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Kyla's Phase 2a Flashcards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define mitral regurgitation

A

Backflow through the mitral valve during systole

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2
Q

Causes of mitral regurgiation

A
  • Functional (LV dilitation)
  • Infective endocarditis
  • Rheumatic fever
  • Annualar calcification (elderly)
  • Mitral valve prolapse
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3
Q

Symptoms of mitral regurgitation

A
  • Dyspnoea
  • Fatigue
  • Palpitations
  • Symptoms of causative factor (e.g. fever)
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4
Q

Signs of mitral regurgitation

A
  • AF
  • Displaced hyperdynamic apex
  • Pansystolic murmur at the apex radiating to the axilia
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5
Q

Tests for mitral regurgitation

A
  • ECG (AF, LVH)
  • CXR (Big LA and LV, Mitral valve calcification, Pulmonary oedema)
  • Transoesophageal echo (diagnostic)
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6
Q

Why use a transoesphogeal echocardiogram with mitral regurgitation

A

Assess LV function and MR severity and aetiology

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7
Q

Causes of mitral stenosis

A
  • Rheumatic fever
  • Congenital
  • Prosthetic valve
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8
Q

When do symptoms and signs of mitral stenosis appear?

A

When the mitral valve orifice area is less than 2cm squared
(usually 4-6cm squared)

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9
Q

How does mitral stenosis present?

A

Pulmonary hypertension causes:
* Dyspnoea
* Haemoptysis
* Chronic bronchitis picture

Pressure from large left atrium on local structures causes:
* Hoarseness (recurrent laryngeal nerve)
* Dysphagia (oesophagus)
* Bronchial obstruction

Also:
* Fatigure
* Palpitations
* Chest pain
* Systemic emboli

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10
Q

Signs of mitral stenosis

A
  • Malar flush on cheeks (due to ↓CO)
  • AF (often due to enlarged LA)
  • Rumbling mid-diastolic murmur
  • Non-displaced apex beat
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11
Q

Tests for mitral stenosis

A
  • ECG (AF, P-mitrale, RVH)
  • CXR (LA enlargement, pulmonary oedema, mitral valave calcification)
  • Transopesophageal echocardiogram (diagnostic)
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12
Q

Causes of aortic stenosis

A
  • Senile calcification (most common)
  • Congenital (bicuspid aortic valve)
  • Rheumatic heart disease
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13
Q

Presentation of aortic stenosis

A

(Think about elderly person with chest pain, exertional dyspnoea or syncope)

Classic triad:
* Angina
* Syncope
* Heart failure

Other:
* Dyspnoea
* Dizziness
* Faints
* Systemic emboli (if IE)
* Sudden death

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14
Q

Signs of aortic stenosis

A
  • Slow rising pulse with narrow pulse pressure (feel for diminished and delayed carotid upstroke -* parvus et tardus*)
  • Non-displaced apex beat (heaving)
  • Ejection systolic murmur (radiates to carotids)
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15
Q

Tests for aortic stenosis

A
  • ECG (LVH with strain pattern, P-mitrale, LBBB or complete AV block (calcified ring))
  • CXR (LVH, calcified aortic valve, post stenotic dilitation of ascending aortic)
  • Echo (diagnostic)
  • Doppler echo (estimate gradient across valves)
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16
Q

Differential diagnosis for aortic stenosis

A
  • Hypertrophic cardiomyopathy
  • Aortic sclerosis
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17
Q

Causes of aortic regurgitation (acute and chronic)

A

Acute:
* Infective endocarditis
* Ascending aortic dissection
* Chest trauma

Chronic:
* Congenital
* Connective tissue disorders (Marfan’s, Ehlers-Danlos syndrome)
* Rheumatic fever

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18
Q

Symptoms of aortic regurgitation

A
  • Exertional dyspnoea
  • Orthopnoea
  • Palpitations
  • Angina
  • Syncope
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19
Q

Signs of aortic regurgitation

A
  • Collapsing pulse
  • Wide pulse pressure
  • Displaced hyperdynamic beat
  • High-pitched early diastolic murmur
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20
Q

Tests for aortic regurgitation

A
  • ECG (LVH)
  • CXR (Cardiomegaly, dilated descending aorta, pulmonary oedema)
  • Echo (diagnostic)
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21
Q

What are cardiac natriuretic peptides? Name them from the artia and ventricles

A

Natriuretic peptides = released from the stretching of atria or ventriculaar muscles/raised atrial or ventricular pressures → causes sodium + water excretion
* Atrial natriuretic peptide → from the atria
- B (brain) natriuretic peptide → from the ventricles

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22
Q

What are the main effects of cardiac natriuretic peptides?

A
  • increase renal excretion of sodium (natriuresis) and water (diuresis)
  • relax vascular smooth muscle (except efferent arterioles of renal glomeruli)
  • increase vascular permeability
  • inhibit release/actions of → aldosterone, ANG2, endothelin, ADH
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23
Q

What are the effects of nitrates?

A
  • Arterial + venous dilation
  • Reducing both preload (venous) and afterload (arteries)
  • Lower blood pressure
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24
Q

When are nitrates used?

A
  • IHD → angina
  • Heart failure
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25
Q

What are the classes of anti-arrhythmic drugs and give an example for each?

A
  • Sodium channel blockers → flecainide, lidocaine
  • Beta adrenceptor antagonists → propanolol (non-selective), metoprolol (Beta-1 selective)
  • Prolong the action potential → amiodarone
  • Calcium channel blockers → verapamil
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26
Q

What is digoxin used for?

A

Used in AF to reduce ventricular response rate OR severe heart failure (becuase its positively inotropic)

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27
Q

What does digoxin cause?

A
  • Bradycardia
  • Slowing AV conduction (vagal tone)
  • Increased ectopic activity
  • Increased force of contraction
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28
Q

What are the side effects of digoxin?

A
  • Nausea
  • Vomiting
  • Diarrhoea
  • Confusion
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29
Q

Which SGLT2 inhibitor (used in diabetes) has a positive effect on heart failure?

A

Dapagliflozin

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30
Q

What are 3 types of acute coronary syndrome?

A
  • Unstable angina
  • STEMI
  • NSTEMI
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31
Q

What is ACS usually caused by?

