Cardiology Flashcards
Non Modifiable CVD risk factors
Older age
Family history
Male
Modifiable CVD risk factors
Raised cholesterol
Smoking
Alcohol
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress
Which Co-morbidities increase the risk of CVD
Diabetes
HTN
CKD
Inflammatory conditions (e.g RA)
Pscyhosis (atypical antipsychotics)
What are the consequences of atherosclerosis
Angina
MI
TIA
Strokes
PAD
Mesenteric ischaemia
What is QRISK3?
Scoring system for primary prevention of CVD. It determines the risk of stroke or MI in next 10 years.
What is the main primary prevention strategy for CVD?
Atorvostatin 20mg at night for pts with CKD, T1DM or with a QRISK score >10%
Significant side effects of statins
Myopathy
Rhabdomyloysis
T2DM
Haemorrhagic strokes
Which drugs interact with statins?
Macrolide antibiotics - pts should stop statins temporarily when prescribed clarithromycin or erythromycin
Secondary prevention of CVD
- Antiplatelet medications (e.g aspirin, clopidogrel, ticagrelor)
- Atorvostatin 80mg
- Atenolol (or bisoprolol)
- ACEi (ramipril)
What is dual antiplatelet therapy
Aspirin 75mg daily (forever) + Clopidogrel/Ticagrelor (for 12 months)
What is Familial Hypercholesterolemia
Autosomal dominant genetic condition causing high cholesterol.
Features of familial hypercholesterolemia
- FHx of premature CVD (e.g MI <60yrs in first-degree relative)
- Very high cholesterol (>7.5mmol/L)
- Tendon xanthomata (hard nodules in tendons, often on back of hand or achilles)
Management of Familial hypercholesterolemia
Statins
What is angina
Narrowing of the coronary arteries leading to reduced blood flow to the myocardium.
Stable vs Unstable Angina
Stable = when symptoms are relieved by rest or GTN
Unstable = When symptoms occur randomly or at rest (considered an ACS)
Gold standard investigation for Angina
CT Coronary angiogram
What are the 4 principles to the management of Angina
RAMP;
Refer to cardiology (urgently if unstable angina)
Advise them about diagnosis, management and when to call ambulance
Medical treatment
Procedural or surgical interventions
Immediate management/Symptomatic relief for Angina
GTN - immediate symptom relief. Take GTN when symptoms occur, can repeat after 5 mins but if pain persists, call an ambulance.
+ Aspirin + Statin
Long-term medical management for angina
1st line = Beta-blocker +/Or Calcium channel blocker (Use Dihydropyridine e.g amlodipine if with beta-blocker or just Verapamil if not. Verapamil can’t be used with beta-blocker as causes complete heart block)
2nd line = Long acting nitrate e.g Isosorbide Mononitrate OR Ivabridine / Nicorandil / Ranolazine)
- Isosorbide mononitrate should be given as asymmetric dosing intervals to maintain a daily nitrate free time of 10-14hrs to minimise tolerance.
Surgical interventions for Angina and their indications
- PCI + Coronary angioplasty = this dilates a blood vessel using a balloon/stent. Indication = “proximal or extensive disease” on angiogram and Age <65
- CABG - Indications = Severe stenosis and Age >65
Why is PCI + Coronary angioplasty preferred over CABG
CABG has a slower recovery and higher complication rate
What is Prinzmetal’s angina
Coronary artery spasm typically occuring at rest without evidence of underlying cardiac disease (hence different to unstable angina). May cause ST elevation.
RF = Female,
What is cardiac syndrome X?
Angina + Positive exercise test despite normal angiography with no evidence of underlying cardiovascular disease. Commonly occurs in peri/post menopausal women. Difficult to treat.
