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
Investigations for pneumothorax (bedside, bloods, imaging)
Whats classified as a large/small pneumothorax?
Bedside
-ECG (rule out)
Bloods
- FBC (useful to look for infection)
- U+E, Baseline clotting, D-Dimer
- ABG
Imaging
-CXR (reduced lung markings)
- small pneumothorax =<2cm between lung and chest wall. Large = >2cm
Management of a PRIMARY pneumothorax
PRIMARY PNEUMOTHORAX
Signs of heamodynamic instability?> straight to chest drain
Size < 2cm and/or patient is not breathless - consider discharge and review in 2-4 weeks
Size > 2cm - aspirate with 16/18G cannula in 2nd intercostal space mid-clavicular line under local anaesthetic
- If aspiration successful, discharge+review in 2-4 weeks
- If aspiration is unsuccessful (still not <2cm or still breathless) then do a chest drain and admit
Management of a SECONDARY pneumothorax
SECONDARY PNEUMOTHORAX (50yrs+/smoking/lung disease)
-If <1cm then admit for oxygen and observe 24 hours
-If 1-2cm ASPIRATE
•if successful and size now <1cm ADMIT with oxygen
•if unsuccessful: chest drain required
then admit with high flow oxygen and 24 hour observation
-If >2cm or breathless then just do chest drain
what is pericarditis?
what causes it?
- Pericarditis is inflammation of the pericardial sac
- Can be idiopathic but cause is often infectious (virus and TB are most common causes)
how does pericarditis present?
-Central chest pain •often worse on breathing (pleuritic) •relieved by sitting forward -Sometimes SOB -Symptoms of underlying illness (fever, cough, rash)
Examination findings in pericarditis
- Pericardial friction rub is pathognomonic - may be positional and transient
- ST elevation across all leads
Investigations and findings for pericarditis
Bedside
- Full cardio exam (pericardial rub) and history (recent viral illness)
- ECG
- Echo
Bloods
- FBC
- ESR and CRP (raised)
- Trop and CK (to exclude concomitant myocardial injury-myopericarditis)
- Could do blood cultures
Imaging
-CXR - large heart, may see pulmonary effusion
(may see cause-malignancies, sarcoidosis, or several infections)
ECG findings in pericarditis
Pericarditis
- ST elevation across all leads (except aVR and often V1)
- Saddle shaped ST segment
- PR depression
Management of pericarditis
- Admit for observation and treat underlying cause
- NSAIDS are mainstay - ibuprofen well tolerated and improves cardiac flow. PPI cover
- Steroids - prednisolone can be used if pain doesn’t settle
- Oral anticoagulants should be discontinued to reduce risk of haemopericardium
NSTEMI: what is it?
Non-ST elevation MI. Closely related to unstable angina (NSTEMI is angina but with myocardial damage)
NSTEMI presentation
Surrounding angina symptoms
- REST angina
- INCREASING angina
- NEW angina
NSTEMI Management
Very similar to that for STEMI - MONAT
- Morphine for analgesia
- Oxygen
- Nitrates
- Aspirin 300mg
- Ticagrelor 180mg
- Fondaparinux (if not going for PCI)
Monitor abs and ECG
What is the PESI score?
What is the PERC rule?
- PESI score (pulmonary embolism severity index) determine the mortality and morbidity of patients with newly diagnosed PE(and determines where they should be managed)
- PERC score is a RULE OUT SCORE for PE (if all points negative and pre clinical suspicion is ≤15%)
What do you see on ECG for PE?
ECG in PE
•Most common is normal
•Most common ABNORMALITY is sinus tachycardia
•Right heart strain (right axis deviation)
• New RBBB
•“S1Q3T3” pattern of acute cor pulmonale (McGinn-White Sign).
Large S wave in lead I. Q wave in lead 3. Inverted T wave in III
What is important to follow up for all patients after PE? (4)
FOLLOW UP AFTER PE
1) ANTICOAGULATION
- initially LMWH (enoxiparin)
- switch to DOAC (e.g. riveroxiban) or warfarin for 3 months/6 months/ lifelong
2) CAUSE-look for cancer
- examination (breast, testicles, PR, lymph nodes)
- urinalysis and biochemistry
- chest x ray
3) RISK ASSSSMENT
- Do a PESI score
4) ECHOCARDIOGRAM at 3 or 4 months
- look for RV strain or pulmonary hypertension
What is a massive PE and what is the management?
What anticoag do you give after treatment?
Massive PE is defined as a PE big enough to cause heamodynamic instability
Treatment:
- thrombolysis with IV alteplase (10mg bolus then infusion)
- after thrombolysis then give unfractionated heparin sub cut
what is virchows triad
Virchows triad- Increased risk of VTE (PE or DVT)
- hypercoagubility
- stasis
- vessel wall injury
Virchows triad- examples of stasis?
STASIS
- AF
- LV dysfunction
- venous obstruction (pregnancy, tumour, obesity)
- varicose veins
- immobility
Virchows triad- examples of hypercoagubility?
HYPERCOAGUBILITY
- major surgery or trauma
- pregnancy
- malignancy
- thrombophilias e.g. antiphospholipid syndrome
- ostrogen therapy COCP, HRT
- autoimmune/inflatmitory conditions (e.g. IBD)
- infection/sepsis
- previous VTE
- Nephrotic syndorme (wee out all anti-thrombotic things)
Virchows triad- examples of vessel wall damage?
