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FinalMB Part I - Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Outline the two main disease processes involved in atherosclerosis? (2)

A
  • Atheromatous plaque formation
  • Scarring and stiffenening of the aterial walls
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2
Q

What is the difference between atherosclerosis and arteriosclerosis

A
  • Atherosclerosis affects the large and medium-sized arteries
  • Arteriosclerosis affects the smaller arterioles
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3
Q

What are the three main components to the aetiology of atherosclerosis

A
  • Endothelial damage
  • Chronic inflammation
  • Activation of the immune system
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4
Q

What are the three main outcomes of untreated atherosclerosis

A
  • Stiffening of the vessels walls leading to hypertension
  • Stenosis of the vessel walls causing stable angina and/or periperal vascular disease
  • Plaque rupture leading to thrombus formation and the development of an acute coronary syndrome
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5
Q

What are the non-modifiable risk factors of cardiovascular disease

A
  • Age
  • Family history
  • Male sex
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6
Q

What are the modifiable risk factors for cardiovascular disease

A
  • Smoking
  • Alcohol consumption
  • Poor diet
  • Lack of exercise
  • Poor sleep
  • Stress
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7
Q

Which co-morbidities can increase the risk of developing cardiovascular disease

A
  • Diabetes (both T1DM and T2DM)
  • Hypertension
  • CKD
  • Inflammatory conditions (RA)
  • Atypical antipsycotics
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8
Q

Which conditions can cardiovascular disease lead to if left untreated

A
  • Stable angina
  • Acute coronary syndromes (unstable angina, STEMI and NSTEMI)
  • Stroke
  • Transient ischaemic attack
  • Peripheral vascular disease
  • Chronic mesenteric ischaemia
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9
Q

What is the first port-of-call in the prevention of a patient developing cardiovascular disease

A

Optimise the modifiable risk factors

  • Inform patient about diet, excercise, smoking etc.
  • Optimise treatment for underlying co-morbidities
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10
Q

What is the difference between primary and secondary prevention of cardiovascular disease

A

Primary prevention - prevents CVD from developing in the first instance

Secondary prevention - prevents reoccurance and/or progression of cardiovascular disease following and ischaemic event

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11
Q

What is the most important step in the primary prevention of cardiovascular disease

A

Perform a Q-RISK3 score - a prediction of the likelihood of an ischaemic event over the next 10 years

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12
Q

If a patients’ Q-RISK3 score is greater than 10, what does this mean

A

This means that there is a greater that 10% chance of the patient having an ischaemic event over the next 10 years

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13
Q

If a patients’ Q-RISK3 score is greater than 10, what primary prevention is indicated

A

Q-RISK3 >10; commence atorvastatin (20mg) taken once a day at night

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14
Q

What dose of statin is indicated in the primary prevention of a patient with a Q-RISK3 score greater than 10?

A

20mg

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15
Q

How is the primary prevention of cardiovascular disease treatment different in patients with CKD or T1DM lasting greater than 10 years?

A

These patients should be started on atorvastatin 20mg regardless of Q-RISK3 score

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16
Q

What is the aim of statin treatment in the primary prevention of cardiovascular disease

A

To reduce non-HDL cholesterol by 40%

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17
Q

What monitoring is required in patients treated with a statin in the primary prevention of cardiovascular disease

A

3 monthly lipid profiling to ensure that a 40% reduction is acheived

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18
Q

What is the mainstay treatments given in the secondary prevention of cardiovascular disease

A

“The Four A’s

  • Aspirin
  • Atorvastatin
  • Atenolol (or bisoprolol)
  • ACE-I (usually ramipril)
    “
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19
Q

What is the treatment dose of statin given to patients in the secondary prevention of cardiovascular disease

A

80mg (this is compared to 20mg in primary prevention)

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20
Q

What are the main side effects of statins?

A
  • Myopathy
  • T2DM
  • Haemorrhagic stroke
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21
Q

A patient on statins presents with muscle ache and pains as well as weakness. What investigation should be carried out?

A

Creatine kinase blood test to look for rhabdomyolysis

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22
Q

What is meant by angina?

A

Angina refers to cardiac-related chest pain that occurs as a result of a narrowing of the coronary arteries that reduces the blood and oxygen supply to the myocardium

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23
Q

What is the difference between stable and unstable angina?

A

Stable angina - cardiac chest pain that only presents on exertion and which are relieved by GTN

Unstable angina - cardiac chest pain that presents spontaneously at rest and occurs as a result of atheromatous plaque rupture

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24
Q

What are the symptoms of angina

A

Constricting chest pain +/- radiation to the jaw/left arm

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25
Q

What is the gold standard investigation for angina

A

CT coronary angiography

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26
Q

What investigations are most appropriate when investigating angina

A
  • Physical exam
  • ECG; looking for old ischaemic changes, rule out PE and other causes of chest pain
  • FBC; looking for signs of anaemia
  • U&Es; indicating renal function prior to commencing ACE-I
  • LFTs; indicating liver function prior to commencing statin
  • Lipid profile; indicating modifiable risk factors and potential benefits of statin therapy
  • TFTs; hypo- and/or hyperthyroidism can be related to angina
  • HbA1C; looking for diabetes which is an optimisible disease risk factor
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27
Q

Outline the management techniques for angina

A

”

_R_eferral – to cardiology

_A_dvice – advise patient about diagnosis, management and when to

_M_edical treatment – symptomatic relief and secondary prevention of subsequent cardiovascular disease

_P_rocedural/surgical treatment – either PCI or CABG
“

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28
Q

What are the three main aims in the medical management of angina

A
  • Immediate symptomatic relief
  • Further symptomatic prevention
  • Secondary prevention
  • Procedural/surgical intervention
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29
Q

Outline the immediate symptomatic relief strategies in the treatment of angina

A

GTN Spray

  • GTN + Rest (5mins)
  • No symptomatic relief –> repeat
  • Still no pain relief after repeat –> ambulance
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30
Q

Outline the further symptomatic prevention strategies in the treatment of angina

A

”- β-blocker (bisoprolol or atenolol, 5mg) OR Ca2+ channel blocker (amlodipine, 5mg)

  • Combine β-blocker AND CCB if symptoms persist
  • Further persistance

o Long-acting nitrates - isosorbide mononitrate

o Funny current (If) blockers - ivabradine

o K+ channel activators - nicorandil (also NO donor)

o Late Na+ current blockers - ranolazine
“

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31
Q

Outline the secondary prevention strategies in the treatment of angina

A

”

The Four A’s

  • Aspirin (75mg)
  • Atorvastatin (80mg)
  • Atenolol (or bisoprolol)
  • ACE-I (usually ramipril)
    “
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32
Q

What are the two options for procedural/surgical intervention in the treatment of angina

A
  • Percutaneous coronary intervention (PCI) with coronary angioplasty
  • Coronary artery bypass grafting (CABG)
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33
Q

When is PCI considered in patients with angina?

A

Offered to patients with proximal (left main stem) or extensive disease indicated by the CTCA

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34
Q

When is CABG considered in patients with angina?

A

Offered to patients with extremely severe stenosis

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35
Q

What is the acute cause of an acute coronary syndrome

A

Thrombus formation usually as a result of atheromatous plaque rupture

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36
Q

What are the key types of acute coronary syndrome

A
  • Unstable angina
  • NSTEMI
  • STEMI
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37
Q

Why are thrombi that occur in acute coronary syndromes treated differently to those that occur in DVT or PE?