A
  • A thrombus from an atherosclerotic plaque blocking a coronary artery
  • Formed mainly of platelets → antiplatelets (aspirin, clopidogrel, ticagrelor)
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32
Q

The RCA curves around the right side + under the heart to supply which regions of the heart?

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area
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33
Q

The LCA becomes what two cornary arteries?

A
  • Circumflex artery
  • Left anterior descending (LAD)
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34
Q

The circumflex artery curves around the top, left and back of the heart and to supply which regions of the heart?

A
  • Left atrium
  • Posterior aspect of the left ventricle
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35
Q

The LAD coronary artery travels down the middle of the heart to supply which regions of the heart?

A
  • Anterior aspect of the left ventricle
  • Anterior aspect of the septum
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36
Q

What group of patients are at risk of silent MIs?

A

Diabtetics

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37
Q

How does ACS usually present?

A
  • Central, constricting chest pain
  • Pain radiating to jaws or arms
  • N + V
  • Sweating + clamminess
  • A feeling of impending doom
  • SOB
  • Palpitations

Symptoms should continue at rest for more than 15 minutes.

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38
Q

ECG changes of a STEMI (2)

A
  • ST elevation
  • New LBBB
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39
Q

ECG changes in a NSTEMI (2)

A
  • ST depression
  • T wave inversion
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40
Q

What do pathological Q waves suggest on an ECG?

A
  • Deep infarction - involving full thickness of the heart muscle (transmural)
  • Typically appear 6 or more hours after onset of symptoms
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41
Q

Name the heart areas supplied by the LCA, RCA, LAD, Cx

A
  • LCA - Anterolateral
  • LAD - anterior
  • Cx - Lateral
  • RCA - Inferior
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42
Q

What is a troponin associated with?

A

Myocardial ischaemia
(They are released from ischaemic muscle tissue)

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43
Q

Troponin results are used to diagnose which ACS?

A

NSTEMI
(STEMI just used ECG + clinical presentation)

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44
Q

Troponin is a non-specific marker, apart form ACS, when can it also rise?

A
  • Chronic kidney disease
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
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45
Q

A high troponin or rising troponin indicates what?

A

NSTEMI

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46
Q

Apart from ECG and troponin levels, what other investigations can be performed for acute coronary syndromes?

A
  • Baseline bloods, including FBC, U&E, LFT, lipids and glucose
  • Chest x-ray to investigate for pulmonary oedema and other causes of chest pain
  • Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function
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47
Q

A patient with acute constricting central chest pain requires what tests to diagnose which ACS?

A
  • ECG
  • Troponin
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48
Q

What is the diagnostic criteria for a STEMI?

A
  • ST elevation
  • New LBBB
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49
Q

What is the diagnostic criteria for an NSTEMI?

A
  • Raised troponin
  • ST depression
  • T wave inversion
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50
Q

Diagnostic criteria for unstable angina

A
  • Normal troponin
  • Normal ECG or ST depression/T wave inversion
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51
Q

If a patient presents with central constricting chest pain and their troponin and ECG return normal, what are the possible diagnoses?

A
  • Unstable angina
  • Other - Musculoskeletal chest pain
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52
Q

What is the mneumonic for the inital management for a patient presenting with ACS symptoms?

A

CPAIN
* C - Call for an ambulance
* P - Perform an12-lead ECG
* A - Aspirin (300mg)
* I - IV morphine for pain if required (with an antiemetic e.g. metoclopramide)
* N - Nitrate (GTN)

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53
Q

What is the management for a STEMI?

A
  • Within 2 hours: Percutaneous Coronary Intervention (PCI) (angiography + angioplasty)
  • After 2 hours: Thrombolysis (fibrinolytic agent - streptokinase, atleplase)
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54
Q

What is the management for a NSTEMI?

A

BATMAN
* B - Beta-blockers (if not contrindicated)
* A- Aspirin (300mg stat dose) - chewed pref.
* T - Ticagrelor (180mg stat dose) (clopidogrel if high bleeding risk)
* M - Morphine (titrated for pain)
* A - Antithrombin therapy (fondaparinux)
* N - Nitrate (GTN)

Give oxygen only if their saturation drops (less than 95% in someone wit

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55
Q

What does the GRACE score indicate?

A

Gives a 6 month probability of death after having an NSTEMI

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56
Q

A patient having an NSTEMI has a 4% on the GRACE score, what risk are they considered to have and what management is then considered?

A
  • Medium to high risk
  • Considered for early angiography with PCI (within 72 hours)
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57
Q

What is the ongoing management for ACS (after intial)?

A
  • Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function
  • Cardiac rehabilitation
  • Secondary prevention
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58
Q

What are the medications involved in the seondary prevention for ACS?

A

The 6As
* Aspirin (75mg OD)
* Another Antiplatelet (ticagrelor, clopidogrel)
* Atorvastatin
* ACEi (ramipril)
* Atenolol (or another beta blocker - usually bisoprolol)
* Aldosterone antagonist (for those with clinical heart failure (eplerenone)

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59
Q

What electrolyte imbalance can ACEis and aldosterone antagonists cause?

A

Hyperkalaemia
(closely monitor renal function)

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60
Q

What are the complications of a myocardial infarction? (mneumonic)

A

DREAD
D - Death
R - Rupture of the heart septum or papillary muscles
E - oEdema (heart failure)
A - Arrhythmia or aneurysm
D - Dressler’s syndrome

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61
Q

What is Dressler’s syndrome?

A

A post-myocardial infarction syndrome → Pericarditis

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62
Q

How does Dressler’s syndrome present?

A
  • Usually occurs 2-3 weeks after an acute myocardial infarction
  • Pleuritic chest pain
  • Low-grade fever
  • Pericardial rub on auscultation

(A pericardial rub is a rubbing, scratching sound that occurs alongside the heart sounds)

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63
Q

What is a complication of Dressler’s syndrome?

A
  • Pericardial effusion
  • Pericardial tamponade (rarely) (pericardial fluid constricts the heart + inhibits its function)
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64
Q

Diagnostic criteria for Dressler’s syndrome

A
  • ECG (global ST elevation + T wave inversion)
  • Echocardiogram (pericardial effusion)
  • Raised inflammatory markers (CRP + ESR)
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65
Q

Management of Dressler’s syndrome

A
  • NSAIDs: aspirin, ibuprofen
  • Severe cases: Prednisolone
  • Pericardiocentesis: Remove fluid from heart - if there is a significant pericardial effusion
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66
Q

What is a STEMI?

