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YEAR 4 - CCC > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is blood pressure normally controlled by?

A

Renin-angiotensin system

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2
Q

Describe how the renin-angiotensin system works

A

1) If renal perfusion is low, kidney juxtaglomerular cells convert pro-renin (present in blood) into renin
2) Renin converts angiotensinogen (secreted by liver) into angiotensin I
3) Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE), released from lungs
4) Angiotensin II is potent vasoconstrictor + promotes adrenal glands to produce aldosterone
5) Aldosterone makes kidneys reabsorb sodium and water into blood (and excrete potassium to maintain electrolyte balance)

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3
Q

What are the stages of hypertension?

A

Stage 1: clinic blood pressure at least 140/90 and subsequent ABPM daytime average of at least 135/85

Stage 2: clinic BP >160/100; ABPM >150/95

Severe hypertension: >180 systolic; >110 diastolic

Accelerated hypertension: >180/110 with signs of papilloedema +/or retinal haemorrhage

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4
Q

What are some secondary causes of hypertension?

A

Renal disease
Endocrine diseases - Cushing’s, Conn’s, phaeochromocytoma, adrenal hyperplasia
Congenital disease - coarctation of the aorta
Pregnancy - pre-eclampsia
Drugs - oestrogen-containing contraceptives, steroids, NSAIDs, EPO

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5
Q

If the blood pressure is raised on a one-off reading, what is required to confirm the diagnosis?

A

ABPM or HBPM

Hypertension is confirmed if:

  • Clinic BP of 140/90 PLUS
  • ABPM/HBPM of >135/85
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6
Q

How do you do home BP monitoring?

A

Twice a day for 7 days
Each of BP recording must be done twice at least 1 minutes apart with patient seated
Discard readings for day 1
Take an average of the rest

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7
Q

What conditions can HTN cause?

A 
Heart failure
Coronary artery disease
Stroke 
CKD
Peripheral arterial disease
Vascular dementia

It is the single biggest risk factor for cardiovascular disease and related disability - half of all MIs and CVA are associated with hypertension

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8
Q

What score is relevant to HTN?

A

QRISK3
Estimates 10-year risk of developing CVD
If over 20%, consider high risk and encourage patient to take statin
Between 10-20% is moderate risk; NICE recommends discussing with patient about starting a statin

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9
Q

What is the drug treatment of hypertension?

A

Step 1: <55 years - ACE inhibitor
> 55 years or black of any age - calcium channel blocker (if CCB not tolerated, use a thiazide diuretic instead)

Step 2: ACE inhibitor + calcium channel blocker

Step 3: ACEi + Ca channel blocker + thiazide diuretic

Step 4 (resistant hypertension): step 3 + further diuretic (e.g. spironolactone) or beta blocker

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10
Q

What is the mechanism of action of thiazides?

A

Inhibit sodium resorption at distal convoluted tubule by binding to Na/Cl co-transporter
This causes increased Na + K excretion

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11
Q

When are thiazides contraindicated?

A

Hyponatraemia - in the elderly, thiazides are a common cause of hyponatraemia
Hypokalaemia
Hypercalcaemia
Renal impairment

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12
Q

What is the mechanism of action of loop diuretics?

How do they compare to thiazides?

A

They inhibit resorption of sodium in ascending loop of Henlé
This causes increased Na+ and K+ excretion

Compared to thiazides:

  • more potent
  • shorter half-life
  • better tolerated in patients with CKD
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13
Q

What is the mechanism of action of potassium-sparing diuretics?

A

Competitively inhibit aldosterone-dependant sodium-potassium exchange channels in the distal convoluted tubule
This action leads to increased sodium and water excretion, but more potassium retention

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14
Q

When are ACE inhibitors contraindicated?

A

Renal artery stenosis

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15
Q

What the side effects of ACE inhibitors?

A

Dry cough
Impotence
Hypotension - take the first one in bed at night

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16
Q

What is decubitus angina?

A

Occurs when lying down

Impaired left ventricular function due to severe coronary artery disease

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17
Q

What is the drug management of coronary artery disease?