A
  • Thrombi that occur in fast flowing arterial vessels consist mostly of platelets and are as such treated with antiplatelets** (DAPT; aspirin + ticagrelor/prasugrel/clopidogrel)
  • Thrombi that occur in slower flowing venous vessels consist mostly of fibrin, hence are treated with anticoagulants** (clotbusters, DOACs, LMWH and Vitamin K antagonists)
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38
Q

Which areas of the heart are supplied by the right coronary artery (RCA)

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area
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39
Q

Which areas of the heart are supplied by the circumflex artery?

A
  • Left atrium
  • Posterior aspect of left ventricle
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40
Q

Which areas of the heart are supplied by the left anterior descending artery (LAD)?

A
  • Anterior aspect of left ventricle
  • Anterior aspect of septum
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41
Q

What is the first port-of-call in the diagnosis of a patient presenting with the symtoms of an acute coronary syndrome?

A

Perform an ECG and look for new ischaemic changes

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42
Q

How is a STEMI diagnosed from an ECG

A

”

  • *Primary Features;**
  • ST segment elevation
  • New LBBB (left axis deviation, QRS > 0.12s, W/negative deflection in V1, M/positive deflection in V6)

Secondary Features - (may be present alongside primary features, if in isolation, consider NSTEMI)

  • ST depression (reciprocal changes)
  • T wave inversion

”

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43
Q

What is the definition of a STEMI?

A
  • ST elevation
  • New LBBB
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44
Q

If an ECG carried out on a patient with symptoms of an acute coronary syndrome reveals no ST elevation and/or new LBB, what is the next appropriate investigation?

A

Perform troponin blood test

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45
Q

What is the definition of NSTEMI

A
  • No ST elevation
  • Raised troponin
  • AND/OR other ischaemic ECG changes (ST depression, T wave inversion or pathological Q waves)
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46
Q

If troponin levels are normal and there are no pathological changes on the ECG of a patient presenting with the symptoms of an ACS, what are the likely diagnoses

A
  • Unstable angina
  • Musculoskeletal chest pain (costochrondritis, pectoralis tear etc.)
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47
Q

What are the symptoms of an acute coronary syndrome

A

Central, constricting chest pain that may be associated with

  • Nausea/vomiting
  • Sweating and clamminess
  • Sense of impending doom
  • SOB
  • Palpitations
  • Pain radiating to jaw or arms
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48
Q

What features of the symptoms of ACS are important in order to diagnose ACS?

A

- Duration; must persist for longer than 20mins

- Relief; not relieved by GTN and/or rest

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49
Q

What is meant by a silent MI

A

This occurs in diabetic patients where peripheral neuropathy prevents the patient from experiencing the classical chest pain associated with an acute coronary syndrome

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50
Q

What ischaemic ECG changes are important to look out for in NSTEMI

A
  • ST depression
  • T wave inversion
  • Pathological Q waves
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51
Q

When using troponin blood tests to diagnose acute coronary syndromes, what do we need to ensure

A

Multiple troponins have been carried out

  • Baseline on admission/indication
    • 6hrs after symptoms developed
    • 12hrs after symptoms developed
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52
Q

What can be said about the specificity and sensitivity of troponin blood tests

A
  • Highly sensitive - hence accurate in detecting raised levels
  • Highly non-specific - hence raised troponins does NOT confirm ACS
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53
Q

What are the non-ACS causes of myocardial ischaemia and hence raised troponin levels

A
  • Chronal renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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54
Q

What investigations should be carried out in a patient suspected to be suffering from an acute coronary syndrome

A
  • Physical exam
  • ECG
  • FBC
  • U&Es
  • LFTs
  • Lipid profiling
  • TFTs
  • HbA1C
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55
Q

What imaging should be carried out for patients suspected of suffering from an acute coronary syndrome

A
  • CXR; to assess for non-cardiac causes
  • Echocardiogram; after the event to assess functional damage
  • CT coronary angiogram; to assess for coronary artery disease
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56
Q

What are the two key treatment options in patients presenting with STEMI and under what conditions should these be used?

A
  • Primary Percutaneous Coronary Intervetnion (PCI) - if available within two hours of presentation
  • Thrombolysis - if PCI not available within two hours of presentation
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57
Q

Outline the steps of PCI used in the treatment of STEMI

A
  • Catheter inserted into femoral/brachial artery
  • Guided up to coronary arteries under X-ray
  • Contrast injected to identify occlusion
  • Balloon inflated to widen the vessel and/or clot aspirated
  • Stent inserted to maintain open vessel
  • Drugs may be eluted to prevent restenosis
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58
Q

Outline the treament options for thrombolysis in patients presenting with a STEMI where PCI is not available within 2hrs

A
  • Streptokinase
  • Alteplase
  • Tenecteplase
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59
Q

What is the acute treatments used for patients presenting with an NSTEMI

A

“(O)BATMAN

  • _B_eta blocker (atenolol or bisoprolol) unless contraindicated (asthma, CCF, pregnancy)
  • Aspirin 300mg stat dose
  • Ticagrelor 180mg (or clopidogrel 300mg)
  • Morphine (titrated up to control pain)
  • Anticoagulant; LMWH such as enoxaparin 1mg/kg twice daily for 2-8 days (or tinzaparin/dalteparin)
  • Nitrates (GTN); to relieve CA spasm

NB: Consider O2 therapy if SpO2< 95%
“

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60
Q

What tool can be used to assess the need for PCI in NSTEMI

A

GRACE Score - gives a 6 month risk of death or repeat MI after having and NSTEMI

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61
Q

How can the GRACE score be used to guide PCI options in patients with NSTEMI

A

GRACE Score;

  • <5% - Low Risk - no need for PCI
  • 5-10% - Medium Risk - consider PCI
  • >10% - High Risk - proceed with PCI within four days
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62
Q

What are the potential complications of MI?

A

“DREAD;

  • Death
  • Rupture of heart septum/papillary muscle
  • Edema secondary to heart failure
  • Arrhythmia and aneurism
  • Dressler’s syndrome
    “
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63
Q

What is Dressler’s syndrome?

A
  • Also known as post-MI syndrome
  • Occurs 2-3 weeks after MI
  • Localised immune response
  • Causes pericarditis
  • Pleuritic chest pain, pericardial rub
  • Can cause pericardial effusion and pericardial tamponade
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64
Q

How can Dressler’s syndrome be diagnosed

A
  • ECG changes; global ST elevation, T wave inversion
  • Echocardiogram; reduced ejection fraction from effusion/tamponade
  • Raised inflammatory markers; CRP and ESR
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65
Q

How can Dressler’s syndrome be managed

A
  • NSAIDs; aspirin or ibuprofen
  • Steroids; prednisolone (more severe cases)
  • Pericardiocentesis
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66
Q

Outline the medical management used in the secondary prevention of MI

A

“The Six A’s (not to be confused with the four A’s for CVD)

  • _A_spirin 75mg; once daily
  • Antiplatelet; clopidogrel/ticagrelor for up to 12 months
  • Atenolol (or bisoprolol); dose titrated as high as tolerated
  • Atorvostatin 80mg; once daily
  • ACE Inhibitor (ramipril); titrated upto 10mg once daily
  • Aldosterone Antagonist (eplerenone); used in patients in heart failure secondary to the MI, titrated up to 50mg once daily
    “
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67
Q

Outline the lifestyle management used in the secondary prevention of MI

A
  • Smoking cessation
  • Reduced EtOH consumption
  • Mediterranean diet
  • Cardiac rehabilitation; specific cardiac exercise regimes
  • Optimisation of other medical conditions; DM and HTN
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68
Q

What are the different classifications of MI

A

Type 1 - traditional MI due to an acute coronary event

Type 2 - ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

Type 3 - sudden cardiac death or cardiac arrest suggestive of an ischaemic event

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

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69
Q

What is meant by acute left ventricular failure (LVF)?

