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Y4 Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Non Modifiable CVD risk factors

A

Older age
Family history
Male

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2
Q

Modifiable CVD risk factors

A

Raised cholesterol
Smoking
Alcohol
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress

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3
Q

Which Co-morbidities increase the risk of CVD

A

Diabetes
HTN
CKD
Inflammatory conditions (e.g RA)
Pscyhosis (atypical antipsychotics)

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4
Q

What are the consequences of atherosclerosis

A

Angina
MI
TIA
Strokes
PAD
Mesenteric ischaemia

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5
Q

What is QRISK3?

A

Scoring system for primary prevention of CVD. It determines the risk of stroke or MI in next 10 years.

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6
Q

What is the main primary prevention strategy for CVD?

A

Atorvostatin 20mg at night for pts with CKD, T1DM or with a QRISK score >10%

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7
Q

Significant side effects of statins

A

Myopathy
Rhabdomyloysis
T2DM
Haemorrhagic strokes

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8
Q

Which drugs interact with statins?

A

Macrolide antibiotics - pts should stop statins temporarily when prescribed clarithromycin or erythromycin

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9
Q

Secondary prevention of CVD

A
  1. Antiplatelet medications (e.g aspirin, clopidogrel, ticagrelor)
  2. Atorvostatin 80mg
  3. Atenolol (or bisoprolol)
  4. ACEi (ramipril)
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10
Q

What is dual antiplatelet therapy

A

Aspirin 75mg daily (forever) + Clopidogrel/Ticagrelor (for 12 months)

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11
Q

What is Familial Hypercholesterolemia

A

Autosomal dominant genetic condition causing high cholesterol.

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12
Q

Features of familial hypercholesterolemia

A
  1. FHx of premature CVD (e.g MI <60yrs in first-degree relative)
  2. Very high cholesterol (>7.5mmol/L)
  3. Tendon xanthomata (hard nodules in tendons, often on back of hand or achilles)
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13
Q

Management of Familial hypercholesterolemia

A

Statins

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14
Q

What is angina

A

Narrowing of the coronary arteries leading to reduced blood flow to the myocardium.

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15
Q

Stable vs Unstable Angina

A

Stable = when symptoms are relieved by rest or GTN
Unstable = When symptoms occur randomly or at rest (considered an ACS)

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16
Q

Gold standard investigation for Angina

A

CT Coronary angiogram

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17
Q

What are the 4 principles to the management of Angina

A

RAMP;
Refer to cardiology (urgently if unstable angina)
Advise them about diagnosis, management and when to call ambulance
Medical treatment
Procedural or surgical interventions

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18
Q

Immediate management/Symptomatic relief for Angina

A

GTN - immediate symptom relief. Take GTN when symptoms occur, can repeat after 5 mins but if pain persists, call an ambulance.
+ Aspirin + Statin

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19
Q

Long-term medical management for angina

A

1st line = Beta-blocker +/Or Calcium channel blocker (Use Dihydropyridine e.g amlodipine if with beta-blocker or just Verapamil if not. Verapamil can’t be used with beta-blocker as causes complete heart block)

2nd line = Long acting nitrate e.g Isosorbide Mononitrate OR Ivabridine / Nicorandil / Ranolazine)
- Isosorbide mononitrate should be given as asymmetric dosing intervals to maintain a daily nitrate free time of 10-14hrs to minimise tolerance.

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20
Q

Surgical interventions for Angina and their indications

A
  1. PCI + Coronary angioplasty = this dilates a blood vessel using a balloon/stent. Indication = “proximal or extensive disease” on angiogram and Age <65
  2. CABG - Indications = Severe stenosis and Age >65
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21
Q

Why is PCI + Coronary angioplasty preferred over CABG

A

CABG has a slower recovery and higher complication rate

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22
Q

What is Prinzmetal’s angina

A

Coronary artery spasm typically occuring at rest without evidence of underlying cardiac disease (hence different to unstable angina). May cause ST elevation.
RF = Female,

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23
Q

What is cardiac syndrome X?

A

Angina + Positive exercise test despite normal angiography with no evidence of underlying cardiovascular disease. Commonly occurs in peri/post menopausal women. Difficult to treat.

