Cardiology p1 Flashcards
SOCRATES for MI
S: Central / behind sternum O: sudden C: crushing, stabbing R: neck, shoulder, jaw A: sweatiness, SOB, nausea T: over mins E: increases with exercise, decreases with rest S: mild-severe
SOCRATES for Aortic dissection
S: central O: sudden C: ripping R: back A: absent or delayed pulses, unequal upper limb BP, distal ischaemia, shock and neurological signs T: seconds E: S: mild-severe
SOCRATES for pleural disease
S: localised to area of chest O: weeks C: sharp R: ?to shoulder A: coughing, pain in shoulder T: E: worse with breathing and coughing S: mild-severe
SOCRATES for oesophageal disease
S: retrosternal O: after meals C: burning R: ? T: after meals E: worse lying down / food or bending over Better with antacids S: mild-severe
SOCRATES for MSK disease
S: Local O: following trauma / causative event C: sharp / sore R: ? A: ? T: ? E: with certain movements S: mild-severe
What conditions are included in ACS?
STEMI
NSTEMI
UA
Describe the pathology of ACS
- atheromatous plaque formation in coronary arteries
- Fissuring/ulceration leads to platelet aggregation
- Localised thrombosis, vasoconstriction and distal thromboembolism
- Leads to ischaemia of myocardium
What is diagnosis of ACS based on?
Cardiac markers - troponin
ECG - ST elevation
Describe the history of a patient presenting with ACS?
Central crushing pain, usually >20 mins
not relieved by GTN
Radiates to left arm, neck and jaw
Associated with: SOB, nausea, fatigue, sweaty, palps
What would be the examination findings of a patient presenting with ACS?
pulse, BP, O2 sats often normal
pale and clammy
tachycardia
What investigations would you do for a patient with ACS?
what might you find?
ECG
Cardiac enzymes: trops (increased in first 4-8 hours, and max at 24 Hours)
FBC, U+E, LFT
glucose (decreases)
lipids (increased)
CXR
Transthoracic echo - helps in ddx of pericarditis, dissection or PE
What is unstable angina?
Angina that occurs at rest
increased frequency
increased severity
What is the cause of UA?
Fissuring of plaques - total vessel occlusion - progress to AMI
How is MI diagnosed?
Increased trops
ECG- ST elevation = STEMI
No ST elevation = NSTEMI
What are the three patterns of MI?
Regional MI (()%) Regional subendocardial infarction Circumferential subendocardial infarction (10%)
What artery causes anterior MI?
Left anterior descending
What are the ECG changes on an anterior MI?
V1-V4
What artery causes inferior MI?
Right coronary
What are the ECG changes on an inferior MI?
II, III, aVF
What artery causes lateral changes?
left circumflex
What are the ECG changes on lateral MI?
lead 1, aVL V5, V6
What are the differences between STEMI and NSTEMI?
STEMI = full thickness whereas NSTEMI = partial thickness
no q waves, but can get ST depression and T-wave inversion
What changes occur in 0-12 hours of MI?
Infarct not visible
Decreased oxidative enzymes
What changes occur in 12-24 hours of MI?
Infarct = pale and blotchy
Intercellular oedema
What changes occur in 24-72 hours of MI?
Infarcted area excites acute inflammatory response
dead area soft/yellow with neutrophil infiltration
What changes occur in 3-10 days of MI?
vascular granulation tissue in infarcted area
What changes occur in 10+ days of MI?
Collagen deposits become scar tissue
What is the management of ACS?
A-E + ECG and trops
MOANA: M - morphine (5mg titrated up) O - oxygen If sats <94% A: anti-emetic - 10mg metoclopramide N: nitrates - GTN spray or IV nitrates A: Aspirin 300mg chewable
What is the management of STEMI?
CHECK local guidelines
PCI: gold standard treatment if available in timely fashion - i.e. under 2 hours -
praugrel + aspirin if not taking oral anticoagulant
Clopidogrel + aspirin if they are taking an oral anticoagulant
If you can’t get PCI in 2 hours, THROMBOLYSIS:
ticagrelor. If ECG after 90 minutes shows this hasn’t worked –> PCI
What is the management of NSTEMI?