Definition of Hypertension
Persistently raised arterial BP >140/90 in clinic or >135/85 at home
What is considered ‘pre-hypertension’
130/85 - 139/89
What is malignant hypertension
Acutely, severely elevated BP with new or progressive organ dysfunction. It is a medical emergency. Generally a BP >180/120
British Hypertension Society Grading Criteria
Grade 1 (mild) = 140/90 to 159/99
Grade 2 (Moderate) = 160/100 to 179/109
Grade 3 (Severe) = >180/110
Risk Factors of essential HTN
FHx
Obesity
High alcohol consumption
High sodium consumption
Stress
Insulin resistance
Low foetal birth weight
Age
Being male (age <65) or Female (65-74yrs)
Black Afrocarribean ethnicity
Poor lifestyle
Causes of Secondary Hypertension (ROPE)
Renal disease - main cause of HTN. if BP does not respond to treatment, consider renal artery stenosis (also causes hypokalemia)
Obesity
Pre-eclampsia
Endocrine - mainly Conn’s syndrome (primary hyperaldosteronism)
1st line investigation for Conn’s syndrome
Renin:aldosterone ratio blood test - this would show high aldosterone but low renin levels (due to negative feedback)
Clinical presentation of HTN
Usually asymptomatic unless very high.
Headaches
Visual disturbances
Seizures
Epistaxis
Gold standard investigation for diagnosis of HTN
24hr ABPM or home blood pressure monitoring
Investigations for new onset HTN (NICE guidance)
Fundoscopy
Blood tests (HbA1C, Renal function, Lipid profile, U&Es)
ECG
Urine ACR + Dipstick (for hypertensive nephropathy)
Keith-Wagener classification (Hypertensive Retinopathy)
Stage 1 = Mild narrowing of arterioles + Silver wiring
Stage 2 = AV nipping (due to sclerosis of arterioles causing compression of veins where they cross)
Stage 3 = Cotton-wool patches, exudates and flame haemorrhages
Stage 4 = Papilledema
Stage 3 + 4 indicate malignant hypertension!!!!
Pharmacological management of HTN
1st line = ACEi / ARB
- ARBs should be used when ACEi can’t be tolerated
due to cough
- ACEi should be used as preference in pts with
diabetes regardless of age
- In pts >55yrs or AfroCarribean descent a CCB
should be used 1st line
2nd line = ACEi/ARB + CCB OR ACEi/ARB + Thiazide-like diuretic (indapamide)
- Pts >55yrs or Afro-Carribean should try CCB +
ARB
- Avoid thiazide diuretics in diabetes as worsenes
glucose tolerance
- CCBs prefered in pts with gout.
3rd line = ACEi/ARB + CCB + Thiazide Diuretic
4th line = Consider adding either Spironolactone (If K+ <4.5) or Alpha/Beta-blocker (K+ >4.5). If no response then refer for specialist input.
What is the BP target for adults age <80 with HTN +/- T2DM
<140/90 or ABPM <135/85
What is the BP target for adults age >80yrs with HTN
<150/90mmHg (or ABPM <145/95)
What is the BP target for pts with CVD + HTN
<130/90mmHg
Complications of Hypertension
IHD
Cerebrovascular event
Hypertensive retinopathy
Hypertensive nephropathy
HF
What monitoring should pts recieving HTN treatment
U&Es - as spirinolactone and ACEi both increase the risk of Hyperkalemia and Thiazide diuretics can cause electrolyte disturbances
ACE inhibitors
Rampiril, Lisinopril
MOA = inhibits the conversion of angiotensin 1 to angiotensin 2
Side effects = Cough, Angiodema, Hyperkalemia
Monitoring = Renal function before starting + after 2wks
ARBs
Losartan, Candesartan
MOA = Inhibits angiotensin II at the AT1 receptor
Side effects = Hyperkalemia
Calcium channel blockers
Amlodipine, Felodipine, Diltiazem
MOA = Inhibits voltage-gated calcium channels + causes smooth muscle relaxation + reduced force of myocardial contraction
Side effects = Flushing, Ankle Oedema, Headaches
Thiazide Diuretics
Bendroflumethiazide, Indapamide
MOA = Inhibits sodium absorption at the beginning of the DCT
Side effects = Hyponatremia, Hypokalemia, Dehydration
Monitoring = monitor serum electrolytes
Potassium-sparing Diuretics
Spirinolactone, Eplerenone
MOA = inhibits aldosterone in the kidneys, causing sodium excretion + potassium reabsorption
Side effects = Hyperkalemia
*useful if thiazide diuretics are causing hypokalaemia
Preload
End diastolic volume. The maximal volume of blood held in the ventricles after atrial systole. (Normal = 130ml)
Afterload
Resistance to blood flow - created by the vascular system
Risk Factors of HF
Old age
Female
Obesity
Diabetes
CKD
Causes of HF
IHD
Dilated cardiomyopathy
Hypertension
Valvular heart disease
Others = Congenital heart disease, alcohol, drugs, tricuspid imcompetence, pericardial disease, arrythmias
Types of HF
Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN.