A

Acute LVF occurs when the left ventricular is unable to adequately move blood through the left side of the heart causing a backlog

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70
Q

What is the result of acute LVF

A

Backlog of blood into the left atrium, pulmonary veins and lungs leading to subsequent pulmonary oedema

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71
Q

What happens as a result of pulmonary oedema

A
  • Impaired gas exchange
  • Decreased SpO2
  • SOB
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72
Q

Outline some of the causes of acute left ventricular failure?

A

”

  • *AIMS;**
  • _I_atrogenic; due to fluid overload from IVF administration in elderly patients
  • Sepsis
  • MI
  • Arrhythmias
    “
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73
Q

What is the typical presentation of acute LVF?

A
  • Rapid onset breathlessness
  • Type 1 respiratory failure (PaO2 < 8kPa with normal or low PaCO2)
  • SOB
  • Looking and feeling unwell
  • Cough; frothy, white/pink sputum
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74
Q

What signs should be looked for when examining a patient in acute LVF?

A
  • *Primary Features;**
  • Increased respiratory rate
  • Reduced SpO2
  • Tachycardia
  • 3rd Heart Sound (S3)
  • Bibasal crackles on auscultation
  • Hypotension in severe cases (cardiogenic shock)

Secondary Features (underlying cause);

  • Chest pain –> ACS
  • Fever –> sepsis
  • Palpitations –> arrhythmia
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75
Q

What clinical signs may be seen in acute LVF that has backed up and caused right sided heart failure?

A
  • Raised JVP
  • Peripheral oedema
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76
Q

What should be considered first when reviewing a patient that has suddenly begun to desaturate

A
  • Assess fluid balance
  • Likely fluid overload
  • Renal function (CKD/AKI)
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77
Q

What investigations should be carried out in a patient expected of being in acute LVF?

A
  • History
  • Clinical exam
  • ECG; looking for arrhythmia/ischaemia as underlying cause
  • Echocardiogram
  • ABG; looking for type 1 respiratory failure or raised lactate in sepsis
  • CXR; looking for pulmonary oedema and to assess for cardiomegaly
  • Bloods; FBC, CRP, U&Es
  • Special Tests; B-type natriuretic peptide (BNP) and/or troponin if MI suspected
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78
Q

When shoudl treatment be initiated in a patient presenting with signs of acute LVF?

A

Commence treatment before diagnosis confirmed with echocardiogram or BNP (i.e. as soon as acute LVF suspected)

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79
Q

What can be said about the sensitivity and specificity of B-type natriuretic peptide (BNP) testing?

A
  • Highly sensitive; hence if not raised, acute LVF can be ruled out
  • Highly non-specific; hence if raised, acute LVF cannot be ruled out, however other causes need to be investigated
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80
Q

Other than acute LVF, what else can cause raised BNP levels?

A
  • Tachycardia
  • Sepsis
  • Pulmonary embolism
  • Renal impairment
  • COPD
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81
Q

When carrying out an echocardiogram in suspected acute LVF, which value is important for conffering the diagnosis

A

Ejection Fraction;

  • >50%; normal
  • <50%; pathological
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82
Q

When carrying out a CXR in suspected actue LVF, which parameters are important to measure?

A

“Cardiothoracic Ratio;

  • Cardiothoracic ratio = width of widest part of heart field/width of widest part of lung fields
  • Cardiomegaly is present when the cardiothoracic ratio >0.5

Upper Lobe Venous Diversion;

  • Increased prominence and diameter of the upper lobe vessels

Fluid Leakage;

  • Bilateral pleural effusions
  • Fluid in interlobar fissures
  • Fluid in septal lines (Kerley lines)
    “
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83
Q

Outline the management for acute left ventricular failure (LVF)

A

“Pour SOD

- Pour; stop IV fluids and monitor fluid balance, may need to fluid restrict

  • _S_it patient upright
  • Oxygen (if SpO2 < 95% and falling); be cautious in COPD
  • Diuretics; furosemide 40mg IV
    “
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84
Q

Outline the management of severe acute LVF causing pulmonary oedema or cardiogenic shock?

A
  • IV Opiates; morphine acts as a vasodilator
  • NIV; CPAP, potential escalation to ITU for intubation and mechanical ventilation
  • Inotropes; noradrenaline
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85
Q

What are the two subtypes of chronic heart failure?

A
  • Systolic Heart Failure; impaired ventricular contraction
  • Diastolic Heart Failure; impaired ventricular relaxation
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86
Q

What are some of the key symptoms a patient in chronic heart failure will present with?

A
  • Breathlessness; worsened on exertion
  • Cough; may be productive with frothy white/pink sputum
  • Orthopnoea; SOB that is worsened upon lying flat
  • Paroxysmal noctural dyspnoea; suddenly awaking at night with severe SOB and cough
  • Peripheral oedema
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87
Q

What causes paroxysmal noturnal dyspnoea (PND)?

A
  • Fluid settling across large area of lungs upon being supine
  • Respiratory cente in medulla less responsive during sleep (hence more severe hypoxia before awakening(
  • Less adrenaline circulation resulting in decreased cardiac output
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88
Q

How is chronic heart failure diagnosed?

A
  • Clinical presentation
  • BNP blood test; specifically N-terminal pro-B-type natriuretic peptide (NT-proBNP)
  • Echocardiogram
  • ECG
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89
Q

What are the main causes of chronic heart failure?

A
  • Ischaemic heart disease (IHD)
  • Valvular heart disease; most often aortic stenosis
  • Hypertension (HTN)
  • Arrhythmias; most often atrial fibrillation
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90
Q

Outline the immediate management steps for chronic heart failure?

A
  • Referral; to specialist (NT-proBNP >2000ng/L is urgent)
  • Discussion; with the patient as to the chronic nature of the condition
  • Medical management; ABAL
  • Surgical management; used in severe aortic stenosis or mitral regurgitation
  • Specialist nurse; consult heart failure nurse for input
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91
Q

Outline the long-term management steps for chronic heart failure?

A
  • Yearly flu and pneumococcal vaccination
  • Smoking cessation
  • Optimisation of co-morbidities
  • Exercise as tolerated
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92
Q

Outline the first-line medical treatment of chronic heart failure?

A

“ABAL;

  • ACE Inhibitor/ARB; ramipril titrated as tolerated up to 10mg OD, candesartan titrated up to 32mg OD
  • Beta Blocker (bisoprolol/atenolol); titrated as tolerated up to 10mg OD
  • Aldosterone Antagonist (spironolactone/eplerenone); added if symptoms persist or if there is reduced ejection fraction
  • Loop Diuretics (furosemide); 40mg OD
    “
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93
Q

What monitoring is required for patients in chronic heart failure who are taking diuretics, ACE inhibitors or aldosterone antagonists

A

Repeat U&Es

  • Potential for electrolyte disturbances
  • Nephrotoxic drugs
  • Avoid AKI/CKD
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94
Q

What is cor pulmonale?

A

Cor pulmonale is another name for right sided heart failure that is caused by respiratory disease

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95
Q

What happens as a result of cor pulmonale?