A
  • Develop a complete occlusion of a MAJOR coronary artery
    previously affected by atherosclerosis
  • This causes full thickness damage of heart muscle (transmural)
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67
Q

What is an NSTEMI?

A
  • Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis
  • This causes** partial thickness damage of heart muscle**
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68
Q

Very brief pathology of an MI

A

Plaque rupture 🡪 development of thrombosis 🡪 total occlusion of coronary artery 🡪 myocardial cell death

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69
Q

Describe the pain associated with ACS

A
  • Longer than 20 mins
  • Not relieved by GTN spray
  • Pain may radiate to left arm, neck and/or jaw
  • Occurs at rest
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70
Q

Differential diagnosis for chest pain

A
  • Cardiac – ACS, Aortic dissection, pericarditis, myocarditis
  • Respiratory – PE, pneumonia, pleurisy, lung cancer
  • MSK – rib fracture, chest trauma, costochondritis (inflammation of the cartilage between the ribs and sternum)
  • GORD
  • Oesophageal spasm
  • Anxiety/panic attacks
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71
Q

What is unstable angina also called and why?

A

Crescendo Angina
(Crescendo pattern of pain → gets worse and worse more readily)

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72
Q

What is unstable (crescendo) angina)

A

An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage

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73
Q

Signs and symptoms of ACS (separately)

A

Signs:
* Pallor
* Increased pulse + reduced BP
* Reduced 4th heart sound
* Tachy/bradycardia
* Peripherial oedema

Symptoms:
* Central, crushing chest pain (elephant sitting on it)
* Pleuritic chest pain
* N + V
* Dyspnoea
* Fatigue
* SOB
* Palpitations

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74
Q

Name two P2Y12 inhibitors (antiplatelet therapy)

A
  • Ticagrelor
  • Clopidogrel
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75
Q

Managment of unstable angina

A
  • Aspirin 300 mg (chewed or dispersed in water)
  • Sublingual glyceryl trinitrate (GTN)
  • Morphine + anti-emetic (metoclopramide)
  • Clopidogrel

Like NSTEMI (this answer is just shorter than BATMAN)

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76
Q

Name some risk factor modifications for ACS

A
  • Smoking cessation
  • Lose weight
  • Healthy diet
  • Exercise
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77
Q

Complications of unstable angina

A

Complications – DARTH VADER

  • Death
  • Arrhythmias
  • Ruptured septum
  • Tamponade
  • HF
  • Valve disease
  • Aneurysm of ventricle
  • Dressler’s syndrome – pericarditis and pericardial effusion after 2-12 weeks
  • Embolism
  • Reoccurrence of ACS
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78
Q

Define angina

A
  • Narrowing of the coronary arteries → reduced blood flow to myocardium
  • During times of high demand such as exercise there is insufficient supply of blood to meet demand.
  • This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms.
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79
Q

What is the difference between stable and unstable angina?

A
  • Stable angina = always relieved glyceryl trinitrate (GTN) or rest
  • Unstable angina = symptoms come on randomly whilst at rest (an ACS)
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80
Q

Sx of stable angina

A

1) chest pressure or squeezing lasting several minutes
2) provoked by exercise or emotional stress,
3) relieved by rest or glyceryl trinitrate

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81
Q

Ix for angina

A
  • 12-lead resting ECG (normal)
  • FBC (anaemia)
  • HbA1c + fasting glucose (diabetes)
  • U&Es (required before starting an ACE inhibitor and other medications)
  • LFTs (required before starting statins)
  • Lipid profile
  • Cardiac stress testing - patient exercise whilst on ECG (or echo, MRI)
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82
Q

What is the gold-standard for determining coronary artery disease? E.g. angina

A

CT coronary angiography (with contrast)

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83
Q

What are the three aims of medical management for stable angina? Example of each

A
  • Symptomatic treatment → GTN spray (headaches, dizziness)
  • Long-term symptomatic relief → beta blocker (bisprolol) + calcium channel blocker (verapamil)
  • Secondary prevention (of CVD) → 4 As (Aspirin 75mg, Atorvastatin, ACEi, Already on a beta blocker for symptomatic relief)
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84
Q

What are the surgical procedures offered to patients with severe stable angina and where treatements do not control symptoms?

A
  • PCI (percutaneous coronary intervention)
  • CABG (coronary artery bypass graft)
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85
Q

What is stable angina also called?

A

Angina Pectoris

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86
Q

Define preload

A

Amount of blood in the left ventricle before contraction

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87
Q

Define afterload

A

Stress on the ventricular wall during systole

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88
Q

What is heart failure with reduced ejection fraction (HFrEF)?

A
  • Systolic HF
  • Inability of the ventricle to contract normally (‘pump dysfunction’) → reduced CO
  • Ejection fraction <40%
  • Causes: Cardiomyopathy, IHD, MI
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89
Q

What is heart failure with preserved ejection fraction (HFpEF)?

A
  • Diastolic HF
  • Inability of the ventricle to relax + fill normall → causing increased filling pressures (‘filling dysfunction)
  • Ejection fraction >50%
  • Causes: Constrictive pericarditis, restrictive cardiomyopathy, obesity
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90
Q

What is the minimum diameter for an AAA?

A

3cm dilated abdominal aorta

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91
Q

Rx and causes of an AAA

A
  • ATHEROSCLEROSIS
  • Inflammation
  • Increased age
  • Hypertension
  • Existing CVD
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92
Q

Brief pathology of AAA

A
  • Degradation of tunica media + adventitia → vessel dilation
  • Most importnat risk factor = atherosclerosis
  • 99% true aneurysms
  • Most occur below renal arteries (AA lacks vasa vasorum → more susceptible to ischaemia)
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93
Q

Most AAAs are what?

A

Asymptomatic

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94
Q

What is the triad of 50% of AAAs?

A
  • Flank, back and (non-specific) back pain
  • Hypotension
  • Pulsatile abdominal mass

Most AAAs are asymptomatic

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95
Q

First line and gold-standard Ix for an AAA

A
  • First line: Aortic ultrasound, FBC, blood cultures
  • Gold standard: CT angiogram (more detailed picture)
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96
Q

Management of AAA

A
  • Surveillance
  • Surgical repair: endovascular aneurysm repair (EVAR)
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97
Q

Where do aortic dissections most commonly affect?