Further divided into;
1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation.
2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS.
Right sided;
Types of HF
Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN.
Further divided into;
1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation.
2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS.
Right sided;
This is when decreased right ventricular function causes a systemic HTN leading to oedema.
Typically occurs due to left-sided HF. Can be related to Pulmonary HTN, Tricuspid/pulmonary valve disease or Pericardial disease
Congestive HF;
When both occur
Symptoms of HF
Fatigue
SOB
Exertional dyspnoea
Cough +/- pink frothy sputum if pulmonary oedema
Orthopnoea
PND
Signs of HF
- Pulmonary oedema - Bibasal fine crackles + Pleural effusion + Tachypnoea + Hypoxia + Cyanosis
- Systemic oedema - Peripheral pitting oedema + tender hepatomegaly + ascites + elevated JVP
- May have signs of underlying heart disease
New York Heart Failure Classification:
Class I = no symptoms + no limitation in ordinary physical activity.
Class II = Mild symptoms (SOB/Angina) + Slight limitation during ordinary activity
Class III = Marked limitation in activity due to Sx in less than ordinary activity
Class IV = Severe limitation. Sx at rest, mostly bedbound
Main diagnostic test for HF
pro-BNP (released by cardiomyocytes in response to excessive stretching)
Interpretation of Pro-BNP values;
If >2000 = Refer to cardiology urgently
If 400-2000 = Refer to cardiology + Echocardiogram within 6 weeks
If <400 = HF diagnosis is less likely. Consider alternative
Besides from HF, what other conditions cause raised BNP?
Tachycardia
Sepsis
PE
Renal impairment
COPD
What are the findings on CXR in HF?
Alveolar oedema
Batwing opacities (Bilateral perihilar lung shadowing) + Kerley B lines
Cardiomegaly
Dilated prominent upper lobe vessels + upper lobe congestion
Effusion (bilateral + transudative)
What lifestyle advice should you give to patients with HF?
Avoid large meals
Exercise regularly (20-30 min walk 3-5times per week)
If congestive heart failure 1-2 days bed rest per week
Annual influenza vaccine + one-off pneumococcal vaccine
Medical therapy of Heart failure (in HF- rEF)
1st line = ACEi + Beta-blocker (Rampril + Bisoprolol/carvedilol)
2nd line = Aldosterone antagonist (e.g spirinolactone - must monitor U&Es for hyperkalemia)
3rd line = Consider use of SGLT-2 inhibitors if HF-rEF (dapagliflozin)
4th line = should be initiated by a specialist. options include;
> If EF <35% give Ivabridine or Subcubitril-valsartan
> If AF is present give Digoxin
> If Afro-Carribean descent give Hydralazine +
Nitrate
> If widened QRS complex = Cardiac
resynchronisation
5th line = Palliative. Consider ionotropes / cardiac transplant / hospice
Which diuretic is best for symptomatic relief of fluid overload (i.e if a patient has preserved EF)
Furosemide 20mg
What is Cor Pulmonale
Right sided HF caused by respiratory disease
Most commonly due to COPD but also PE, Interstitial lung disease, CF, Primary pulmonary HTN
Pathophysiology of cor pulmonale
Existing pulmonary disease leads to an increased stiffness of pulmonary arteries resulting in pulmonary HTN. This causes an increased afterload in the right ventricle leading to right ventricular hypertrophy and therefore a reduced right ventricle ejection fraction. This leads to a back pressure of blood in the right atrium, vena cava and systemic system (leading to systemic HTN)
Clinical features of Cor Pulmonale
Often asymptomatic in early stages.
1. Signs of lung disease = SOB + Exertional dyspnoea + Hypoxia + Cyanosis
2. Signs of R sided HF = Peripheral oedema, Syncope, Raised JVP, S3 gallop, Pan-systolic murmur (tricuspid regurg / Pulmonary HTN) + Hepatomegaly + Ascites.
Management of Cor Pulmonale
Treat underlying cause
Alleviate hypoxia - with long term oxygen therapy
Medical management as for HF
Aortic stenosis murmur
Ejection systolic, high-pitched murmur with a cresendo-decresendo pattern heard best over the aortic area with radiation to the carotids.