A

20mg artovastatin to those with >10% risk of CV disease (calculated with QRisk3)

80mg artovastatin if previous MI, Hx of type 2 diabetes, current ACS symptoms (e.g. angina, total cholesterol >4, LDL>2)

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18
Q

What is the mechanism of action of statins?

A

Inhibit HMG Co-A reductase which limits the rate of cholesterol synthesis

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19
Q

How can you describe heart failure?

A

When the cardiac output is inadequate for the body’s metabolic requirements leading to peripheral hypoperfusion

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20
Q

What is high output cardiac failure?

What are some causes of high output heart failure?

A

This is when the heart is working at normal/increased rate but needs of the body are beyond that which heart can supply

AAPPTT

  • Anaemia
  • Arteriovenous malformation
  • Paget’s disease
  • Pregnancy
  • Thyrotoxicosis
  • Thiamine deficiency (wet Beri-Beri)
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21
Q

What is the difference between systolic and diastolic low output heart failure?

A

Systolic

  • Inability of the ventricle to contract normally resulting in reduced cardiac output
  • Ejection fraction <40%

Diastolic

  • Inability of the ventricle to relax and fill normally causing increased filling pressures
  • Ejection fraction >50%
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22
Q

What are some causes of systolic heart failure?

A
  • Ischaemic heart disease
  • Dilated cardiomyopathy
  • Myocarditis
  • Infiltration (e.g. in haemochromatosis or sarcoidosis)
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23
Q

How does left sided heart failure present?

A

Symptoms caused by pulmonary congestion…

  • Shortness of breath on exertion
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Nocturnal cough (± pink frothy sputum)

Failure of the left side of the heart causes blood to back up into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood

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24
Q

What are the signs and symptoms of right side heart failure?

A 
Symptoms of venous congestion…
• Ankle swelling
• Weight gain
• Abdominal distension and discomfort,
• Anorexia/nausea.
Signs of venous congestion…
• Raised JVP
• Pitting ankle/sacral oedema
• Tender smooth hepatomegaly
• Ascites
• Transudative pleural effusions (typically bilateral)

failure of the right ventricle leads to congestion of systemic capillaries, which generates excess fluid accumulation in the body

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25
Q

What is the blood pressure like in heart failure?

A

Low BP with narrow pulse pressure

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26
Q

What is the pulse like in left heart failure?

A

Pulse alternans - alternate strong and weak beats

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27
Q

What would you feel on palpation of heart failure?

A

Displaced apex beat - LV dilated

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28
Q

What would you hear on auscultation of LVF?

A

Gallop rhythm due to presence of S3

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29
Q

What investigations should be done in suspected heart failure if no previous MI? What levels indicate what?

A

B-type natriuretic peptide (BNP) - initial test

  • It is released when the myocardium is stressed and is related to left ventricular pressure
  • It distinguishes heart failure from other causes of dyspnoea

· High: >2000 pg/ml – urgent ECHO within 2 weeks
· Raised: 400-2000 pg/ml – 6 week referral for ECHO
Normal: <400 pg/ml – normal

ECHO - confirms the presence and degree of ventricular dysfunction

  • <40% = HF with reduced ejection fraction
  • > 40% with raised BNP = HF with preserved ejection fraction
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30
Q

What chest X-Ray signs do you see in pulmonary oedema?

A

A:Alveolaroedema (with ‘batwing’ perihilar shadowing)
B:Kerley Blines (caused by interstitial oedema)
C:Cardiomegaly(cardiothoracic ratio >0.5)
D: upper lobe blooddiversion (increased vasculature in the upper lobes)
E:Pleural effusions(typically bilateral transudates)
F:Fluid in the horizontal fissure

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31
Q

What is the criteria used to diagnose congestive cardiac failure?

A

Framingham criteria

1 major + 2 minor criteria

Major criteria:

  • PND
  • Crepitations
  • Neck vein distention
  • S3 gallop
  • Hepatojugular reflex
  • Cardiomegaly
  • Increased CVP
  • Weight loss >4.5kg over 5 days

Minor criteria:

  • Bilateral ankle oedema
  • Dyspnoea on normal exertion
  • Tachycardia > 120bpm
  • Nocturnal cough
  • Hepatomegaly
  • Pleural effusion
  • Decreased vital capacity by 1/3
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32
Q

What is the management of acute heart failure (i.e. pulmonary oedema)?

