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Cardiology Flashcards

1
Q

What is atherosclerosis?

A

Combination of atheromas (fatty deposits in artery walls) and sclerosis (hardening / stiffening of blood vessel walls)

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2
Q

Which arteries does atherosclerosis affect?

A

Medium and large arteries

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3
Q

What is atherosclerosis caused by?

A

Chronic inflammation and activation of immune system in artery wall (causes deposition of lipids in artery wall followed by development of fibrous atheromatous plaques)

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4
Q

What is the result of atheromatous plaques?

A

Stiffening of artery wall leading to hypertension (raised blood pressure) and strain on the heart

Stenosis = reduced blood flow - angina

Plaque rupture giving off thrombus blocking distal vessel leading to ischaemia

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5
Q

What are some non-modifiable risk factors for atherosclerosis?

A

Older age

FH

Male

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6
Q

What are some modifiable risk factors for atherosclerosis?

A

Smoking

Alcohol consumption

Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption)

Low exercise

Obesity

Poor sleep

Stress

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7
Q

Which medical co-morbidities increase risk of atherosclerosis?

A

Diabetes

HTN

CKD

Inflammatory conditions e.g. Rheumatoid artheritis

Atypical antipsychotics

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8
Q

What are the end results of atherosclerosis?

A

Angina

MI

TIA

Stroke

PVD

Mesenteric ischaemia

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9
Q

What is the difference between primary prevention and secondary prevention for CVD?

A

Primary - never had CVD in past

Secondary - had angina, MI, TIA, stroke or PVD

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10
Q

How to optimise modifiable risk factors for CVD?

A

Advice on diet, exercise and weight loss

Stop smoking

Stop drinking alcohol

Tightly treat any co-morbidities e.g. diabetes

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11
Q

What is the QRISK 3 score and when should a statin be offered?

A

Risk that a patient will have a stroke or MI in next 10 years (give atorvastatin 20mg at night)

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12
Q

Who else should be offered a statin?

A

Patients with CKD and T1DM for more than 10 years

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13
Q

What reduction in non-HDL cholesterol should be aimed for on statin treatment?

A

Check lipids at 3 months and aim for greater than 40% reduction in non-HDL cholesterol (always check adherance before increasing)

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14
Q

What bloodsshould becheckedafter starting astatin?

A

LFTs within 3 months and again at 12 months (don’t need to check after that if normal - can cause transient rise in ALT and AST in first few weeks, dont need to stop if rise is less than 3 times upper limit)

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15
Q

What is the secondary prevention of CVD?

A

Aspirin (plus second antiplatelet e.g. clopidogrel)

Atorvostatin 80mg

Atenolol (or other beta-blocker commonly bisoprolol) titrated to max dose

Ace inhibitor (commonly ramipril) titrated to max tolerated dose

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16
Q

What are some notable side effects of statins?

A

Myopathy (check creatine kinase in patients with muscle pain / weakness)

T2DM

Haemorrhagic stroke (very rarely)

(Atorvastatin = newer statin, mostly well tolerated)

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17
Q

What is angina?

A

Narrowing of coronary arteries reducing blood flow to myocardium causing chest pain during periods of high demand e.g. exercise

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18
Q

What is the difference between stable and unstable angina?

A

Stable = relieved by rest / glyceryl trinitrate (GTN)

Unstable = symptoms come on randomly (considered an acute coronary syndrome)

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19
Q

What is the gold standard investigation for angina?

A

CT Coronary Angiography (injecting contrast and taking CT images timed with heart beat - highlighting narrowing)

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20
Q

What other investigations should be performed for angina?

A

Physical examination (heart sounds, signs of heart failure, BMI)

ECG

FBC (for anaemia)

U&Es (prior to ACEi and other meds)

LFTs (prior to statins)

Lipid profile

TFT (check for hypo/hyper thyroid)

HbA1C and fasting glucose (for diabetes)

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21
Q

What forms the management of angina?

A

Refer to cardiology (urgently if unstable)

Advise about diagnosis, management and when to call ambulance

Medical treatment (short term / long term)

Procedural or surgical interventions

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22
Q

What can be used for immediate symptomatic relief for angina?

A

GTN and repeat after 5 mins (if still pain 5 mins after this then call ambulance)

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23
Q

What can be used for long term symptomatic relief of angina?

A

Beta blocker (e.g. bisoprolol 5mg once daily - best if HF)

OR

CCB (e.g. amlodipine 5mg once daily)

(can be used in combo)

Other options (not first line): long acting nitrates (e.g. isosorbide mononitrate - may develop tolerance), ivabradine, nicorandil, ranolazine

don’t use verapamil if HF or with BBs (risk of complete heart block)

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24
Q

What can be used for secondary prevention of angina?

A

Aspirin (i.e. 75mg once daily)

Atorvastatin 80mg once daily

ACE inhibitor

Already on beta-blocker for symptomatic relief

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25
Q

What procedural / surgical intervention can be performed for stable angina?

A

Percutaneous coronary intervention (PCI) = dilating blood vessel with balloon and / inserting stent - offered to patients with proximal / extensive disease on CT coronary angiography - catheter inserted into patient’s brachial or femoral artery (contrast inserted looking for stenosis)

Coronary artery bypass graft (CABG) for severe stenosis = open chest along sternum causing midline sternotomy scar - using graft vein (usually great saphenous vein) and sewing it onto affected artery - recovery slower and complication rate higher than PCI

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26
Q

What normally causes acute coronary syndrome?