*May have reduced/absent S2 in moderate/severe disease
Pulse characteristics in Aortic Stenosis
Slow rising pulse + Narrow pulse pressure (pulse pressure <25% of SBP)
Symptoms of Aortic stenosis
Exertional syncope due to difficulty maintaining good blood flow to brain
Chest pain
SOB
Causes of Aortic stenosis
Age related calcification (most common)
Bicuspid aortic valve (most common congenital heart disease 1-2%, most common cause in <65yrs)
Rheumatic heart disease
William’s syndrome (supravalvular AS)
HOCM (subvalvular)
Complications of Aortic stenosis
Left bundle branch block (usually present on ECG)
Aortic sclerosis
Thickening / Calcification of the aortic valve without obstruction of blood flow.
Consider this when Ejection systolic murmur + No ECG changes + No carotid radiation
Mitral stenosis murmur
Mid-diastoic low pitched rubmling murmur, best heard on expiration with pt in the left lateral decubitus position.
Signs + Symptoms of Mitral stensosis
Malar flush
Haemoptysis / Dyspnoea
AF - L atrium struggles to push blood through stenotic valve leading to strain + electrical disruption
Low volume pulse
Loud S1 + Opening snap (thick valves require large systolic force to shut)
Tapping apex beat (palpable closure of mitral valve)
ECG changes = P mitrale (late stage sign due to atrial hypertrophy)
Causes of Mitral stenosis
Rheumatic heart disease (most common + main complication of rheumatic HD)
Congenital
Left atrial Myxoma
Connective tissue disorder
Mucopolysaccharidosis
Aortic regurgitation murmur
Early diastolic soft murmur with decrescendo pattern
How can you emphasise an aortic regurg murmur?
Get pt sat up, leant forward and hold expiration or handgrip manoeuvre
Austin flint murmur
This is the murmur that can be heard in severe AR. It is an early diastolic rumbling murmur heard over the apex.
Caused by a backflow of blood through the aortic valve and some over mitral valve (causing it to vibrate)
5 Clinical signs of Aortic regurgitation
- Corrigans sign = visible distension and collapse of carotid arteries in neck
- De Musset’s sign = head bobbing with each heart beat
- Quincke’s sign = pulsations in nail bed with each heartbeat when nail bed is lightly compressed
- Traube’s sign = pistol shot sound heard when stethoscope placed over femoral artery during systole and diastole
- Mullers sign = Uvula pulsations are seen with each heartbeat
Pulse characteristics in Aortic regurgitation
Corrigan’s pulse (Collapsing pulse) = rapidly appearing and disappearing pulse at carotid.
Also wide pulse pressure
Causes of Aortic regurgitation
- Valvular disease - congenital bicuspid aortic valve, Rheumatic heart disease, Infective endocarditis
- Aortic root dilation = Aortic dissection, Connective tissue disease (marfans), Aortitis.
Main complication of aortic regurg
Heart failure
Mitral regurgitation murmur
Pan systolic, high-pitched, whistling murmur with radiation to the left axilla.
How to emphasise a mitral regurgitation murmur
Left lateral decubitus position, on expiration
Causes of mitral regurgitation
- Infective endocarditis
- Acute MI (papillary muscle rupture)
- Rheumatic heart disease
- Congenital defect of valve
- Cardiomyopathy
What is the gold standard investigation for Aortic stenosis?
Transoesophageal echocardiogram
Gold standard Invx for Mitral stenosis / Regurg and Aortic regurg
Doppler transthroacic echocardiogram
Management of acute aortic regurgitation
Medical emergency!
Ionotropes + Vasodilators + Aortic valve replacement
Management of chronic aortic regurg
If asyptomatic / EF >50% - Yearly review
If symptomatic / EF <50% - Aortic valve replacement. if not surgical candidate then vasodiators + ACEi
Acute management of Mitral regurg
Emergency mitral valve replacement
Management of Aortic stenosis
If asymptomatic then 3-5 year monitoring
If symptomatic (or LV dysfunction/+ve exericse tolerance test or valvular gradient >40mmHg) then Aortic valve replacement is needed. If high risk pt then can do a transcatheter replacement (TAVI)
Management of symptomatic mitral stenosis
Diuretic + Balloon valvotomy/replacement
Treat rheumatic heart disease or AF.
