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Phase 3 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe the stages of congestive heart failure

A
  • Stage 1: redistribution, PCWP 13-18 mmHg
    > Redistribution of pulmonary vessels
    > Cardiomegaly
  • Stage 2: interstitial oedema, PCWP 18-25 mmHg
    > Kerley B lines
    > Peribronchial cuffing
    > Hazy contours of vessels
    > Thickened interlobar fissures
  • Stage 3: alveolar oedema, PCWP > 25 mmHg
    > Consolidation
    > Cotton wool appearance
    > Pleural effusion: fluid within potential space between parietal and visceral pleura
    » Seen as homogeneous lower zone opacity with a curvilinear upper border
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2
Q

Describe how impulses are conducted in the heart

A
  • Sinoatrial node (SA node): near the entrance of the SVC
    > Initiates heartbeat and determines heart rate: cardiac pacemaker
    > Impulse from SA node spreads throughout atria, stimulating contraction
  • Impulse reaches atrioventricular (AV) node, which delays passage of electrical impulses to the ventricles
  • AV node passes impulse into the atrioventricular bundle (bundle of His)
    > divided into right and left bundle branches, which conduct impulses towards apex of heart
  • Signals are passed onto Purkinje fibres, which ascend through ventricular myocardium, triggering contraction
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3
Q

Describe the morphology of the ECG waveforms

A
  • P wave: atrial contraction
  • PR segment: time taken for impulses to travel from SA node to AV node
  • QRS complex: firing of AV node and ventricular depolarisation
  • ST segment: plateau in myocardial action potential - ventricular contraction (systole)
  • T wave: ventricular repolarisation immediately before ventricular relaxation (diastole)
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4
Q

Describe the different chest leads used in the 12-lead ECG

A
  • Anterior view: V1, V2, V3, V4
  • Inferior view: Leads II, III, aVF
  • Lateral view: Lead I, aVL, V5, V6
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5
Q

What is the QRS axis? What is its normal range?

A

The QRS axis is used to determine the average direction of ventricular depolarisation

> Normal QRS axis ranges from -30º to +90º, predominantly positive QRS in I and II

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6
Q

How do you determine heart rate on an ECG?

A
  • 300 / number of large squares between each QRS complex
  • Number of QRS complexes across ECG x 6
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7
Q

Describe the patterns of right axis and left axis deviation on an ECG

A
  • Right axis deviation: +90º to +180º
    > Predominantly negative QRS in I and aVL
    > Can be pathological - cor pulmonale secondary to COPD - but also common in young, fit males
  • Left axis deviation: -30º to -90º
    > Predominantly negative QRS in II and aVF
    > Common in ischaemic heart disease or conduction problems
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8
Q

Describe the patterns seen in AV block on an ECG

A
  • Complete heart block
    > Complete dissociation between P wave and QRS complex
    > Regular & slow rate
  • 2nd degree AV block
    > Classic (Mobitz type 2): fixed prolongation of PR segment, non-conducted P wave with return to normal conduction at regular intervals
    » 2:1 block indicates every second P wave is non-conducted

> Wenckebach (Mobitz type 1): progressive prolongation of PR segment

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9
Q

Describe the patterns seen in bundle branch block on ECG

A
  • Right bundle branch block (RBBB) - MarroW
    > Conduction through right bundle will be delayed so predominant conduction through left bundle on ECG
    > Small positive deflection followed by larger deflection in V1 (M shape)
    > Small negative deflection > large positive deflection > negative deflection in V6 (W shape)
  • Left bundle branch block (LBBB) - WilliaM
    > V1: 2 negative deflections (1st smaller, 2nd deeper) - W shape
    > V6: 2 positive deflections (1st smaller, 2nd larger) - M shape
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10
Q

Describe the algorithm used to identify tachycardias on ECG

A
  • Fast & irregular
    > Narrow QRS: AF
    > Broad QRS: pVT or pre-excited AF; AF bundle branch block
  • Fast & regular
    > Narrow QRS: sinus rhythm or supraventricular tachycardia
    > Broad QRS: ventricular tachycardia or supraventricular tachycardia bundle branch block
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11
Q

Describe the ECG changes seen in pericarditis

A
  • Clinical history not consistent with MI
  • Concave ST elevation
  • No specific territory (often global)
    > No reciprocal change
    > PR depression
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12
Q

Define atrial fibrillation as well as its symptoms

A
  • Commonest sustained cardiac arrhythmia especially in the elderly
  • Increases risk of stroke (5x)
  • Symptoms
    > Asymptomatic
    > Palpitations
    > Dyspnoea
    > Rarely, chest pain or syncope
    > Complications e.g. stroke (blood clots form in left atrial appendage)
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13
Q

Describe the investigations used in atrial fibrillation

A
  • Irregularly irregular pulse
  • Confirmed by 12-lead ECG
    > Rate variable
    > Irregular, narrow QRS
    > No P waves
  • Echocardiogram
  • Thyroid function tests: thyrotoxicosis can cause AF
  • Liver function tests
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14
Q