A
  1. Sit the patient up
  2. High flow oxygen therapy via rebreathe mask
  3. IV furosemide 40mg (with further doses as necessary) and close fluid balance (aiming for a negative balance to reduce cardiac preload)
  4. IV diamorphine 2.5mg - vasodilator, alleviates distress and anxiety, small dose to reduce risk of respiratory depression

If systolic BP<100, send to ICU

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33
Q

What is the pharmacological management of chronic heart failure?

A

First line - ACEi + beta-blocker

  • these improve mortality
  • avoid ACEi in valve disease
  • if intolerant of ACEi, give ARB
  • hydralazine + nitrate in africans/caribbeans

Second line - add spironolactone if still symptomatic

Third line - consider digoxin if still symptomatic and in AF (it worsens mortality but improves mortality)

Loop diuretic to treat symptoms (but does not improve mortality)

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34
Q

What are some complications of heart failure?

A

Cardiogenic shock
AKI
Pleural effusion
CKD

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35
Q

What are the most common causes of AF?

A

Ischaemic heart disease
Hypertension
Valvular heart disease
Hyperthyroidism

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36
Q

Define the different types of AF:

1) Acute
2) Paroxysmal
3) Persistent
4) Permanent

A
  • Acute - <48 hours
  • Paroxysmal - < 7 days and is intermittent
  • Persistent - >7 days but is amenable to cardioversion
  • Permanent - >7 days and is not amenable to cardioversion
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37
Q

How do you investigate suspected paroxysmal AF?

A

ambulatory ECG

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38
Q

What are some symptoms of AF?

A 
Often asymptomatic 
Palpitations
Chest pain
Dyspnoea
Fatigue
Light-headedness or syncope
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39
Q

What does an ECG of AF show?

A

Absent p waves
Irregular QRS complexes
Irregular RR intervals

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40
Q

What score is relevant to AF?

A

CHA2DS2VASc score - calculates the risk of stroke in AF

o Congestive HF/LVSD 1
o Hypertension 1
o Age ≥75 years 2
o Diabetes mellitus 1
o Stroke/ TIA/ thromboembolism Hx 2
o Vascular disease 1
o Age 65-74 years 1
o Sex category (female) 1
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41
Q

When should you consider anticoagulation in AF?

A

If their CHADSVASc score is greater than or equal to 2

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42
Q

What is the first line therapy for AF?

A

Rate control drugs such as:

Beta-blockers e.g. atenolol, bisoprolol (but not sotalol)

Calcium channel blockers e.g. verapamil or diltiazem

Digoxin (only consider in sedentary patients and heart failure)

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43
Q

What is the second line therapy for AF?

A

Rhythm control - consider if symptoms persist after rate control

Flecainide - Na+ channel blocker

Amiodarone (only given to older, sedentary patients)

Sotalol - beta-blocker with additional K+ channel blocker action

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44
Q

What is warfarin?

A

Vitamin K antagonist

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45
Q

What drugs reduce the concentration of warfarin in the body?

A

It is metabolised by the CYP450 system - concentration is reduced by CYP450 inducers

Carbamazepine
Rifampicin
Barbituates
Phenytoin
St John's wort
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46
Q

What drugs increase the concentration of warfarin in the body?

A

It is metabolised by the CYP450 system - concentration is increased by CYP450 inhibitors

Sodium valproate
Ciprofloxacin
Sulphonamide
Cimetidine/omeprazole
Antifungals
Amiodarone
Isoniazid
Erythromycin/clarithromycin
Grapefruit juice
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47
Q

What do NOACs do?

A

Inhibit factor Xa

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48
Q

What score is relevant to anticoagulation?

A

HAS-BLED score

Hypertension - 1
Abnormal renal and liver function - 1 point each
Stroke - 1
Bleeding - 1
Labile INRs - 1
Elderly >65 - 1
Drugs or alcohol - 1 point each

Max 9 points

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49
Q

What conditions are NOACs contraindicated in?