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24
Q

Definition of Hypertension

A

Persistently raised arterial BP >140/90 in clinic or >135/85 at home

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25
Q

What is considered ‘pre-hypertension’

A

130/85 - 139/89

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26
Q

What is malignant hypertension

A

Acutely, severely elevated BP with new or progressive organ dysfunction. It is a medical emergency. Generally a BP >180/120

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27
Q

British Hypertension Society Grading Criteria

A

Grade 1 (mild) = 140/90 to 159/99
Grade 2 (Moderate) = 160/100 to 179/109
Grade 3 (Severe) = >180/110

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28
Q

Risk Factors of essential HTN

A

FHx
Obesity
High alcohol consumption
High sodium consumption
Stress
Insulin resistance
Low foetal birth weight
Age
Being male (age <65) or Female (65-74yrs)
Black Afrocarribean ethnicity
Poor lifestyle

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29
Q

Causes of Secondary Hypertension (ROPE)

A

Renal disease - main cause of HTN. if BP does not respond to treatment, consider renal artery stenosis (also causes hypokalemia)
Obesity
Pre-eclampsia
Endocrine - mainly Conn’s syndrome (primary hyperaldosteronism)

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30
Q

1st line investigation for Conn’s syndrome

A

Renin:aldosterone ratio blood test - this would show high aldosterone but low renin levels (due to negative feedback)

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31
Q

Clinical presentation of HTN

A

Usually asymptomatic unless very high.
Headaches
Visual disturbances
Seizures
Epistaxis

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32
Q

Gold standard investigation for diagnosis of HTN

A

24hr ABPM or home blood pressure monitoring

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33
Q

Investigations for new onset HTN (NICE guidance)

A

Fundoscopy
Blood tests (HbA1C, Renal function, Lipid profile, U&Es)
ECG
Urine ACR + Dipstick (for hypertensive nephropathy)

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34
Q

Keith-Wagener classification (Hypertensive Retinopathy)

A

Stage 1 = Mild narrowing of arterioles + Silver wiring
Stage 2 = AV nipping (due to sclerosis of arterioles causing compression of veins where they cross)
Stage 3 = Cotton-wool patches, exudates and flame haemorrhages
Stage 4 = Papilledema

Stage 3 + 4 indicate malignant hypertension!!!!

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35
Q

Pharmacological management of HTN

A

1st line = ACEi / ARB
- ARBs should be used when ACEi can’t be tolerated
due to cough
- ACEi should be used as preference in pts with
diabetes regardless of age
- In pts >55yrs or AfroCarribean descent a CCB
should be used 1st line

2nd line = ACEi/ARB + CCB OR ACEi/ARB + Thiazide-like diuretic (indapamide)
- Pts >55yrs or Afro-Carribean should try CCB +
ARB
- Avoid thiazide diuretics in diabetes as worsenes
glucose tolerance
- CCBs prefered in pts with gout.

3rd line = ACEi/ARB + CCB + Thiazide Diuretic

4th line = Consider adding either Spironolactone (If K+ <4.5) or Alpha/Beta-blocker (K+ >4.5). If no response then refer for specialist input.

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36
Q

What is the BP target for adults age <80 with HTN +/- T2DM

A

<140/90 or ABPM <135/85

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37
Q

What is the BP target for adults age >80yrs with HTN

A

<150/90mmHg (or ABPM <145/95)

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38
Q

What is the BP target for pts with CVD + HTN

A

<130/90mmHg

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39
Q

Complications of Hypertension

A

IHD
Cerebrovascular event
Hypertensive retinopathy
Hypertensive nephropathy
HF

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40
Q

What monitoring should pts recieving HTN treatment

A

U&Es - as spirinolactone and ACEi both increase the risk of Hyperkalemia and Thiazide diuretics can cause electrolyte disturbances

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41
Q

ACE inhibitors

A

Rampiril, Lisinopril

MOA = inhibits the conversion of angiotensin 1 to angiotensin 2
Side effects = Cough, Angiodema, Hyperkalemia
Monitoring = Renal function before starting + after 2wks

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42
Q

ARBs

A

Losartan, Candesartan

MOA = Inhibits angiotensin II at the AT1 receptor
Side effects = Hyperkalemia

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43
Q

Calcium channel blockers

A

Amlodipine, Felodipine, Diltiazem

MOA = Inhibits voltage-gated calcium channels + causes smooth muscle relaxation + reduced force of myocardial contraction
Side effects = Flushing, Ankle Oedema, Headaches

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44
Q

Thiazide Diuretics

A

Bendroflumethiazide, Indapamide

MOA = Inhibits sodium absorption at the beginning of the DCT
Side effects = Hyponatremia, Hypokalemia, Dehydration
Monitoring = monitor serum electrolytes

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45
Q

Potassium-sparing Diuretics

A

Spirinolactone, Eplerenone

MOA = inhibits aldosterone in the kidneys, causing sodium excretion + potassium reabsorption
Side effects = Hyperkalemia

*useful if thiazide diuretics are causing hypokalaemia

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46
Q

Preload

A

End diastolic volume. The maximal volume of blood held in the ventricles after atrial systole. (Normal = 130ml)

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47
Q

Afterload

A

Resistance to blood flow - created by the vascular system

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48
Q

Risk Factors of HF

A

Old age
Female
Obesity
Diabetes
CKD

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49
Q

Causes of HF

A

IHD
Dilated cardiomyopathy
Hypertension
Valvular heart disease
Others = Congenital heart disease, alcohol, drugs, tricuspid imcompetence, pericardial disease, arrythmias

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50
Q

Types of HF

A

Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN.
Further divided into;
1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation.
2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS.

