Cardiology

Outline 4 types of angina

1. Decubitus angina: pain worse when lying down, stable, atherosclerotic

2. Prinzmetal's or variant angina: ST elevation due to coronary vasospasm

3. Syndrome X: ST depression on exercise ECG but normal angiogram, sign of microvascular disease

4. St. Vincent's angina: pharyngitis caused by ulcerative gingivitis

Other than atherosclerosis, what are 2 causes of angina?

Aortic valve disease

Cardiomyopathy

List the risk factors for coronary disease

Hyperlipidaemia

Diabetes

Smoking

Hypertension

Obesity

CKD

Outline the investigations for coronary artery disease

Anatomical: CTCA (+ calcium score), invasive coronary angiography

Functional:

• exercise stress test/ echo

• myocardial perfusion scan

• cardiac MRI with stress perfusion

• exercise ECG

Outline the treatment of angina

Treat risk factors

GTN spray for acute relief

1st line BB's or CCB

2nd line long acting nitrates (if GTN responsive) or nicorandil, ivabradine or ranolizine

75 mg aspirin + statin

Consider CABG and PCI

Outline the A-E steps of assessment

Airway- own, patent

Breathing- RR, saturation (pulmonary oedema due to LVF? hypoxia)

Circulation- HR/BP (bradycardia= inferior MI, hypotension= cardiogenic shock/RV infarction, murmur)

Disability- GCS, glucose

Exposure- pain, inspection, bleeding, temp

List the causes of high serum troponin

Myo/pericarditis

CKD

PE

Cardiomyopathy

Atrial fibrillation/tachyarrhythmia

List the ECG changes in acute coronary syndrome

ST segment deviation (elevation or depression)

T wave inversion

Bundle branch block (delayed QRS)

Localisation

How do you look for ST segment deviation on an ECG?

Locate J point- inflection point between QRS and following segment

ST segment can be above or below point

Outline the immediate symptomatic management of ACS

Pain- morphine + nitrates

O2 if hypoxic

Outline the prognostic treatment for ACS

Dual antiplatelet therapy: aspirin (lifelong) + P2Y12 inhibitors

Atorvastatin 80mg

Cardio-selective BB (bisoprolol)

ACE inhibitor (ramipril) or ARB

PPI (if above 65yrs and/or history of GORD/ peptic ulcer disease/ dyspepsia etc)- aspirin can cause stomach bleeds

Describe the definitive management of ACS

Coronary angiography

• if STEMI, do immediately

• if NSTEMI, do within 72 hrs

PCI

Emergency CABG

Define ACS

Encompasses range of conditions including STEMI, NSTEMI and stable angina that are all due to sudden myocardial ischaemia

Outline the complications of ACS

DARTH VADER

Death

Arrhythmia- sinus brady, SVT, heart block, V fib

Rupture (free ventricular wall, ventricular septum + papillary muscles)

Tamponade

Heart failure

VSD

Aneurysm of ventricles- seen as persistent ST elevation without chest pain

Dressler’s syndrome- pleuritic pain, pericarditis, fever, pericardial effusion; 10-14 days after MI

thromboEmbolism (mural thrombus= attached to endocardium)

Recurrence/ mitral Regurgitation

Compare infarction vs injury

Myocardial injury= trop > 99th percentile e.g. myocarditis

Infarction= injury due to myocardial damage from ischaemia e.g. MI

Describe Takotsubo's cardiomyopathy

Presents as STEMI with heart failure symptoms + chest pain

Catecholamine mediated stress CM in post-menopausal women

Myocardial stunning

Findings: unobstructed coronaries + transient LV impairment with sparing of top of ventricle

AKA broken heart syndrome

Myocardial INJURY

Distinguish between type 1 and 2 MI vs myocardial injury

Type 1: acute ischaemia, atherosclerosis + thrombosis

• triggered by plaque rupture/erosion :. requires PCI, CTCA

Type 2: acute ischaemia, O2 supply + demand imbalance e.g. severe hypertension, sustained tachyarrhythmia

Myocardial injury: without acute ischaemia e.g. acute heart failure, myocarditis

:. treat underlying causes

Outline the signs and symptoms of mitral regurgitation

Symptoms:

• dyspnoea

• fatigue

• RHF (ankle oedema, abdomen distension)

Signs:

• full volume pulse

• AF

• pansystolic murmur

• tachycardia

• ST depression

• bilateral crackles on auscultation (pulmonary oedema)

Outline the management of severe mitral regurgitation as a result of flail posterior mitral valve leaflet

Furosemide- for pulmonary oedema

LMWH + IV amiodarone- for AF

Referred for urgent surgery

Outline the causes of mitral regurgitation

Congenital

Rheumatic

Myxomatous degeneration

Endocarditis

CAD

CM (dilated LV)

AF (dilated LA)

CREAM CupCake

Describe the pathophysiology of mitral regurgitation

LV volume overload-> increased LV emptying

Increased LA pressure

Increased LV filling pressure

Increased LV end diastolic damage

LV stretches-> failure

Outline the causes of mitral stenosis

Rheumatic fever

Severe annulus calcification

LA myxoma (benign tumour)/thrombus

Congenital

Outline the signs and symptoms of mitral stenosis

Dyspnoea

Palpitations

AF

Mitral facies (flushed cheeks, cyanotic lips)

Opening snap (mitral valves tensing + go into LV due to high pressure

Mid-diastolic rumbling murmur when lying on left

Presystolic murmur

Describe the pathophysiology of mitral stenosis

Blood unable to flow to LV due to leaflet rigidity

Increased LA pressure to maintain CO

LA dilation-> AF

Increased pulmonary pressure-> Outline the causes of mitral regurgitationpulmonary congestion

R + LHF

Describe the pathophysiology of aortic stenosis

Progressive narrowing of valve due to calcific degeneration

Compensatory LVH to maintain SV

Pressure overload -> LVF (SOB, angina, syncope)

Outline the management of aortic stenosis

Surgical or percutaneous valve replacement

Poor prognosis if symptomatic

Describe the pathophysiology of aortic regurgitation

AR leads to compensatory LV dilation + hypertrophy to maintain SV

LV dilation -> LVF (no LV dilation in acute AR)

List the causes of aortic regurgitation

Valvular:

• infective endocarditis

• rheumatic

• degenerative

• bicuspid AV

• trauma

Aortic root:

• hypertension

• dissection

• aortopathy e.g. in Marfan's

Outline the signs and symptoms of aortic regurgitation

Early diastolic murmur

• left sternal edge

• leaning forward

• end expiration

Wide pulse pressure (collapsing due to increased SV)

Outline the signs and symptoms of tricuspid regurgitation

Ascites

Raised JVP

Peripheral oedema

Abdo pains

Hepatomegaly (liver congestion)

Define heart failure

The inability of the heart to generate a sufficient CO to meet metabolic demands

WITHOUT an increased filling pressure

This is secondary to an underlying cause e.g. CAD and hypertension

Describe chronic HF

Breathlessness with impaired exercise tolerance

Slowly progressive + had periods of acute decompensation (suddenly worse)

State of fluid retention and overload

Describe acute HF

Can be dramatic with flash pulmonary oedema

Or gradual deterioration of chronic HF due to

• fluid accumulation

• low exercise tolerance + fatigue

• orthopnoea + nocturnal dyspnoea

Compare systolic and diastolic HF

Systolic: HR with reduced ejection fraction (HFrEF) or mildly reduced (HFmrEF)

Normal EF= ABOVE 55%

Diastolic: HF with preserved EF (HFpEF)

• stiffness of ventricular wall

• impaired filling

• reduced CO

• echo shows LVH, LA dilation + abnormal relaxation

Compare high output HF and low output HF

High output:

• heart overworked

• can be physiological (athletes, pregnant) or pathological (sickle cell, thyrotoxicosis)

Low output:

• capillary refill slow

• increasing breathlessness

List the top 3 causes of heart failure

Ischaemic heart disease (35-40%)

Dilated CM (30-35%)

Hypertensive heart disease (15-20%)

Other- valvular disease, HCM, uncontrolled tachyarrhythmias, viral myocarditis, COPD

Outline the signs and symptoms of heart failure

Symptoms:

• breathlessness (on exertion or at rest, orthopnoea, paroxysmal nocturnal dyspnoea)

• fatigue

• reduced exercise tolerance

• palpitations

• angina

Signs:

• raised JVP

• 3rd heart sound

• pulmonary crepitations

• hepatomegaly

• peripheral/sacral oedema

• cachexia (weight loss/wasting, loss of appetite)