A

Ascending aortic and aortic arch

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98
Q

What system is used to classify aortic dissections?

A

Stanford system
* Type A: ascending aorta
* Type B: descending aorta

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99
Q

What is an aortic dissection?

A
  • Separation in the aortic wall intima
  • → causing blood flow into a new false channel composed of the inner + outer layers of the media.
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100
Q

Causes and Rx of aortic dissection

A
  • Bicuspid aortic valve (BAV)
  • Coarctation of aorta
  • Hypertension
  • Marfan syndrome
  • Ehlers-Danlos syndrome
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101
Q

What is the pain associated with an aortic dissection?

A
  • Sudden onset, severe ‘ripping’ or ‘tearing’ chest pain
  • Anterior chest pain → ascending aorta is affected
  • Back pain → descending aorta is affected.
  • The pain may change location (migrate) over time.
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102
Q

Signs and symptoms of an aortic dissection

A

Signs:
* Hypertension → hypotension
* Differences in BP between arms (more than 20 mmHg)
* Radial pulse deficit in one arm

Symptoms:
* Severe chest AND abdominal pain
* Collapse (syncope) - red flag

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103
Q

First line Ix (+ gold standard) for aortic dissection

A
  • CT angiogram (initial Ix to confirm the diagnosis)
  • ECG + CXR (exclude MI)
  • High-sensitivity troponin, FBC, CRP, blood gas
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104
Q

Differentials for aortic dissection

A
  • Acute coronary syndrome
  • Pericarditis
  • Aortic aneurysm (Aortic dissection = chest + abdominal pain)
  • Musculoskeletal pain
  • Pulmonary embolus
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105
Q

First line treatment for an aortic dissection

A
  • Beta-blockers (metoprolol IV) → BP + HR control
  • Thoracic endovaascular aortic repair (TEVAR)
  • IV morphine
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106
Q

Complications of aortic dissection

A
  • MI
  • Stroke
  • Death
107
Q

A man aged around 60 with a background of hypertension, presenting with a sudden onset tearing chest pain. Possible diagnosis and risk factors?

A
  • Aortic dissection
  • Ehlers-Danlos and Marfan’s syndrome
108
Q

What ECG change is seen in first-degree heart block?

A
  • PR interval prolongation (>0.2s)
  • Delayed conduction athrough the AV node
  • (Every P wave followed by a QRS complex)

Asymptomatic therefore no Tx

109
Q

What is second-degree heart block? And what are the two types?

A
  • Some atrial impulses = do not make it through the AV node to the ventricles
  • Some P waves are not followed by QRS complexes
  • Mobitz type 1 (Wenkebach phenomenom)
  • Mobitz type 2
110
Q

What is Mobitz type 1 and how does it present on an ECG?

A
  • Conduction through AV node takes progressively longer until it fails and resets, cycle restarts
  • Increasing PR interval until a P wave is not followed by a QRS complex
  • The PR interval then returns to normal, cycle repeats itself
111
Q

What is Mobitz type 2 and how does it present on an ECG?

A
  • Intermittent failure of conduction through the AV node - with an absence of QRS complezes following P waves
  • Usually a set ratio of P waves to QRS complexes (e.g. 3 P waves to each QRS complex (3:1 block))
  • PR interval = remains normal
  • Risk of asystole with Mobitz type 2
112
Q

What is third-degree heart block and how does it present on an ECG?

A
  • Complete heart block
  • No relationship between the P waves and the QRS complexes
  • Significant risk of asystole
113
Q

What drugs can cause first and second degree heart block?

A
  • Beta-blockers
  • Calcium channel blockers
  • Digoxin
114
Q

What are the Sx of 1st degree heart block?

A

Asymptomatic

115
Q

What are the Sx of the 2nd degree heart blocks?

A
  • Mobitz type 1: Syncope
  • Mobitz type 2: Syncope, chest pain, SOB
116
Q

Treatment for 2nd degree heart block

A

Pacemaker

117
Q

What can cause third degree heart block?

A
  • Acute MI
  • HTN
  • Structural heart disease
118
Q

Treatment of third degree heart block

A
  • IV atropine
  • Permanent pacemaker
119
Q

What are the causes of second degree heart block?

A
  • Drugs (verapamil, calcium channel blockers, digoxin)
  • Inferior MI
  • Rheumatic fever
120
Q

What is bundle branch block (BBB)?

A

Block of Bundle of His

121
Q

What are the causes of right BBB?

A
  • Underlying lung pathology (pulmonary emboli, COPD)
  • Ischaemic heart disease
  • Congential heart disease (ASD)
122
Q

In RBBB, what happens to the ventricular contraction?

A

RV contraction is later than LV

123
Q

What does RBBB look like on an ECG?

A
  • MaRRoW (V1 and V6)
  • QRS >120ms (3 small squares)
  • Wide, slurred S wave in V6 (lateral leads)
124
Q

What causes LBBB?

A
  • Ischaemic heart disease
  • Valvular heart disease
125
Q

What does LBBB look like on an ECG?

A
  • WiLLiaM
  • QRS duration > 120ms (3 small squares)
  • Prolonged R wave (>60 ms) in V5-V6 leads
126
Q

What BP is considered normotensive and what is high?

A

Hypertension:
* Above 140/90 in clinic
OR
* 135/85 with ambulatory or home readings

Normotensive:
* Less than 140/90 mmHg

127
Q

What is malignant hypertension?

A

Rapid rise in BP leading to vascular damage

128
Q

What are the symptoms of malignant hypertension?

A
  • Headache
  • Visual disturbance
129
Q

What are the causes of secondary hypertension?

A

ROPED:
* R - Renal disease e.g. renal artery stenosis (most common)
* O - Obesity
* P - Pregnancy-induced hypertension pr Pre-eclampsia
* E - Endocrine (Hyperaldosterone, Conn’s syndrome)
* D - Drugs (alcohol, steroids, NSAIDs, oestrogen)

130
Q

What BP is considered malignant hypertension? And other signs?

A
  • Systolic > 180 mmHg
  • Diastolic > 120 mmHg
  • With retinal haemorrhages or papilloedema (require FUNDOSCOPY)
131
Q

What are some complications of malignant hypertension?