Right sided;

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50
Q

Types of HF

A

Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN.
Further divided into;
1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation.
2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS.

Right sided;
This is when decreased right ventricular function causes a systemic HTN leading to oedema.
Typically occurs due to left-sided HF. Can be related to Pulmonary HTN, Tricuspid/pulmonary valve disease or Pericardial disease

Congestive HF;
When both occur

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51
Q

Symptoms of HF

A

Fatigue
SOB
Exertional dyspnoea
Cough +/- pink frothy sputum if pulmonary oedema
Orthopnoea
PND

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52
Q

Signs of HF

A
  1. Pulmonary oedema - Bibasal fine crackles + Pleural effusion + Tachypnoea + Hypoxia + Cyanosis
  2. Systemic oedema - Peripheral pitting oedema + tender hepatomegaly + ascites + elevated JVP
  3. May have signs of underlying heart disease
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53
Q

New York Heart Failure Classification:

A

Class I = no symptoms + no limitation in ordinary physical activity.
Class II = Mild symptoms (SOB/Angina) + Slight limitation during ordinary activity
Class III = Marked limitation in activity due to Sx in less than ordinary activity
Class IV = Severe limitation. Sx at rest, mostly bedbound

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54
Q

Main diagnostic test for HF

A

pro-BNP (released by cardiomyocytes in response to excessive stretching)

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55
Q

Interpretation of Pro-BNP values;

A

If >2000 = Refer to cardiology urgently
If 400-2000 = Refer to cardiology + Echocardiogram within 6 weeks
If <400 = HF diagnosis is less likely. Consider alternative

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56
Q

Besides from HF, what other conditions cause raised BNP?

A

Tachycardia
Sepsis
PE
Renal impairment
COPD

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57
Q

What are the findings on CXR in HF?

A

Alveolar oedema
Batwing opacities (Bilateral perihilar lung shadowing) + Kerley B lines
Cardiomegaly
Dilated prominent upper lobe vessels + upper lobe congestion
Effusion (bilateral + transudative)

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58
Q

What lifestyle advice should you give to patients with HF?

A

Avoid large meals
Exercise regularly (20-30 min walk 3-5times per week)
If congestive heart failure 1-2 days bed rest per week
Annual influenza vaccine + one-off pneumococcal vaccine

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59
Q

Medical therapy of Heart failure (in HF- rEF)

A

1st line = ACEi + Beta-blocker (Rampril + Bisoprolol/carvedilol)
2nd line = Aldosterone antagonist (e.g spirinolactone - must monitor U&Es for hyperkalemia)
3rd line = Consider use of SGLT-2 inhibitors if HF-rEF (dapagliflozin)
4th line = should be initiated by a specialist. options include;
> If EF <35% give Ivabridine or Subcubitril-valsartan
> If AF is present give Digoxin
> If Afro-Carribean descent give Hydralazine +
Nitrate
> If widened QRS complex = Cardiac
resynchronisation
5th line = Palliative. Consider ionotropes / cardiac transplant / hospice

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60
Q

Which diuretic is best for symptomatic relief of fluid overload (i.e if a patient has preserved EF)

A

Furosemide 20mg

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61
Q

What is Cor Pulmonale

A

Right sided HF caused by respiratory disease
Most commonly due to COPD but also PE, Interstitial lung disease, CF, Primary pulmonary HTN

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62
Q

Pathophysiology of cor pulmonale

A

Existing pulmonary disease leads to an increased stiffness of pulmonary arteries resulting in pulmonary HTN. This causes an increased afterload in the right ventricle leading to right ventricular hypertrophy and therefore a reduced right ventricle ejection fraction. This leads to a back pressure of blood in the right atrium, vena cava and systemic system (leading to systemic HTN)

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63
Q

Clinical features of Cor Pulmonale

A

Often asymptomatic in early stages.
1. Signs of lung disease = SOB + Exertional dyspnoea + Hypoxia + Cyanosis
2. Signs of R sided HF = Peripheral oedema, Syncope, Raised JVP, S3 gallop, Pan-systolic murmur (tricuspid regurg / Pulmonary HTN) + Hepatomegaly + Ascites.

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64
Q

Management of Cor Pulmonale

A

Treat underlying cause
Alleviate hypoxia - with long term oxygen therapy
Medical management as for HF

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65
Q

Aortic stenosis murmur

A

Ejection systolic, high-pitched murmur with a cresendo-decresendo pattern heard best over the aortic area with radiation to the carotids.