A

Thrombus from atherosclerotic plaque blocking coronary artery (made up mostly of platelets - anti-platelets are preventative: aspirin, clopidogrel and ticagrelor)

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27
Q

Label the following:

What does the left coronary artery become?

A

LCA becomes circumflex and left anterior descending

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28
Q

What does the right coronary artery supply?

A

Right atrium

Right ventricle

Inferior aspect of left ventricle

Posterior septal area

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29
Q

Where does the circumflex artery supply?

A

Left atrium

Posterior aspect of left ventricle

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30
Q

What does the LAD supply?

A

Anterior aspect of left ventricle

Anterior aspect of septum

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31
Q

What are the three types of ACS?

A

Unstable angina

STEMI

NSTEMI

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32
Q

What investigations for patients with ACS symptoms?

A

Perform an ECG:

ST elevation / new LBBB = STEMI

No ST elevation = troponin blood tests:

Raised / if other ECG changes e.g. ST depression or T wave investion or pathological Q waves = NSTEMI

Normal levels and no ECG changes = unstable angina / MSK pain

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33
Q

What are the symptoms of ACS?

A

Central constricting chest pain associated with:

  • Nausea and vomiting
  • Sweating and clamminess
  • Feeling of impending doom
  • SoB
  • Palpitations
  • Pain radiating to jaw or arms

Symptoms should continue at rest for more than 20 mins (if settle = angina)

Diabetic patients may not experience typical chest pain (‘silent MI’)

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34
Q

What are the ECG changes in STEMI?

A

ST segment elevation in leads consistent with area of ischaemia

New LBBB

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35
Q

What are the ECG changes in NSTEMI?

A

ST segment depression in a region

Deep T wave inversion

Pathological Q waves (suggesting deep infarct - late sign)

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36
Q

Complete the following:

A
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37
Q

How is ACS typically diagnosed?

A

Rise in serial troponins (proteins in cardiac muscle): baseline and 6 or 12 hours after onset

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38
Q

What are the alternative causes of raised troponin?

A

Chronic renal failure

Sepsis

Myocarditis

Aortic dissection

PE

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39
Q

What are the investigations for ACS?

A

ALL STABLE ANGINA INVESTIGATIONS

  • Physical examination (heart sounds, signs of heart failure, BMI)
  • ECG
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • TFTs (check for hypo / hyper thyroid)
  • HbA1C and fasting glucose (for diabetes)

PLUS

  • CXR (look for other causes / pulmonary oedema)
  • Echo (assess functional damage)
  • CT coronary angio
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40
Q

What is the treatement of STEMI presenting within 12 hours of onset?

A

Primary PCI (if available within 2 hours of presentation - balloons, or aspirate blockage then usually stent)

Thrombolysis (if PCI not available)

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41
Q

How is thrombolysis performed? Give examples?

A

Injecting fibrinolytic medication (breaks down fibrin)

Risk of bleeding

E.g. streptokinase, alteplase and tenecteplase

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42
Q

What is the treatment of acute NSTEMI?

A

BATMAN

Beta-blockers (unless contraindicated)

Aspirin 300mg stat dose

Ticagrelor 180mg stat dose (clopidogrel 300mg is alternative)

Morphine titrated to control pain

Anticoagulant: LMWH at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)

Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if sats dropping (<95%)

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43
Q

What is the GRACE Score?

A

Assessing for PCI in NSTEMI:

Scoring system for 6-month risk of death / repeat MI after NSTEMI

< 5% low risk

5-10% medium risk

>10% high risk

If medium / high = early PCI (within 4 days of admission)

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44
Q

What are the complications of MI?

A

Death

Rupture of heart septum / papillary muscles

Edema (heart failure)

Arrhythmia and Aneurysm

Dressler’s Syndrome

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45
Q

What is Dressler’s syndrome?

A

Aka post MI syndrome: 2-3 weeks after MI

Caused by localised immune response and causes pericarditis (less common as management of ACS becomes more advanced)

Pleuritic chest pain, low grade fever and pericardial rub

Can cause pericardial effusion and pericardial tamponade

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46
Q

How is Dressler’s syndrome diagnosed?

A

ECG (global ST elevation and T wave inversion)

Echocardiogram (pericardial effusion)

Inflammatory markers (raised CRP and ESR)

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47
Q

What is the management of Dressler’s syndrome?

A

NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone)

Pericardiocentesis (remove fluid from around heart)

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48
Q

What form secondary prevention following ACS?

A

Aspirin 75mg once daily

Another antiplatelet e.g. clopidogrel or ticagrelor for up to 12 months (dual anti platelet duration will vary following PCI procedure depending on type of stent used due to higher risk of thrombus formation with different stents)

Atorvastatin 80mg once daily

ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)

Atenolol (or other BB titrated as high as tolerated)

Aldosterone antogonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

Dual antiplatelet duration varies following PCI procedures depending on type of stent (some have higher risks of thrombus)

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49
Q

What are the advisable lifestyle changes following ACS?

A

Stop smoking

Reduce alcohol

Mediterranean diet

Cardiac rehab (specific exercise regime for patients post MI)

Optimise treatment of other medical conditions (e.g. HTN and diabetes)

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50
Q

What are the types of MI?