A
  • Hypertensive emergencies e.g. acute kidney injury, HF and encephalopathy
  • Cardiac failure - with left ventricular hypertrophy + dilatation
  • Blurred vision - due to papilloedema with retinal haemorrhages
  • Severe headache + cerebral haemorrhage
132
Q

What is the treatment for malignant hypertension?

A

Sodium nitroprusside IV
Glyceryl trinitrate (GTN)

133
Q

What Ix can you perform to assess end-organ damage as a result of hypertension?

A
  • Fundoscopy (hypertnesive retinopathy)
  • ECG + echocardiogram (cardiac abnormalities)
  • Bloods (HbA1c, renal function (eGFR), lipids)
  • Urine albumin:creatinine ratio (for proteinuria)
  • Urinalysis (haematuria)
134
Q

Define white coat effect

A

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

135
Q

General management style for hypertension

A
  • Establish a diagnosis
  • Investigate for potential causes + end-organ damage
  • Advise on lifestyle
136
Q

When do you use angiotensin receptor blockers instead of ACEi

A
  • Patient is black, African or African-Caribbean descent
  • Patient does not tolerate ACEis (commonly due to dry cough)
137
Q

When is medical management offered for hypertension?

A
  • All patients with stage 2 hypertension
  • Patients under 80 with stage 1 hypertensopm - that also have a QRISK score pf 10% or more, renal disease, diabetes, CVD, end-organ damage
138
Q

What are some complications of hypertension?

A
  • Left ventricular hypertrophy
  • Ischaemic heart disease (angina and acute coronary syndrome)
  • Cerebrovascular accident (stroke or intracranial haemorrhage)
  • Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Vascular dementia
  • Heart failure
139
Q

What are the clinic readings and ambulatory/home readings for stage 1, 2, 3 hypertension?

A

Clinic:
* Stage1: Above 140/90
* Stage 2: Above 160/100
* Stage 3: Above 180/120

Home:
* Stage 1: Above 135/85
* Stage 2: Above 150/95

140
Q

What does the Wells Score predict?

A

Wells score = predicts the risk of a patient presenting woth symptoms having a DVT or PE

141
Q

What is the driving force in thrombosis formation in the arterial and venous circulation?

A
  • Arterial circulation → platelets (high-pressure)
  • Venous circulation → fibrin (low pressure)
142
Q

Causes of arterial thrombosis

A
  • ATHEROSCLEROSIS
    • Hypercholesterolaemia
    • Hypertension
    • Smoking
    • Plaque deposition → rupture → thrombosis
  • Inflammatory
  • Infective
  • Trauma
143
Q

How might an arterial thrombosis present?

A
  • MI
  • CVA
  • Peripheral cardiovascular diease
144
Q

Treatment of coronary arterial thrombosis

A
  • Aspirin (300mg), other antiplatelets (inhibits platelet function)
  • LMWH or Fondaparinux
  • Thrombolytic therapy → streptokinase (tissue plasminogen activator) - generates plasmin + degrades fibrin
  • Reperfusion → catheter-directed treatments + stents
145
Q

What is the treatment for a cerebral arterial thrombosis?

A
  • Aspirin, other antiplatelets
  • Thrombolysis (streptokinase)
  • Reperfusion
146
Q

Why is the use of heparin avoided in cerebral arterial thrombosis?

A
  • Risk of haemorrhage → catastrophic complications
  • Acute cerebral occlusion = treated less aggressively
147
Q

What are the components of Virchow’s triad?

A
  • Hypercoagulability (preggo, antiphospholipid syndrome, sepsis)
  • Endothelial injury (smoking, trauma)
  • Venous stasis (immobility - long flights, after surgery)
148
Q

What is the underlying pathology of arterial and venous thrombosis formation?

A
  • Arterial → atherosclerosis + rupture of plaque
  • Venous → Virchow’s triad (+ underlying coagulation disorders)
149
Q

Name an underlying condition that increases coagulability, increasing chances of a venous thrombosis

A

Antiphospolipid syndrome

150
Q

Basic treatment for arterial and venous thrombosis

A
  • Arterial → anti-platelets (aspirin)
  • Venous → anti-coagulation
    • Heparin (IV or S/C) + oral agents
    • Coagulation cascade → fibrin at the end
151
Q

Portal hypertension can increase the risk of what CVD event?

A

Thrombosis

152
Q

What are the long-term effects of damage to the venous circulation?

A

Post-thrombotic limb:
* Long-term leg swelling
* Venous circulation

153
Q

What do you monitor and what level does it need to be at when using unfractionated heparin?

A

Activated partial thrombin time (APTT)
Needs to be twice as normal

154
Q

How is unfractionated heparin given and why?

A
  • Continuous infusion
  • Very short-life (4 hours)
155
Q

Why is low molecular weight heparin used instead of unfractionated heparin?

A
  • Longer half-life (12 hours)
  • Don’t need to monitor them
  • Given subcutaneously (weight-adjusted)
  • Less risk of heparin-induced thrombocytopaenia (HIT)
156
Q

How does warfarin work and what needs to be monitored?

A
  • Warfarin = orally active
  • Prevents the synthesis of factors 2,7,9,2 (1972)
  • 36 hours half-life
  • Warfarin = anatgonist of vitamin K
  • Warfarin = prolongs the prothrombin time
  • International normalised ratio (INR) - derived from the prothrombin time
    • Usual target range: 2-3
157
Q

What does NOAC/DOAC mean?

A
  • New Oral Anticoagulant Drugs
  • Direct-acting Oral Anticoagulant Drugs
158
Q

What do DOACs act on and do they need to monitored?

A
  • Directly acting on factor 2 or 10 (II or X)
  • No blood tests/monitoring needed
159
Q

Why and which conditions are DOACs used?

A
  • DOACs = used to extend thromboprophylaxis
  • AF and DVT/PE
160
Q

Contraindications forDOACs

A
  • Pregnancy
  • Metal heart valves (use heparin instead)
161
Q

What does fondaparinux inhibit?