BROMANCE: Beta blocker Reassurance O2 Morphine 5mg Aspirin 300mg Nitrates Clopidogrel 300mg Enoxaparin - NOTE NOW FONDAPARINOUX
Assess using grace score.
Only give oxygen if sats below 95%
What is the GRACE score?
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
> 3% = PCI within 72 hours
<3%: Ticagrelor
What is the management if the grace score indicates high risk?
(>5-10% in 6 months, increased troponin or ST depression, diabetes)
Semi-elective PCI as inpatient
What is the management if the grace score = low risk?
Discharge with long term meds
Outpatient stress test/angiography or elective PCI
What is the long term management of ACS?
48 hours bed rest daily U+Es and cardiac enzymes thromboprophylaxis (fondaparinoux) Aspirin 75mg for life Clopidogrel 75mg for 1 year Bisoprolol statin + ACEi
Oral nitrates
D/c on COBRAA
COBRAA?
5-7 days post discharge: Clopidogrel (75mg) - N.B. now ticagrelor Omega 3 Bisoprolol Ramipril (2.5mg) Atorvastatin (80mg) Aspirin 75mg
What lifestyle advice immediately after MI?
Smoking cessation
No sex for 1 month
No air travel for 2 months
diet + exercise
What are the immediate complications of Acute MI?
Cardiac arrest - VF (most common cause of death)
VF
Bradyarrhythmia
What are the short term complications of MI?
Pulmonary oedema
Cardiogenic shock
Thromboembolism
VSD –> pan systolic murmur
Ruptured chordae tendinea –> Mitral regurg
Ruptured ventricle wall –> cardiac tamponade
How does pulmonary oedema occur following MI?
LH fails to pump
Dilation of LV causes back pressure on pulmonary veins causing Extravasation of low protein fluid into the alveoli
How does cardiogenic shock occur following MI?
Decreased BP and decreased coronary flow = pump failure
What are the long term complications of MI?
Heart failure
Dressler’s syndrome (immune mediated pericarditis)
Pericarditis
Ventricular aneurysm - Thrombus may form within the aneurysm increasing the risk of stroke
What is Dressler’s syndrome?
Immune-mediated pericarditis
Sharp chest pian, increased lying down
What is the management of Dressler’s?
high dose aspirin and NSAIDs - n.b. now aspirin and colchicine
What is angina caused by?
Narrowing of the coronary arteries reduces blood flow to the myocardium. During times of exercise, there is inefficient blood to meet the demands causing pain.
Therefore, exertional chest pain
What causes decreased perfusion in angina?
Atheroma Embolus Thrombosis Inflammation of coronary arteries Decreased BP
How does tissue demand increase in Angina?
Cardiac hypertrophy
Increased CO
What is the cause of stable angina?
Decreased flow in atherosclerotic coronary arteries
Describe the Pathology of stable angina?
Arteriosclerosis: thickening and hardening of walls, decreased contractility and elasticity and decreased blood flow
Atheroma: thickening and hardening of walls so decreased tissue perfusion
How does atheroma formation occur?
Damage to endothelium
Entry of LDLs in the intima, macrophages form a fatty streak
Cytokines stimulated by macrophages: collagen deposition –> plaque
What are the risk factors for stable angina?
Increasing age Males FH Smoking Diet high in fat / low in fruit obesity increased BP lipidaema DM
How is diagnosis of angina done?
Clinical: mild ache - severe pain
Sweating/fear
increased with exercise, meals, cold, emotion
fades after rest
CT Coronary Angiography - Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing
What ix would you do for ?angina?
Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes)
What is the NICE tool for CAD?
clinical assessment of CAD: >90% - stable angina treatment 61-70%: coronary angiography indicated 31-60: SPECT myocardial scan, exercise echo, stress MRI 10-30: CT calcium scoring <10: investigate other cause
What are the indications for Stress ECG?
If resting ECG normal
ST depression >1mm shows ischaemia
+ve within 6 mins - angiography indicated
What is the first management of Angina?
Immediate: GTN N.B. nitrates are contraindicated in aortic stenosis
Long term: Beta-blocker / Calcium channel blocker (verapamil or diltiazem if mono therapy)
If disease not treated with one, add the other
(refractory disease - nicorandil)
Secondary prevention: Aspirin (75mg), atorvastatin, ACEi and they are already on beta blocker
What is given for secondary prevention of Angina?