Describe the risk factors for stroke and thromboembolism in non-valvular AF (CHA2DS2-VASc scoring system)

A

Major
- Previous stroke / TIA / thromboembolism
- Age > 75

Non-major
- Congestive heart failure / LV dysfunction
- Hypertension
- Diabetes mellitus
- Vascular disease
- Age 65-74
- Female sex

CHA2DS2-VASc
C: congestive heart failure/left ventricular dysfunction (1)
H: hypertension (1)
A2: age >=75 (2 points)
D: diabetes mellitus (1)
S2: stroke / TIA / thromboembolism (2 points)
V: vascular disease (1)
A: age 65-74 (1)
Sc: sex category (1)

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15
Q

Describe the management of atrial fibrillation

A
  • Warfarin
  • DOACs e.g. dabigatran, rivaroxaban
  • Rhythm control
    > Direct current cardioversion (persistent AF)

> Antiarrhythmic drugs (used in combination with a beta blocker)
> Class 1: sodium channel blockers (flecainide, propafenone)
> Class 3: potassium channel blockers - prolong action potential duration / QT interval; sotalol (beta blocker w/ class 3 activity), amiodarone
> Multichannel blockers e.g. dronedarone

> Catheter ablation: radiofrequency current - burning - or cryoablation - freezing with NO
(triggers for paroxysmal AF can be found in the pulmonary veins so pulmonary vein isolation can be curative)

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16
Q

Describe the different types of AF and the goals of treatment

A
  • Paroxysmal - intermittent (prolonged ambulatory ECG used to detect)
  • Persistent - requiring intervention to terminate the arrhythmia e.g. IV antiarrhythmic drug injection or DC cardioversion
  • Permanent

Goals of treatment: target heart rate is <110/min or if still symptomatic, <80/min

> Patients without heart failure should be started on a beta blocker e.g. bisoprolol or atenolol, or rate-limiting calcium channel antagonist e.g. verapamil, diltiazem (digoxin as second-line)

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17
Q

Define atrial flutter and the changes seen on ECG

A
  • Atrial flutter is related to atrial fibrillation - atrial rhythm is variable (regular or irregular) at 240-300bpm
  • Characteristic sawtooth pattern seen in inferior leads (II, III, aVF)
  • Re-entry around the tricuspid valve with variable ventricular rate
  • ECG
    > Regular narrow QRS
    > Sawtooth atrial activity 300bpm
    > Variable AV block
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18
Q

Define hypertension and its complications

A
  • Persistently elevated arterial blood pressure > 140/90 mmHg
  • Linear relationship between blood pressure and CV events such as MI, stroke, heart failure & PVD
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19
Q

Describe the 2 types of hypertension as well as their causes

A
  • Primary (aka essential or idiopathic, 90-95%)
    > Risk factors include
    » Non-modifiable: age, gender, race, genetic factors
    » Modifiable: diet, physical activity, obesity, excess alcohol, stress
  • Secondary (5-10%)
    > Endocrine
  • Hyperaldosteronism, phaeochromocytoma, thyroid disease, Cushing’s syndrome

> Vascular
- Coarctation of aorta

> Renal
- Renal artery stenosis, renal parenchymal disease

> Drug
- NSAIDs, herbal remedies, cocaine, exogenous steroid use

> Other
- Obstructive sleep apnoea

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20
Q

Describe the pathophysiology of hypertension

A

BP = CO x TPR (cardiac output x total peripheral resistance)

  • Defects in renal sodium homeostasis:
    > Overactive renin-angiotensin-aldosterone system (RAAS) leads to salt & water retention
    > Increase in total blood volume leads to increased cardiac output
  • Functional vasoconstriction:
    > Decreased baroreceptor sensitvity
    > Vascular tone may be elevated due to increased alpha adrenoceptor stimulation (overactive nervous system and RAAS system - vasoconstriction)
  • Defects in vascular smooth muscle growth and structure
    > Growth factors such as angiotensin and endothelins can increase vascular smooth muscle leading to remodelling
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21
Q

Describe the investigations used in the diagnosis of hypertension

A
  • Assessment:
    > History e.g. risk factors, age of onset, medications, symptoms, family history and lifestyle

> Physical examination: BP both arms >2 readings on 2+ occasions, out of office BP measurement, BMI, examination of heart & lungs, auscultation of carotid, abdominal and femoral bruits, examination of thyroid gland and abdomen, palpation of the lower extremities (oedema and pulses), optic fundi examination, neurological exam & cognitive status assessment

> Investigations:
- Routine metabolic panel and lipids: hyperglycaemia or hyperlipidaemia
- Renal function: eGFR and creatinine
- FBC: Hb
- Urinalysis: ACR or PCR (albumin:creatinine ratio)
- ECG
- If investigations are unclear: echocardiogram & carotid dopplers, sleep study, phaeochromocytoma screen, TFTs, plasma renin/aldosterone, renal artery imaging