A

Xa inhibitor

162
Q

Name some anti-platelets

A
  • Aspirin

P2Y12 inhibitors:
* Clopidogrel
* Ticagrelor

163
Q

Rx for DVT

A
  • Surgery
  • Immobility
  • OC pill, pregnancy, HRT
  • Long haul flights
  • Inherited thrombophilia
  • THINK VIRCHOW’S TRIAD
164
Q

Sign and symptoms of a DVT

A

Symptoms:
* Leg pain
* Tenderness

Signs:
* Calf or leg swelling
* Warmth
* Discolouration
* Unilateral (almost always)
* Dilated superficial veins

165
Q

Why does DVT lead to ischaemia?

A
  • All of the small veins are thrombosed
  • Increased compartment pressures
  • Causes compression of the arterioles → causes ischaemia
166
Q

Give an example of LWMH

A

Dalteparin

167
Q

What are the Ix for a DVT?

A
  • D-Dimer level (sensitive - but not specific) - not diagnostic
  • Doppler ultrasound (with compression) = diagnostic

Other:
* CT or MR venogram - catheter venogram

168
Q

What investigation can diagnose a pulmonary embolism?

A
  • D-Dimer
  • CT pulmonary angiogram (CTPA)
169
Q

What is the first line treatment you should use immediately for a DVT or PE?

A

Apixaban

170
Q

What are the signs and symptoms of a pulmonary embolism?

A
  • Sudden onset pleuritic chest pain
  • Dyspnoea

Signs:
* Tachycardic
* Hypotensive
* Raised JVP
* Ankle oedema

171
Q

What are the Wells score for a PE and DVT?

A

PE: More than 4
DVT: More than 1

172
Q

Ix for a pulmonary embolsim

A
  • D-Dimer (raised)
  • CT pulmonary angiogram (CTPA) = diagnostic
  • ECG (sinus tachycardia)
173
Q

Management for a massive PE and not massive PE (most common)

A
  • Massive PE: Thrombolysis → alteplase
  • Not massie PE: Apixaban
174
Q

What is the immediate first line management for DVT?

A
  • Apixaban (DOAC (anticoagulant))
175
Q

What is a differential diagnosis for a DVT?

A

Cellulitis
* (Skin infection, staphylococcus aureus + streptococcus pyogenes)
* Will show LEUKOCYTOSIS

176
Q

What are the 2 shockable rhythms?

A
  • Ventricular tachycardia
  • Ventricular fibrillation
177
Q

What are the 2 non-shockable rhythms?

A
  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
178
Q

What is narrow complex tachycardia?

A
  • Fast HR (tachycardia)
  • QRS complex less than 0.12s (2 small squares)
179
Q

What is broad complex tachycardia?

A
  • Fast HR (tachycardia)
  • QRS comple = more than 0.12 seconds (3 small squares)
180
Q

Name the 4 supraventricular tachycardias

A
  • Atrial fibrillation
  • Atrial flutter
  • AVRT (Wolff-Parkinson White Syndrome)
  • AVNRT
181
Q

Name the ventricular tachycardias

A
182
Q

Name the 3 ventricular tachycardias

A
  • Ventricular ectopics
  • Prolonged QT syndrome
  • Torsades de Pointes
183
Q

How is atrial fibrillation described?

A
  • Irregularly irregular atrial firing rhythm
  • HR = 300-600 bpm → HR = 120-180 bpm
184
Q

What are the causes of atrial fibrillation? mneumonic

A

Mrs SMITH:
* S - Sepsis
* M - Mitral valve pathology (stenosis or regurgitation)
* I - Ischaemic heart disease
* T - Thyrotoxicosis
* H - Hypertension/Heart failure

185
Q

Describe the pathology of atrial fibrillation

A
  • Disorganised electrical activity in SA node → lack of coordinated atrial electrical activity = leads to irregular conduction of electrical impulses to the ventricles - results:
    • Irregularly irregular ventricular contractions
    • Tachycardia
    • HF - due to poor filling of the ventricles - during systole
    • Risk of stroke
  • Atrial action 300-600/minute
  • Only a proportion of the impulses conducted to the ventricles → due to the refractory period of AVN
  • HR 120-180 bpm
186
Q

Why is AF associated with an increased risk of stroke?

A

Tendency of blood to collect in the atria → forms blood clots → emboli → occlude cerebral arteries → ischaemic stroke

187
Q

What is the appearance of AF on an ECG?

A
  • No P waves
  • Irregularly irregular ventricular rhythm
  • Narrow QRS complex tachycardia
  • (Absence of isoelectric baseline)
188
Q

What are the types of AF?

A
  • Paroxysaml AF (episodic, resolve back to sinus rhythm)
  • Persistent (longer than 7 days)
  • Permanent (sinus rhythm unrestorable)
189
Q

Signs and symptoms of AF

A
  • Asymptomatic
  • Palpitations
  • Fatigue
  • Dyspnoea and/or chest pain
  • Heart failure
  • Other conditions: Thromboemboli (‘ischaemic stroke’), stroke, thyrotoxicosis, sepsis
190
Q

What are the two aims of AF management?

A
  • Rate or rhythm control
    • Rate control = unless contraindicated
  • Anticoagulation
    • To prevent stroke
191
Q

REALLY USEFUL CARD

What is the most common form of treatment for AF?

If stuck on exam

A
  • Beta-blocker (bisoprolol)
  • DOAC (apixaban)
192
Q

What does rate control in AF aim to do?

A
  • Get the HR below 100 bpm
  • Extending the time during dystole for the ventricles to fill with blood
193
Q

What are the contraindications for rate control in AF?

A
  • A reversible cause of AF
  • New onset AF (within 48 hours)
  • Heart failure (caused by AF)
  • Symptoms (despite being effectively rate controlled)
194
Q

What is the first line for rate control in AF (and others as alternative)

A
  • Beta-blockers (atenolol)
  • Calcium channel blockers - not in HF
  • Digoxin (only in sedentary patients)
195
Q

What is the aim of rhythm control in AF? What is it achieved through?

A
  • Return the patinet to normal sinus rhythm
  • Achieved through:
    • Cardioversion
    • Long-term rhythm control (medications)
196
Q

What are the two typoes of cardioversion used in AF? Which one is first line?

A
  • Pharmacological (first line)
    • Flecanide
    • Amiodarone (for structural heart disease)
  • Electrical
    • Sedation or general anaesthetic
    • Cardiac defibrillator (attempt to restore sinus rhythm)
197
Q

What are the 3 options for long term rhythm control in AF? Which one is first line?