Statin
Low dose aspirin
ACEi
How should the patient be counselled when starting a nitrate
sublingual GTN
Advise to sit down after spray
wait 5 mins and spray again
999 if still in pain after 10 mins - may be having an MI
Can use prophylactically
Nitrate free period if standard release isosorbide mononitrate
How do nitrates act?
Cause venorelaxation (decrease pre-load) beware of venous pooling therefore dizziness on standing
Decreased aortic pressure
overall decreased O2 requirement of myocardium
coronary vasodilation - increased O2 delivery
How do b-blockers work?
work on b1 receptors to decrease HR and SV
What are the S/E of b-blockers
bronchoconstriction - don’t use in asthma, COPD
cardiac depression / bradycardia
hypoglycaemia
fatigue
Give some examples of CCB
dihydropyridines: amlodipine or nifedipine
rate limiting agents: verapamil/diltiazem
How do CCB work?
prevent SM contractions: decreased after load and CA vasodilation
Acton AVN to decrease HR
What are the S/E of CCB?
flushing
headache
ankle swelling
What are the procedural / surgical treatments for angina?
Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent: catheter into brachial or femoral artery, feeding that up to the coronary arteries under xray guidance + contrast This can then be treated with balloon dilatation followed by insertion of a stent
PCTA
Co-prescribe aspirin and clopidogrel
CABG
What are the risks of angioplasty?
local dissection or CA or CA occlusion
1% mortality, 2% AMI
increased symptoms but no prognostic benefit
What are the indications for CABG?
Severe stenosis: symptom control for patients unsuitable for PCI
improved survival after MI
What are the employment and driving limitations following ACS?
2 months return to work
(not pilots/drivers, and heavy labour should seek lighter work)
Travel - avoid air travel for 2 months
sex - 1 month off
Driving: PCI - 1 week, and if not, 4 weeks
Angina - stop
What are the driving limitations for AAA?
notify DVLA if >6cm
Disqualified if >6.5cm
What does the left circumflex artery supple?
Left atrium and left ventricle
What does the right coronary artery supply?
Right atrium and right ventricle
What does the left anterior descending artery supply?
left ventricle and inter ventricular septum
what does the left marginal artery supply?
left ventricle
What does the tricuspid valve separate
RA and RV
What does the mitral valve separate?
LA and LV
What does the left heart go to?
AORTA - BODY
What does the right heart go to?
pulmonary artery - lungs
What are the major branches of the aortic arch?
BCC: right CC and subclavian
Left common carotid
left subclavian
What is the management of blunt cardiac trauma?
CXR in resus
CT often needed
ECG
conservative
What is the management of Penetrating cardiac trauma?
complex ix and management
surgery
CXR
What is the presentation of cardiac tamponade?
Becks triad: hypotension
JVP increased
muffled heart sounds
CXR- rounded heart border
ECG: alternans QRS
Confirm with USS
Mx - pericardiocentesis and sternotomy and repair
What is myxoma? what are the signs?
Cardiac tumour Signs - similar to infective endocarditis MS confirm on echo mx = excision
What are the causes of constrictive pericarditis?
What are the signs?
Tx?
TB, RA, trauma
dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive
Excision of pericardium
What are the differences between cardiac tamponade and constrictive pericarditis?
JVP: Absent Y descent. X and Y present in constrictive pericarditis
pulsus paradox - present in cardiac tamponade, absent in constrictive pericarditis
Kussmaul sign: rare in cardiac tamponade but present in constrictive pericarditis
What is the pathophysiology of pulmonary oedema?
Increase in fluid in the alveolar wall
most common = LVF
increased pressure in alveolar capillaries and leakage of fluid
What is the presentation of pulmonary oedema?
dyspnoea
paroxysmal nocturnal SOB
orthopnoea
cough - frothy, blood stained sputum
ACUTE PRES: SOB, cough, anxiety, cheyne stokes breathing
What are the examination features of pulmonary oedema?
increased RR increased HR and gallop rhythm increased venous pressure peripheral shut down widespread crackles / wheeze
What investigations would you do for pulmonary oedema? What might you find?