What is the normal diameter of the aortic valve
3-4cm
what is the diameter of the aortic valve in severe aortic stenosis
<1cm
Causative agent of rheumatic fever
Streptococcus pyogenes
Clinical features of rheumatic fever
- Erythema marginatum (rash which quickly dissapears)
- Sydenham’s chorea / st Vitus dance
- Polyarthritis
- Carditis + Valvulitis (think mitral stenosis)
- Subcutaneous nodes
- Pyrexia
Investigations for Rheumatic fever
Bloods = raised inflammatory markers
Raised Anti-streptococcal antibody titre
Treatment for Rheumatic fever
Oral Penecillin + NSAIDs
Diagnostic criteria for Rheumatic fever
Jones criteria;
1. Evidence of recent group A streptococcal infection (e.g +ve throat swab, raised ASO)
2. 2 major or 1 major + 1 minor criteria
Major = ‘JONES’
- Joint involvement
- myOcarditis
- Nodules (subcutaneous)
- Erythema marinatum
- Sydenham Chorea
Minor = ‘Cafe Pal’
- CRP raised
- Arthralgia
- Fever
- ESR raised
- Prolonged PR interval
- Anaemensis of rheumatism
- Leukocytosis
Causes of pericarditis
- Mainly idiopathic
- Viral - Cocksackie B or echo virus, HIV. Very painful
- Post-MI (Dressler’s syndrome)
- Uremic (secondary to CKD)
- Bacterial - e.g staphyloccocus aureus (rare)
- Tuberculosis - usually constrictive pericarditis. pts will have TB symptoms
- Malignant - secondary to lung/breast/hodgkins lymphoma
- Other = radiation, fungus, hypothyroidism
Risk factors for pericarditis
Male, Age 20-50, autoimmune disease, past cardiac surgery, previous MI, Dialysis
Clinical presentation of pericarditis
Chest pain - may be pleuritic in nature + may radiate to neck or shoulders. Typically relieved by sitting forwards, exacerbated by lying flat
Pericardial friction rub - best heard at left lower sternal edge with pt leaning forward and expiring
Pyrexia + Leukocytosis (if infective)
Dyspnoea
Tachypnoea
Tachycardia
ECG changes in pericarditis
Global + widespread changes.
1. ST elevation which is saddle-shaped (concave + upwards) in all leads
2. PR depression in all leads
Management of pericarditis
NSAIDs + Colchine (until symptoms resolution or normalisation of inflammatory markers)
Treat underlying cause
Avoid strenuous physical activity
What is brugada syndrome + What is the inheritence?
An inherited (Autosomal dominant) CVD which may present with sudden death.
Due to a mutation in the SCN5A gene
Features of Brugada syndrome
Convex elevation / Down-sloping ST segment (mainly in V1-V3)
Partial RBBB
What is the investigation of choice for Brugada syndrome
Injection of flecainide or ajmaline - this will make ECG changes more pronounced.
Management of brugada syndrome
implantable cardioverter-defibrillator
Features of Tetralogy of Fallot
- Ventricular septal defect
- Pulmonary valve stenosis
- Misplaced aorta
- Right ventricular hypertrophy
If a younger patient is presenting with chest pain on a history of recent viral illness what must you consider as a cause?
Myocarditis
Causes of Myocarditis
Viral : Coxsackie, HIV
Bacteria : Diptheria, Clostridia
Lyme disease
Chaga disease
Toxoplasmosis
Autoimmune
Doxarubicin antracycline chemotherapy agent.
Clinical Features of myocarditis
Typically younger pt with a history of a recent viral illness with new chest pain.
May also have dyspnoea, signs of acute HF (Pulmonary oedema or orthopnoea) and arrythmias
Investigation findings in myocarditis
May have elevated tropnin, BNP and inflammatory markers.
Tachycardia
ECG may show focal ST elevation (e.g V1-V4) or global T wave inversion
What are the RF of infective endocarditis
Prior endocarditis
Prior heart survery
Prosthetic heart valves
Valvular heart disease
Dental procedures or poor dental hygeine
IV catheter or implanted pacemaker
IVDU
Cardiomyopathy
Most common causes of Infective endocarditis
- Staphylococcus aureus: esp in IVDU
- Streptococcus viridians: associated with dental procedures or poor dental hygiene
- Steptococcus epidermis: in first 2 months following prosthetic heart valve surgery
- Streptococcus bovis: in colorectal cancer
Which valve is most commonly affected by Infective endocarditis + what type of murmur does it case?