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22
Q

Describe the management of hypertension

A
  • Lifestyle modification
    > Education, sodium reduction, dietary approaches to stop hypertension (DASH) diet, weight loss, increased physical activity, limited alcohol consumption, smoking cessation
  • Antihypertensive drugs
    > Diuretics: loop, thiazide, mineralocorticoid receptor antagonists e.g. spironolactone
    > ACE inhibitors or angiotensin receptor blocker (ARB)
    > Vasodilators: calcium channel blockers, beta blockers, alpha blockers
    > Others: methyldopa, hydralazine, monoxidine
  • Device based therapies
    > Renal sympathetic denervation - clinical trials
    > Baroreflex activation therapy (BAT) - feasibility studies
  • Electrical stimulation of carotid sinus baroreceptor system
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23
Q

Describe infective endocarditis including the vegetation formed

A
  • Infection of the endocardium
  • Formation of a vegetation which results in damage to the cusps of the valves
    > Most commonly mitral (followed by aortic, tricuspid & pulmonary valves)
  • The vegetation consists of a fibrin mesh, platelets, white blood cells, RBC debris and organisms
    > Consists of a mass of different components forming a biofilm (adhere to foreign materials, treatment of infection often requires removal of the material)
  • Organisms communicate via quorum sensing: production of chemical messages which instruct other organisms to divide or become biochemically inert
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24
Q

List the organisms causing endocarditis

A
  • Bacterial

> Gram positive
> Rods
> Cocci
- Staphylococci
> Staphylococcus aureus (coagulase positive staph) e.g. MRSA (methicillin resistant staph aureus) or MSSA (methicillin sensitive staph aureus)

> > Coagulase negative staphylococci (CoNS)

  • Streptococci
    » Streptococci viridans, enterococci

> Gram negative
> HACEK organisms: haemophilus, aggregatibacter, cardiobacterium, eikenella, kingella
> Enterobacteriales (Coliforms) e.g. E. Coli
> Pseudomonas aeruginosa

> Fungal, e.g. candida species - Candida albicans

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25
Q

Describe Q fever

A

Zoonotic bacterial infection with Coxiella burnetii

Common in sheep farmers

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26
Q

Describe the classification of endocarditis and the organisms which usually cause it

A
  • Native valve endocarditis (NVE)
    > Commonly caused by S. viridans, S.aureus or gram negative
  • Endocarditis in IVDUs (intravenous drug users)
    > S. aureus, S. viridans or fungi
  • Prosthetic valve endocarditis (PVE)
    > CoNS - S. epidermis, gram negative, fungi
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27
Q

Describe risk factors for endocarditis

A
  • Increasing age
  • IV drug use
  • Male sex
  • Specific for NVE: underlying valve abnormalities

> Aortic stenosis: caused by age-related calcification, calcification of congenitally abnormal valve or rheumatic fever

> Mitral valve prolapse

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28
Q

Describe rheumatic heart disease

A
  • Caused by group A Strep infection (causes strep throat)
  • Streptococcus pyogenes has an M surface protein
    > Treatment of infection via immune system or antibiotics leads to release of M protein following bacterial lysis
    > Anti-M antibodies produced against M protein
  • Through molecular mimicry, cardiac valves share similar antigenic structure to M protein
    > So body’s own anti-M antibodies attack heart valves leading to stenosis or regurgitation
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29
Q

Describe the clinical features of endocarditis in IVDU

A
  • Tricuspid valve endocarditis is more common than aortic or mitral
  • Clinical features
    > Acute: toxic presentation
    » Progressive valve destruction and metastatic infection developing in days-weeks
    » Commonly S. aureus

> Subacute: mild toxicity
> Presentation over weeks to months
> Rarely leads to metastatic infection; commonly Strep viridans or enterococcus

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30
Q

Describe the clinical features of endocarditis

A
  • Early manifestations of infection
    > Incubation period is 2 weeks; longer in PVE
    > Fever + murmur is infective endocarditis until proven otherwise
    > Fatigue & malaise
  • Embolic events
    > Can take days-weeks to occur but seen earlier in acute endocarditis

> Small emboli: petechiae, splinter haemorrhages, haematuria

> Larger emboli: CVA, renal infarction

> Right-sided endocarditis (especially in IVDUs) - septic pulmonary emboli

  • Late effects of infection
    > Osler’s nodes: painful palpable lesions found on hands & feet
    > Immunological reaction: splenomegaly, nephritis, vasculitis lesions of skin & eye, clubbing
    > Tissue damage: valve destruction, valve abscess
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31
Q

Describe the diagnosis of infective endocarditis

A
  • Blood cultures (3 sets from 3 different sites)
  • Echocardiograph
    > Transthoracic (TTE): non-invasive, transducer placed at front of chest, 50% sensitivity

> Transoesophageal (TOE): invasive, transducer placed in oesophagus, 85-100% sensitivity

  • Duke criteria (positive if 2 major criteria or 1 major & 3 minor or 5 minor)

> Major:
> Typical organism in 2 separate blood cultures
> Positive echocardiogram or new valve regurgitation