A
  • Pulmonary arterial hypertension
  • Right ventricular hypertrophy
  • Peripheral oedema
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96
Q

What are the most common causes of cor pulmonale?

A
  • COPD; by far the most common
  • PE
  • Interstitial lung disease
  • Cystic fibrosis
  • Primary PAH; genetics
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97
Q

How do patients with cor pulmonale often present?

A
  • Often asymptomatic
  • SOB; may be masked as a symptom of the underlying respiratory disease superimposed over the right sided heart failure
  • Periperhal oedema
  • Increased breathlessness on exertion
  • Syncope
  • Chest pain
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98
Q

What signs should be looked out for when examining a patient suspected of suffering for cor pulmonale

A
  • Hypoxia
  • Cyanosis
  • Raised JVP
  • Peripheral oedema
  • 3rd heart sound (S3)
  • Murmurs; ESM –> aortic stenosis, PSM –> mitral regurgitation
  • Hepatomegaly; due to back pressure in hepatic vein
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99
Q

How can cor pulmonale be managed?

A
  • Treating underlying caused (i.e. the respiratory disease)
  • Long-term oxygen therapy
  • Poor prognosis
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100
Q

What is the NICE definition of clinical and ambulatory hypertension?

A
  • Clinic blood pressure >140/90mmHg
  • Ambulatory blood pressure >135/85mmHg
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101
Q

What is the primary cause of hypertension

A

Primary hypertension is the most common form (95%) and is also known as essential hypertension; this has no known cause

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102
Q

Outline the secondary causes of hypertension

A

“ROPE;

  • Renal disease; renal artery stenosis
  • Obesity
  • Pregnancy induced (pre-eclampsia if alongside proteinuria)
  • Endocrine; hyperaldosteronism (Conn’s syndrome), neuroendocrine (phaechromatocytoma)
    “
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103
Q

What are the major complications of hypertension?

A
  • IHD
  • Cerebrovascular accident; stroke or haemorrhage
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Heart failure
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104
Q

Outline how the diagnosis of hypertension is reached?

A
  • Patients with clinic blood pressure >140/90mmHg offered ambulatory blood pressure monitoring (ABPM)
  • If these patients are found to have an ABPM that is >135/85mmHg then the diagnosis can be made
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105
Q

What are the stages of hypertension?

A

Stage 1;

  • CBP >140/90mmHg
  • ABPM >135/85mmHg
  • *Stage 2;**
  • CBP >160/100mmHg
  • ABPM >150/95mmHg
  • *Stage 3;**
  • CBP >180/120mmHg
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106
Q

All patients with newly diagnosed hypertension should undergo investigation for end-organ damage, what does this involve?

A
  • Urine albumin:creatinine ratio; looking for proteinuria and kidney damage
  • Urine dipstick; looking for haematuria and kidney damage
  • Ophthalmoscopy (fundus examination); looking for hypertensive retinopathy
  • ECG; looking for cardiac abnormailities
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107
Q

What dose of ramipril should a patient be on if being treated for hypertension?

A

Ramipril; 1.25mg - 10mg OD

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108
Q

What dose of bisoprolol should a patient be on if being treated for hypertension?

A

Bisoprolol; 5mg - 20mg OD

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109
Q

What dose of amlodipide should a patient be on if being treated for hypertension?

A

Amlodipine; 5mg - 10mg OD

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110
Q

What dose of indapamide should a patient be on if being treated for hypertension?

A

Indapamide; 2.5mg OD

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111
Q

What dose of candesartan should a patient be on if being treated for hypertension?

A

Candesartan; 8mg - 32mg OD

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112
Q

Outline the initial management for a patient with suspected hypertension?

A
  • Establish a diagnosis; essential or secondary
  • Investiage possible end-organ damage
  • Advise on lifestyle
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113
Q

What is the treatment targets in terms of blood pressure when treating a patient for hypertension that is below the age of 80?

A

SBP < 140mmHg

DBP < 90mmHg

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114
Q

What is the treatment targets in terms of blood pressure when treating a patient for hypertension that is above the age of 80?

A

SBP < 150mmHg

DBP < 90mmHg

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115
Q

What is atrial fibrillation?

A

Atrial fibrillation - where the contraction of the atria is uncoordinated, rapid and irregularly irregular

116
Q

What causes atrial fibrillation?

A

Atrial fibrillation arises due to disorganised electrical activity that overrides the normal, organised activity of the sinoatrial node

117
Q

What changes may be seen on the ECG of a patient with atrial fibrillation?

A

Absent P Waves

118
Q

What is the effect of atrial fibrillation on the contraction of the ventricles?

A

AF leads to irregular conduction of electrical impulses to the ventricles, causing irregularly irregular ventricular contractions

119
Q

What conditions can occr as a result of atrial fibrillation?

A
  • Tachycardia
  • Heart failure; due to poor filling of the ventricles during diastole
  • Risk of stroke; due to thrombosis
120
Q

Why can atrial fibrillation result in ischaemic stroke?

A

Atrial fibrillation increases the tendency for blood to collect in the atria and form blood clots. These may embolise to the cerebral arteries and cause an ischaemic stroke

121
Q

How to patients with atrial fibrillation often present?

A
  • Palpitations
  • SOB
  • Syncope; either dizziness or fainting
  • Symptoms of associated; stroke, sepsis or thyrotoxicosis
122
Q

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

A
  • Atrial fibrillation
  • Ventricular ectopics
123
Q

How can atrial fibrillation and ventricular ectopics be distinguished on ECG?

A
  • Ventricular ectopics disappear when the heart rate increases above a certain threshold; hence measurement after exercise may be useful
  • Ventricular beats will also have widended QRS complex (>120ms)
124
Q

Outline the ECG features of atrial fibrillation?

A
  • Absent P waves
  • Narrow QRS Complex Tachycardia
  • Irregularly irregular ventricular rhythm
125
Q

What is meant by valvular atrial fibrillation, how does this differ from non-valvular AF?

A
  • Valvular atrial fibrillation is defined as patients with AF who also have moderate or servere mitral stenosis and/or mechanical heart valves
  • It is thought that valvular pathology itself leads to the atrial fibrillation
  • Non-valvular AF can be used to refer to AF in the absence of vavle pathology or with alternative valve pathology (mitral regurgitation/aortic stenosis)
126
Q

Outline the most common causes of atrial fibrillation?

A

“MRS SMITH;

  • Sepsis
  • Mitral valve pathology; either stenosis or regurgitation
  • Ischaemic heart disease
  • Tyrotoxicosis
  • Hypertension
    “
127
Q

What are the two principles used in the treatment of atrial fibrillation?

A
  • Rate OR Rhythm Control
  • Anticoagulation; to minimise risk of stroke
128
Q

What are the indications for rhythm control as first line over rate control in patients with atrial fibrillation?

A
  • Reversible cause for the AF
  • AF is of new onset; within the last 48hrs
  • AF is causing heart failure
  • Patient remains symptomatic despite effective rate control
129
Q

What is most often used as the first line treatment in patients with atrial fibrillation?

A

Rate control is most often the first line therapy apart from in a few exceptions

130
Q

What are the pharmacological options for rate control in atrial fibrillation?

A

- β-blockers (atenolol); 50-100mg OD

- Calcium Channel Blockers (diltiazem); not preferable in heart failure

- Digoxin; only used in sedentary people, requires monitoring as carries risk of toxicity

131
Q

What is the aim of rhythm control in the treatment of atrial fibrillation?