A

Type 1: Traditional MI due to acute coronary event

Type 2: Ischaemia due to increased demand / reduced supply oxygen (severe anaemia, tachycardia, hypotension)

Type 3: Sudden cardiac death / cardiac arrest suggestive of ischaemic event

Type 4: MI associated with PCI / coronary stunting / CABG

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51
Q

What is the result of acute left ventricular failure?

A

Pulmonary oedema

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52
Q

What can trigger acute LVF?

A

Iatrogenic (e.g. aggressive IV fluids in frail elderly patient)

Sepsis

Myocardial infarction

Arrhythmias

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53
Q

How does acute LVF present?

A

Rapid onset breathlessness (exacerbated by lying flat)

T1RF (low O2 with normal CO2)

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54
Q

What are the symptoms of acute LVF?

A

SoB

Looking and feeling unwell

Cough (frothy white / pink sputum)

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55
Q

What may be found on examination for acute LVF?

A

Increased RR

Reduced O2 sats

Tachycardia

3rd heart sound

Bilateral basal crackles (sounding wet on auscultation)

Hypotension in severe cases (cardiogenic shock)

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56
Q

What signs of underlying cause may be found in acute LVF?

A

Chest pain in ACS

Fever in sepsis

Palpitation in arrhythmias

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57
Q

What are the signs of right sided heart failure?

A

Raised JVP

Peripheral oedema (ankles, legs, sacrum)

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58
Q

What may cause an elderly patient who has recieved lots of IV fluid desaturate? What can be prescribed?

A

Acute LVF

IV furosemide

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59
Q

How to initally investigate possible acute LVF?

A

History

Clinical examination

ECG (to look for ischaemia / arrhythmias)

ABG

CXR

Bloods (routine for infection, kidney function, BNP and consider troponin)

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60
Q

What are the investigations for acute LVF?

A

B-type natriuretic peptide (BNP blood test - hormone released from ventricles when myocardium is stretched too far)

Echo - to assess function of LV (ejection fraction - should be > 50%) and any structural abnormalities

CXR findings:

  1. cardiomegaly (cardiothoracic ratio > 50%)
  2. upper lobe venous diversion (usually when standing erect lower lobe veins contain more blood than upper - in LVF the upper lobe veins also fill = engorged)
  3. bilateral pleural effusions
  4. fluid in interlobar fissures
  5. fluid in septal lines (Kerley lines)
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61
Q

What is the action of BNP and when else can it be released (sensitive but not specific)

A
  1. Relax smooth muscle - reducing systemic vascular resistance
  2. Act on kidneys to promote excretion of more water
  • Tachycardia
  • Sepsis
  • PE
  • Renal impairment
  • COPD
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62
Q

What is the standard management of acute LVF?

A

Pour SOD

Pour away (stop IV fluids)

Sit up (moving fluid to bases)

Oxygen (if falling <95% - caution in COPD)

Diuretics (IV furosemide 40mg stat) - reducing circulating volume meaning heart is less overloaded

Monitor fluid balance (fluid intake, urine output, U&E bloods and daily body weight)

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63
Q

What are the further treatment options in acute LVF?

A

IV opiates (e.g. morphine - acts as vasodilator)

NIV - CPAP (or full intubation / ventilation)

Inotropes e.g. infusion of noradrenaline - strengthen force of heart contraction (in local coronary care unit / high dependency unit / ICU)

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64
Q

What is chronic heart failure caused by?

A

Impaired LV contraction (‘systolic heart failure’)

Impaired LV relaxation (‘diastolic heart failure’)

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65
Q

How does chronic heart failure present?

A

Breathlessness (worse on exertion)

Cough - may produce frothy white / pink sputum

Orthopnoea (SoB when lying flat)

Paroxysmal nocturnal dyspnoea (waking up with severe SoB, cough, wheeze, improves over minutes)

Peripheral oedema (swollen ankles)

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66
Q

What may cause PND?

A
  • Fluid settles across large surface area (stand up and upper lungs clear)
  • During sleep resp centre in brain is less responsive so RR / effort doesnt increase in response to reduced O2 sats allowing more significant pulmonary congection and hypoxia before waking up
  • Less adrenalin means myocardium is more relaxed worsening cardiac output
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67
Q

How is chronic heart failure diagnosed?

A

Clinical presentation

BNP blood test (specifically N-terminal pro-B-type natriuretic peptide” - NT - proBNP)

Echo

ECG

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68
Q

What may cause chronic heart failure?

A

Ischaemic heart disease

Valvular heart disease (commonly aortic stenosis)

HTN

Arrhythmias (commonly atrial fibrillation)

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69
Q

What is the initial management of chronic heart failure?

A

Refer to specialist (NT-proBNP > 2,000 = urgent referral)

Discussion and explanation

Medical management

Surgical treatment for severe aortic stenosis or mitral regurgitation

Heart failure specialist nurse

In addition: yearly flu and pneumococcal vaccine, stop smoking, optimise co-morbidities, exercise as tolerated

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70
Q

What is the first line medical treatment for chronic heart failure?