*May have reduced/absent S2 in moderate/severe disease

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66
Q

Pulse characteristics in Aortic Stenosis

A

Slow rising pulse + Narrow pulse pressure (pulse pressure <25% of SBP)

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67
Q

Symptoms of Aortic stenosis

A

Exertional syncope due to difficulty maintaining good blood flow to brain
Chest pain
SOB

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68
Q

Causes of Aortic stenosis

A

Age related calcification (most common)
Bicuspid aortic valve (most common congenital heart disease 1-2%, most common cause in <65yrs)
Rheumatic heart disease
William’s syndrome (supravalvular AS)
HOCM (subvalvular)

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69
Q

Complications of Aortic stenosis

A

Left bundle branch block (usually present on ECG)

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70
Q

Aortic sclerosis

A

Thickening / Calcification of the aortic valve without obstruction of blood flow.
Consider this when Ejection systolic murmur + No ECG changes + No carotid radiation

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71
Q

Mitral stenosis murmur

A

Mid-diastoic low pitched rubmling murmur, best heard on expiration with pt in the left lateral decubitus position.

72
Q

Signs + Symptoms of Mitral stensosis

A

Malar flush
Haemoptysis / Dyspnoea
AF - L atrium struggles to push blood through stenotic valve leading to strain + electrical disruption
Low volume pulse
Loud S1 + Opening snap (thick valves require large systolic force to shut)
Tapping apex beat (palpable closure of mitral valve)
ECG changes = P mitrale (late stage sign due to atrial hypertrophy)

73
Q

Causes of Mitral stenosis

A

Rheumatic heart disease (most common + main complication of rheumatic HD)
Congenital
Left atrial Myxoma
Connective tissue disorder
Mucopolysaccharidosis

74
Q

Aortic regurgitation murmur

A

Early diastolic soft murmur with decrescendo pattern

75
Q

How can you emphasise an aortic regurg murmur?

A

Get pt sat up, leant forward and hold expiration or handgrip manoeuvre

76
Q

Austin flint murmur

A

This is the murmur that can be heard in severe AR. It is an early diastolic rumbling murmur heard over the apex.

Caused by a backflow of blood through the aortic valve and some over mitral valve (causing it to vibrate)

77
Q

5 Clinical signs of Aortic regurgitation

A
  1. Corrigans sign = visible distension and collapse of carotid arteries in neck
  2. De Musset’s sign = head bobbing with each heart beat
  3. Quincke’s sign = pulsations in nail bed with each heartbeat when nail bed is lightly compressed
  4. Traube’s sign = pistol shot sound heard when stethoscope placed over femoral artery during systole and diastole
  5. Mullers sign = Uvula pulsations are seen with each heartbeat
78
Q

Pulse characteristics in Aortic regurgitation

A

Corrigan’s pulse (Collapsing pulse) = rapidly appearing and disappearing pulse at carotid.
Also wide pulse pressure

79
Q

Causes of Aortic regurgitation

A
  1. Valvular disease - congenital bicuspid aortic valve, Rheumatic heart disease, Infective endocarditis
  2. Aortic root dilation = Aortic dissection, Connective tissue disease (marfans), Aortitis.
80
Q

Main complication of aortic regurg

A

Heart failure

81
Q

Mitral regurgitation murmur

A

Pan systolic, high-pitched, whistling murmur with radiation to the left axilla.

82
Q

How to emphasise a mitral regurgitation murmur

A

Left lateral decubitus position, on expiration

83
Q

Causes of mitral regurgitation

A
  1. Infective endocarditis
  2. Acute MI (papillary muscle rupture)
  3. Rheumatic heart disease
  4. Congenital defect of valve
  5. Cardiomyopathy
84
Q

What is the gold standard investigation for Aortic stenosis?

A

Transoesophageal echocardiogram

85
Q

Gold standard Invx for Mitral stenosis / Regurg and Aortic regurg

A

Doppler transthroacic echocardiogram

86
Q

Management of acute aortic regurgitation

A

Medical emergency!
Ionotropes + Vasodilators + Aortic valve replacement

87
Q

Management of chronic aortic regurg

A

If asyptomatic / EF >50% - Yearly review
If symptomatic / EF <50% - Aortic valve replacement. if not surgical candidate then vasodiators + ACEi

88
Q

Acute management of Mitral regurg

A

Emergency mitral valve replacement

89
Q

Management of Aortic stenosis

A

If asymptomatic then 3-5 year monitoring
If symptomatic (or LV dysfunction/+ve exericse tolerance test or valvular gradient >40mmHg) then Aortic valve replacement is needed. If high risk pt then can do a transcatheter replacement (TAVI)

90
Q

Management of symptomatic mitral stenosis

A

Diuretic + Balloon valvotomy/replacement

Treat rheumatic heart disease or AF.