Mitral valve (regurg)
Then aortic valve (regurg)
Signs + Symptoms of Infective endocarditis
mneumonic = ‘For James’
Fever
Osler’s nodes
Roth spots
Janeway lesions
Anemia
Murmur (mitral/aortic regurg)
Emboli
Splinter haemorrhages
Modified Duke’s Criteria for IE
Diagnosis based on either +ve Pathological criteria / 2 major criteria / 1 Major + 3 minor / 5 minor
Major = 2 x blood cultures +ve / +ve Echocardiogram / New valvular regurg
Minor = Predisposing heart condition / Fever >38 / Signs + symptoms / immunological phenomenon e.g GN
Management of Infective endocarditis
1st line = Amoxicillin +/- Gentamycin
(if pen allergic or severe sepsis/MRSA - Vancomycin + gentamicin)
If prosthetic heart valve = Vancomycin + Rifampicin + Gentamicin
Poor prognostic factors in infective endocarditis
- Staphylococcus aureus +ve
- Prosthetic heart valve
- Culture -ve
- Low complement levels
Clinical features of cardiac tamponade
Beck’s triad;
1. Hypotension
2. Raised JVP
3. Muffled heart sounds
Additional: Dyspnoea, Tachycardia, Chest pain, Pulsus paradoxus
ECG findings and JVP characteristic in Cardiac tamponade
Absent Y descent on JVP
ECG = electrical alternans (alternating amplitude/axis of QRS complex)
What diagnosis should be considered in a patient presenting with shock but no tension pneumothorax
Cardiac tamponade
Gold standard investigation for cardiac tamponade
Echocardiogram - will show a pericardial effusion / ventricular collapse
Management of Cardiac tamponade
Definitive treatment = Thoracotomy
Unless pt is in peri-arrest = perform urgent needle pericardiocentesis to buy some time.
Gold standard invx for aortic injury
CT with contrast
CXR findings in aortic injury
Widened mediastinum (>8cm)
Loss of aortic knuckle
Tracheal deviation to the R
Troponin guidelines in suspected MI
Troponin on admission + repeat after 6-12hours.
If <14 after 6+ hours then can exclude NSTEMI/STEMI
If 14-30 then should repeat in 3 hours (If inc by 50% then STEMI/NSTEMI)
if >30 = STEMI/NSTEMI
For how long does troponin stay elevated for
10-14 days
Other causes of raised troponin (other than MI)
CKD
Sepsis
PE
Aortic dissection
Myocarditis
Evolution of ECG changes in STEMI
Initially = tall, pointed upright T waves and ST elevation
After a few hours = T wave inversion and R wave voltage decreases. Q waves begin to develop
After a few days = ST elevation returns to normal
After a few weeks = Pathological Q waves develop and T wave returns to normal
Initial management of suspected NSTEMI/STEMI
Aspirin 300mg
02 via nasal cannula 2-4l/min
Morphine if severe pain (+/- antiemetic)
Nitrates (Sublingual GTN x2)
Gain IV access and take bloods. Do ECG.
What is a GRACE score
Global registry of acute coronary events
Used to estimate 6 month mortality in NSTEMI/Unstable angina
Definitive management of NSTEMI/Unstable angina
High risk/haemodynamically unstable = urgent CA + PCI + Dual antiplatelets
Intermediate risk = Early coronary angiography + PCI (<72hrs)
Low risk = BATMAN
1. Beta-blockers
2. Aspirin 300mg stat
3. Ticagrelor
4. Morphine
5. Anticoagulant (e.g fondiparinaux)
6. Nitrates (E.g GTN - avoid in HTN)
Management of STEMI
- Dual antiplatelet therapy = Aspirin + Presagurel / ticagrelor (or clopidogrel if already taking anticoagulant e.g apixaban)
- PCI (should be done <2hrs) - give unfractionated heparin before
- If PCI can’t be done, thrombolyse with tPA then recheck ECG after 60 mins.