A

ABAL

Ace inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)

Beta blocker (e.g. bisoprolol up to 10mg as tolerated)

Aldosterone antagonist if not controlled with A and B (spirololactone or eplerenone)

Loop diuretics improve symptoms (e.g. furosemide 40mg once daily)

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71
Q

What can be used instead of ACE inhibitors if they’re not tolerated?

A

Candesartan titrated up to 32mg OD (avoid ACEi in patients with valvular heart disease)

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72
Q

When are aldosterone antagonists used?

A

Reduced ejection fraction and symptoms not controlled with ACEi and BB

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73
Q

What should be closely monitored when on diuretics, ACEi, and aldosterone antagonists?

A

U&Es (all cause electrolyte disturbances)

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74
Q

What is cor pulmonale?

A

Right sided heart failure caused by respiratory disease (pulmonary hypertension)

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75
Q

What are the respiratory causes of cor pulmonale?

A

COPD - most common

PE

Interstitial lung disease

Cystic fibrosis

Primary pulmonary hypertension

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76
Q

How does cor pulmonale present?

A

Often asymptomatic - main presenting complaint is SoB (also SoB from chronic lung disease)

  • Peripheral oedema
  • Increased breathlessness on exertion
  • Syncope (dizziness and fainting)
  • Chest pain
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77
Q

What are the examination signs of cor pulmonale?

A

Hypoxia

Cyanosis

Raised JVP (due to back-log of blood in jugular veins)

Peripheral oedema

Third heart sound

Murmurs (e.g. pan systolic in tricuspid regurg)

Hepatomegaly due to back pressure in hepatic vein (pulsatile in tricuspid regurgitation)

78
Q

What is the management of cor pulmonale?

A

Treat symptoms and underlying cause (LTOT often used)

Prognosis is poor (unless reversible cause)

79
Q

What BP do NICE suggest diagnosis of HTN?

A

Above 140/90 in clinic or 135/85 with ambulatory

80
Q

What are the causes of hypertension?

A

Essential (95% of HTN)

ROPE

Renal disease (most common cause, BP is very high / no response to treatement = renal artery stenosis)

Obesity

Pregnancy induced / pre-eclampsia

Endocrine (hyperaldosteronism - Conns syndrome - renin:aldosterone ratio blood test)

Consider these in patients under 40

81
Q

What are the complications of HTN?

A

Ischaemic heart disease

CVA (stroke / haemorrhage)

Hypertensive retinopathy

Hypertensive nephropathy

Heart failure

82
Q

How often should BP be measured?

A

Every 5 years to screen (more often in patients on borderline - 140/90 and every year in T2DM)

If between 140/90 and 180/120 then have 24 hour ambulatory BP / home readings to confirm

Measure in both arms if difference is more than 15mmHg then use reading from arm with higher blood pressure

83
Q

What is the white coat effect?

A

More than 20/10 mmHg difference in blood pressure between clinic and ambulatory / home readings

84
Q

Complete the following:

A
85
Q

How to examine for end organ damage in hypertension?

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage

Bloods for HbA1c, renal function and lipids

Fundus examination for hypertensive retinopathy

ECG for cardiac abnormalities

86
Q

How to initially manage HTN?

A

Establish diagnosis

Investigate for possible causes and end organ damage

Advise on lifestyle (healthy diet, stop smoking, reduce alcohol, reduce caffeine and salt intake, take regular exercise)

87
Q

Who is medically managed for HTN?

A

All patients with type 2 HTN

All patients under 80 with stage 1 and QRISK score >10%, diabetes, renal disease, CVD or end organ damage

88
Q

What is the medical management of HTN?

A

ACEi e.g. ramipril

Beta blocker e.g. bisoprolol

Calcium channel blocker (e.g. amlodipine

Diuretic (thiazide-like e.g. indapamide)

AiiRB e.g. candesartan (if not tolerating ACEi - dry cough or black - not used with ACEi)

Step 1: < 55 and non black use A but if > 55 or black use C

Step 2: A + D or C + D

Step 3: A + C + D

Step 4: A + C + D + additional

Additional = if serum potassium < 4.5 mmol/l give potassium sparing diuretic e.g. spironolactone if > 4.5 then give alpha blocker e.g. doxazosin or a beta blocker e.g. atenolol

89
Q

What is spirolonactone? How does it work? What is the risk?

A

“potassium-sparing diuretic“working byblockingaction ofaldosteroneinkidneysresulting insodium excretionandpotassium reabsorption(helpful whenthiazidediuretics are causinghypokalaemia)

Risk = hyperkalaemia (ACEi also cause this, thiazide-like cause electrolyte disturbances - monitor U&Es regularly)

90
Q

Complete this:

A
91
Q

What is the first heart sound (S1) caused by?

A

Closing of AV valves (tricuspid and mitral) at start of systolic contraction of the ventricles

92
Q

What is the second heart sound (S2) caused by?

A

Closing of semilunar valves (pulmonary and aortic) once systolic contraction is complete

93
Q

When is the third heart sound heard?

A

Roughly 0.1 seconds after second heart sound - rapid ventricular filling causing chordae tendineae to pull to their full length and twang - normal in young healthy people, older patients = heart failure

94
Q

What is the fourth heart sound?

A

Heart directly before S1 - always abnormal and relatively rare - indicates stiff / hypertrophic ventricle - caused by turbulent flow from atria contracting against non-compliant ventricle

95
Q

What side of the stethoscope do you use?