ABG: T1RF or T2 due to impaired gas exchange
Bloods - FBC, U+E. glucose, D-dimer and CRP to rule out.
BNP
CXR: diffuse haziness/batwing oedema / Kerley B lines
ECG: tachycardia, arrhythmias
Echo
What are the causes of pulmonary oedema?
- Increased capillary pressure: LVF, valve disease, arrhythmia, VSD, pulmonary venous obstruction, MI
fluid overload - Increased capillary permeability: ARDS, infection, DIC, toxins
- Decreased plasma oncotic pressure: Renal/liver failure - hypoalbuminaemia
- Lymph obstruction - tumour
- Other: neuro/head injury / raised ICP
PE, altitude
What is the management of pulmonary oedema?
A-E
POUR SOD: Pour away fluids PLUS:
Sit upright
Oxygen
Diuretics - IV furosemide
If severe IV diamorphine IV furosemide GTN spray 2 puffs NIV
SBP >100: IV infusion of nitrate and CPAP if no improvement
DBP <100: treat as cardiogenic shock
alert ICU
What are the complications of ARDS?
Prolonged oedema –> pulmonary HTN which leads to irreversible structural changes to pulmonary arteries
Increased pressure to RV leads to RV hypertrophy leading to RHF and Cor Pulmonale
What is ARDS caused by?
Lungs responding to direct inhalation or blood-bourne insults.
Direct:
aspiration of gastric contents, smoke/toxins
pneumonia
near drowning
Indirect: sepsis trauma pancreatitis transfusion reaction anaphylaxis
What is the pathophysiology of ARDS?
damage to type 2 pneumocystis - surfactant depletion and alveolar collapse
non-cardiogenic pulmonary oedema
What are the features of ARDS?
Decreased O2
absence of increased arterial pressure
CXR: bilateral ground glass appearace
decreased lung compliance
What is the management of ARDS?
Admit to ICU 100% O2 CPAP IV nitrates IV furosemide Morphine and metoclopramide Aminophylline if bronchospasm
What is open heart surgery?
How is this different from closed heart surgery?
Any surgery requiring cardio-pulmonary bypass, whereas closed heart surgery does not require a bypass
What is the function of a cardiopulmonary bypass?
Takes over the function of the heart and lungs, allowing a motionless blood-free field for operation
What happens during a cardiopulmonary bypass?
Ascending aorta is clamped and cannulated and a venous Line inserted into the right atrium to drain venous blood
System involves a heat exchanger to regulate temperature, an oxygenator, an arterial pump and a filter
How is potential for ischaemic damage minimised in cardiopulmonary bypass?
(no coronary blood supply)
potential for ischaemic damage is minimised by arresting the heart in a high potassium solution and also cooling the myocardium to between 4 and 12 degrees
What are the main complications of a cardiopulmonary bypass?
Due to activation of the clotting cascade, within the bypass machine, with consumes clotting factors and platelets
This is prevented with high dose systemic heparin biro cannulation, reversed after this operation with protamine sulphate
Blood products may also be needed to reverse this
What is a median sternotomy?
Most common approach for operations on The heart and aortic arch - with any chamber or surface of the heart operable
When might an anterolateral thoracotomy be used?
Access to the right side of the heart
When might a Posterolateral thoracotomy be used?
Access to the distal aortic arch and descending thoracic aorta
When might a bilateral transverse thoracotomy be used?
Double lung transplants or heart-lung transplants
Which is better - CABG or PCI?
CABG provides better symptomatic relief and requires fewer late re-interventions than PCI
How is CABG performed?
Median sternotomy incision with CPB
Left internal mammary artery os the most common artery used as a conduit - harvested from the chest wall
Enlarges in response to demand, resistant to atheroma formation
Which vein was previously used for CABG?
Saphenous vein harvest - good secondary targets, however results are less good than IMA
What are the complications of CABG?
MI bleeding stroke arrhythmias tamponade aortic dissection respiratory / systemic complications
What are the two different types of valves?
Man made: ball in cage / bileaflet
durable BUT thrombogenic and require anti-coagulation with warfarin
Tissue valves: homographs / xenographs
Anticoagulation not required BUT more prone to degenerative failure