A

Return the patient to normal sinus rhythm

132
Q

What are the two options for rhythm control in the treatment of atrial fibrillation?

A
  • Single cardioversion event; pharmacological or electrical
  • Long-term medical rhythm control; pharmacological
133
Q

What are the two different types of cardioversion and when are they used?

A

“Immediate Cardioversion; used if the AF has been present <48hrs or the patient is severely haemodynamically unstable

Delayed Cardioversion; used if the AF has been present for >48hrs and the patient is stable
“

134
Q

When is delayed cardioversion given and what caveats are there to its used?

A
  • Delayed cardioversion is given following anticoagulant therapy
  • Given after three weeks anticoagulant therapy
  • In the meantime, the patient must be given rate control
135
Q

What are the two options for pharmacological cardioversion?

A

“- Flecainide (use-dependant Na+ channel blocker)

**- Amiodarone** (class III antidysrhythmic)
"
136
Q

Outline the process of electrical cardioversion in the treatment of atrial fibrillation?

A
  • Sedation of patient
  • Administration of general anaesthetic
  • Delivery of rapid electrical shock using a cardiac defibrillator
137
Q

What pharmacological options are available for the long-term medical rhythm control of atrial fibrillation?

A

- β-blockers (atenolol/bisoprolol); first-line

- Dronedarone (class III antidysrhythmic); second-line, in patients post-cardioversion

- Amiodarone (class III antidysrhythmic); used in patients with heart failure or left ventricular dysfunction

138
Q

What is paroxysmal atrial fibrillation and how is it managed?

A
  • AF that transiently comes and goes
  • Treated with pill-in-the-pocket approach
  • Flecanide is often the drug of choice
139
Q

What are the conditions required for a pill-in-the-pocket approach with paroxysmal AF?

A
  • Infrequent episodes
  • No underlying structural heart disease
140
Q

When should flecanide not be used in the treatment of paroxysmal atrial fibrillation?

A

Contraindicated in atrial flutter as it can cause 1:1 AV conduction and susequent tachycardia

141
Q

What is the aim of anticoagulant therapy in the treatment of atrial fibrillation?

A

To prevent thrombus formation

142
Q

Without anticoagulation, what is the risk of stroke per year in a patient with atrial fibrillation?

A

5%

143
Q

With anticoagulation, what is the risk of stroke per year in a patient with atrial fibrillation?

A

1-2%

144
Q

By what degree does anticoagulation reduce that chances of stroke in patients with atrial fibrillation?

A

2/3rds

145
Q

What scoring system is used to determine whether to commence anticoagulant therapy in a patient with atrial fibrillation?

A

“CHA2DS2VASc Score;

  • Congestive heart failure = 1
  • Hypertension = 1
  • Age >75 = 2
  • Diabetes = 1
  • Stroke or TIA previously = 2
  • Vascular disease = 1
  • Age 65-74 = 1
  • Sex category (female) = 1
    “
146
Q

How can the CHA2DS2VASc score be used to inform whether to commence anticoagulant therapy in atrial fibrillation?

A
  • CHA2DS2VASc Score = 0; no anticoagulation
  • CHA2DS2VASc Score = 1; consider anticoagulation
  • CHA2DS2VASc Score = >1; offer anticoagulation
147
Q

What is the risk of patients on anticoagulants for AF developing a signifcant bleed?

A

3% per year

148
Q

What scoring system can be used to assess the risk of serious bleeds in patients who are anticoagulated for the treatment of atrial fibrillation?

A

“HAS-BLED Score;

  • Hypertension = 1
  • Abnormal renal and/or liver function = 1 for each
  • Stroke previously = 1
  • Bleed previously = 1
  • Labile INRs (whilst on warfarin) = 1
  • Elderly = 1
  • Drugs or alcohol = 1 for each
    “
149
Q

How can the HAS-BLED Score be used to assess the risk of serious bleeds in patients who are anticoagulated for the treatment of atrial fibrillation?

A

HAS-BLED Score < 3; low risk

HAS-BLED Score 3 - 6; high risk

HAS-BLED Score > 6; very high risk

150
Q

What is meant by the INR, how does this relate to the coagulation properties of a patients’ blood sample?

A
  • INR = international normalised ratio
  • Comparison of the prothrombin time (PT) between test patient and a normal healthy adult
  • Prothrombin time indicates the time taken for the patients’ blood to clot
  • An INR of 2 indicates that the patient has a prothrombin time twice that of a healthy adult
151
Q

What is the target INR for patients treated with warfarin for atrial fibrillation?

A

An INR of between 2 - 3 is ideal for the treatment of atrial fibrillation

152
Q

Which anticoagulants are now being used in the treatment of atrial fibrillation to prevent stroke?

A

DOACs;

  • Rivaroxaban; half-life of 7-15hrs
  • Apixaban; half-life of 12hrs
  • Endoxaban; half-life of 7-15hrs
  • Dabigatran; direct thrombin inhibitor
153
Q

What are the benefits of using DOACs in the prevention of stroke in patients with AF?

A
  • Shorter half-lives compared to warfarin; hence only needed to be taken once daily
  • No monitoring required
  • No major drug or food interactions
  • Equal or slightly better than warfarin in preventing stroke in AF
  • Equal or slightly less risk of bleeding that warfarin
154
Q

What is the cause of the first heart sound (S1)

A

Closure of the atrioventricular valves (mitral and triscuspid) at the start of ventricular systole

155
Q

What is the cause of the second heart sound (S1)

A

Closure of the semilunar valves (aortic and pulmonary) at the end of ventricular systole just prior to ventricular relaxation (diastole)

156
Q

What is the root cause of a third heart sound (S3)

A
  • Rapid ventricular filling
  • Sound itself is generated by ‘plucking’ of the chordae tendinae
157
Q

When can an S3 heart sound be heard, what is it indicative of?

A
  • Heard 0.1s after S2
  • Normal in young healthy patients <40y/o
  • Pathological in elderly patients; heart failure
158
Q

When can a fourth heart sound (S4) be heard and what does it indicate?

A
  • S4 is heard immediately before S1
  • Always patholgoical
  • Indicates a stiff/hypertrophic ventricle
  • Sound itself results from turbulent flow between atria and non-compliant ventricle
159
Q

What manoeuvre can be used to enhance the auscultation of a pansystolic mumur?

A
  • PSM = Mitral regurgitation
  • Roll patient onto left hand side
160
Q

What manoeuvre can be used to enhance the auscultation of aortic regurgitation?

A
  • Sit patient up and lean them forward forward
  • Inhale, deeply exhale and hold
161
Q

What aspects of a murmur should be assessed

A

“SCRIPT;

  • Site; location
  • Character; soft, blowing, crescendo, decrescendo
  • Radiation; carotids (aortic stenosis), left axilla (mitral regurgitation)
  • Pitch; high, low, indicates velocity
  • Timing; systiolic or diastolic
    “
162
Q

How can murmurs be classified depending on grade?

A
  • Grade 1; difficult to hear
  • Grade 2; quiet
  • Grade 3; loud
  • Grade 4; loud with palpable thrill
  • Grade 5; as above + with stethoscope just off chest
  • Grade 6; as above + with stethoscope away from chest
163
Q

What kind of valve defect causes hypertrophy?

A
  • Stenosis
164
Q

What kind of valve defect causes dilatation?

A
  • Regurgitation
165
Q

What kind of valve defect causes left atrial hypertrophy?

