Cardiology 1 Flashcards

1
Q

Define abdominal aortic aneurysm

A

A localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal diameter.

o NOTE: normal diameter of the aorta = 2 cm

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2
Q

Explain the aetiology/risk factors for AAA

A
  • There are NO specific identifiable causes
  • Risk Factors

o Severe atherosclerotic damage to aortic wall

o Family history

o Smoking

o Male

o Age

o Hypertension

o Hyperlipidaemia

o Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome

o Inflammatory disorders: Behcet’s disease, Takayasu’s arteritis

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3
Q

Recognise the presenting symptoms of AAA

A
  • Unruptured

o NO SYMPTOMS

o Usually an incidental finding

o May have pain in the back, abdomen, loin or groin

  • RUPTURED

o Pain in the abdomen, back or loin

o Pain may be sudden or severe

o Syncope

o Shock

  • NOTE: degree of shock depends on site of rupture and whether it is contained
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4
Q

Recognise the signs of AAA on physical examination

A
  • Pulsatile and laterally expansile mass on bimanual palpation of the abdominal aorta
  • Abdominal bruit
  • Retroperitoneal haemorrhage can cause Grey-Turner’s sign
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5
Q

Identify appropriate investigations for AAA

A
  • Bloods

o FBC, clotting screen, renal function and liver function

o Cross-match if surgery is planned

  • Scans

o Ultrasound - can detect aneurysm but CANNOT tell whether it is leaking or not

o CT with contrast - can show whether an aneurysm has ruptured

o MRI angiography

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6
Q

Define Aortic Dissection

A
  • A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, creating a false lumen
  • Classification of aortic dissection:

o Type A: ASCENDING aorta (MOST COMMON)

o Type B: DESCENDING aorta (distal to the left subclavian artery)

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7
Q

Explain the aetiology/risk factors of aortic dissection

A
  • Aortic dissection is usually preceded by degenerative changes in the smooth muscle of the aortic media
  • Common causes and risk factors:

o HYPERTENSION

o Aortic atherosclerosis

o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos, SLE)

o Congenital cardiac abnormalities (e.g. coarctation of the aorta)

o Aortitis

o Iatrogenic (e.g. during angioplasty/angiography)

o Trauma

o Crack cocaine

  • NOTE: expansion of the false lumen can lead to obstruction of the subclavian, carotid, coeliac and renal arteries

o Hypoperfusion of the target organs of these major arteries can give rise to other symptoms (e.g. carotid artery –> collapse)

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8
Q

Summarise the epidemiology of aortic dissection

A
  • Most common in males aged 40-60 yrs
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9
Q

Recognise the presenting symptoms of aortic dissection

A
  • MAIN SYMPTOM: sudden central ‘tearing’ pain, it may radiate to the back in between the shoulder blades (it can mimic MI)
  • Other symptoms caused by obstruction of branches of the aorta:

o Carotid artery –> hemiparesis, dysphasia, blackout

o Coronary artery –> chest pain (angina or MI)

o Subclavian artery –> ataxia, loss of consciousness

o Anterior spinal artery –> paraplegia

o Coeliac axis –> severe abdominal pain (due to ischaemic bowel)

o Renal artery –> anuria, renal failure

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10
Q

Recognise the signs of aortic dissection on physical examination

A
  • Murmur on the back (below the left scapula), descending to the abdomen
  • Hypertension
  • Blood pressure difference between the two arms > 20 mm Hg
  • Wide pulse pressure
  • Hypotension may suggest tamponade
    o Check for pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration

o This may indicate:

  • Tamponade
  • Pericarditis
  • Chronic sleep apnoea
  • Obstructive lung disease
  • Signs of Aortic Regurgitation
    o High volume collapsing pulse
    o Early diastolic murmur over aortic area
  • Unequal arm pulses
  • There may be a palpable abdominal mass
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11
Q

Identify appropriate investigations for aortic dissection

A
  • Bloods

o FBC

o X-match 10 units of blood

o U&E - check renal function

o Clotting screen

  • CXR

o Widened mediastinum

  • ECG

o Often NORMAL

o If the ostia of the right coronary artery is compromised you may get signs of:

  • Left ventricular hypertrophy
  • Inferior MI
  • CT Thorax

o Shows false lumen

  • Echocardiography

o Transoesophageal allows visualisation

  • Cardiac catheterisation and aortography
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12
Q

Define aortic regurgitation

A

Reflux of blood from the aorta into the left ventricle during diastole. Also known as aortic insufficiency