> Minor:
> Predisposition (heart condition or IVDU)
> Fever >38ºC
> Vascular phenomena e.g. septic emboli
> Immunological phenomena e.g. Osler’s nodes
> Positive blood cultures not meeting major criteria

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32
Q

Describe the management of infective endocarditis

A
  • Medical
    > Antimicrobial therapy
    » Bactericidal agents at high doses
    » Duration of therapy: NVE is 4 weeks, PVE is 6 weeks

> > Streptococcus: benzylpenicillin +/- gentamicin
Enterococcus: amoxicillin/vancomycin +/- gentamicin
S. aureus MSSA: flucloxacillin +/- gentamicin
S. aureus MRSA: vancomycin +/- gentamicin
CoNS: vancomycin +/- gentamicin +/- rifampicin

  • Surgical intervention
    > If heart failure
    > If uncontrollable infection e.g. abscess, persisting fever + positive blood cultures > 7 days, multi-drug resistant organism
    > If needed to prevent embolism e.g. large vegetations or embolic episode
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33
Q

Define adult congenital heart disease and describe its prevalence

A
  • Abnormal development within foetal heart resulting in birth defects
    > Commonest birth defect: 1 in 145 live births
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34
Q

Describe the morphology of the heart

A
  • Right atrium
    > Sinoatrial node
    > Broad appendage
  • Left atrium
    > Narrow, long appendage
  • Right ventricle
    > Trabeculated endocardium
    > Insertion of chordae to interventricular septum
    > Moderator band
    > Tricuspid valve
  • Left ventricle
    > Smooth endocardium
    > Ellipsoid cavity
    > Mitral valve (no septal connection)
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35
Q

Describe the pathophysiology and treatment of an atrial septal defect (ASD)

A
  • Defect or hole in the atrial septum
  • Types
    > Secundum: most common, hole in the middle of the atrial septum

> Primum: more complex, partial atrioventricular septal defect (AVSD)

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36
Q

Describe ventricular septal defects, including complications and management

A
  • If haemodynamically significant in early life can lead to pulmonary vascular disease
  • Shunts left to right when in isolation - leads to left heart volume loading
  • Examination: occasionally no murmur or pansystolic murmur
  • Complications:
    > Left ventricular failure
    > Aortic valve regurgitation
    > Right ventricular outflow tract obstruction
    > Arrhythmias
    > Pulmonary hypertension
    > Eisenmenger syndrome
  • Management:
    > Spontaneous closure
    > Intervention - pulmonary band deployed, transcatheter closure device
    > Surgery
37
Q

Describe the clinical features of aortic coarctation

A
  • Highly variable in severity - shelf-like or tubular stenosis in lumen of aorta
  • Tends to form after left subclavian artery in a juxta-ductal position (forms where patent ductus arteriosus has been)
  • Clinical features
    > Bicuspid aortic valve
    > Rib notching may be present on CXR due to retrograde flow from high pressure anterior intercostal arteries to low pressure posterior
    > Collateral blood flow to bypass coarctation e.g. dilated ITA
38
Q

Discuss the complications and management of aortic coarctation

A

Complications
- Upper body hypertension: difference between 2 arms
- Berry aneurysms
- Claudication
- Renal insufficiency
- Accelerated coronary artery disease

Management
- Surgical repair via thoracotomy: subclavian flap, end to end, jump graft
- Stent

39
Q

What is meant by “Tetralogy of Fallot”?

A

Cyanotic congenital heart disease caused by deviation of part of ventricular septum

  1. Ventricular septal defect
  2. Overriding aorta
  3. Right ventricular outflow tract obstruction
  4. Right ventricular hypertrophy
40
Q

Discuss the operative strategy for Tetralogy of Fallot including complications

A
  • BT shunt: in child with low oxygen saturations (approximately surgery at 1 year)
    > Repair involves closing the ventricular septal defect & opening the RV outflow tract and pulmonary valve
    > This helps pulmonary arteries develop properly
  • Complete repair

Complications after repair:
> Significant pulmonary regurgitation; RV dilatation +/- dysfunction
> Arrhythmia: ventricular tachycardia
> Pulmonary arterial/branch PA stenoses

41
Q

Describe the transposition of the great arteries and how this condition might be managed

A
  • Great arteries (aorta & pulmonary artery) run parallel to each other instead of crossing over
  • Diagnosis in utero (foetal echocardiography) & surgery within days of life

> Patent ductus arteriosus starts to close within first few days of life (allows mixing of circulation to sustain life) can be kept open by giving prostaglandins

  • Management:
    > Atrial switch: obsolete procedure where blood is switched at atrial level so oxygenated blood is pumped by right ventricle

> Arterial switch: trunk arteries are switched around from original position; aorta is attached to left side of circulation & coronary arteries are mobilised too