A
  • Mitral stenosis
166
Q

What kind of valve defect causes left ventricular hypertrophy?

A
  • Aortic stenosis
167
Q

What kind of valve defect causes left atrial dilatation?

A
  • Mitral regurgitation
168
Q

What kind of valve defect causes left ventricular dilatation?

A
  • Aortic regurgitation
169
Q

What are the causes of mitral stenosis?

A
  • Rheumatic heart disease
  • Infective endocarditis
170
Q

What symptoms/signs is mitral stenosis associated with?

A
  • Malar flush; due to back-pressure of blood into pulmonary system, resulting in CO2 retention and subsequent vasodilatation
  • Atrial fibrillation; caused by the left atrium struggling to push blood through the stenotic valve
171
Q

What condition can mitral regurgitation lead to?

A

Congestive cardiac failure (CCF); due to reduced ejection fraction as a result of backlog of blood

172
Q

What are the causes of mitral regurgitation?

A
  • Idiopathic weakening; increases with age
  • Ischaemic heart disease
  • Infective endocarditis
  • Rheumatic heart disease
  • Connective tissue disorders; Ehlers Danlos Syndrome (EDS) or Marfan Syndrome
173
Q

What is the nature of the murmur heard in mitral regurgitation?

A
  • Pan-systolic murmur
  • High pitched
  • Radiates to the left axilla
  • Heard alongside S3
174
Q

What is the nature of the murmur heard in aortic stenosis?

A
  • Ejection systolic murmur
  • Crescendo-decrescendo
  • Radiates to the carotid arterties
175
Q

Other than an ejection systolic murmur, what other signs may be seen in a patieint with aortic stenosis?

A
  • Slow rising pulse
  • Narrow pulse pressure
  • Exertional syncope
176
Q

What are the causes of aortic stenosis?

A
  • Idiopathic age-related calcification
  • Rheumatic heart disease
  • Bicuspid aortic valve
177
Q

What is the nature of the heart murmur caused by aortic regurgitation?

A
  • Early diastolic murmur
  • Soft in character
178
Q

What is meant by Corrigan’s pulse sign?

A

Collapsing pulse, rapidly appearing and disappearing

179
Q

What condition can arise as a result of aortic regurgitation?

A

Heart failure

180
Q

What is meant by an Austin-Flint murmur?

A

Austin-Flint Murmur; early diastolic murmur heard at the apex of the heart that resembles a rumble that is caused by the backflow of blood through the aortic valve and over the leaflets of the mitral valve causing a vibration

181
Q

What are the causes of aortic regurgitation?

A
  • Idiopathic age-related weakness
  • Connective tissue disease; Ehlers Danlos Syndrome or Marfan Syndrome
182
Q

What kind of heart murmur can be heard here?

[sound:1.0.m4a]

A

Aortic Regurtation

183
Q

What kind of heart murmur can be heard here?

[sound:2.0.m4a]

A

Aortic Stenosis

184
Q

What kind of heart murmur can be heard here?

[sound:3.0.m4a]

A

Mitral Regurgitation

185
Q

What kind of heart murmur can be heard here?

[sound:4.0.m4a]

A

Mitral Stenosis

186
Q

Which kinds of scars may be seen in patients that have undergone valve replacement procedures?

A

Midline sternotomy; most often, could also indicate previous CABG

Right-sided mini-thoracotomy; minimally invasive mitral valve replacements

187
Q

What are the two types of prosthetic valves?

A

Bioprosthetic valves; porcine valves

Mechanical valves; Starr-Edwards, Tilting-disc or St Jude

188
Q

How do the lifespan of bioprosthetic and mechanical valves differ?

A
  • Bioprosthetic valves; last up to 10 years
  • Mechanical valves; last over 20 years
189
Q

What is the caveat to using mechanical valves?

A
  • Patients require lifelong anticoagulation with warfarin
  • Target INR; 2.5 - 3.5
190
Q

What is the target INR for a patient with a prosthetic mechanical valve who is anticoagulated with warfarin?

A

Target INR; 2.5 - 3.5

191
Q

What are the major complications associated with mechanical valves?

A
  • Thrombus; formation, blood stagnates and clots
  • Infective endocarditis; infection in prosthesis
  • Haemolysis; blood gets churned up in the valve causing anaemia
192
Q

Which heart sound is replaced by a mechanical click as a result of a prosthetic mitral valve?

A

S1

193
Q

Which heart sound is replaced by a mechanical click as a result of a prosthetic aortic valve?

A

S2

194
Q

When can a transcatheter aortic valve implantation be used?

A
  • Treatment for severe aortic stenosis
  • Patients high risk for open valve replacement
195
Q

Outline the steps involved in transcatheter aortic valve replacement (TAVI)?

A
  • Local or general anaesthetic
  • Catheter inserted into femoral artery
  • Fed wire up under X-Ray guidance
  • Balloon inflated to stretch the stenosed valve
  • Biprosthetic valve implanted into the located of the aortic valve
196
Q

What kind of valve is used in a TAVI?

A

Bioprosthetic valve

197
Q

What is the first-line valve replacement procedure offered in younger and/or healthy patients?

A

Open valve replacement

198
Q

What is the long-term benefit of TAVI procedures?

A

Patients do not require life-long anticoagulation as the valve is bioprosthetic

199
Q

What percentage of patients who have undergone open valve replacement go on to develop infective endocarditis?

A

2.5%

200
Q

What percentage of patients who have undergone TAVI valve replacement go on to develop infective endocarditis?

A

1.5%

201
Q

What is the mortality in patients who have developed infective endocarditis secondary to valve replacement?

A

15%

202
Q

What are the most common organisms responsible for infective endocarditis in patients who have undergone valve replacement?

A

“Gram Positive Cocci;

  • Staphylococcus
  • Streptococcus
  • Enterococcus
    “
203
Q

Where are pacemakers most commonly implanted?

A
  • Left anterior chest wall
  • Left axilla
204
Q

How long do the batteries in modern pacemakers last for?

A

Around 5 years

205
Q

What electrical interventions are contraindicated in patients that have had pacemakers fitted?

A
  • TENS machines
  • Diathermy in sugery
206
Q

What are the main indications for the insertion of a pacemaker?

A
  • Symptomatic bradycardias
  • Mobitz type 2 (AV) heart block
  • 3rd degree heart block
  • Severe heart failure; for biventricular pacemakers
  • Hypertrophic obstructive cardiomyopathy; implantable cardioverter defibrillator (ICD)
207
Q

What are the different types of pacemaker?

A
  • Single chamber pacemakers
  • Dual chamber pacemakers
  • Biventricular (triple-chamber) pacemakers
208
Q

Where in the heart can a single-chamber pacemaker be fitted?

A

Right atrium or right ventricle

209
Q

When are single chamber pacemakers placed in the right atrium?

A

If AV conduction is normal and there is a problem with the SAN

210
Q

When are single chamber pacemakers placed in the right ventricle?

A

Where there is a problem with AV conduction, and the ventricles need to be stimulated directly

211
Q

Where are the leads in dual chamber pacemakers implanted?

A

Right atrium and right ventricle

212
Q

Where are the leads in a biventricular (triple-chamber) pacemakers implanted?

A

Right atrium, right ventricle and left ventricle

213
Q

When are biventricular (triple chamber) pacemakers used?

A
  • In patients with heart failure
  • Used to synchronise the contractions to maximise heart function
214
Q

What is the other term for biventricular (triple-chamber) pacemakers?