A

Mitral stenosis

Chronic kidney disease

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50
Q

In which AF patients should rate control not be used as the first line strategy?

A

Those whose AF has reversible cause
Those who have heart failure due to AF
Those with new onset AF
For whom a rhythm control strategy is more suitable based on clinical judgement e.g. paroxysmal atrial fibrillation

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51
Q

What does catheter ablation do in AF?

A

Creates an electrically inexcitable ‘scar’ around the pulmonary veins which blocks pulmonary vein ectopics from entering the left atrium

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52
Q

When should you anticoagulate if performing cardioversion?

A

if AF>48hours, consider amiodarone 3 weeks before + 4 weeks after to eliminate clots that may have formed in heart

if AF<48hrs, can perform without cardioversion

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53
Q

What medication is commonly used for patients in AF who are also in heart failure or are hypotensive?

A

Digoxin

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54
Q

What is the effect of digoxin on the heart?

A

It inhibits the sodium potassium adenosine triphosphatase ([Na+/K+ ATPase) ion pump in the myocardium and also has parasympathetic effects on the AV node

It is thereforenegatively chronotropic and positively ionotropic(i.e. slows heart rate but increases contractility).

55
Q

What characteristic ECG changes are seen in patients taking digoxin?

A
  • Downsloping ST depression
  • T wave inversion
  • Biphasic or flattened and shortened QT interval

(The morphology of the QRS complex / ST segment is described as either “slurred”, “sagging” or “scooped” and resembling either a “reverse tick” or “hockey stick”)

56
Q

What are the symptoms of digoxin toxicity?

A 
Nausea/vomiting
Diarrhoea
Blurred vision
Yellow/green visual discolouration
Haloes in vision
Confusion 
Palpitations
Syncope
57
Q

What lifestyle modification improves mortality in heart failure?

A

Salt and fluid restriction

58
Q

What are the adverse effects of spironolactone?

A 
Hyperkalaemia
Renal impairment
Gynaecomastia
Breast tenderness/hair growth in women
Changes in libido
59
Q

In suspected heart failure, what is the reason for doing an ECHO? What results show what?

A

To confirm the presence and degree of ventricular dysfunction

Ventricular dysfunction is measured by the ejection fraction

<40% = heart failure

> 40% but raised BNP = heart failure with preserved ejection fraction

60
Q

Aside from NT-proBNP, what blood tests should be ordered in ? heart failure?

A

U+Es to assess renal function (for medication) and to look for hyponatraemia

LFTs for hepatic congestion

TFTs to check for hyperthyroidism

Glucose and lipid profile to assess modifiable cardiovascular risk factors

FBC to check for anaemia

61
Q

What are the 4 classes in the New York Heart Association classification of Heart Failure?

A
  • Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitation or dyspnoea.
  • Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitation and/or dyspnoea.
  • Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
  • Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
62
Q

What are some causes of diastolic heart failure?

A

This is when there is impaired ventricular filling during diastole

  • Hypertrophic obstructive cardiomyopathy
  • Restrictive cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
63
Q

What is a significant cause of heart failure in Central/South America?

A

Chagas disease - a parasitic disease also known as American trypanosomiasis

64
Q

What is the most common valvular heart disease and what most commonly causes it?

A

Mitral regurgitation

Mitral valve prolapse (5% cases)

65
Q

What else can cause mitral regurgitation?

A

Ischaemic MR - papillary muscle rupture secondary to MI

Non-ischaemic MR - ruptured chordae tendinae
• Myxomatous disease (mitral prolapse)
• Infective endocarditis
• Rheumatic heart disease - acute or chronic
• Trauma
• Spontaneous rupture

66
Q

How does mitral regurgitation present?

A

Fatigue and exertional dyspnoea - most common symptoms

Signs of heart failure e.g. pulmonary oedema and peripheral oedema

May be asymptomatic until there is significant systolic dysfunction

67
Q

Describe the murmur in mitral regurgitation

A 
Systolic murmur
Loudest at the apex
Pansystolic in nature
Radiates to the axilla
Louder of expiration
Louder on rolling to the left
68
Q

How is mitral regurgitation diagnosed?