A
  • Beta blocker (first line)
  • Dronedarone (scond line)
  • Amiodarone (patients with HF or left ventricular dysfunction)
198
Q

What medication is used in paroxysmal atrial fibrillation? And what is the term given?

A
  • Flecanide
  • ‘Pill-in-pocket’ approach
  • Paroxysmal AF = infrequent episodes without structural heart defects
199
Q

What is the risk of flecanide use in paroxysmal AF?

A

Converting AF into atrial flutter (with 1:1 AV conduction to the ventricles)

200
Q

Should patients with paroxysmal AF be anticoagulated?

A

Yes
Based on their CHA2DS2-VASc score

201
Q

In AF where rate and rhythm control is inadequate, what is the two next options for treatment?

A
  • Left atrial ablation (radiofrequency ablation)
  • Atrioventricular node ablation + permanent pacemaker
202
Q

What is the first and second line treatment for anticoagulation in AF?

A
  • First line: DOACs (direct-acting oral anticoagulants)
  • Second line: Warfarin (if DOACs are contraindicated)
203
Q

What are the most common indications for DOACs?

A
  • Stroke prevention in patients with AF
  • Treatment of DVT and PE
  • Prophylaxis of venous thromboembolism (DVTs and PEs) after a knee or hip replacement
204
Q

Why are some antibiotics contraindicated in warfarin use?

A

Wafarin = affected by CYP450

205
Q

Advanatages of DOACs

A
  • No monitoring required
  • No major interaction problems
  • Equal or slightly better than warfarin at preventing strokes in AF
  • Equal or slightly less risk of bleeding than warfarin
206
Q

What is the CHA2DS2VASc Score used for?

A

Assessing whether an AF patient should be started on anticoagulation
Estimating risk of stroke
(No role for aspirin in preventing stroke)

207
Q

What are the categories of CHA2DS2VASc?

A
  • Score 0 = negligible risk of stroke
  • Score 1 = 1.3%/y risk of stroke
  • Score 2 or more: >2.2% (high risk)
  • SCORE 2 or MORE = ANTICOAGULATION
208
Q

What does CHA2DS2VASc standard for?

A
  • C - Congestive heart failure (LV systolic dysfunction)
  • H - Hypertension
  • A2 - Age (75 and above)
  • D - Diabetes
  • S2 - Prior Stroke or TIA or thromboembolism
  • V - Vascular disease (peripheral artery disease, MI)
  • A - Age 65-74 years
  • Sc - Sex category (female = 1 point)
209
Q

What is ORBIT Tool or HAS-BLED used for?

A

Assess patient’s risk of major bleeding whilst on anticoagulation

210
Q

What does HAS-BLED and ORBIT scan for? What score requires regular reviews?

A

HAS-BLED Score of 3 and aboves = requires regular reviews

HAS-BLED:
* H–Hypertension
- A–Abnormal renal and liver function
- S–Stroke
- B–Bleeding
- L–Labile INRs (whilst on warfarin)
- E–Elderly
- D–Drugs or alcohol

ORBIT Tool:
O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication

211
Q

What are some complications of atrial fibrillation?

A
  • Embolic events - stroke
  • Heart failure
  • Cardiomyopathy
212
Q

Difference between AF and ventricular ectopics
(Both are irregularly irregular pulse)

A

Just do an ECG:
- Ventricular ectopics
- Disappear when the HR gets over a certain threshold
- Regular HR during exercise = suggests a diagnoses of ventricular ectopics

213
Q

Define atrial flutter

A
  • Irregular organised atrial firing (atrial rate = approx. 300 bpm)
  • Atrial flutter = ‘re-entrant rhythm’ in ether atrium
    • This is where the electrical signal re-circulates in aself-perpetuating loop - due to an extra electrical pathway.
  • Less common + less severe than AF
214
Q

What is the appearance of atrial flutter on an ECG?

A
  • F wave ‘Sawtooth appearance’
  • Narrow complex tachycardia
  • Often with a 2:1 conduction (2 paves for every QRS complex)
215
Q

Sx for atrial flutter

A
  • Palpitations
  • Chest pain
  • Syncope
  • Fatigue
216
Q

Causes of atrial flutter

A
  • Idiopathic
  • HTN
  • Percarditis
  • Obesity
217
Q

What is the treatment for atrial flutter?

A
  • Rate/rhythm control → beta-blockers or cardioversion
    • IV amiodarone (restore rhythm)
    • Beta-blocker (suppress further arrhythmias)
  • DOACs for anticoagulation (based on CHA2DS2VASc score)
  • **Radiofrequncy ablation **
218
Q

What is the other name of atrioventricular re-entry tachycardia (AVNT)?

A

Wolff-Parkinson White Syndrome
Pre-excitation syndrome

219
Q

What is AVRT (Wolff-Parkinson-White syndrome)?

A
  • Additional accessory pathy (Bundle of Kent)
  • Allows electrical activity to pass between the atria and ventricles - bypasssing the AV node
  • Excites the ventricles earlier → get delta waves
220
Q

Sx for AVRT (Wolff-Parkinson-Wgite syndrome)

A
  • Palpitations
  • Chest pain
  • Dyspnoea
  • Syncope
221
Q

What dos AVRT (Wolf-Parkinson-White) look like on an ECG?

A
  • Shortened PR interval <0.12s
  • Slurred DELTA waves
  • Wide QRS >0.12s

Early depolarisation of part of the ventricle

222
Q

First, second line and definitive management for AVRT (Wolf-Parkinson-White Syndrome)

A
  • First line: Carotid massage or valsalva manoeuvre
  • Second line: IV adenosine
  • Third: IV Verapamil or a beta blocker
  • Fourth: Synchronised DC cardioversion
  • ?Definitive management: Radiofrequency ablation of Bundle of Kent
223
Q

Biggest complication of Wolff-Parkinson-White

A

Prone to developing ventricular fibrillation

224
Q

How does adenosine work?

A
  • Slows the cardiac conduction (primarily through the AV node)
  • It interrupts the AV node or accessory pathyway during SVT and ‘resets’ it to sinus rhythm
225
Q

When is adenosine avoided?

A
  • Asthma
  • COPD
  • Heart failure
  • Heart block
  • Severe hypotension
  • Potential atrial arrhythmia with underlying pre-excitation
226
Q

What is atrioventricular nodaal re-entrant tachycardia?