Describe the 4 classes of heart failure (NYHA)

1= no symptoms

2= symptoms on exertion

3= symptoms on minimal exertion

4= symptoms at rest

Outline the possible investigations for heart failure

Routine bloods- FBC, iron, glucose, cholesterol, Ig's, BNP, uric acid

ECG- BBB, STEMI

CXR- pulmonary oedema

Transthoracic echo

Cardiac MRI

Outline the management of heart failure

ACUTE

-high flow oxygen (MONA- morphine, oxygen, nitrate/GTN, aspirin)

• furosemide if fluid overload

• ECG monitoring

• ventilatory support if needed

• find cause

CHRONIC

• prevent decompensation

• maintain or improve symptoms

• increase longevity

• device (pacemaker, implantable cardiac defibrillators) or surgical therapy

• drug therapy- BBs, ARB, ACEi

• LVAD (left ventricular assist device) carried in backpack

List the most common causes of secondary hypertension

Primary kidney disease

Primary aldosteronism

Renal artery stenosis

Pheochromocytoma (vascular tumour of adrenal medulla)

Cushing's

Obstructive sleep apnea

Coarctation of aorta

Drugs- NSAIDs, contraceptives, antidepressants

What are the diagnostic values for hypertension?

Clinic BP 140/90

ABPM/home monitoring (day time) 135/85

Outline the management of hypertension

ACD D(squared)

A= ACEi (dry cough) or ARB

C= CCBs e.g. verapamil

D= thiazide diuretics

D^2= loop diuretics e.g. spironolactone (oestrogen side effects e.g. gynaecomastia)

Which antihypertensives are specific to pregnancy?

Labetolol

Methyl dopa

Nifedepine

Outline the assessment of primary tachycardia

Assess using A-E approach

Monitor O2 saturation + give O2 if needed

Adverse features?

• e.g. shock, syncope, myocardial ischaemia, HF

If unstable-> synchronised cardioversion shock then specialist + amiodarone

If stable- is QRS narrow (<0.12ms)?

Is rhythm regular?

Describe supraventricular tachycardia and list the 3 types

Tachycardia that originates above the ventricles e.g. atria

Atrial fibrillation/flutter/tachycardia

Atrio-ventricular nodal reentrant tachycardia (AVNRT)

Atrio-ventricular reentrant tachycardia

Which drug can be used to treat AVNRT and AVRT?

Adenosine 6mg

Both conditions affect nodes, interrupted with drug

Describe broad complex tachycardia and give an example

Occurs when ventricular activation is not via normal specialised conduction system e.g. SAN

E.g. ventricular tachycardia where the activation comes from within ventricles + distribution is not even

Compare acute pericarditis and STEMI ECGs

Pericarditis- saddle shaped T wave inversion (smiley face)

STEMI- ST depression (sad face)

List the 4 Plasmodium agents that cause malaria

Most common:

1. Plasmodium Vivax

2. Plasmodium Falciparum (most lethal, drug resistant)

Less common:

3. Plasmodium Malariae (mildest)

4. Plasmodium Ovale

Outline the clinical features of malaria and its major risk factors

Clinical features:

• fever

• headaches, muscle aches, diarrhoea or vomiting

Risk Factors:

• foreign travel within last 12 months

• pregnancy status

• immunocompetence status (HIV, cancer, transplant recipients)

• drug history (previous prophylaxis, allergies, potential drug interactions)

List the signs of severe malaria

List 4 antimalarials and their mechanism of action

1. Quinoline derivatives e.g. chloroquine

   1. accumulate in parasite food vacuole and form cytotoxic complex with heme

2. Antifolates e.g. sulfonamides

   1. target enzymes involved in folate synthesis required for parasite DNA synthesis

3. Antimicrobials e.g. tetracycline, doxycycline

   1. target prokaryotic protein synthesis :. slow effect

4. Artemisinin derivatives e.g. artemether

   1. binding iron and breaking down peroxide bridges

Name 2 iron tests that are most useful in monitoring haemochromatosis and why

Ferritin and transferrin saturation

Both tests can track response to treatment

Ferritin= measure of total iron stores

Transferrin saturation= measures how much serum iron is bound to the proteins in the blood