VESSEL WALL DAMAGE
- MI
- atherosclerosis
- trauma
- cellulitis
What are the cardiac territories in ECG? What vessels supply these areas?
INFERIOR-right coronary artery
-II, III, AVF (f=foot)
ANTERIOR-left anterior descending
- septal: V1 and V2
- anterior: V3 and V4
LATERAL-left circumflex artery
I, aVL, V5, V6 (1 and L= Lateral)
What vessel is occluded most often in posterior MI?
POSTERIOR DESCENDING ARTERY — a branch of the RIGHT CORONARY ARTERY in 80% of individuals
What do POSTERIOR changes on ECG look like?
What should you do?
-Deep ST depression and tall R waves in anterior leads V1,V2,V3
- Take off V4 V5 V6 and put on back
- May be a posterior MI- need re-perfusion
What is the difference in the type of occlusion AND infarction between NSTEMI and STEMI
NSTEMI
- partial occlusion
- subendocardial infarction
STEMI
- complete occlusion
- transmural infarction
What does pathological Q wave indicate?
-May indicate current or past MI (most likely STEMI) (25% height of QRS)
what do GRACE scores indicate?
GRACE score for ACS (mortality risk and likelihood of needing angiogram)
Clinically unstable: Angiogram immediately
Intermediate-high risk: Angiogram within 72 hours
Low risk: medical managment
What are some complications of myocardial infarction? (< 2 weeks and >2weeks)
<2 weeks
- Cardiac arrest
- Cardiogenic shock (ventricle damage reduces ejectionF)
- Arrhytmias (VT most common, also VF/AF)
- VSD
- Mitral regurg (papillary muscle rupture)
- Ventricular wall rupture (presents like ACUTE HEART FAILURE secondary to cardiac TAMPONADE)
- Pericarditis (first 48 hours)
> 2 weeks
- heart failure
- dresslers syndrome (autoimmune) (fever, pericarditis, pericardial effusion, pleuritic pain and ↑ESR). It is treated with NSAIDs.
- ventricular aneurysm (persistent ST elevation and symptoms of LVF, may present with stroke)
What anticoagulants would a patient with unstable angina/NSTEMI be put on?
- Normally Fondaparinux
- However must be on UFH if angiography planned within 24 hours or if patients creatinine is > 265 µmol/l)
Contraindications for thrombolysis (ACS)
Contraindications for thrombolysis (Alteplase/streptokinase)
- Neurosurgery, head trauma or ischemic stroke in past 3 months
- Current or past intracranial heamorrage
- Active internal bleeding (GI bleed)
- Coagulation disorders
- Uncontrolled hypertension (>185 mmHg SBP or >110 mmHg DBP)
- Known intracranial arteriovenous malformation, neoplasm, or aneurysm
What anticoagulant is used for when people are having PCI?
If <12 hours since onset and PCI available within 2 hours
-Do PCI with with unfractionated heparin (shorter half-life than other anticoagulants)
In pneumothorax managment, explain aspiration and chest drain locations
ASPIRATION - mid clav line 2nd IC space with 16G needle
CHEST DRAIN - mid-ax line 5th IC
What signs would you find in cardiac tamponade?
Treatment?
Cardiac tamponade
Becks triad
-muffled heart sounds, raised JVP and hypotension
Kussmals sign (raise in JVP with inspiration)
Pulsus paradoxus
-drop in systolic BP of 15 with inspiration
Treatment:pericadocentesis
Pneumothroax
- where do you aspirate?
- where do you do a chest drain?
Aspirate
-decompression with 16/18G cannula in 2nd intercostal space mid-clavicular line under local anaesthetic
• if >2cm primary
• 1-2cm secondary
Chest drain
- 5th intercostal space mid-axillary line and admit patient
What types of emboli exist? (PE)
Septic emboli from endocarditis - IVDU (or from complication of tonsillitis)
Fat - long-bone fractures
Air - surgery, trauma
Neoplastic cells - prostate/breast cancers most commonly
Parasites
Amniotic fluid embolism
Foreign bodies - IVDU, iatrogenic
If a patent has an UNPROVOKED PE what should you do ? (bedside, bloods, imaging)
Unprovoked PE=CANCER SCREEN
Bedside
- A full history and physical examination
- Urinalysis
Bloods
-Blood tests, (FBC, Calcium, LFT)
Imaging
-CT TAP
Who do you give if someone needs 300mg aspirin, but they already take 75mg?
Give 225mg
What is fondaparinux? when would you give in an MI?
- Fondaparinux is a factor 10a inhibitor
- Give when CANT go for PCI (or give LMMW-enoxaparin)
What is delta troponin?
% difference between trop levels within 3-8 hour time period
if greater than 20%= MI
Driving rules following ACS
successful PCI=1 week stop
no PCI= 4 week stop
truck driver=6 weeks
An inferior myocardial infarction plus aortic regurgitation murmur. What are you thinking?
An inferior myocardial infarction and AR murmur should raise suspicions of an ascending aorta dissection rather than an inferior myocardial infarction alone.
In ST elevation, what is the first changes to see on ECG?
What are the last to stay?
ST elevation Normal initially (require constant ECG monitoring) 1. Big T wave 2. Then ST elevation 3. Then pathological Q wave 4. Then Inverted T wave (Q gets bigger)
Then after
- ST normalises (days)
- T wave normalises (weeks)
- Pathological Q wave remains