91
Q

What is the normal diameter of the aortic valve

A

3-4cm

92
Q

what is the diameter of the aortic valve in severe aortic stenosis

A

<1cm

93
Q

Causative agent of rheumatic fever

A

Streptococcus pyogenes

94
Q

Clinical features of rheumatic fever

A
  1. Erythema marginatum (rash which quickly dissapears)
  2. Sydenham’s chorea / st Vitus dance
  3. Polyarthritis
  4. Carditis + Valvulitis (think mitral stenosis)
  5. Subcutaneous nodes
  6. Pyrexia
95
Q

Investigations for Rheumatic fever

A

Bloods = raised inflammatory markers
Raised Anti-streptococcal antibody titre

96
Q

Treatment for Rheumatic fever

A

Oral Penecillin + NSAIDs

97
Q

Diagnostic criteria for Rheumatic fever

A

Jones criteria;
1. Evidence of recent group A streptococcal infection (e.g +ve throat swab, raised ASO)
2. 2 major or 1 major + 1 minor criteria

Major = ‘JONES’
- Joint involvement
- myOcarditis
- Nodules (subcutaneous)
- Erythema marinatum
- Sydenham Chorea

Minor = ‘Cafe Pal’
- CRP raised
- Arthralgia
- Fever
- ESR raised
- Prolonged PR interval
- Anaemensis of rheumatism
- Leukocytosis

98
Q

Causes of pericarditis

A
  1. Mainly idiopathic
  2. Viral - Cocksackie B or echo virus, HIV. Very painful
  3. Post-MI (Dressler’s syndrome)
  4. Uremic (secondary to CKD)
  5. Bacterial - e.g staphyloccocus aureus (rare)
  6. Tuberculosis - usually constrictive pericarditis. pts will have TB symptoms
  7. Malignant - secondary to lung/breast/hodgkins lymphoma
  8. Other = radiation, fungus, hypothyroidism
99
Q

Risk factors for pericarditis

A

Male, Age 20-50, autoimmune disease, past cardiac surgery, previous MI, Dialysis

100
Q

Clinical presentation of pericarditis

A

Chest pain - may be pleuritic in nature + may radiate to neck or shoulders. Typically relieved by sitting forwards, exacerbated by lying flat
Pericardial friction rub - best heard at left lower sternal edge with pt leaning forward and expiring
Pyrexia + Leukocytosis (if infective)
Dyspnoea
Tachypnoea
Tachycardia

101
Q

ECG changes in pericarditis

A

Global + widespread changes.
1. ST elevation which is saddle-shaped (concave + upwards) in all leads
2. PR depression in all leads

102
Q

Management of pericarditis

A

NSAIDs + Colchine (until symptoms resolution or normalisation of inflammatory markers)
Treat underlying cause
Avoid strenuous physical activity

103
Q

What is brugada syndrome + What is the inheritence?

A

An inherited (Autosomal dominant) CVD which may present with sudden death.
Due to a mutation in the SCN5A gene

104
Q

Features of Brugada syndrome

A

Convex elevation / Down-sloping ST segment (mainly in V1-V3)
Partial RBBB

105
Q

What is the investigation of choice for Brugada syndrome

A

Injection of flecainide or ajmaline - this will make ECG changes more pronounced.

106
Q

Management of brugada syndrome

A

implantable cardioverter-defibrillator

107
Q

Features of Tetralogy of Fallot

A
  1. Ventricular septal defect
  2. Pulmonary valve stenosis
  3. Misplaced aorta
  4. Right ventricular hypertrophy
108
Q

If a younger patient is presenting with chest pain on a history of recent viral illness what must you consider as a cause?

A

Myocarditis

109
Q

Causes of Myocarditis

A

Viral : Coxsackie, HIV
Bacteria : Diptheria, Clostridia
Lyme disease
Chaga disease
Toxoplasmosis
Autoimmune
Doxarubicin antracycline chemotherapy agent.

110
Q

Clinical Features of myocarditis

A

Typically younger pt with a history of a recent viral illness with new chest pain.
May also have dyspnoea, signs of acute HF (Pulmonary oedema or orthopnoea) and arrythmias

111
Q

Investigation findings in myocarditis

A

May have elevated tropnin, BNP and inflammatory markers.
Tachycardia
ECG may show focal ST elevation (e.g V1-V4) or global T wave inversion

112
Q

What are the RF of infective endocarditis

A

Prior endocarditis
Prior heart survery
Prosthetic heart valves
Valvular heart disease
Dental procedures or poor dental hygeine
IV catheter or implanted pacemaker
IVDU
Cardiomyopathy

113
Q

Most common causes of Infective endocarditis

A
  1. Staphylococcus aureus: esp in IVDU
  2. Streptococcus viridians: associated with dental procedures or poor dental hygiene
  3. Steptococcus epidermis: in first 2 months following prosthetic heart valve surgery
  4. Streptococcus bovis: in colorectal cancer
114
Q

Which valve is most commonly affected by Infective endocarditis + what type of murmur does it case?