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13
Q

Explain the aetiology and risk factors of aortic regurgitation

A
  • Aortic valve leaflet abnormalities or damage

o Bicuspid aortic valve

o Infective endocarditis

o Rheumatic fever

o Trauma

  • Aortic root/ascending aorta dilatation

o Systemic hypertension

o Aortic dissection

o Aortitis

o Arthritides (e.g. rheumatoid arthritis, seronegative arthritides)

o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos)

o Pseudoxanthoma elasticum

o Osteogenesis imperfecta

  • Pathophysiology

o Reflux of blood into the left ventricle results in left ventricular dilatation

o This means increased end diastolic volume and increased stroke volume

o The combination of increased stroke volume and low end-diastolic AORTIC pressure may explain the high-volume collapsing pulse

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14
Q

Summarise the epidemiology of aortic regurgitation

A
  • Chronic AR often begins in the late 50s

* It is most frequently seen in patients > 80 yrs

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15
Q

Recognise the presenting symptoms of aortic regurgitation

A
  • Chronic AR

o Initially ASYMPTOMATIC

o Later on, the patient may develop symptoms of heart failure (e.g. exertional dyspnoea, orthopnoea, fatigue)

  • Severe Acute AR

o Sudden cardiovascular collapse (left ventricle cannot adapt to the rapid increase in end-diastolic volume)

  • Symptoms related to aetiology (e.g. chest or back pain caused by aortic dissection)
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16
Q

Recognise the signs of aortic regurgitation on examination

A
  • Collapsing (water-hammer) pulse
  • Wide pulse pressure
  • Thrusting and heaving displaced apex beat
  • Early diastolic murmur over the aortic valve region

o Heard better at the left sternal edge when the patient is sitting forward with the breath held at the top of expiration

  • NOTE: an ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume)
  • Austin Flint mid-diastolic murmur

o Heard over the apex

o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis

  • Rare signs associated with aortic regurgitation:

o Quincke’s Sign - visible pulsation on nail bed

o de Musset’s Sign - head nodding in time with the pulse

o Becker’s Sign - visible pulsation of the pupils and retinal arteries

o Muller’s Sign - visible pulsation of the uvula

o Corrigan’s Sign - visible pulsation in the neck

o Traube’s Sign - pistol shot (loud systolic and diastolic sounds) heard on auscultation of the femoral arteries

o Duroziez’s Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the stethoscope

o Rosenbach’s Sign - systolic pulsations of the liver

o Gerhard’s Sign - systolic pulsations of the spleen

o Hill’s Sign - popliteal cuff systolic pressure exceeding brachial pressure by > 60 mm Hg

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17
Q

Identify appropriate investigations for aortic regurgitation

A
  • CXR

o Cardiomegaly

o Dilatation of ascending aorta

o Signs of pulmonary oedema (if accompanied by left heart failure)

  • ECG

o May show left ventricular hypertrophy

  • Deep S in V1/2
  • Tall R in V5/6
  • Inverted T waves in lead I, aVL, V5/6
  • Left axis deviation
  • Echocardiogram

o May show underlying cause (e.g. aortic root dilatation, bicuspid aortic valve)

o May show the effects of aortic regurgitation (e.g. left ventricular dilatation, fluttering of the anterior mitral valve leaflet)

o Doppler echocardiogram can show AR and indicate severity

o Repeat echos allow monitoring of progression (LV size and function)

  • Cardiac catheterisation with angiography

o If there is any uncertainty about the functional state of the ventricle or the presence of coronary artery disease

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18
Q

Define aortic stenosis

A

Narrowing of the left ventricular outflow at the level of the aortic valve

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19
Q

Explain the aetiology and risk factors of aortic stenosis

A
  • Stenosis can be secondary to rheumatic heart disease (MOST COMMON WORLDWIDE)
  • Calcification of a congenital bicuspid aortic valve
  • Calcification/degeneration of a tricuspid aortic valve in the elderly
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20
Q

Summarise the epidemiology of aortic stenosis

A
  • Present in 3% of 75 yr olds
  • More common in males
  • Those with bicuspid aortic valve present earlier
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21
Q

Recognise the presenting symptoms of aortic stenosis

A
  • May be ASYMPTOMATIC initially
  • Angina (due to increased oxygen demand of the hypertrophied left ventricle)
  • Syncope or dizziness on exercise (due to outflow obstruction)
  • Symptoms of heart failure (e.g. dyspnoea, orthopnoea)
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22
Q