Secondary prevention after MI
Aspirin
Anti-platelet (Ticagrelor or Clopidogrel for 12 months)
Atorvastatin 80mg
Acei
Atenolol / beta-blocker
Aldosterone antagonist (if HF) e.g spirinolactone
Driving rules following MI
Cannot drive for 4 weeks
or 1 week if succesfully treated with angioplasty
Complications of MI
Think ‘Drreaad’
Death
Regurg (mitral)
Rupture (septum or Left ventricular wall)
Edema
Arrythmia (VT / VF / Bradyarrythmia)
Aneurysm (in left ventricle)
Dresslers syndrome
Dressler’s syndrome
Localised immune response leading to pericarditis
Occurs 2-6 weeks post MI
Sx = pleuritic chest pain, worse on lying flat, low grade fever, pericardial rub.
Investigations for Dressler’s syndrome
ECG shows saddle-shaped global ST elevation + PR depression
Echocardiogram = pericardial effusion
Management of Dresslers syndrome
NSAIDs + Pericardiocentesis
What investigation can you do to confirm if a patient with recent ACS has had a reinfarct
CK-MB
Causes of Atrial Fibrillation
‘MRS SMITH’
Mitral Rerug/Stenosis
Sepsis
MI / IHD
Thyrotoxicosis
HTN
Acute rate/rhythm control in AF
Two principles = Rate/rhythm control + Anticoagulation
- Rate control 1st line (unless a reversible cause, new onset or associated HF) = Beta-blockers.
If Beta-blockers don’t work/contraindicated then give CCB (diltiazem) or Digoxin (only in sedentary people) - Rythm control - if reversible / new onset / associated HF / failure to respond = Cardioversion
- This should be done within 48hrs if new onset + stable
- Pharmacological = Flecainide / Amiodarone (if structural HD)
- Electrical cardioversion - if haemodynamically unstable
Long-term management in AF
Think Rate/rhythm control + Anticoagulation
1st line = beta-blockers
2nd line = Drondedarone / Amiodarone (if HF of LVF)
Anticoagulate with DOACs (e.g apixaban or rivoraxoabn) or give Warfarin if can’t have DOAC (i.e severe hepatic disease)
What food/drink must patients on warfarin avoid?
Vit K rich foods (e.g leafy greens)
CYP450 enzyme effectors (e.g Cranberry juice + Alcohol)
Management of Peri-arrest tachycardia
If life-threatening (i.e haemodynamic instability):
1. Synchronised DC shock. Give up to 3 attempts. must be sedated or anaesthetised if conciouss.
2. If unsuccessful give 300mg Amiodarone IV infusion over 10-20 mins then shock again.
Broad complex (>0.12ms);
1. Regular rhythm = Assume VT + Give 300mg Amiodarone IV followed by 24hr infusion
2. Irregular rhythm = seek help (could be AF + BBB or TdP)
Narrow complex (<0.12ms);
1. Regular rhythm = Vagal manoevre + IV Adenosine. 6mg, then 12mg, then 18mg. If unsuccessful consider atrial flutter and try beta-blocker / verapamil
2. Irregular = probably AF so consider cardioversion.
Management of SVT
If Unstable = DC Cardiovert
If stable;
1. Valsava manoevre
2. Carotid sinus massage
3. Adenosine - 6mg, then 12mg, then 18mg.
4. Verapamil
5. DC cardioversion
Contraindications to adenosine
asthma / COPD / Heart failure / Heart block / Severe HTN
Main side effect of adenosine
Sense of impending doom
Management of peri-arrest bradycardia
If stable = observe
If unstable =
1. IV Atropine 500mcg - can be repeated up to 6 times 3mg total
2. If still no improvement try Ionotropes (e.g noradrenaline / Isoprenaline) or transcutaneous cardiac pacing + defib
main side effects of atropine
Pupil dilation
Dry eyes
Urinary retention
Constipation
Because it is an antimuscarinic
Management of Acute Left ventricular failure
‘pour SOD’
- ‘pour away’ or stop their IV fluids
- Sit up
- Oxygen
- Diuretics - IV 40mg Furosemide
If severe shock = Ionotropes (dobutamine) or Vasopressors (norepinhephrine)
If severe Pulmonary oedema = CPAP
*also monitor fluid balance
Debakey classification of Aortic dissection
Type 1 = originates in ascending aorta, propagates to atleast the aortic arch and possibly beyond (most lethal)
Type 2 = Originates in and is confined to ascending aorta
Type 3 = Originates in descending aorta, extends distally
Management of Type B Aortic dissection
Type B = descending aorta
Observe, Bed rest + IV Labetalol to prevent progression
Management of Type A aortic dissection
Type A = ascending aorta
Management = HTN control with IV labetaolol + Surgical repair (usually thoracic endovascular aortic repair)
Main side effects of Nicorandil
Headache
Flushing
GI ulcers, anal ulceration + eye ulceration
Which medications commonly reduce hypoglycemic awareness
Beta-blockers
Anti-dote for dabigatran
Inadrucizumab
= monoclonal antibody which binds directly to dabigatran with greater affinity than thrombin.