A

Bell = low pitched sounds

Diaphragm = high pitched

96
Q

Where can you listen to the different valves?

A

Pulmonary: 2nd I.C.S left sternal boarder

Aortic: 2nd I.C.S right sternal boarder

Tricuspid: 5th I.C.S left sternal boarder

Mitral: 5th I.C.S mid clavicular line (apex area)

97
Q

Where is the best area for listening to heart sounds?

A

Erb’s point (3rd intercostal space on left sternal border)

98
Q

What can be done to emphasise the murmur heard in mitral stenosis?

A

Patient on lhs

99
Q

How can murmur in aortic regurgitation be exaggerated?

A

Sit patient up

Lean forward

Hold exhalation

100
Q

How to assess a murmur?

A

SCRIPT

Site: where is it loud?

Character: soft / blowing / crescendo / decrescendo

Radiation: hear murmur over carotids (AS) or left axilla (MR)

Intensity: what grade is murmur

Pitch: high / low pitched (indicates velocity)

Timing: systolic / diastolic

101
Q

How to grade a murmur? (quite subjective)

A
  1. Difficult to hear
  2. Quiet
  3. Easy to hear
  4. Easy to hear with a palpable thrill
  5. Can hear with stethoscope barely touching chest
  6. Can hear with stethoscope off the chest
102
Q

Give an example script for describing a murmur?

A

“This patient has a harsh / soft / blowing, Grade …, systolic / diastolic murmur, heard loudest in the aortic / mitral / tricuspid / pulmonary area, that does not / radiates to the carotids / left axilla. It is high / low pitched and has a crescendo / decrescendo / crescendo-decrescendo shape. This is suggestive of a diagnosis of mitral stenosis / aortic stenosis”

103
Q

What is the difference between hypertrophy and dilatation?

A

Hypertrophy = thickening both outwards and into chambeer

Dilatation = thinning and expanding

104
Q

What changes to myocardium does mitral stenosis and aortic stenosis cause?

A

Mitral stenosis = left atrial hypertrophy

Aortic stenosis = left ventricular hypertrophy

105
Q

What changes to the myocardium does mitral regurgitation and aortic regurgitation cause?

A

Mitral regurgitation = left atrial dilatation

Aortic regurgitation = left ventricular dilatation

106
Q

What causes mitral stenosis?

A

Rheumatic heart disease

Infective endocarditis

107
Q

What kind of murmur does mitral stenosis cause?

A

Mid-diastolic, low pitched“rumbling” murmur due to a low velocity of blood flow

Loud S1 due to thick valves requiring a large systolic force to shut then shutting suddenly

Palpate a tapping apex beat due to loud S1

108
Q

What is mitral stenosis associated with?

A

Malar flush - due to back-pressure of blood into pulmonary system causing rise in CO2 and vasodilation

AF - caused by left atrium struggling to push blood through stenotic valve causing strain, electrical disruption and resulting fibrillation

109
Q

What is mitral regurgitation?

A

Incompetent mitral valve allows blood to leak back through during systolic contraction of the left ventricle - causing congestive cardiac failure (leaking valve causes reduced ejection fraction)

Causing pan-systolic, high pitched“whistling” murmur due to high velocity blood flow though leaky valve

Radiates to left axilla (may hear 3rd heart sound)

110
Q

What are the causes of mitral regurg?

A

Idiopathic weakening of valve with age

IHD

Infective endocarditis

Rheumatic heart disease

Connective tissue disorder e.g. Ehlers Danlos syndrome or Marfan syndrome

111
Q

Describe the murmur in aortic stenosis?

A

Ejection-systolic, high-pitched murmur

Crescendo-decrescendo due to speed of blood during different periods of systole

112
Q

What are the other signs in aortic stenosis?

A

Radiates to carotids as turbulence continues up neck

Slow rising pulse and narrow pulse pressure

Exertional syncope (light headedness and fainting when exercising) due to difficulty maintaining good flow to brain

113
Q

What are the causes of aortic stenosis?

A

Idiopathic age related calcification

Rheumatic heart disease

114
Q

What is the murmur heard in aortic regurgitation?

A

Early diastolic, soft murmur (assoicated with Corrigan’s pulse - collapsing pulse - blood pumped out by ventricles then immediately flows back)

115
Q

What does aortic regurgitation result in?

A

Heart failure

116
Q

What other murmur can aortic regurgitation result in?

A

Austin-flint - heard at apex and is early diastolic‘rumbling’ murmur - caused by blood flowing back through aortic valve and over mitral causing vibrations

117
Q

What are some causes of aortic regurgitation?

A

Idiopathic age related weakness

Connective tissue disorder e.g. Ehlers Danlos syndrome or Marfan syndrome

118
Q

What scar will patients who have had valve replacement have?

A

Midline sternotomy scar - down middle of sternum (mitral or aortic valve replacement or CABG)

Right sided mini-thoracotomy (minimally invasive mitral valve replacement)

119
Q

What are the different types of replacement valves?

A

Bioprosthetic (e.g. porcine from a pig) - last for 10 years

Mechanical valves - over 20 years - require lifelong anticoagulation with warfarin (target INR = 2.5 - 3.5)

120
Q

What are the types of mechanical heart valves?