A

ECHO - it is diagnostic and also allows measurement of severity by assessing size of valve lesions and pressure of regurgitant jet

69
Q

What is the definitive management for symptomatic mitral regurgitation?

A

Surgical - there are 2 options:

  1. Mitral valve repair (mitral valvuloplasty) - this is preferable as is preserves all components of the native valve and avoids use of prostheses
  2. Mitral valve replacement - offers the choice between a mechanical valve (lifelong anticoagulation but long-lasting), and a bioprosthetic valve (limited durability but no need for anticoagulation)
70
Q

What are the examination findings in mitral valve prolapse?

A

A non-ejection click - due to snapping of the mitral chordae during systole when the valve bows into the atrium

Mitral regurgitation murmur

71
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease - streptococcal antigens secondary to bacterial infection cross-react with the valve tissue causing damage

72
Q

How does mitral stenosis typically present?

A

Gradual exertional dyspnoea - most common symptom
Reduced exercise tolerance
Palpitations - AF is common in mitral stenosis

73
Q

Describe the murmur in mitral stenosis

A

Diastolic murmur (low pitched rumble)
Most prominent at apex
Loudest on expiration
Heard best with patient lying on left side using stethoscope bell

74
Q

What are the other signs of mitral stenosis?

A
  • Mitral facies (malar flush) - cutaneous vasodilation due to carbon dioxide retention
  • Low volume pulse
  • Atrial fibrillation
  • Raised JVP
  • R ventricular heave (suggestive of pulmonary hypertension)
  • Inspiratory crepitations (pulmonary oedema) and other signs of right heart failure
75
Q

How is progression of disease measured in patients with mitral stenosis?

A

Echocardiography

76
Q

What are the surgical management options for symptomatic patients with mitral stenosis?

A
  • Balloon valvuloplasty - only appropriate if valve is pliable and non-calcified
  • Percutaneous mitral valvotomy - for patients with moderate disease
  • Open valve repair/replacement - for patients with severe disease who are not too high risk for surgery but are not candidates for percutaneous intervention, due to valve morphology. Valves are more likely to be metal than bioprosthetic.
77
Q

What are the two most common causes of acute aortic regurgitation?

A

Infective endocarditis - the valve is destroyed and can get perivalvular abscesses which can rupture into the left ventricle

Aortic dissection - valve closure is impeded

78
Q

What are the two categories of causes of chronic aortic regurgitation? Give examples of these

A

Chronic valvular causes of AR include:
• Calcific aortic valve disease (age related)
• Myxomatous degeneration
• Congenital disease e.g. bicuspid aortic valve
• Rheumatic heart disease - most common cause in the developing world
• Infective endocarditis
• Rheumatic causes e.g. rheumatoid arthritis, antiphospholipid syndrome

Aortic root dilation, leading to incomplete valve closure, can be caused by the following:
• Congenital bicuspid aortic valve
• Genetic syndromes e.g. Marfan’s, Ehlers-Danlos, osteogenesis imperfecta
• Systemic vasculitides e.g. giant cell arteritis (GCA), Takayasu’s arteritis

79
Q

Describe the murmur heard in aortic regurgitation?

A
  • Early diastolic murmur

* Heard best in the aortic area whilst the patient isleant forwardand onexhalation

80
Q

What are the other signs found in aortic regurgitation?

A
  • “Waterhammer” pulse (Corrigan’s pulse)
  • De Musset’s sign - bobbing of the head in synchrony with the beating of the heart
  • Quincke’s sign - Pulsation of the nail beds
  • Traube’s sign - “Pistol shot” like bruit heard on auscultation of the femoral pulse
  • Müller’s sign - Pulsation or bobbing of the uvula
  • Widened pulse pressure (low diastolic pressure) is usually present
81
Q

What is the most common cause of aortic stenosis?

A

Calcification of a congenital bicuspid valve

82
Q

What is the classical triad of aortic stenosis?