Anti-dote for factor Xa inhibitors (Apixaban or Rivoroxaban)
Andexanet alfa
Anti-dote for Warfarin
Phytomedandione (vitamin K)
Anti-dote for heparin
Protamine
= Peptide which binds and sequesters heparin modules
Pulseless electrical activity management
1mg Adrenaline ASAP!!!
CPR 30:2
Secure airway + ventilate
Recheck rhythm after 2 minutes, if no response then repeat 1mg Adrenaline every 3-5 minutes + continue CPR
Anticoagulation in pts with AF post-stroke
2 weeks post stroke = Warfarin of DOAC (e.g 5mg Apixaban BD)
what causes a slurred upstroke on QRS complex
Wolf-Parkinson White syndrome
How can you differentiate between an aortic stenosis and pulmonary stenosis murmur
Pulmonary stenosis is louder on inspiration and does not radiated (unlike AS which radiates to carotids and is loudest on expiration)
Lateral MI ECG territories and arteries
I, aVL and V5,V6
Left circumflex artery
Inferior MI ECG territories
II, III, aVF
Right coronary artery
Anterolateral/Septal MI ECG territories + arteries
V1 - V4
sometimes V1-V6 + aVL
Left Anterior Descending (LAD)
Posterior MI ECG territories and Arteries
V1-V3 ST DEPRESSION!!!
Also often causes horizontal ST depression, Tall broad R waves, upright T waves + Q waves in posterior leads (V7-V9)
Usually left circumflex or right coronary
HOCM murmur
Ejection systolic murmur, louder on valsalva maneouvre + Quieter on squatting
cause of worsening renal function in a young pt shortly after starting ACEi for hypertension
Bilateral renal artery stenosis - if ACEi are started before diagnosis of this it can cause significant renal impairment
How can you distinguish between tricuspid regurgitation and mitral regurg?
Both cause pansystolic murmur however TR is loudest on inspiration and is best heard at left lower sternal border and radiates to right lower sternal border
Whereas MR is best heard at apex and in left lateral decubitus position.
ECG changes in PE
Most often sinus tachycardia is seen
S1Q3T3 is seen in 20% of patients. this is when there is a large S wave in lead 1, Q wave in lead 3 and a inverted T wave in Q3.
ECG findings in hypercalcemia
Short QT interval
What causes persistent ST elevation months after an MI
Left ventricular thromboembolism/aneurysm
Loop diuretics side effects
e.g Furosemide, Bumetanide
SE’s;
- Ototoxicity
- Hypotension
- Hyponatremia
- Hypokalemia
- Hypomagnesemia
- Hypochloremic acidosis
- Hypocalcemia
- Renal impairment
- Hyperglycemia (not as much as thiazide diuretics)
- Gout
Which medications can cause torsades de pointes?
- Macrolide antibiotics (e.g azithromycin / Clarithromycin)
- Antiarrythmics e.g amiodarone, sotalol
- TCAs
- Antipsychotics
- erythromycin
- Chloroquine
Causes of a raised JVP
Pulmonary HTN / PE / PS / Pericardial effusion (CT)
Quantity of fluid (i.e fluid overload)
RVF
SVC obstruction
Tamponade / TR
Why must ACEi be stopped prior to starting subcutril-valsartan?
Subcutrl-valsartan contains valsartan (ARB). Using both together increases the risk og angiodema as it would result in higher levels of bradykinin (as they both inhibit bradykinin degredation)
36 hour wash out period must be done.