A

Mitral valve (regurg)
Then aortic valve (regurg)

115
Q

Signs + Symptoms of Infective endocarditis

A

mneumonic = ‘For James’
Fever
Osler’s nodes
Roth spots
Janeway lesions
Anemia
Murmur (mitral/aortic regurg)
Emboli
Splinter haemorrhages

116
Q

Modified Duke’s Criteria for IE

A

Diagnosis based on either +ve Pathological criteria / 2 major criteria / 1 Major + 3 minor / 5 minor

Major = 2 x blood cultures +ve / +ve Echocardiogram / New valvular regurg

Minor = Predisposing heart condition / Fever >38 / Signs + symptoms / immunological phenomenon e.g GN

117
Q

Management of Infective endocarditis

A

1st line = Amoxicillin +/- Gentamycin
(if pen allergic or severe sepsis/MRSA - Vancomycin + gentamicin)

If prosthetic heart valve = Vancomycin + Rifampicin + Gentamicin

118
Q

Poor prognostic factors in infective endocarditis

A
  1. Staphylococcus aureus +ve
  2. Prosthetic heart valve
  3. Culture -ve
  4. Low complement levels
119
Q

Clinical features of cardiac tamponade

A

Beck’s triad;
1. Hypotension
2. Raised JVP
3. Muffled heart sounds

Additional: Dyspnoea, Tachycardia, Chest pain, Pulsus paradoxus

120
Q

ECG findings and JVP characteristic in Cardiac tamponade

A

Absent Y descent on JVP
ECG = electrical alternans (alternating amplitude/axis of QRS complex)

121
Q

What diagnosis should be considered in a patient presenting with shock but no tension pneumothorax

A

Cardiac tamponade

122
Q

Gold standard investigation for cardiac tamponade

A

Echocardiogram - will show a pericardial effusion / ventricular collapse

123
Q

Management of Cardiac tamponade

A

Definitive treatment = Thoracotomy
Unless pt is in peri-arrest = perform urgent needle pericardiocentesis to buy some time.

124
Q

Gold standard invx for aortic injury

A

CT with contrast

125
Q

CXR findings in aortic injury

A

Widened mediastinum (>8cm)
Loss of aortic knuckle
Tracheal deviation to the R

126
Q

Troponin guidelines in suspected MI

A

Troponin on admission + repeat after 6-12hours.

If <14 after 6+ hours then can exclude NSTEMI/STEMI
If 14-30 then should repeat in 3 hours (If inc by 50% then STEMI/NSTEMI)
if >30 = STEMI/NSTEMI

127
Q

For how long does troponin stay elevated for

A

10-14 days

128
Q

Other causes of raised troponin (other than MI)

A

CKD
Sepsis
PE
Aortic dissection
Myocarditis

129
Q

Evolution of ECG changes in STEMI

A

Initially = tall, pointed upright T waves and ST elevation
After a few hours = T wave inversion and R wave voltage decreases. Q waves begin to develop
After a few days = ST elevation returns to normal
After a few weeks = Pathological Q waves develop and T wave returns to normal

130
Q

Initial management of suspected NSTEMI/STEMI

A

Aspirin 300mg
02 via nasal cannula 2-4l/min
Morphine if severe pain (+/- antiemetic)
Nitrates (Sublingual GTN x2)

Gain IV access and take bloods. Do ECG.

131
Q

What is a GRACE score

A

Global registry of acute coronary events
Used to estimate 6 month mortality in NSTEMI/Unstable angina

132
Q

Definitive management of NSTEMI/Unstable angina

A

High risk/haemodynamically unstable = urgent CA + PCI + Dual antiplatelets
Intermediate risk = Early coronary angiography + PCI (<72hrs)

Low risk = BATMAN
1. Beta-blockers
2. Aspirin 300mg stat
3. Ticagrelor
4. Morphine
5. Anticoagulant (e.g fondiparinaux)
6. Nitrates (E.g GTN - avoid in HTN)

133
Q

Management of STEMI

A
  1. Dual antiplatelet therapy = Aspirin + Presagurel / ticagrelor (or clopidogrel if already taking anticoagulant e.g apixaban)
  2. PCI (should be done <2hrs) - give unfractionated heparin before
  3. If PCI can’t be done, thrombolyse with tPA then recheck ECG after 60 mins.
134
Q