A
  1. Syncope
  2. Angina
  3. Dyspnoea

SAD

83
Q

Describe the murmur heard in aortic stenosis

A

Ejection systolic murmur
Heard best at the second intercostal space on the right
Described as ‘harsh’
Radiates to the carotids

84
Q

What are the two options for surgical management of aortic stenosis?

A
  • Transcatheter aortic valve implantation (TAVI)

* Surgical aortic valve replacement (SAVR)

85
Q

In which patients is transcatheter aortic valve favoured in for the surgical management of severe aortic stenosis?

A

Basically patients that will not make it through open heart surgery

  • Severe comorbidities
  • Previous heart surgery
  • Frailty
  • Restricted mobility
  • > 75 years old
86
Q

What 3 features of chest pain typically define stable angina?

A
  1. Constriction like pain in chest/neck/arm/jaw
  2. Brought on by physical activity
  3. Alleviated by rest or GTN within minutes
87
Q

What are the first line investigations in stable angina?

A

ECG

Routine bloods - FBC to exclude anaemia; TFTs to exclude hyperthyroidism

88
Q

What investigation can be carried out if ECG shows ischaemic changes or if the diagnosis is not clear from the history when investigating stable angina?

A

CT coronary angiography

89
Q

What are the first line pharmacological treatments for stable angina?

A

Symptomatic relief

  • GTN spray
  • Beta-blocker OR cardiac selective calcium channel blocker

Secondary prevention

  • Aspirin 75mg OD
  • Statin
90
Q

What information should be given to a patient when starting GTN spray?

A

Side effects - headaches, flushing, dizziness

Take another dose if the pain has not subsided after 5 minutes.

Emergency help should be sought if the pain has not subsided after 2 doses of GTN as this may indicate ACS

91
Q

If the patient continues to experience symptoms of stable angina despite first line treatments, what can be given second line?

A

Combination of beta blocker and amlodipine (long-acting dihydropyridinecalcium channel blocker)

92
Q

What can be offered for high risk patients suffering from stable angina that is not adequately managed by full medical therapy?

A

Revascularisation

  • CABG (coronary artery bypass graft)
  • PCI (percutaneous coronary intervention)
93
Q

What is the order of frequency of valve involvement in infective endocarditis?

A

Mitral > aortic > tricuspid > pulmonary

94
Q

What are the most common causative organisms of infective endocarditis and who most commonly gets which?

A
  • Staph. Aureus - most common for all groups
  • Strep. Viridans - most common after dental procedures
  • Enterococci - following UTI
  • Staph. Epidermidis - infected cannulas
  • Strep. bovis- often in patients with colonic lesions, e.g. IBD or colorectal cancer
  • Fungi - immunosuppressed patients
  • HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) - poor dental hygiene
95
Q

What classic presentation should always raise the suspicion of infective endocarditis?

A

A patient with a fever and new murmur

90% of patients have fever and chills

96
Q

What are the extra-cardiac manifestations of infective endocarditits?

A

FROM JANE

(Fever)
Roth spots - exudative haemorrhagic retinal lesions with pale centres
Osler nodes - tender subcutaneous nodules on the finger pads and toes
(Murmur)
Janeway lesions - nontender macules on palms and soles
Anaemia
Nail bed haemorrhage
Emboli

97
Q

What two investigations are required to diagnose infective endocarditis?

A
  • Blood cultures - at least 3 sets of blood cultures should be taken at different times from various sites
  • Transoesophageal echocardiogram - most sensitive diagnostic test
98
Q

What are the major criteria in Dukes criteria for diagnosing infective endocarditis?

A
  1. Blood culture positive for IE

2. Imaging positive for IE

99
Q

What are the minor criteria in Dukes criteria for diagnosing infective endocarditis?

A
  1. Predisposition e.g. predisposing heart condition or IVDU
  2. Fever > 38.0°C
  3. Vascular phenomena e.g. arterial emboli, infarcts, intracranial or conjunctival haemorrhages, Janeway lesions
  4. Immunological phenomena e.g. glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
  5. Microbiological evidence e.g. blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE
100
Q

How many major and minor Dukes criteria must be present in order to diagnose infective endocarditis?