A

Starr-Edwards valve - bell in cage, very successful but no longer used, highest risk of thrombus formation

Tilting disc valve - single tilting disc

St Judes valve - two tilting metal discs, bileaflet valve, least risk of thrombus formation

121
Q

What are the major complications of mechanical heart valves?

A

Thrombus formation (blood stagnates and clots)

Infective endocarditis

Haemolysis (blood churns in valve)

122
Q

What type of click does mechanical heart valve cause?

A

S1 click for metallic mitral valve

S2 click for metallic aortic valve

123
Q

What is the surgical treatment for severe aortic stenosis?

A

TAVI (transcatheter aortic valve implantation)

Local / general anaesthetic - catheter inserted to femoral artery and under x-ray guidance going to the aortic valve - inflating balloon to stretch valve and implanting bioprosthetic valve in the location of the aortic valve

Long term outcome = still not clear (relatively new procedure) - typically do not require warfarin as valve is bioprosthetic

124
Q

What is a complication with surgical valve replacement? What organisms are implicated normally?

A

Infective endocarditis (2.5% of patients)

Gram +be cocci organisms:

  • Staphylococcus
  • Streptococcus
  • Enterococcus

Used to take abx for routine dental procedures - no longer case

125
Q

What is the result of atrial fibrillation?

A

Irregularly irregular ventricle contractions

Tachycardia

Heart failure due to poor filling of the ventricles during diastole

Risk of stroke (blood collects in atria and forms blood clots)

126
Q

How does atrial fibrillation present?

A

Asymptomatic usually

  • Palpitations
  • SoB
  • Syncope (dizziness or fainting)
  • Symptoms of associated conditions (e.g. stroke, sepsis, or thyrotoxicosis)
127
Q

What are the two differential diagnoses of an irregularly irregular pulse?

A

Atrial fibrillation

Ventricular ectopics (disappear when HR gets over certain threshold - if regular during exercise = ventricular ectopics)

Differentiated using ECG

128
Q

How does AF appear on an ECG?

A

Absent P waves

Narrow QRS Complex Tachycardia

Irregularly irregular ventricular rhythm

129
Q

What is valvular AF?

A

Patients with AF who have moderate / severe mitral stenosis or mechanical heart valve

130
Q

What are the most common causes of AF?

A

Sepsis

Mitral valve pathology (stenosis / regurgitation)

Ischaemic heart disease

Thyrotoxicosis

Hypertension

131
Q

What are the two principles of treating AF?

A

Rate or rhythm control

Anticoagulation to prevent stroke

132
Q

What should patients with AF have first line?

A

Rate control unless:

  • Reversible cause of AF
  • New onset (within last 48 hrs)
  • AF causing heart failure
  • Remain symptomatic despite effective rate control
133
Q

What can be given for rate control in AF?

A

Beta blocker (e.g. atenolol 50-100mg OD)

CCB (e.g. diltiazem - not in HF)

Digoxin (only in sedentary people, needs monitoring and risk of toxicity)

134
Q

When is rhythm control given to patients with AF?

What are the two options?

A

Reversible cause

New onset (48rs)

Causing heart failure

Symptomatic despite rate control

  • Single cardioversion event that puts the patient back into sinus rhythm or long term medical rhythm control
135
Q

What are the two choices for timing of cardioversion?

A

Immediate - present for less than 48 hrs / severely haemodynamically unstable

Delayed - present for more than 48 hrs and haemodynamically stable (should be anticoagulated for 3 weeks prior to cardioversion - may have developed a blood clot in atria and cardioversion mobilises causing stroke, should have rate control whilst waiting)

136
Q

What are the two options for cardioversion?

A

Pharmacological (first line) - flecanide, amiodarone (choice in structural heart disease)

Electrical - shock heart back into sinus rhythm involving sedation / GA and using defibrillator

137
Q

What are the options for long term medical rhythm control?

A

Beta blockers - rhythm control

Dronedarone - second line for maintaining normal rhythm where successful cardioversion

Amiodarone - if HF or left ventricular dysfunction

138
Q

What is warfarin and how does it work?

A

Warfarin is a vitamin K antagonist (needed for clotting factors)

Prolonging PT (time for blood to clot)

139
Q

What does an INR of 2 mean?

A

Prothrombin time twice that of a normal healthy adult

140
Q

What is the target INR in AF? When is warfarin given?

A

2-3

Given in evening in hosp (6pm) and INR taken before

141
Q

What foods affect warfarin / cytochrome P450 (and as such metabolism)?

A

Those containing vitamin K e.g. leafy green vegetables

Those that affect P450 e.g. cranberry juice and alcohol

142
Q

What is the half life of warfarin and how can it be reversed?

A

1-3 days (reversibel with vitamin K in event INR is very high / bleeding)

143
Q

What are NOACs now known as? Give some examples? What are they reversed with?

A

NOvel AntiCoagulants are now known as Direct acting Oral AntiCoagulants (DOACs)

E.g.

Apixaban, rivaroxaban (Andexanet Alfa)

Dabigatran (Idarucizumab)

Currently on patent so more expensive than warfarin (e.g. £27 versus £1, apixaban comes off in 2022)

144
Q

How are DOACs taken?

A

Apixaban and dabigatran are taken twice daily

Rivaroxaban is taken once daily

No way to reverse effect however lower blleding risk and short half life (7-15 hours)

145
Q

What are the advantages of DOACs compated to warfarin?