Secondary prevention after MI

A

Aspirin
Anti-platelet (Ticagrelor or Clopidogrel for 12 months)
Atorvastatin 80mg
Acei
Atenolol / beta-blocker
Aldosterone antagonist (if HF) e.g spirinolactone

135
Q

Driving rules following MI

A

Cannot drive for 4 weeks
or 1 week if succesfully treated with angioplasty

136
Q

Complications of MI

A

Think ‘Drreaad’

Death
Regurg (mitral)
Rupture (septum or Left ventricular wall)
Edema
Arrythmia (VT / VF / Bradyarrythmia)
Aneurysm (in left ventricle)
Dresslers syndrome

137
Q

Dressler’s syndrome

A

Localised immune response leading to pericarditis
Occurs 2-6 weeks post MI
Sx = pleuritic chest pain, worse on lying flat, low grade fever, pericardial rub.

138
Q

Investigations for Dressler’s syndrome

A

ECG shows saddle-shaped global ST elevation + PR depression
Echocardiogram = pericardial effusion

139
Q

Management of Dresslers syndrome

A

NSAIDs + Pericardiocentesis

140
Q

What investigation can you do to confirm if a patient with recent ACS has had a reinfarct

A

CK-MB

141
Q

Causes of Atrial Fibrillation

A

‘MRS SMITH’
Mitral Rerug/Stenosis
Sepsis
MI / IHD
Thyrotoxicosis
HTN

142
Q

Acute rate/rhythm control in AF

A

Two principles = Rate/rhythm control + Anticoagulation

  1. Rate control 1st line (unless a reversible cause, new onset or associated HF) = Beta-blockers.
    If Beta-blockers don’t work/contraindicated then give CCB (diltiazem) or Digoxin (only in sedentary people)
  2. Rythm control - if reversible / new onset / associated HF / failure to respond = Cardioversion
    - This should be done within 48hrs if new onset + stable
    - Pharmacological = Flecainide / Amiodarone (if structural HD)
    - Electrical cardioversion - if haemodynamically unstable
143
Q

Long-term management in AF

A

Think Rate/rhythm control + Anticoagulation

1st line = beta-blockers
2nd line = Drondedarone / Amiodarone (if HF of LVF)

Anticoagulate with DOACs (e.g apixaban or rivoraxoabn) or give Warfarin if can’t have DOAC (i.e severe hepatic disease)

144
Q

What food/drink must patients on warfarin avoid?

A

Vit K rich foods (e.g leafy greens)
CYP450 enzyme effectors (e.g Cranberry juice + Alcohol)

145
Q

Management of Peri-arrest tachycardia

A

If life-threatening (i.e haemodynamic instability):
1. Synchronised DC shock. Give up to 3 attempts. must be sedated or anaesthetised if conciouss.
2. If unsuccessful give 300mg Amiodarone IV infusion over 10-20 mins then shock again.

Broad complex (>0.12ms);
1. Regular rhythm = Assume VT + Give 300mg Amiodarone IV followed by 24hr infusion
2. Irregular rhythm = seek help (could be AF + BBB or TdP)

Narrow complex (<0.12ms);
1. Regular rhythm = Vagal manoevre + IV Adenosine. 6mg, then 12mg, then 18mg. If unsuccessful consider atrial flutter and try beta-blocker / verapamil
2. Irregular = probably AF so consider cardioversion.

146
Q

Management of SVT

A

If Unstable = DC Cardiovert
If stable;
1. Valsava manoevre
2. Carotid sinus massage
3. Adenosine - 6mg, then 12mg, then 18mg.
4. Verapamil
5. DC cardioversion

147
Q

Contraindications to adenosine

A

asthma / COPD / Heart failure / Heart block / Severe HTN

148
Q

Main side effect of adenosine

A

Sense of impending doom

149
Q

Management of peri-arrest bradycardia

A

If stable = observe
If unstable =
1. IV Atropine 500mcg - can be repeated up to 6 times 3mg total
2. If still no improvement try Ionotropes (e.g noradrenaline / Isoprenaline) or transcutaneous cardiac pacing + defib

150
Q

main side effects of atropine

A

Pupil dilation
Dry eyes
Urinary retention
Constipation

Because it is an antimuscarinic

151
Q

Management of Acute Left ventricular failure

A

‘pour SOD’

  1. ‘pour away’ or stop their IV fluids
  2. Sit up
  3. Oxygen
  4. Diuretics - IV 40mg Furosemide

If severe shock = Ionotropes (dobutamine) or Vasopressors (norepinhephrine)
If severe Pulmonary oedema = CPAP