Recognise the signs of aortic stenosis on examination

A
  • Narrow pulse pressure
  • Slow-rising pulse
  • Thrill in the aortic area (only if severe)
  • Forceful sustained thrusting undisplaced apex beat
  • Ejection systolic murmur at the aortic area, radiating to the carotid artery
  • Second heart sound may be softened or absent (due to calcification)
  • A bicuspid valve may produce an ejection click
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23
Q

Identify appropriate investigations for aortic stenosis

A
  • ECG

o Signs of left ventricular hypertrophy

  • Deep S in V1/2
  • Tall R in V5/6
  • Inverted T waves in I, aVL and V5/6
  • Left axis deviation

o LBBB

  • CXR

o Post-stenotic enlargement of ascending aorta

o Calcification of aortic valve

  • Echocardiogram

o Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar)

o Estimation of aortic valve area and pressure gradient across the valve in systole

o Assess left ventricular function

  • Cardiac angiography

o Allows differentiation from other causes of angina (e.g. MI)

o Allows assessment of concomitant coronary artery disease

  • NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease
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24
Q

Define arterial ulcer

A

A localised area of damage and breakdown of skin due to inadequate arterial blood supply. Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.

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25
Q

Explain the aetiology/risk factors of arterial ulcers

A
  • The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities
  • Risk Factors

o Coronary heart disease

o History of stroke or TIA

o Diabetes mellitus

o Peripheral arterial disease (e.g. intermittent claudication)

o Obesity and immobility

26
Q

Summarise the epidemiology of arterial ulcers

A
  • 22% of leg ulcers

* Prevalence increases with age and obesity

27
Q

Recognise the presenting symptoms of arterial ulcers

A
  • Often DISTAL - at the dorsum of the foot or between the toes
  • Punched-out appearance
  • Often elliptical with clearly defined edges
  • The ulcer base contains grey, granulation tissue
  • NIGHT PAIN - hallmark of arterial ulcers

o Pain is worse when supine (because arterial blood flow is further reduced when supine)

o Pain is relieved by dangling the affected leg off the end of the bed

28
Q

Recognise the signs of arterial ulcers on physical examination

A
  • Night pain
  • Punched-out appearance
  • Hairlessness
  • Pale skin
  • Absent pulses
  • Nail dystrophy
  • Wasting of calf muscles
29
Q

Identify appropriate investigations for arterial ulcers

A
  • Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
  • ABPI
  • Percutaneous angiography
  • ECG
  • Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor)
  • FBC - anaemia can worsen the ischaemia
30
Q

Define atrial fibrillation

A
  • Characterised by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into:

o Permanent

o Persistent

o Paroxysmal

31
Q

Explain the aetiology and risk factors of atrial fibrillation

A
  • There may be no identifiable cause
  • Secondary causes lead to an abnormal atrial electrical pathway that results in AF
  • Systemic Causes

o Thyrotoxicosis

o Hypertension

o Pneumonia

o Alcohol

  • Heart Causes

o Mitral valve disease

o Ischaemic heart disease

o Rheumatic heart disease

o Cardiomyopathy

o Pericarditis

o Sick sinus syndrome

o Atrial myxoma

  • Lung Causes

o Bronchial carcinoma

o PE

32
Q

Summarise the epidemiology of atrial fibrillation

A
  • VERY COMMON in the elderly
  • Present in 5% of those > 65 years
  • May be paroxysmal
33
Q

Recognise the presenting symptoms of atrial fibrillation

A
  • Often ASYMPTOMATIC
  • Palpitations
  • Syncope (if low output)
  • Symptoms of the cause of AF
34
Q

Recognise the signs of atrial fibrillation on physical examination

A
  • Irregularly irregular pulse
  • Difference in apical beat and radial pulse
  • Check for signs of thyroid disease and valvular disease
35
Q

Identify appropriate investigations for atrial fibrillation

A
  • ECG

o Uneven baseline with absent p waves

o Irregular intervals between QRS complexes

o Atrial flutter = saw-tooth

  • Bloods

o Cardiac enzymes

o TFT

o Lipid profile

o U&Es, Mg2+ and Ca2+

  • Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia
  • Echocardiogram

o May show:

  • Mitral valve disease
  • Left atrial dilatation
  • Left ventricular dysfunction
  • Structural abnormalities
36
Q

Generate a management plan for atrial fibrillation

A

First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection)

There are TWO main components to AF management:

  • RHYTHM CONTROL

o If > 48 hrs since onset of AF

  • Anticoagulate for 3-4 weeks before attempting cardioversion

o If < 48 hrs since onset of AF

  • DC cardioversion (2 x 100 J, 1 x 200 J)
  • Chemical cardioversion: flecainide or amiodarone
  • NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease

o Prophylaxis against AF

  • Sotalol
  • Amiodarone
  • Flecainide
  • Consider pill-in-the-pocket (single dose of a cardioverting drug (e.g. flecainide) for patients with paroxysmal AF) strategy for suitable patients
  • RATE CONTROL

o Chronic (Permanent) AF

  • Control ventricular rate with:
  • Digoxin
  • Verapamil
  • Beta-blockers
  • Aim for ventricular rate ~ 90 bpm
  • STROKE RISK STRATIFICATION

o LOW RISK patients can be managed with aspirin

o HIGH RISK patients require anticoagulation with warfarin

o This is based on the CHADS-Vasc Score

o Risk factors include:

  • Previous thromboembolic event
  • Age > 75 yrs
  • Hypertension
  • Diabetes
  • Vascular disease
  • Valvular disease
  • Heart failure
  • Impaired left ventricular function
37
Q

Identify the possible complications of atrial fibrillation

A
  • THROMBOEMBOLISM

o Embolic stroke risk of 4% per year

o Risk is increased with left atrial enlargement or left ventricular dysfunction

  • Worsening of existing heart failure
38
Q

Summarise the prognosis for patients with atrial fibrillation

A

Chronic AF in a disease heart does not usually return to sinus rhythm

39
Q

Define cardiac arrest

A

Acute cessation of cardiac function

40
Q

Explain the aetiology and risk factors of cardiac arrest

A

The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts

  • FOUR Hs

o Hypothermia

o Hypoxia

o Hypovolaemia

o Hypokalaemia/Hyperkalaemia

  • FOUR Ts

o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))

o Thromboembolic

o Tamponade

o Tension pneumothorax

41
Q

Recognise the presenting symptoms of cardiac arrest

A
  • Management precedes or is concurrent to history

* Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness

42
Q

Recognise the signs of cardiac arrest on physical examination

A
  • Unconscious
  • Not breathing
  • Absent carotid pulses
43
Q

Identify appropriate investigations for cardiac arrest

A
  • Cardiac Monitor

o Allows classification of the rhythm

  • Bloods

o ABG

o U&E

o FBC

o X-match

o Clotting

o Toxicology screen

o Blood glucose

44
Q

Generate a management plan for cardiac arrest

A
  • SAFETY IS IMPORTANT

o Approach any arrest scene with caution

o The cause of the arrest may pose a threat

o Defibrillators and oxygen are hazards

  • Basic Life Support

o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist)

o Clear and maintain the airway with head tilt, jaw thrust and chin lift

o Assess breathing by look, listen and feel

  • If they are not breathing, give two rescue breaths

o Assess circulation at carotid pulse for 10 seconds

  • If absent - give 30 chest compressions at around 100/min
  • Continue cycle of 30 chest compressions for every 2 rescue breaths

o Proceed to advanced life support as soon as possible

  • Advanced Life Support

o Attach cardiac monitor and defibrillator

o Assess rhythm

  • If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)
  • Defibrillate once (150-360 J biphasic, 360 J monophasic)
  • Make sure no one is touching the patient or the bed
  • Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF
  • Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins
  • If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
  • If pulseless electrical activity (PEA) or asystole (non-shockable rhythms)
  • CPR for 2, and then reassess rhythm
  • Administer adrenaline (1 mg IV) every 3-5 mins
  • Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm

o During CPR:

  • Check electrodes, paddle positions and contacts
  • Secure airway
  • Once secure, give continuous compressions and breaths
  • Consider magnesium, bicarbonate and external pacing
  • Stop CPR and check pulse only if change in rhythm or signs of life
  • Treatment of REVERSIBLE causes

o Hypothermia - warm slowly

o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels

o Hypovolaemia - IV colloids, crystalloids and blood products

o Tamponade - pericardiocentesis

o Tension Pneumothorax - aspiration or chest drain

o Thromboembolism - treat as PE or MI

o Toxins - use antidote for given toxin

45
Q

Identify the possible complications of cardiac arrest

A
  • Irreversible hypoxic brain damage

* Death

46
Q

Summarise the prognosis for patients with cardiac arrest

A
  • Resuscitation is less successful if cardiac arrest happens outside the hospital
  • Increased duration of inadequate effective cardiac output –> poor prognosis
47
Q