A

No monitoring is required

No major interaction problems

Equal / better than warfarin at preventing strokes in AF

Equal / less risk of bleeding than warfarin

146
Q

What is the tool for assessing whether to initiate anticoagulation? (risk of stroke / TIA)

A

CHA2DS2-VASc (if one or more then consider / start)

Congestive heart failure

Hypertension

Age > 75 (scores 2)

Diabetes

Stroke / TIA / MI previously (score 2)

Vascular disease

Age 65-74

Sex (female)

147
Q

What is the assessment tool for assessing risk of major bleed whilst on anticoagulation?

A

HAS-BLED (don’t need to know inside out - usually risk of stroke outweighs risk of bleeding)

Hypertension

Abnormal renal and liver function

Stroke

Bleeding

Labile INRs (whilst on warfarin)

Elderly

Drugs or alcohol

148
Q

What are the four cardiac arrest rhythms?

A

Shockable: VT, VF

Non-shockable: PEA (including sinus rhythm without pulse), asystole

149
Q

What is the treatment of tachycardia in unstable / stable (broad / narrow)

A

Unstable: consider 3 syncronised shocks / amiodarone infusion

Stable:

Narrow complex (QRS < 0.12s)

Atrial fibrillation - rate control with BB / diltiazem

Atrial flutter - control rate with BB

Supraventricular tachycardias - treat with vagal manoeuvres and adenosine

Broad complex (QRS > 0.12s)

Ventricular tachycardia or unclear - amiodarone

If known SVT with BBB treat as normal SVT

If irregular may be AF variation - seek expert help

150
Q

What causes atrial flutter how does it appear on ECG?

A

Re-entrant rhythm in either atrium (re-circulates in self perpetuating loop due to extra electrial pathway)

Atria contract at 300bpm - signal is conducted every second lap due to refractory period at AV node (150bpm)

Sawtooth appearance on ECG with P wave after P wave

151
Q

Which conditions are associated with atrial flutter?

A

Hypertension

Ischaemic heart disease

Cardiomyopathy

Thyrotoxicosis

152
Q

What is the treatment of atrial flutter?

A

Similar to AF:

  • Rate / rhythm control with BB / cardioversion
  • Treat underlying condition e.g. hypertension / thyrotoxicosis
  • Radiofrequency ablation of the re-entrant rhythm
  • Anticoagulation based on CHA2DS2VASc
153
Q

What is a supraventricular tachycardia caused by?

How does it appear?

A

Electrical signals re-entering atria from ventricles (normally can only go from atria to ventricles)

Causing fast narrow complex tachycardia (QRS < 0.12)

QRS followed by T followed by QRS followed by T…

154
Q

What is paroxysmal SVT?

A

SVT reoccurs and remits in same patient over time

155
Q

What are the three main types of SVT? (based on source of electrical signal)

A

Atrioventricular nodal re-entrant tachycardia (re-entry back through AV node)

Atrioventricular re-entrant tachycardia (re-entry is an accessory pathway - Wolff-Parkinson-White syndrome)

Atrial tachycardia - electrical signal originates in atria somewhere other than SAN node (ectopic electrical activity causes atrial rate of >100bpm)

156
Q

What can be done to acutely manage SVT?

A

Valsalva manoeuvre - blow hard against resistance e.g. into plastic syringe

Carotid sinus massage - on one side with two fingers

Adenosine

Alternative to adenosine is verapamil

Direct current cardioversion (if all other treatment fails)

^ try in stepwise fashion

157
Q

How does adenosine work?

A

“Resets rhythmn”

Slows cardiac conduction through AV node (interrupting AV node / accessory pathway during SVT - needs to be given as rapid bolus to ensure reaches heart with enough impact - causes brief period of asystole / bradycardia - quickly metabolised)

158
Q

When to avoid adenosine?

What to warn about?

A

If patient has asthma / COPD / heart failure / heart block / severe hypotension

Feeling of dying / impending doom

159
Q

How to give adenosine?

A

Fast IV bolus into antecubital fossa (initially 6mg, then 12mg then futher 12mg if no improvement between doses)

160
Q

What can be given to manage SVT?

A

Medication (beta blocker, CCB, or amiodarone)

Radiofrequency ablation

161
Q

What is Wolff-Parkinson White syndrome?

A

Extra electrical pathway connecting atria and ventricles (normally only AV node connects)

(Often called bundle of kent)

162
Q

What is the definitive treatment of WPW syndrome?

A

Radiofrequency ablation of the accessory pathway

163
Q

What are the ECG changes on WPW syndrome?

A

Short PR interval (<0.12 seconds)

Wide QRS complex (>0.12)

Delta wave - slurred upstroke of QRS

164
Q

What is the risk with AF / atrial flutter and WPW?

A

Electrical activity can pass through accessory pathway causing polymorphic wide complex tachycardia

Antiarrhythmic medications (e.g. BB, CCB and adenosine) increase risk by reducing contraction through AV node and promoting through accessory (contraindicated in patients with WPW who develop AF / flutter)

165
Q

How does radiofrequency ablation work?

A

Catheter ablation performed in cath lab (local / GA) interting catheter into femoral veins and guiding to heart under xray guidance (placed against different areas of heart looking for electrical signals) - radiofrequency ablation (heat) used in abnormal areas of electrical activity leaving scar tissue

166
Q

What is radiofrequency ablation used for?