42
Q

Describe the foetal circulation

A
  • In utero oxygenation is by maternal placenta
  • Pulmonary circulation is minimal and at high resistance
  • Oxygenated blood returns to RA via IVC
  • It then bypasses the RV/PA via the foramen ovale
    > Of the blood that is pumped to the pulmonary arteries by the right ventricle, most passes to the aorta via the ductus arteriosus
43
Q

Describe a univentricular heart and its treatment

A
  • Heart with one functioning ventricle reliant on shunts for mixing of deoxygenated and oxygenated blood
  • Treatment
    > Aim of surgery is to create 2 functioning ventricles

> If not feasible then a Fontan circulation will be created
> Where there is a single functioning ventricle, this is used to support systemic circulation
> Plug in systemic venous return (IVC & SVC) directly to pulmonary vessels
> Leave oxygenated blood to return to single ventricular mass & pumped out through aorta

44
Q

Describe the issues associated with Fontan circulation

A
  • Pulmonary circulation is dependent on high systemic venous pressure and low pulmonary vascular resistance
  • Anything that causes an imbalance can cause haemodynamic compromise
    > Pulmonary embolism
    > Arrhythmia
    > Dehydration
    > Bleeding
45
Q

Describe heart failure and its causes

A

Failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of tissues

Causes
- Common
> Coronary artery disease (MI)
> Hypertension
> Idiopathic
> Toxins - alcohol, chemotherapy
> Genetics

  • Less common
    > Valve disease
    > Infections - virus, Chaga’s
    > Congenital heart disease
    > Metabolic - haemochromatosis, amyloid, thyroid disease
    > Pericardial disease e.g. TB
46
Q

Discuss the main types of heart failure

A
  • HF-rEF aka systolic HF
    > Reduced ejection fraction
    > Younger, male, often coronary aetiology
  • HF-pEF aka diastolic HF
    > Preserved ejection fraction
  • Chronic (Congestive)
  • Acute (decompensated)
47
Q

Explain the pathophysiology of heart failure

A
  • Myocardial injury (MI)

> Leads to left ventricular systolic dysfunction

> Perceived reduction in circulating volume and pressure

> Maladaptive neurohumoral activation
> SNS
> RAAS
> ET, AVP
> Natriuretic peptides

> Systemic vasoconstriction

> Renal sodium and water retention

48
Q

List the signs and symptoms of heart failure

A

Symptoms
- Dyspnoea: orthopnoea, paroxysmal nocturnal dyspnoea, cough
- Ankle swelling: legs, abdomen
- Fatigue/tiredness

Signs
- Peripheral oedema: ankle, legs, sacrum, abdomen (ascites)
- Elevated JVP
- Third heart sound (S3)
- Displaced apex beat: cardiomegaly
- Pulmonary oedema: lung crackles
- Pleural effusion

49
Q

Describe the New York Heart Association (NYHA) Functional Classification

A
  • Class I: no symptoms, no limitation in ordinary physical activity
  • Class II: mild shortness of breath + angina, slight limitation during ordinary activity
  • Class III: marked limitation in activity due to symptoms even during normal activity, comfortable only at rest
  • Class IV: severe limitations, symptoms even while at rest - mostly bedbound patients
50
Q

List the investigations used for heart failure

A
  • ECG: MI, left ventricular hypertrophy, rhythm, rate, QRS duration
  • CXR: exclude lung pathology, pulmonary oedema
  • Echocardiogram: chamber size, systolic/diastolic function, valves
  • Blood chemistry: U&Es, Cr, urea, LFTs, urea (gout)
  • Haematology: Hb (anaemia), RDW
  • Natriuretic peptides: BNP, NT-proBNP
  • Selected patients: coronary angiography, exercise test, ambulatory ECG monitoring, myocardial biopsy, genetic testing
51
Q

Describe the diagnosis of heart failure

A
  • Suspected heart failure: risk factors, symptoms/signs, abnormal ECG
  • Measure NT-proBNP, BNP
  • Echocardiography
  • Confirmed heart failure
    > Define heart failure phenotype based on LVEF measurement
52
Q

Describe the medical management of HF-rEF

A

ALL patients:
- ACE inhibitor (ACE-I) e.g. enalapril or angiotensin receptor blocker-neprolysin inhibitor (ARNI) e.g. sacubitril valsartan

  • Beta-blocker e.g. bisoprolol
  • Mineralocorticoid receptor antagonists e.g. spironolactone
  • SGLT2 inhibitor e.g. dapagliflozin

Additional medications:
- Diuretics
- If AF: anticoagulation
- IV iron: IDA

  • Class II recommendation
    > Ivabradine: sinus node inhibition (If inhibitor)
    > Hydralazine + isosorbide dinitrate (vasolidator used in African-American populations)
53
Q

Describe the mechanism of action of ARNIs

A

Angiotensin receptor blocker e.g. Candesartan, Losartan
> Blocks angiotensin II binding to AT1 receptor
> Reduces vasoconstriction, sodium/water retention and fibrosis/hypertrophy

Sacubitril blocks neprolysin , the enzyme which blocks natriuretic peptides
> Leads to vasodilation, natriuresis, diuresis, inhibition of pathologic growth/fibrosis