A

Cardiac resynchronisation therapy (CRT) pacemakers

215
Q

Other than pacing-related pacemakers, what other type of pacemaker is there?

A

Implantable cardioverter defibrillator (ICD)

216
Q

What is an implantable cardioverter defibrillator?

A

Implantable pacemakers that continually monitor the heart and apply a defibrillator shock to cardiovert the patient back to sinus rhythm if they identify a shockable arrhythmia

217
Q

What ECG changes will be seen if a patient has been fitted with a single chamber pacemaker?

A
  • In right atrium; vertical line either before the P wave
  • In right ventricle; vertical line before the QRS complex
218
Q

What ECG changes will be seen if a patient has been fitted with a dual chamber pacemaker?

A

A vertical line before both the P wave and the QRS complex

219
Q

What are the four cardiac arrest rhythms?

A
  • Ventricular tachycardia (VT)
  • Ventricular fibrillation (VF)
  • Pulseless electrical activity (PEA)
  • Asystole
220
Q

What are the two shockable cardiac arrest rhythms?

A
  • Ventricular fibrillation (VF)
  • Ventricular tachycardia (VT)
221
Q

What are the two non-shockable cardiac arrest rhythms?

A
  • Pulseless electrical activity (PEA); all electrical activity except VT/VF where there is not a pulse
  • Asystole; no significant electrical activity
222
Q

Pulseless electrical activity (PEA) can include normal sinus rhythm, T or F?

A

T - patients can be in a normal sinus rhythm without any palpable pulse, this is still a non-shockable rhythm

223
Q

How is tachycardia treated in unstable patients?

A
  • Consider up to 3 synchronised shocks
  • Consider amiodarone infusion
224
Q

What are the three types of narrow complex tachycardia?

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardia (SVT)
225
Q

What are the three types of broad complex tachycardia?

A
  • Ventricular tachycardia
  • Supraventricular tachycardia (SVT) with bundle branch block
  • Irregular AF variant
226
Q

What is meant by a narrow complex tachycardia?

A
  • Tachycardia with narrow QRS complex
  • Indicates non-ventricular rhythm
  • QRS < 120ms (3x small squares)
227
Q

What is meant by broad complex tachycardia?

A
  • Tachycardia with widened QRS complex
  • Indicates a ventricular rhythm
  • QRS > 120ms (3x small squares)
228
Q

Outline the treatment of atrial fibrillation in a stable patient?

A

Rate control with β-blocker (atenolol) or calcium channel blocker (diltiazem)

229
Q

Outline the treatment for atrial flutter in a stable patient?

A

Rate control with β-blocker (atenolol/bisoprolol)

230
Q

Outline the treatment for supraventricular tachycardia in a stable patient?

A
  • Vagal manoeuvres; carotid massage
  • Adenosine bolus
231
Q

Outline the treatment for ventricular tachycardia in a stable patient?

A

Amiodarone infusion

232
Q

Outline the treatment for unclear broad complex tachycardias in a stable patient?

A

Amiodarone infusion

233
Q

Outline the treatment for SVT with bundle branch block in a stable patient?

A
  • Vagal manoeuvres; carotid massage
  • Adenosine bolus
234
Q

What sort of rhythm causes atrial flutter?

A
  • Atrial flutter is caused by re-entrant electrical activity in the atria
  • Creates a self-perpetuating loop of electrical activity
  • Due to an extra electrical pathway
235
Q

What are the ECG features that are consistent with atrial flutter?

A
  • Atrial contraction at 300bpm; indicated by P waves spaces by one large box (0.2s)
  • Ventricular contraction at 150bpm; QRS complexes separated by two large boxes (0.4s)
  • Saw-tooth appearance; due to sucessive P waves
236
Q

What do the atria and ventricles fire at different rates in atrial flutter?

A
  • Re-entrant electrical activity leads to self-perpetuating loop in the atria (300bpm)
  • Signal makes it through to the ventricles every second lap
  • Due to the long refractory period of the AV node (150bpm)
237
Q

What conditions are associated with atrial flutter?

A
  • Hypertension
  • Ischaemic heart disease
  • Cardiomyopathy
  • Thyrotoxicosis
238
Q

Outline the treatment options in atrial flutter?

A

Similar to that of atrial fibrillation;

  • Rate/rhythm control; β-blockers or cardioversion
  • Treat underlying condition; HTN, IHD, cardiomyopathy
  • Radiofrequency ablation; long-term prevention
  • Anticoagulation; based on the CHA2DS2VASc core
239
Q

What physical intervention/procedure can be used to ablate the abnormal rhythm in atrial fibrillation?

A

Radiofrequency ablation

240
Q

What electrical activity causes a supraventricular tachycardia (SVT)?

A
  • This occurs when electrical activity re-enters the atria from the ventricles
  • This electrical activity then passes back through the AVN into the ventricles
241
Q

What kind of arrhythmia is caused by supraventricular tachycardia (SVT)?

A

Narrow complex tachycardia

242
Q

How does SVT look on an ECG?

A
  • Self-perpetuating loop
  • QRS –> T –> QRS –> T….
  • Narrow QRS (<0.12s)
  • No P waves
243
Q

What is meant by paroxysmal SVT?

A
  • Transient periods of SVT
  • SVT reoccurs and remits in the same patient
244
Q

What are the three types of SVT?

A
  • Atrioventricular nodal re-entrant tachycardia; re-entry occurs through the AV node directly
  • Atrioventricular re-entrany tachycardia; re-entry occurs through an accessory pathway
  • Atrial tachycardia; signal originates in the atria elsewhere from the SAN, not re-entry but abnormal electrical activity (atrial rate >100bpm)
245
Q

What condition causes an atrioventricular re-entrant tachycardia?

A

- Wolff-Parkinson-White syndrome

  • Accessory pathway between the ventricles and the atria (Bundle of Kent)
  • Electrical acitivity conducted back from the ventricles to the atria
246
Q

Outline the acute management of SVT in a stable patient?

A

- Valsalva manoeuvre

- Carotid sinus massage

- Adenosine or verapamil

- Direct current cardioversion

247
Q

What is the mechanism of action of adenosine in patients with SVT?

A
  • Slows cardiac conduction through the AVN
  • Interrupts AVN directly or the accessory pathway
248
Q

How is adenosine given in patients with SVT?

A
  • Rapid bolus
  • Ensure reaches the heart with enough impact to interrupt the pathway
  • Will often cause brief period of asystole or bradycardia (counsel the patient on this)
249
Q

What considerations need to be taken into account when deciding whether to give adenosine in the treatment of SVT?

A

- Contraindications; asthma, COPD, heart failure, heart block, severe hypotension

- Counsel the patient; regarding the scary period of bradycardia or asystole

  • Fast IV bolus into large proximal cannula; grey cannula in ACF
250
Q

What dose of adenosine can be given to treat SVT?

A
  • Initially 6mg rapid bolus into large cannula in ACF
  • If not sucessful in restoring sinus rhythm repeat with 12mg rapid bolus

- If not sucessful in restoring sinus rhythm repeat again with another 12mg rapid bolus

  • If unsuccessful consider alternate
251
Q

Outline the long-term management for patients with paroxysmal SVT?

A
  • Medication; β-blockers, CCBs or amiodarone
  • Radiofrequency abblation
252
Q

What ECG changes can be seen in a patient with Wolff-Parkinson-White syndrome?