Briefly outline the differentials of acute chest pain for the main body systems

Cardiac- ACS, aortic dissection, pericarditis/myocarditis

Respiratory- PE, pneumothorax, pneumonia

GI- GORD, peptic ulcer disease, acute pancreatitis, oesophageal spasm/rupture

Other- MSK, shingles

Outline the features of complete heart block

Syncope

HF

Sinus bradycardia (30-50)

Wide pulse pressure (large difference between systolic and diastolic)

JVP

Variable intensity of S1

Briefly outline the treatment steps of angina

1. Aspirin + statin

2. GTN spray

3. BB or CCB

   1. CCB monotherapy- verapamil or diltiazem (rate-limiting)

4. BB + CCB combination- amlodipine or modified-release nifedipine

5. Still symptomatic

   1. long-acting nitrates e.g. ivabradine, nicorandil, ranolazine

6. PCI or CABG

Outline the NICE guidelines for diagnosing hypertension

Always ABPM to rule out ‘white coat HTN’

Which drugs should be taken for the secondary prevention of an MI?

BRATS

BB

Ramipril

Aspirin

Ticagrelor

Statin

How do you identify RBBB and LBBB on an ECG?

LBBB: W in V1, M in V6

WiLLiaM

RBBB: M in V1, W in V6

MaRRoW

How do you differentiate between unstable angina and NSTEMI?

Both: ST depression and T wave inversion

Take troponin levels at 3hrs and 6hrs

IF ELEVATED→ NSTEMI

Normal troponin= unstable angina

How is anemia classified?

Describe hereditary spherocytosis- signs, tests, blood film and treatment

Genetic mutation resulting in defective RBC membrane

Usually hypochromic microcytic anemia

Increased destruction of RBCs

Describe aplastic anemia- clinical features, tests, blood film, treatment

Reduction or absence of hemopoietic precursors in all 3 cell lineages

Production issue

Outline the diagnosis of sickle cell disease

Clinical:

• family history

• recurrent pain

Lab:

• FBC- anemia

• haemolysis (high bilirubin, high LDH, raised reticulocytes, undetectable haptoglobin)

• blood film

• Hb electrophoresis/ sickle solubility test

Describe the emergency presentations of sickle cell disease

Briefly outline the 5 types of sickle cell crises

1. Thrombotic

   1. AKA vaso-occlusive crisis

   2. precipitated by infection, dehydration, deoxygenation

   3. can occur in various organs e.g. bones, lungs, spleen, brain

2. Sequestration

   1. sickling within organs e.g. spleen or lungs :. causes pooling of blood

   2. associated with increased reticulocyte count

   3. mainly in young children

3. Acute chest syndrome

   1. VOC within pulmonary microvasculature :> infarction in lung parenchyma

   2. SSx- SOB, chest pain, pulmonary infiltrates on CXR, low pO2

   3. management- pain relief, O2, antibiotics, transfusion

4. Aplastic

   1. infection with parvovirus (HPV B19)

   2. sudden fall in Hb

   3. bone marrow suppression causes reduced reticulocyte count

5. Haemolytic

   1. rare

   2. fall in Hb due to increased rate of haemolysis

Briefly outline the main transfusion reactions

Acute haemolytic reaction

Delayed haemolytic reaction: 7-10 days after transfusion

Febrile non-haemolytic reaction: during or soon after transfusion

Anaphylaxis

TRALI: anti-leukocyte antibodies in donor react with recipient WBCs, within 6hrs

TACO: pulmonary oedema/respiratory compromise due to volume overload, within 12 hours

Outline the signs and symptoms of acute haemolytic reaction

Outline the management and prevention of transfusion reactions

Outline how rheumatic fever typically presents

JONES criteria

Joints (arthritis)

O- carditis + pan-systolic murmur (looks like heart!!)

Nodules

Erythema marginatum (rash)

Sydenham’s chorea (late feature)- rapid, jerky, irregular movements

Outline the management of rheumatic fever

Oral penicillin IV

NSAIDs

Treat complications e.g. heart failure

Outline the features of hypercalcaemia

Bones, stones, groans and psychic moans

Corneal calcification

Shortened QT interval

HTN

Describe pulsus paradoxus

When there is an abnormally large drop in BP during inspiration

Usually presents in cardiac tamponade

Which artery is the preferred site for primary PCI?

Radial access

Next is Femoral

List 4 drugs recommended for reducing stroke risk in AF

DOACs e.g.

