) admit and do an immediate CTPA
- If Wells is <4 do a D dimer. If D dimer is -ve consider alternate diagnosis. If D dimer is +ve immediate CTPA
What is CTPA?
How long do you have to do CTPA?
Alternate scan for pregnancy?
CT pulmonary angiogram (CTPA) is gold standard for PE
- Dye is put through pulmonary arteries and this is then visualised on CT (arterial phase)
- Sensitivity and Specific >90%
- MUST DO WITHIN 1 hour of massive PE and 24 hours of normal PE. **Give LMWH if there will be a delay for CTPA (e.g. enoxaparin)
- V/Q scan (under 40 or pregnant)
Management of PE
think about what problems you have and what medical treatment would help
ABCDEG and stabilise
- Hypotension: Start IV fluids (2 wide bore cannulas - get baseline bloods + d-dimer)
- Hypoxia: Give oxygen 15L NRBM
- Pain: Analgesia: NSAIDs. Use opioid with caution (vasodilation may worsen hypotension)
Treating the actual PE
-Thrombolysis if MASSIVE PE (heamo instability) -Alteplase
-LMWH e.g. enoxaparin (as per guidelines) for 5 days: Target INR 2-3 (unfractionated if renal impairment)
- Long term DOAC or warfarin for maintenance therapy
•3 months if provoked
• 6 months if caused by unprovoked (or malignancy)
• lifelong if thrombophilia or repeat
Presentation of pneumothorax
PNEUMOTHORAX
- Sudden onset of unilateral pleuritic chest pain
- SOB-progressivly worsening
- Tension - history of trauma
Examination findings in pneumothorax (and addition signs seen in tension)
PNEUMOTHORAX
- Unequal expansion
- Hyper-resonance
- Decreased breath sounds
- Decreased tactile vocal fremitus and vocal resonance
Tension
-Deviation of mediastinum and trachea in tension (away)
-Haemodynamic instability
• Tachypnoea and tachycardia
• Dizzy/syncope
-Pulsus paradoxicus - pulse slows on inspiration
- Raised JVP and distended neck veins (compression from mediastinal deviation)
RFx for pneumothorax (primary and secondary)
What is the pathophysiology of tension pneumothorax?
Primary - thin, young, tall men.
Secondary - to lung pathology:
Connective tissue disease
- Marfan’s syndrome
- Ehlers-Danlos syndrome
Obstructive lung disease
- Asthma
- COPD (can get tension)
Infective lung disease
- TB
- Pneumonia
Fibrotic lung disease
- Cystic fibrosis
- Idiopathic pulmonary fibrosis
Neoplastic disease
- Bronchial carcinoma
Trauma
- Penetrating trauma
- Blunt trauma with rib fracture
Iatrogenic
-aspiration, mechanical ventilation (positive pressure), central line