A

Two major criteria

OR

One major + three minor

OR

All five minor

101
Q

What is the mainstay of treatment of infective endocarditis?

A

Long-term IV antibiotics - approx 6 weeks minimum

Initially broad-spectrum e.g. vancomycin + gentamicin

102
Q

What investigations must be done in every patient with hypertension to look for evidence of target organ damage?

A

Bloods:

  • HbA1c
  • Creatinine and urea (for eGFR)
  • Cholesterol

Urinalysis – dip for haematuria and proteinuria and send to lab for albumin:creatinine ratio (ACR)

ECG – for left ventricular hypertrophy

Check fundi for evidence of retinopathy

103
Q

What are the pros and cons of DOACs as anticoagulants?

A

Do not require monitoring

Less bleeding risk than warfarin

12 hour half-life so if patient misses dose, they are not covered

104
Q

What are the pros and cons of warfarin?

A

Requires cover with LMWH for 5 days when initiating treatment because warfarin is initially pro-thrombotic

Requires regular INR monitoring and it can be affected by many drugs/food

40 hour half-life so anticoagulant effect lasts days

105
Q

What are the 3 main types of cardiomyopathy?

A
  1. Dilated cardiomyopathy
  2. Hypertrophic cardiomyopathy
  3. Restrictive cardiomyopathy
106
Q

What can cause dilated cardiomyopathy?

A 
• Idiopathic in 50% cases
• Genetic predisposition
• Ischaemic heart disease
• Alcohol
• Cocaine use
• Beriberi - thiamine deficiency 
• Peripartum - last trimester and up to 6 months postpartum 
• Infective causes
- Coxsackie B virus myocarditis
- Chagas disease
- HIV
- Rheumatic heart disease
• Valvular heart disease
107
Q

Summarise the pathophysiology behind dilated cardiomyopathy

A

Damage to the myocardial cells causes necrosis and chronic fibrosis - the remaining myocardial tissue then dilates and hypertrophies to compensate

108
Q

How does dilated cardiomyopathy present?

A 
Gradual development of heart failure presentation
• Exertional dyspnoea
• Fatigue
• Peripheral oedema
• Raised JVP
• Loud 3rd and 4th heart sounds
109
Q

What is the approach to diagnosis of dilated cardiomyopathy?

A
  1. Investigate underlying cause
  2. Assess cardiac function
  3. Assess structural remodelling

Echocardiography assesses both cardiac function and structural remodelling

110
Q

What investigation can be done to rule out myocarditis, amyloidosis and sarcoidosis in dilated cardiomyopathy?

A

Cardiac muscle biopsy

111
Q

What would an echo show in dilated cardiomyopathy?

A
  • Atrial or ventricle dilatation
  • Reduced LVEF
  • Hypokinetic chambers
  • Rules out primary valve disorders
112
Q

How is dilated cardiomyopathy managed?

A

Treat the underlying cause

Same treatment as heart failure - ACE inhibitors + beta-blockers +/- diuretics if symptomatic

Implantable cardioverter defibrillator (ICD) if LVEF < 35%

Heart transplantation - final solution for patients < 60

113
Q

What do patients with dilated cardiomyopathy usually die from?

A

Thrombus formation (due to large dilated chambers)

Sudden arrhythmia (dilated atria leads to atrial fibrillation and AV node block)

114
Q

Which cardiomyopathy is often the cause of sudden cardiac death in young people and athletes?

A

Hypertrophic cardiomyopathy

115
Q

What causes hypertrophic cardiomyopathy in young people?

A

Autosomal dominant genetic disorder

A mutation of one or more of the 12 genes that code for cardiac proteins

Troponin T mutations are most significant - more likely to cause sudden cardiac death, often occurring without any left ventricular hypertrophy

116
Q

What part of the heart is most commonly affected by hypertrophy in hypertrophic cardiomyopathy?

A

Anterior ventricular septum

117
Q

How can hypertrophic cardiomyopathy present?