A

Atrial fibrillation

Atrial flutter

SVT

WPW syndrome

167
Q

What is Torsades des pointes?

A

Polymorphic (multiple shape) ventricular tachycardia - looks like normal VT on ECG but variable QRS heights

Occurs in patients with prolonged QT interval

168
Q

How does torsades de pointes progress?

A

Terminate spontaneously

If progress into ventricular tachycardia leading to cardiac arrest

169
Q

What are some causes of prolonged QT?

A

Long QT syndrome (inherited)

Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotic)

Electrolyte disturbance (hypokalaemia, hypomagnesaemia, hypocalaemia)

170
Q

What is the acute management of Torsades de pointes?

A

Correct the cause (electrolyte disturbances / medications)

Magnesium infusion (even if normal serum magnesium)

Defibrillation if VT occurs

171
Q

What is the long term management of prolonged QT syndrome?

A

Avoid medications that prolong QT

Correct electrolyte disturbance

BB (not sotalol)

Pacemaker / implantable defibrillator

172
Q

What are ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharge from outside the atria = random brief palpitations (relatively common at all ages and in healthy patients - more common in pre-existing heart conditions (e.g. ischaemic heart disease / heart failure)

173
Q

How do ventricular ectopics appear on an ECG?

A

Appear as individual random, abnormal, broad QRS complexes on a background of normal ECG

174
Q

What is bigemy?

A

Ventricular ectopics occur so frequently (after every sinus beat)

ECG looks like normal sinus beat followed immediately by ectopic, then normal beat and so on

175
Q

What is the management of ventricular ectopics?

A

Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities

Reassurance & no treatment in otherwise healthy people

Expert advise if heart conditions / concerning features (chest pain, syncope, murmur, FH of sudden death)

176
Q

What is first degree heart block?

A

Delayed AV condition (every P wave has a QRS complex)

PR interval > 0.20 seconds (5 small or 1 big square)

177
Q

What is second degree heart block? What are the types?

A

Some atrial impulses don’t make it through AV node:

Mobitz type 1 (Wenckebach’s phenomenon) = atrial impulses become gradually weaker until it doesn’t pass - ECG shows increasing PR intervals until QRS complex is missed

Mobitz type 2 = Intermitted failure of AV conduction - usually ratio e.g. 3:1 (3 p’s to each QRS) risk of asystole

2:1 block = caused by mobitz type 1 / 2 (difficult to tell which)

178
Q

What is third degree heart block?

A

Aka complete heart block (no relationship between P waves and QRS) significant risk of asystole with 3rd degree heart block

179
Q

What is the treatment of bradycardias / AV node blocks?

What is an unstable / risk of asystole rhythmn?

A

Stable = observe

Unstable / risk of asystole (Mobitz type 2, complete heart block / previous asystole) =

Atropine 500mcg (first line)

Repeat atropine up to 6 times (total 3mg)

Other inotropes (e.g. noradrenaline)

Transcutaneous cardiac pacing (using defib)

Temporary transvenous cardiac pacing (if high risk of asystole - electrode on wire inserted into vein and fed through venous system to right atrium to stimulate directly)

Permanent implantable pacemaker when available

180
Q

What is atropine? What are the side effects?

A

Antimuscarinic - inhibits the parasympathetic nervous system causing pupil dilatation / urinary retention / dry eyes / constipation

181
Q

What are the components to a pacemaker?

A

Pulse generator (pacemaker box)

Pacing leads (carry electrical impulses to heart)

182
Q

Where is the pacemaker implanted?

A

Left anterior chest wall / axilla and wires implanted into relevant chambers of heart

183
Q

How long do pacemaker batteries last? When are they contraindicated?

A

5 years

MRI scans (due to powerful magnets - some are MRI compatible) and electrical interventions e.g. TENS machines and diathermy

184
Q

When should pacemakers be removed at death?

A

Prior to cremation - on “cremation form” the most important task is to state if it’s been removed

185
Q

When is pacemaker indicated?

A

Symptomatic bradycardia

Mobitz Type 2 AV block

Third degree heart block

Severe heart failure (biventricular pacemakers)

Hypertrophic obstructive cardiomyopathy (ICDs)

186
Q

How do single-chamber pacemakers work?

A

Leads in a single chamber either right atrium or right ventricle

Placed in right atrium if problem with SA node (AV conduction is normal) or right ventricle if AV conduction is abnormal

187
Q

How do dual chamber pacemakers work?

A

Leads in both right atrium and right ventricle allowing pacemaker to syncronise

188
Q

What is a biventricular (triple-chamber) pacemaker? When is it given? What are they also called?

A

Leads in right atrium, right ventricle, and left ventricle

Usually in heart failure

Cardiac resynchronisation therapy (CRT) pacemakers

189
Q

What are implantable cardioverter defibrillators (ICDs)?

A

Monitor heart and apply defib shock to cardiovert patient back to sinus rhythmn

190
Q

Describe the ECG changes with:

Single chamber pacemakers

Dual chamber pacemakers

A
191
Q

When should a statin not be prescribed?

A

Pregnant

Ceased during macrolide meds (increased risk of rhabdomyolysis)

Medicine (12 decks)

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