Define cardiac failure

A

Inability of the cardiac output to meet the body’s demands despite normal venous pressures

48
Q

Explain the aetiology and risk factors of cardiac failure

A
  • LOW OUTPUT Cardiac Failure (reduced cardiac output)

o Left Heart Failure

  • Ischaemic heart disease
  • Hypertension
  • Cardiomyopathy
  • Aortic valve disease
  • Mitral regurgitation

o Right Heart Failure

  • Secondary to left heart failure (in which case it is called congestive cardiac failure)
  • Infarction
  • Cardiomyopathy
  • Pulmonary hypertension/embolus/valve disease
  • Chronic lung disease
  • Tricuspid regurgitation
  • Constrictive pericarditis/pericardial tamponade

o Biventricular Failure

  • Arrhythmia
  • Cardiomyopathy (dilated or restrictive)
  • Myocarditis
  • Drug toxicity
  • HIGH OUTPUT Cardiac Failure (increased demand)

o Anaemia

o Beri beri

o Pregnancy

o Paget’s disease

o Hyperthyroidism

o Arteriovenous malformation

49
Q

Summarise the epidemiology of cardiac failure

A

10% > 65 yrs old

50
Q

Recognise the presenting symptoms of cardiac failure

A
  • Left Heart Failure - symptoms caused by pulmonary congestion

o Dyspnoea - divided based on the New York Heart Association classification:

  • 1 - no dyspnoea
  • 2 - dyspnoea on ordinary activities
  • 3 - dyspnoea on less than ordinary activities
  • 4 - dyspnoea at rest

o Orthopnoea

o Paroxysmal nocturnal dyspnoea

o Fatigue

  • Acute Left Ventricular Failure

o Dyspnoea

o Wheeze

o Cough

o Pink frothy sputum

  • Right Heart Failure

o Swollen ankles

o Fatigue

o Increased weight (due to oedema)

o Reduced exercise tolerance

o Anorexia

o Nausea

51
Q

Recognise the signs of cardiac failure on physical examination

A
  • Left Heart Failure

o Tachycardia

o Tachypnoea

o Displaced apex beat

o Bilateral basal crackles

o S3 gallop (caused by rapid ventricular filling)

o Pansystolic murmur (due to functional mitral regurgitation)

  • Acute Left Ventricular Failure

o Tachypnoea

o Cyanosis

o Tachycardia

o Peripheral shutdown

o Pulsus alternans

  • Arterial pulse waveforms showing alternating strong and weak beats
  • Sign of left ventricular systolic impairment
  • Explanation:
  • In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume
  • This causes an increase in end-diastolic volume
  • This means that the left ventricle is stretched more for the next contraction
  • Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction
  • This results in a stronger systolic pulse

o Gallop rhythm

o Wheeze (cardiac asthma)

o Fine crackles throughout lung

  • Right Heart Failure

o Raised JVP

o Hepatomegaly

o Ascites

o Ankle/sacral pitting oedema

o Signs of functional tricuspid regurgitation

52
Q

Identify appropriate investigations for cardiac failure

A
  • Bloods

o FBC

o U&E

o LFTs

o CRP

o Glucose

o Lipids

o TFTs

  • In ACUTE Left Ventricular Failure

o ABG

o Troponin

o BNP

  • Raised plasma BNP suggests diagnosis of cardiac failure
  • Low plasma BNP rules out cardiac failure (90% sensitivity)
  • CXR

o Alveolar shadowing

o Kerley B lines

o Cardiomegaly

o Upper Lobe Diversion

o Pleural Effusion

  • ECG

o May be normal

o May show ischaemic changes (pathological q waves, t wave inversion)

o May show arrhythmia or left ventricular hypertrophy

  • Echocardiogram

o Assess ventricular contraction

o Systolic dysfunction = LV ejection fraction < 40%

o Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect

  • Swan-Ganz Catheter

o Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures

53
Q

Generate a management plan for cardiac failure

A
  • Acute Left Ventricular Failure

o Treating Cardiogenic Shock:

  • This is severe cardiac failure with low blood pressure
  • Requires the use of inotropes (e.g. dobutamine)
  • Managed in ITU

o Treating Pulmonary Oedema:

  • Sit the patient up
  • 60-100% Oxygen (and consider CPAP)
  • Diamorphine (venodilator + anxiolytic)
  • GTN infusion (venodilator –> reduced preload)
  • IV furosemide (venodilator and later diuretic effect)
  • Monitor:
  • BP
  • Respiratory rate
  • Oxygen saturation
  • Urine output
  • ECG
  • TREAT THE CAUSE! (e.g. MI, arrhythmia)
  • Chronic Left Ventricular Failure

o TREAT THE CAUSE (e.g. hypertension)

o TREAT EXACERBATING FACTORS (e.g. anaemia)

o ACE Inhibitors

  • Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
  • They slow down the progression of heart failure and improve survival

o Beta-Blockers

  • Blocks the effects of a chronically activated sympathetic system
  • Slows progression of heart failure and improves survival
  • The benefits of ACE inhibitors and beta-blockers are additive

o Loop Diuretics

  • Alongside dietary salt restriction, can correct fluid overload

o Aldosterone Antagonists

  • Improves survival in patients with NYHA class III/IV symptoms on standard therapy
  • Monitor K+ (as these drugs may cause hyperkalaemia)

o Angiotensin Receptor Blockers

  • May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers
  • Monitor K+ (as these drugs may cause hyperkalaemia)

o Hydralazine and a Nitrate

  • May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers

o Digoxin

  • Positive inotrope
  • Reduces hospitalisation but does NOT improve survival

o N-3 Polyunsaturated Fatty Acids

  • Provide a small beneficial advantage in terms of survival

o Cardiac Resynchronisation Therapy

  • Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms
  • These patients are also candidates for implantable cardioverter defibrillator (ICD)
  • They may receive a combined device

o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)

54
Q

Identify the possible complications of cardiac failure

A
  • Respiratory failure
  • Cardiogenic shock
  • Death
55
Q

Summarise the prognosis for a patient with cardiac failure

A

50% with cardiac failure die within 2 years

56
Q

Define cardiomyopathy

A

Primary disease of the myocardium. Cardiomyopathy may be:

o Dilated (ventricle dilates and gets bigger)

o Hypertrophic (heart muscle gets bigger and ventricle space gets smaller)

o Restrictive (the muscle wall becomes stiff and rigid and there’s no efficient blood flow)

57
Q

Explain the aetiology/risk factors of cardiomyopathy

A
  • The majority are IDIOPATHIC
  • Dilated Cardiomyopathy

o Post-viral myocarditis

o Alcohol

o Drugs (e.g. doxorubicin, cocaine)

o Familial

o Thyrotoxicosis

o Haemochromatosis

o Peripartum

  • Hypertrophic Cardiomyopathy

o Up to 50% are genetic

  • Restrictive Cardiomyopathy

o Amyloidosis

o Sarcoidosis

o Haemochromatosis

58
Q

Summarise the epidemiology of cardiomyopathy

A
  • Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20%
  • Restrictive is even rarer
59
Q

Recognise the presenting symptoms of cardiomyopathy

A
  • Dilated

o Symptoms of heart failure

o Arrhythmias

o Thromboembolism

o Family history of sudden death

  • Hypertrophic

o Usually NO SYMPTOMS

o Syncope

o Angina

o Arrhythmias

o Family history of sudden death

  • Restrictive

o Dyspnoea

o Fatigue

o Arrhythmias

o Ankle or abdominal swelling

o Family history of sudden death

60
Q

Recognise the signs of cardiomyopathy on physical examination

A
  • Dilated

o Raised JVP

o Displaced apex beat

o Functional mitral and tricuspid regurgitations

o Third heart sound

  • Hypertrophic

o Jerky carotid pulse

o Double apex beat

o Ejection systolic murmur

  • Restrictive

o Raised JVP

  • Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles

o Palpable apex beat

o Third heart sound

o Ascites

o Ankle oedema

o Hepatomegaly

61
Q

Identify appropriate investigations for cardiomyopathy

A
  • CXR

o May show cardiomegaly

o May show signs of heart fail

  • ECG

o All Types

  • Non-specific ST changes
  • Conduction defects
  • Arrhythmias

o Hypertrophic

  • Left-axis deviation
  • Signs of left ventricular hypertrophy
  • Q waves in inferior and lateral leads

o Restrictive

  • Low voltage complexes
  • Echocardiography

o Dilated

  • Dilated ventricles with global hypokinesia

o Hypertrophic

  • Ventricular hypertrophy (asymmetrical septal hypertrophy)

o Restrictive

  • Non-dilated non-hypertrophied ventricles
  • Atrial enlargement
  • Preserved systolic function
  • Diastolic dysfunction
  • Granular or sparkling appearance of myocardium in amyloidosis
  • Cardiac Catheterisation
  • Endomyocardial Biopsy
  • Pedigree or Genetic Analysis