A

”- Shortened PR interval; PR < 0.12s (3 small boxes)

- Wide QRS complex; QRS > 0.12s (3 small boxes)

- Delta waves; slurred upstroke of Q wave

”

253
Q

When are antiarrhythmic medications such as β-blockers, CCBs and adenosine, contraindicated in Wolff-Parkinson-White syndrome?

A
  • If the patient has also developed atrial flutter or atrial fibrillation on the background of Wolff-Parkinson-White
  • Risk of choatic electrical activity through the accessory pathway
  • May result in polymorphic wide-complex tachycardia
254
Q

Outline the steps involved in the radiofrequency ablation of arrhythmias

A
  • Catheter ablation performed in a cath lab
  • Local or general anaesthetic
  • Catheter inserted into the femoral veins
  • Guided through venous system under X-ray
  • Electrical signals tested in different parts to identify location of accessory pathway
  • Radiofrequence ablation (heat) applied to the area
  • Scar tissue forms which can no longer conduct the electrical activity
255
Q

Which arrhythmias can radiofrequency ablation (RFA) be used to cure?

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardias
  • Wolff-Parkison-White Syndrome
256
Q

What is Torsades de pointes

A
  • A type of polymorphic ventricular tachycardia
  • Twisting tips
  • Looks like normal VT
  • QRS is twisting around the baseline
257
Q

What ECG changes are seen in patients with Torsades de pointes?

A

”- Ventricular tachycardia

  • QRS twisting around baseline
  • QRS complex height gradually decreases and then increases again
  • Prolonged QT interval

”

258
Q

What causes the prolonged QT interval in torsades de pointes?

A

Prolonged repolarisation after a contraction

259
Q

Outline what happens in Torsades de pointes?

A
  • Prolonged repolarisation
  • Afterderpolarisations; random spontaneous depolarisations prior to proper repolarisation
  • Ventricular contraction before proper repolarisation
  • Recurrent ventricular contractions
260
Q

What can Torsades de pointed lead to?

A
  • Usually self-limiting
  • However, can progress to VT
  • Cardiac arrest
261
Q

What are the causes of a prolonged QT interval?

A

- LongQT syndrome; inherited mutations in cardiac ion channels

- Medications; antipsychotics, citalopram, flecanide, sotalol, amiodarone, macrolide antibiotics

- Eletrolyte disturbances; hypokalaemia, hypocalcaemia, hypomagnesaemia

262
Q

Outline the acute management options of Torsades de pointes?

A

- Correct the underlying cause; electrolyte disturbances or medications

- Magnesium infusion; even if serum magnesium is normal

- Defibrillation; if it progresses to VT

263
Q

Outline the long-term management options in Torsades de pointes?

A
  • Avoid QT-prolonging medications
  • Correct electrolyte disturbances
  • β-blockers; however NOT sotalol
  • Pacemaker or ICD
264
Q

What are ventricular ectopic beats?

A

Premature ventricular beats caused by electrical activity generated from outside the atria

265
Q

How can patients with ventricular ectopic beats often present?

A

Brief palpitations

266
Q

What conditions predispose a patient to ventricular ectopics?

A
  • IHD
  • Heart disease
  • Heart failure
267
Q

How can ventricular ectopics be diagnosed on ECG?

A
  • Individual, random QRS complexes
  • Background normal sinus rhythm
  • Broadened QRS complex (>0.12s)
268
Q

What is bigeminy?

A

Type of ventricular ectopic beat where these ventricular ectopics occur after every sinus beat

269
Q

Outline the management options for patients with ventricular ectopics?

A

- Bloods; anaemia, electrolyte disturbances, thyroid function

- Reassurance; no treatment in otherwide healthy patients

- Expert help; in patients with a background of heart disease or concering clinical findings

270
Q

What is meant by first degree heart block?

A

PR Interval > 0.2s (5 small squares, 1 big square)

271
Q

What are the three types of second degree heart block?

A

- Mobitz Type 1; increasing PR interval, cycle of skipped QRS

- Mobitz Type 2; constant PR interval, no pattern of skipped QRS

- Fixed Ratio Blocks (2:1, 3:1 etc.); contant PR interval, clear pattern of skipped QRS

272
Q

What is meant by second degree heart block?

A

Where not all of the electrical impulses generated in the SAN make it through the AV node into the ventricles

273
Q

What is meant by Wenckebach’s phenomenon?

A
  • This is Mobitz Type 1 second degree heart block
  • Gradually increasing PR interval until one P wave fails to elicit a QRS complex
  • After the dropped ventricular contraction (QRS) the PR interval is restored and generates a QRS again
  • This cycle repeats
274
Q

What is Mobitz Type 2 second degree heart block?

A
  • Intermittent non-conductive P waves
  • No change in PR interval
  • No pattern in skipped QRS complexes
275
Q

What is the major risk of Mobitz Type 2 second degree heart block?

A

Asystole

276
Q

What is 2:1 heart block?

A
  • 2 P waves for every QRS complex
277
Q

What is 3rd degree heart block?

A
  • Complete heart block
  • No relationship between P waves and QRS complexes
278
Q

What is the major risk in 3rd degree heart block?

A

Asystole

279
Q

Outline the management options in stable patients with bradycardias and/or heart block?

A
  • Observation
  • No treatment may be sufficient
280
Q

Outline the management options in unstable patients with bradycardias and/or heart block and/or who have a risk of asystole?

A

- Atropine 500μg IV

  • If no improvement repeat upto 6 doses
  • Other inotropes; noradrenaline
  • Transcutaneous cardiac pacing; using a defibrillator
281
Q

Outline the management options in unstable patients with bradycardias/heart block and have a severe risk of asystole?

A

- Temporary transvenous cardiac paceing; electrode inserted through the venous system into the RA or RV to stimulate contraction directly

  • Permanent implantable pacemaker; when available
282
Q

Outline the management steps for NSTEM/unstable angina?

A

“DEFG;

  • DAPT; aspirin (300mg) + ticagrelor/clopidogrel
  • Enzymes; troponins (TnT)
  • Fondaparinux (Xa inhibitor)
  • GRACE Scoring; to predict mortalility and/or need for PCI
    “
283
Q

Outline all the secondary prevention strategies post-MI to prevent further cardiovascular disease?

A

“ABCD;

  • A’s; medical management with the 6 A’s
  • β-blocker; if not atenolol as part of 6 A’s
  • Cardiac rehabilitation and cessation of smoking
  • Driving, diet and alcohol
    “
284
Q

What kind of rhythm are patients who have had inferior myocardial infarctions particularly at risk of developing?

A
  • Total (3rd degree) heart block
  • As a result of ischaemia of the AVN as a result of RCA occlusion
285
Q

Outline the different types of aetiology that lead to the development of atrial fibrillation

A

Cardiac Causes;

  • HTN
  • IHD
  • Valvular disease
  • Cardiomyopathy

Non-Cardiac Causes;

  • Alcohol and drugs
  • Infection
  • Hyperthyroidism
  • Electrolyte disturbances
286
Q

How does the treatment of atrial fibrillation differ depending on when the arrhythmia developed?

A
  • AF developed definitively within the last 48hrs; consider cardioversion
  • AF likely to have been present for longer than 48hrs; anticoagulate for minimum of 3 weeks (to alleviate blood pooling) and/or perform a trans-oesophageal echo (TOE) prior to cardioversion
287
Q

What are the indications for valve replacement in severe aortic stenosis?

A

”- Syncope

  • Chest pain
  • Dyspnoea
  • LVEF >50%

”

FinalMB Part I - Medicine (12 decks)

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