A
  • Most cases are asymptomatic
  • Exertional dyspnoea
  • Chest pain (angina)
  • Syncope on exertion
  • Palpitations
  • Sudden cardiac death
118
Q

What can be heard on auscultation in hypertrophic cardiomyopathy? What exacerbates this and what reduces it?

A

Systolic ejection murmur best heard at left sternal edge 4th intercostal space - does not radiate to neck

Exacerbated by Valsalva manoeuvre
Reduced when squatting

119
Q

What 2 criteria must there be to diagnose hypertrophic cardiomyopathy?

A
  1. Left ventricular non-dilated hypertrophy

2. Absence of other cardiac/systemic disease that could explain hypertrophy

120
Q

What is the best initial and diagnostic test for hypertrophic cardiomyopathy? What would it show?

A

Echocardiogram

  • Asymmetrical septal hypertrophy > 15mm
  • Ratio of septal wall to posterior wall > 1.4:1
  • Non-dilated left ventricular cavity
  • Normal systolic function
  • Absence of valvular disease
121
Q

What investigation is used to assess functional capacity and response to therapy in hypertrophic cardiomyopathy?

A

Treadmill exercise testing

  • Observe for development of symptoms
  • BP monitoring for any hypotension
  • ECG tracings to pick up any arrhythmias or ischaemia
122
Q

What investigation can be done if echo findings are inconclusive in hypertrophic cardiomyopathy?

A

Cardiac MRI - good at evaluating ventricular morphology

123
Q

What lifestyle changes do you need to counsel a patient with hypertrophic cardiomyopathy about?

A
  • Avoid dehydration
  • Maintain healthy body weight
  • Avoid excess alcohol
  • Avoid strenuous exercise
  • Avoid situations that will likely cause vasodilation e.g. high temps
124
Q

What is the goal of medical treatment in hypertrophic cardiomyopathy? What is first and second line?

A

The goal is to slow the heart rate to alleviate symptoms

First - beta-blockers

Second - non-dihydropyridine calcium channel blockers e.g. verapamil

125
Q

What drugs should generally be avoided in hypertrophic cardiomyopathy?

A

Drugs that reduce pre-load because they can decrease chamber size and exacerbate symptoms

Diuretics
ACE inhibitors
Digoxin
Nitrates

126
Q

What surgical interventions can be done for hypertrophic cardiomyopathy?

A
  • Implantable cardioverter defibrillator for those at high risk of sudden death
  • Surgical myectomy for severe symptoms (Morrow procedure)
  • Heart transplant in end-stage non-obstructive HCM when LVEF < 50%
127
Q

What are the main signs that someone with hypertrophic cardiomyopathy is at risk of sudden cardiac death?

A 
Unexplained syncopal events
Episode of VF or VT
Abnormal BP response to exercise
Family history of sudden cardiac death
Age < 30
128
Q

What diseases can cause restrictive cardiomyopathy?

A

Amyloidosis - most common in western world
Sarcoidosis
Haemochromatosis
Loffler’s syndrome - tropical disease causing eosinophilic infiltration of myocardium

129
Q

What does restrictive cardiomyopathy do to the heart?

A

It decreases the elasticity of the myocardium which decreases ventricular compliance (i.e. how stretchy the muscle is to allow filling of blood during diastole)
This leads to atrial congestion and enlargement
Ultimately it results in systemic venous congestion

130
Q

What is the most common symptom of restrictive cardiomyopathy?

A

Dyspnoea

131
Q

What is the best initial test for restrictive cardiomyopathy? What would it show?

A

Echocardiography to confirm restrictive cardiomyopathy

  • Normal systolic function but signs of diastolic dysfunction
  • Atrial enlargement and dilation
  • Wall thickening may be present
  • Distinguishes from restrictive pericarditis in which the pericardium would be thickened
132
Q

What ECG change in particularly seen in amyloidosis in restrictive cardiomyopathy?

A

Low voltage

133
Q

How is restrictive cardiomyopathy managed?

A 
Treating underlying condition
Palliative treatment 
Beta-blockers to maintain sinus rhythm
Cardioselective CCB to increase ventricular filling time
ACE inhibitors to decrease preload

YEAR 4 - CCC (7 decks)

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