• Apixaban

• Dabigatran

• Edoxaban

• Rivaroxaban

Outline Takayasu’s arteritis- features, associations, investigation and management

Large vessel vasculitis

More common in younger females

Features: systemic features, unequal BP in upper limbs, absent/weak peripheral pulses, AR

Associations: renal artery stenosis

Investigations: magnetic resonance angiography (MRA) or CTA

Treatment: steroids

How does HOCM cause sudden death?

Ventricular tachycardia secondary to ischaemia

Occurs after extreme exertion

What are the echo findings in HOCM?

MR SAM ASH

Mitral regurgitation

Systolic anterior motion of the anterior mitral valve leaflet

Asymmetric hypertrophy

Briefly outline the main side effects of loop diuretics

Hypotension

Hypo→ Na+, Mg2+, Ca2+ and Cl-

Hyperglycaemia

Renal impairment

Ototoxicity

When is cardioversion used for AF?

1. If the patient is haemodynamically unstable

2. New onset AF that presents within 48hrs

   1. lower risk of thrombus that could be dislodged

What is the first line management for a patient that is over 55yrs with stage 2 HTN and a QRISK score >10%?

CCB, statin and lifestyle advice

Outline the 4 steps of HTN management

1: A or C

2: A + C or A + D or C + D

3: A + C + D

4: K+< 4.5 → spironolactone

K+ > 4.5 → alpha or BB

Outline the management of HOCM

ABCDE

Amiodarone

Beta-blockers or verapamil for symptoms

Cardioverter defibrillator

Dual chamber pacemaker

Endocarditis prophylaxis

AVOID: nitrates, ACE-Is or inotropes (adrenaline, dobutamine)

Outline the secondary prevention of ACS

5A’s

Aspirin

And another antiplatelet

Atorvastatin

ACE-I/ARB

Atenolol (or other BB)

How are ACE-Is used in renal disease?

Should be stopped in AKI

They are reno-protective in CKD

Which biomarkers are most useful for confirming a reinfarction?

CK-MB: elevated 3-4 days following infarction

Troponin: elevated for 10 days following infarction

Outline the adverse effects of amiodarone

Indication: terminates SVT

• chest pain

• bronchospasm

• transient flushing

Outline the management of acute NSTEMI

BATMAN

Beta blockers (unless contra-indicated)

Aspirin 300mg stat

Ticagrelor 180mg stat

Morphine

Anticoagulant (LMWH e.g. enoxaparin 1mg/kg)

Nitrates (GTN)

How should a patient with gout be treated for HTN?

ACE-I

if not controlled with ACE, add CCB over thiazide (even if low K+)

How does malignant hypertension typically present?

Severe HTN (>180 systolic)

Papilloedema

Retinal bleeding

Raised ICP

Which drug should patients be given before fibrinolysis?

Anti-thrombin drug e.g. fondaparinux

List the adverse effects of adenosine

Indication: terminates SVT

Chest pain

Bronchospasm

Transient flushing

Compare the ECG changes in bifascicular and trifascicular block

Bifascicular: RBBB and left axis deviation

Trifascicular: RBBB, left axis deviation and 1st degree heart block

Describe the ECG changes in hypothermia

Jesus Quist Its Bloody Freezing

J waves

QT interval prolonged

Irregular rhythm

Bradycardia

First degree heart block

Briefly outline the mechanism of warfarin

Oral anticoagulant used for VTE management + reducing stroke risk in AF

Inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form

:. acts as a cofactor for clotting factor II, VII, IX and X (1972) and protein C

Taking warfarin increases INR :. takes longer for blood to clot

List the warfarin inducers

Inducers: decrease INR (increase effect of warfarin)

SCARS

Smoking

Chronic alcohol intake

Antiepileptics (phenytoin, carbamazepine, barbiturates)

Rifampicin

St. John’s Wort

List the inhibitors of warfarin

Inhibitors: cause increase in INR (counter effect of warfarin)

ASS-ZOLES

Antibiotics (ciprofloxacin, erythromycin, isoniazid, clarithromycin)

SSRIs

Sodium valproate

Zoles- omeprazole, ketoconazole, fluconazole

When should amiodarone be used?

Pharmacological cardioversion of AF if there is structural heart disease

Typically more chronic AF

Which ECG abnormality is commonly seen in hypercalcaemia?

Short QT interval

Painful bones, renal stones, abdominal groans and psychic moans