54
Q

List the surgical approaches including devices used in the management of HF-rEF

A
  • Cardiac resynchronisation therapy (CRT)
  • Implantable cardioverter defibrillator (ICD)
  • Left ventricular assist device (LVAD)
  • Heart transplant
  • CABG for atherosclerotic patients
  • Total artificial heart
55
Q

Describe cardiac resynchronisation therapy (CRT)

A
  • Used in left bundle branch block (LBBB) - prolonged QRS to improve synchronisation between ventricles & improve CO
    > Leads going to right atrium, right ventricle and left ventricle

> CRT-P: pacemaker; CRT-D: combined with defibrillator

> Higher NYHA class patients

56
Q

Describe the mechanism of action of the implantable cardioverter defibrillator (ICD)

A
  • Pacemaker that detects abnormal ventricular arrythmia
  • Shocks into normal rhythm
  • 1 lead into right ventricle

> Lower NYHA class patients especially in ischaemic aetiology e.g. MI

57
Q

Describe the function of a left ventricular assist device (LVAD)

A
  • Pumps blood out of the left ventricle into the aorta - continuous flow
  • Risk of infection, clots
  • Used as transition treatment for heart failure
58
Q

Describe the management of the decompensating patient in acute heart failure

A
  • Ultrafiltration: natriuresis
  • Nitrates, nitroprusside, dobutamine: arterial vasodilation
    > Reduce afterload (pressure the heart has to pump against)
    > Increased inotropy
  • Nitrates, morphine: venodilation
    > Reduce preload (venous return), reduce work
  • Furosemide: natriuresis - reduce fluid
  • Dobutamine, dopamine, milrinone: increased inotropy
  • Bilevel or continuous positive airway pressure (CPAP): preload reduction
59
Q

Describe the symptoms associated with hypoperfusion and congestion in heart failure

A

Hypoperfusion
- Cold sweated extremities
- Oliguria
- Mental confusion
- Dizziness
- Narrow pulse pressure

Congestion
- Pulmonary congestion
- Orthopnoea/paroxysmal nocturnal dyspnoea
- Peripheral bilateral oedema
- Jugular venous dilatation
- Congested hepatomegaly
- Gut congestion, ascites
- Hepatojugular reflux

60
Q

Describe the management of heart failure patients depending on their perfusion and congestion status

A

Warm-dry: well
- Adjust oral therapy

Warm-wet: congestion but adequate perfusion
- Vasodilators
- Diuretics
- Maybe ultrafiltration

Cold-wet: congested and hypoperfused
- Vasodilators
- Diuretics
- Inotropes
- Consider mechanical circulatory support

Cold-dry: hypoperfused, not congested
- Diuretics
- Inotropes
- Add mechanical support?

61
Q

Describe the semilunar valves and some congenital abnormalities which may affect them

A

Aortic valves
- Lies between left ventricular outflow tract and aorta
- 3 cusps: trileaflet
- Right, left, non-coronary
> Bicuspid aortic valve: prone to premature dysfunction due to turbulent flow, associated with aortic abnormalities such as coarctation; can have a genetic component

Pulmonary valves
- 3 leaflets
- Lies between right ventricular outflow tract & pulmonary artery

62
Q

Describe the atrioventricular valves

A
  • Chordae tendinae attach papillary muscles to front aspects of leaflets - leading to closure of valves
  • Mitral: lies between LA and LV
    > 2 leaflets: anterior (more mobile, divided into 3, A1-A3); posterior (divided into 3 by clefts, P1-P3)
  • Tricuspid: AV valve, 3 leaflets, lies between RA & RV
63
Q

List the causes of valvular heart disease

A

Valve leaflets
- Calcification
- Thickening
- Degeneration
- Infection
- Prolapse

Apparatus/annulus
- Annular dilatation
- Annular calcification
- Apparatus tethering/thickening/tupture
- Regional wall motion abnormality

64
Q

Describe the causes, signs and symptoms of aortic stenosis

A

Causes: thickening, calcification, rheumatic valve disease, congenital
> Leads to increased LV cavity pressure, resulting in LV hypertrophy

Symptoms
- Dyspnoea
- Presyncope/syncope
- Chest pain
- Reduced exercise capacity

Signs
- Ejection systolic murmur
- Soft/quiet second heart sound
- Narrowed pulse pressure
- Heaving apex beat (LVH)
- Signs of heart failure

Do NOT give GTN - vasodilation can cause collapse

65
Q

Describe the causes, signs and symptoms of aortic regurgitation

A

Causes: degeneration, rheumatic valve disease, aortic root dilatation, systemic disease e.g. Marfan’s syndrome, Ehlers-Danlos syndrome, ankylosing spondilitis, SLE; endocarditis

Symptoms: dyspnoea, reduced exercise capacity

Signs:
> Early diastolic murmur
> Increased pulse pressure
> Collapsing pulse
> Signs of heart failure
> Eponymous signs
» Corrigan’s: carotid pulsation
» Quinke’s: nail bed pulsation
» De Musset’s: head nodding