*also monitor fluid balance

152
Q

Debakey classification of Aortic dissection

A

Type 1 = originates in ascending aorta, propagates to atleast the aortic arch and possibly beyond (most lethal)
Type 2 = Originates in and is confined to ascending aorta
Type 3 = Originates in descending aorta, extends distally

153
Q

Management of Type B Aortic dissection

A

Type B = descending aorta

Observe, Bed rest + IV Labetalol to prevent progression

154
Q

Management of Type A aortic dissection

A

Type A = ascending aorta
Management = HTN control with IV labetaolol + Surgical repair (usually thoracic endovascular aortic repair)

155
Q

Main side effects of Nicorandil

A

Headache
Flushing
GI ulcers, anal ulceration + eye ulceration

156
Q

Which medications commonly reduce hypoglycemic awareness

A

Beta-blockers

157
Q

Anti-dote for dabigatran

A

Inadrucizumab
= monoclonal antibody which binds directly to dabigatran with greater affinity than thrombin.

158
Q

Anti-dote for factor Xa inhibitors (Apixaban or Rivoroxaban)

A

Andexanet alfa

159
Q

Anti-dote for Warfarin

A

Phytomedandione (vitamin K)

160
Q

Anti-dote for heparin

A

Protamine
= Peptide which binds and sequesters heparin modules

161
Q

Pulseless electrical activity management

A

1mg Adrenaline ASAP!!!
CPR 30:2
Secure airway + ventilate
Recheck rhythm after 2 minutes, if no response then repeat 1mg Adrenaline every 3-5 minutes + continue CPR

162
Q

Anticoagulation in pts with AF post-stroke

A

2 weeks post stroke = Warfarin of DOAC (e.g 5mg Apixaban BD)

163
Q

what causes a slurred upstroke on QRS complex

A

Wolf-Parkinson White syndrome

164
Q

How can you differentiate between an aortic stenosis and pulmonary stenosis murmur

A

Pulmonary stenosis is louder on inspiration and does not radiated (unlike AS which radiates to carotids and is loudest on expiration)

165
Q

Lateral MI ECG territories and arteries

A

I, aVL and V5,V6
Left circumflex artery

166
Q

Inferior MI ECG territories

A

II, III, aVF
Right coronary artery

167
Q

Anterolateral/Septal MI ECG territories + arteries

A

V1 - V4
sometimes V1-V6 + aVL
Left Anterior Descending (LAD)

168
Q

Posterior MI ECG territories and Arteries

A

V1-V3 ST DEPRESSION!!!
Also often causes horizontal ST depression, Tall broad R waves, upright T waves + Q waves in posterior leads (V7-V9)
Usually left circumflex or right coronary

169
Q

HOCM murmur

A

Ejection systolic murmur, louder on valsalva maneouvre + Quieter on squatting

170
Q

cause of worsening renal function in a young pt shortly after starting ACEi for hypertension

A

Bilateral renal artery stenosis - if ACEi are started before diagnosis of this it can cause significant renal impairment

171
Q

How can you distinguish between tricuspid regurgitation and mitral regurg?

A

Both cause pansystolic murmur however TR is loudest on inspiration and is best heard at left lower sternal border and radiates to right lower sternal border
Whereas MR is best heard at apex and in left lateral decubitus position.

172
Q

ECG changes in PE

A

Most often sinus tachycardia is seen
S1Q3T3 is seen in 20% of patients. this is when there is a large S wave in lead 1, Q wave in lead 3 and a inverted T wave in Q3.

173
Q

ECG findings in hypercalcemia

A

Short QT interval

174
Q

What causes persistent ST elevation months after an MI

A

Left ventricular thromboembolism/aneurysm

175
Q

Loop diuretics side effects

A

e.g Furosemide, Bumetanide

SE’s;
- Ototoxicity
- Hypotension
- Hyponatremia
- Hypokalemia
- Hypomagnesemia
- Hypochloremic acidosis
- Hypocalcemia
- Renal impairment
- Hyperglycemia (not as much as thiazide diuretics)
- Gout

176
Q

Which medications can cause torsades de pointes?

A
  1. Macrolide antibiotics (e.g azithromycin / Clarithromycin)
  2. Antiarrythmics e.g amiodarone, sotalol
  3. TCAs
  4. Antipsychotics
  5. erythromycin
  6. Chloroquine
177
Q

Causes of a raised JVP

A

Pulmonary HTN / PE / PS / Pericardial effusion (CT)
Quantity of fluid (i.e fluid overload)
RVF
SVC obstruction
Tamponade / TR

178
Q

Why must ACEi be stopped prior to starting subcutril-valsartan?

A

Subcutrl-valsartan contains valsartan (ARB). Using both together increases the risk og angiodema as it would result in higher levels of bradykinin (as they both inhibit bradykinin degredation)

36 hour wash out period must be done.

Y4 Medicine (22 decks)

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