66
Q

Describe the causes, symptoms and signs of mitral stenosis

A

Causes: rheumatic valve disease, congenital
> Leads to pressure overload, dilated LA
> Results in atrial fibrillation, pulmonary hypertension and secondary right heart dilatation

Symptoms:
- Dyspnoea
- Palpitation
- Chest pain
- Haemoptysis
- Right heart failure syndrome

Signs:
- Diastolic murmur
- Quiet second heart sound
- Heaving apex
- Signs of heart failure

67
Q

Describe the signs and symptoms of mitral regurgitation

A

Mitral regurgitation leads to LV and LA dilatation, pulmonary hypertension, secondary right heart dilatation and atrial fibrillation

Symptoms
- Shortness of breath
- Palpitation
- Right heart failure symptoms

Signs
- Pansystolic murmur
- Quiet first heart sound
- Displaced apex beat
- Signs of heart failure

68
Q

Describe the medical treatment for valvular heart disease

A

Medication is used to reduce symptoms by controlling heart rate and preventing arrhythmias

> Beta-blockers
Digoxin
Calcium channel blockers

69
Q

Describe the surgical interventions used in the treatment of valvular heart disease

A

Valve repair
> Resect parts of redundant leaflet to reduce regurgitation and add a support ring

Valve replacement
> Ball & cage
> Bileaflet tilting disc prosthetic valve
> Metal valves: last longer, anticoagulation needed
> Tissue valves: don’t last long but no anticoagulation needed: resected animal valves made of pericardium

Other surgical options:
> Open heart surgery
> Minimal incision valve surgery
> TAVI (transcatheter aortic valve implantation) of a tissue valve in a self-expanding frame
> Mitraclip: patients not fit for open heart mitral valve replacement; pliable mitral valve leaflets are clipped & inserted
> Valvuloplasty

70
Q

Define MI and outline the different types of MI there are

A
  • Any elevation in troponin in clinical setting consistent with myocardial ischaemia
  • Isolated troponin elevation does not equal MI

Different types:
- Type 1: spontaneous MI due to a primary coronary event (coronary artery rupture & thrombus formation)

  • Type 2: increased oxygen demand/decreased oxygen supply
    > Heart failure, sepsis, anaemia, arrhythmia, hypertension/hypotension
    > Fixed atherosclerosis & supply-demand imbalance, or supply-demand imbalance alone
  • Type 3: sudden cardiac death
  • Type 4a: MI associated with a PCI
  • Type 4b: MI stent thrombosis documented by angiography
  • Type 5: MI associated with CABG
71
Q

Describe the signs and symptoms of a myocardial infarction

A

Symptoms
- Chest, back or jaw pain
- Indigestion
- Sweatiness, clamminess
- Shortness of breath
- None - diabetes/dementia
- Death

Signs
- Distressed patient
- Tachycardia
- Heart failure - crackles/raised JVP
- Shock
- Arrhythmia
- None

72
Q

Describe the investigations used in acute MI

A
  • Electrocardiograph
    > Evidence of ST segment deviation - biomarker of myocardial ischaemia
  • Bloods
    > Cardiac troponin: integral part of the cardiac myocyte, 3 types: TnI, TnT, TnC; release into blood stream is a marker of myocyte necrosis
  • CXR and echocardiogram
    > Evidence of acute heart failure/left ventricular systolic dysfunction
    > Coronary angiogram: coronary artery anatomy
73
Q

Describe the HEART score for chest pain patients

A

History
> Highly suspicious, moderately suspicious, slightly suspicious

ECG
> Significant ST deviation or non-specific repolarisation disturbance, LBBB…

Age
> 65y
> 45-65
< 45y

Risk factors
>1-3 from the following: hypercholesterolaemia, hypertension, diabetes, smoking, family history, obesity OR history of atherosclerotic disease

Troponin

74
Q

Describe non-coronary causes of elevated troponin

A

Causes of type 2 MIs
- Acute congestive heart failure
- Tachyarrhythmias - SVT, AF, VT
- Pulmonary embolism
- Sepsis
- Apical ballooning syndrome (Takotsubo cardiomyopathy)
- Anything that stresses the heart: critically unwell patient

Chronic elevation of troponin
> Renal failure, chronic heart failure, infiltrative cardiomyopathies e.g. amyloidosis, haemochromatosis, sarcoidosis

75
Q

Describe the pathophysiology of a type 1 MI

A
  • Rupture of the plaque exposes the subendothelial tissue triggering thrombus formation
    > This blocks the arterial lumen and restricts blood flow acutely
  • ST elevation indicates complete blockage; if untreated it will completely infarct
    > Reciprocal ST depression is characteristic of MI
76
Q

State the coronary arteries which may be blocked in a myocardial infarction depending on its location

A
  • Inferior STEMI: RCA (right coronary artery - mostly) or LCx (circumflex)
  • Posterior STEMI: LCx (mostly) or RCA
  • Lateral STEMI: LCx
  • Anteroseptal STEMI: LAD (left anterior descending)
77
Q

Describe the ECG features seen in a posterior infarct

A
  • ST elevation not seen due to location
    > Anterior leads are directly opposite & will see the opposite of any current generated at the posterior wall
    > Posterior ST elevation = anterior ST depression
    > Do posterior ECG
78
Q

Describe the management of acute coronary syndrome

A
  • STEMI
    > ABCs + put in ambulance attached to defibrillator
    > Oxygen if hypoxic (< 94% O2 sats)
    > Aspirin 300mg PO
    > Unfractionated heparin 5000U IV
    > Morphine 5-10mg IV, GTN infusion 2nd line
    >Anti-emetics
    > Clopidogrel (ambulance)
    > Ticagrelor (hospital)
    > Activate PPCI team

> Reperfusion therapy:

> > Primary percutaneous coronary intervention (PCI) if <120 mins
- Transfer patient to cath lab rapidly, use transradial approach, insert catheter wire with balloon & deploy stent

> If not eligible - thrombolysis IV (alteplase, tenecteplase) + fondaparinux

79
Q

Monitor in Coronary Care Unit for complications of MI

A

Drugs for secondary prevention
> ACE inhibitors
> Beta blockers
> Statins
> Eplerenone
> Aspirin (lifelong) / clopidogrel (6 months to a year)
» Shorter duration of anti-platelets if elderly, falls risk, GI bleed, major malignancy

> Echocardiogram for LV function & cardiac structure
Cardiac rehabilitation

If left ventricular systolic dysfunction at >9 months consider primary prevention ICD

80
Q

Describe the complications associated with myocardial infarction

A
  • Arrhythmias
    > VT/VF - DC conversion
    > AF
  • Heart failure
    > Diuretics, inotropes, vasodilators
  • Cardiogenic shock
    > Intra-aortic balloon-pump, ventricular assist device
  • Myocardial rupture
    > Septum - VSD - surgery
    > Papillary muscle - mitral regurgitation - surgery
    > Free wall - tamponade - usually fatal
  • Psychological
    > Anxiety/depression
    > Cardiac rehabilitation
81
Q

Describe the GRACE score risk model

A

Used for triage and prioritisation, predicts complications in hospital and post-discharge

> Low risk: discharge on medical treatment
Intermediate risk: discharge to be readmitted for angiogram
High risk: urgent inpatient angiogram

82
Q

What is one of the main side effects of simvastatin?

A

Muscle pain caused by myositis, producing elevated creatine kinase, confusion and fever

83
Q

What is the most accurate method for assessing left ventricular ejection fraction?

A

Cardiac magnetic resonance imaging

84
Q

List the different types of bradyarrhythmias

A
  • Sinus bradycardia
  • Junctional bradycardia
  • AV block
    > Complete (third degree): complete dissociation betwwen P wave & QRS complex
    > 2nd degree: every second P wave is non-conducted
    >1st degree: prolonged PR interval but all P waves are conducted
85
Q

Define the characteristics of junctional bradycardia as seen on ECG

A
  • HR is 60bpm
  • Absent P waves - no atrial activity due to SA node dysfunction or suppression due to high vagal tone
  • Regular, narrow QRS complexes
86
Q

Describe the NICE guidelines for the treatment of hypertension

A

Hypertension with type 2 diabetes: ACEi or ARB

Hypertension w/o T2DM, age <55 & not black African/African-Caribbean family origin
> ACEi or ARB
» ACEi or ARB + CCB or thiazide diuretic
»> ACEi or ARB + CCB + thiazide diuretic
»» resistant hypertension, consider adding low dose spironolactone (low potassium) or alpha blocker/beta blocker (high potassium)

Hypertension w/o T2DM, age >55 or black African/African-Caribbean family origin
> Calcium channel blocker (CCB)
» CCB + ACEi or ARB or thiazide diuretic
»> ACEi or ARB + CCB + thiazide diuretic
»» resistant hypertension, as above

87
Q

Describe the signs of pericarditis on examination, including a syndrome which may appear after MI

A

ECG: widespread ST elevation, horseshoe shape

If pericardial effusion: cardiac tamponade

Auscultation: pericardial rub, muffled heart sounds

Dressler’s syndrome: pericarditis following an MI (pericardial effusion due to cardiac injury)
> Can present with chest pain, relieved by leaning forward

88
Q

Describe the troponin levels and ECG changes associated with 1) unstable angina 2) NSTEMI 3) STEMI

A

1) Unstable angina
- Normal troponin
- Normal ECG; possible ST depression

2) NSTEMI
- Normal ECG
- ST depression
- T wave inversion

3) STEMI
- ST elevation
- Reciprocal ST depression
- T wave inversion
- New LBBB (anteroseptal MI)

89
Q

Describe the ECG changes seen in a PE patient

A

S1 Q3 T3 pattern, sinus tachycardia, RBBB

Phase 3 (14 decks)

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