A
  • Re-entry point is back through the atrioventricular node
227
Q

Supraventricular tachycardia (SVT) causes what type of tachycardia?

A

Narrow complex tachycardia

228
Q

What is the most common type of SVT?

A

AVNRT
Commonest cause of palpitations in patients with structurally normal hearts

229
Q

What are the signs and symptoms of AVNRT?

A
  • Typically paroxysmal
  • Occur spontaneously or w/ triggers: Exertion, caffeine, alcohol, beta-agonists (salbutamol)
  • Presyncope or syncope
  • Regular rapid palpitations (abrupt onset + sudden termination)
  • Neck pulsation (JV pulsations)
  • Chest pain + SOB
  • Polyuria (due to the release of ANP in response to increased atrial pressure during tachycardia)
230
Q

What are the EGG changes seen in AVNRT?

A
  • Regular tachycardia (140-280 bpm)
  • P waves not visible OR immediately before or after the QRS complex
  • Narrow QRS complexes <120 ms
231
Q

What is the treatment of AVRT and AVNRT?

A
  • Vagal maoeuvres (carotid massage or valsalva maneouvres)
  • IV adenosine
  • IV verapamil or beta-blocker
232
Q

What is the long term management for paroxysaml SVT?

A
  • beta blockers
  • Calcium channel blockers
  • Amioderone
233
Q

What is acute left ventricular failure?

A

An acute event results in the left ventricle being unable to move blood efficiency through the left side of the heart into the systemic circulation

234
Q

SV x HR = ?

A

Cardiac output

235
Q

Why does pulmonary oedema occur in left ventricular heart failure?

A
  • As the blood can’t flow efficiently through the left side of the heart → backlog of blood in the left atrium, pulmonary veins + lungs
  • The high pressure in these areas → leak fluid → pulmonary oedema
236
Q

What Sx does pulmonary oedema cause?

A
  • Interferes with gas exchange in lungs
  • SOB + reduced oxygen saturation
237
Q

Causes of left ventricular heart failure

A
  • IHD
  • Hypertension
  • Cardiomyopathy
  • Aortic stenosis
238
Q

Symptoms of left ventricular heart failure

A
  • (Acute) SOB → Exacerbated by lying flat + improves sitting up

OPEN:
* Orthopnoea (SOB when lying down)
* Paroxysmal nocturnal dyspnoea
* Extertional dyspnoea
* Nocturnal cough (pink, frothy sputum)

239
Q

What are the causes of pericarditis and give an example of each?

A
  • Viral (Coxsackie viruses)
  • Bacterial (TB)
  • Fungal (immunocompromised patient)
  • Non-infectious:
    • Autoimmune (RA)
    • Dressler’s syndrome (post-MI)
    • Neoplastic
240
Q

A patient presents with sharp pleuritic chest pain and radiates to left shoulder tip. It is relieved by sitting forwards. Possible diagnosis?

A

Pericarditis

241
Q

Signs and symptoms of pericarditis

A

Signs:
* Pericardial friction rub (scratching sound) heard by ausculation
* Raised JVP

Symptoms:
* Central chest: Pleuritic, worse on lying down and breathing in
* Dyspnoea
* Fever
* Hiccups (phenic involvement)

242
Q

What is the first line and diagnostic Ix for pericarditis? What does it show?

A

ECG:
* Concave (saddle-shaped) ST segment elevation (global ST elevation)
* PR depression

  • PeRicardiTiS
243
Q

Apart from an ECG what other tests can you perform for pericarditis?

A
  • CXR: ‘water bottle’ heart (cardiomegaly) , bacterial (pneumonia)
  • Bloods: Raised ESR (autoimmune), FBC - raised WBC (infective)
244
Q

What are differential diagnoses for pericarditis?

A
  • Angina
  • MI - rule out pleuritic pain, and pericardial rub ioon auscultation
  • Pneumonia, GI reflux, peritonitis
  • Aortic dissection
245
Q

What treatment do you give for pericarditis? Viral + idiopathic, bacterial, Autoimmune

A
  • Viral + idiopathic = NSAIDs (aspirin) + PPI + Colchicine
  • Bacterial = Antibiotics (RIPE for TB)
  • Autoimmune = Prednisolone
246
Q

What is colchicine used for?

A

In pericarditis
Inhibits migration of neutrophils to site of inflamaation
(Reduces risk of occurrence)

247
Q

What are 3 complications for pericarditis?

A
  • Pericardial effusion
  • Cardiac tamponade
  • Chronic constrictive pericarditis
248
Q

What is a pericardial effusion and a cardiac tamponade?

A
  • Pericardial effussion = collection of fluid within the pericardial sac
  • Cardiac tamponade = when a large volume compromises ventricular filling - impacting circulation
249
Q

What are the signs and symptoms of a cardiac tamponade?

A
  • Becks triad: Hypotension; Raised JVP; Muffled heart sounds
  • Pulsus paradoxus (A fall in BP of more than 10mmHg on inspiration)
  • High pulse - but low BP

Kussmaul’s sign = rise in JVP + increased neck distension during inspiration

250
Q

What is Beck’s triad and what does it indicate?

A
  • Hypotension
  • Muffled heart sounds
  • Raised JVP
251
Q

Ix for cardiac tamponade and pericardial effusion

A
  • CXR → Large globular heart
  • ECG → Low-voltage QRS complexes + sinus tachycardia
    * Echocardiogram → echo-free zone surrounding the heart
252
Q

Management for a cardiac tamponade

A
  • Pericardiocentesis
    • Drain the fluid → relieving the pressure on the heart
    • Send fluid for culture → Ziehl-Nielsen stain and cytology
253
Q

What is infective endocarditis?

A
  • Infection of the endocardium (including valves, chordae tendineae, septal defect sites, pacemaker leads, surgical patches) - typically affects valves
    • Endocardium becomes inflamed secondary to infection
  • A really bad infection, plus showers of infectious material around your bloodstream, and/or damaging the heart valves to cause heart failure.
254
Q

Rx for infective endocarditis

A
  • Male
  • Prosthetic heart valves or cardiac devices
  • Congenital HD
  • Poor dental hygeine
  • IV drug use
  • Immunosuppression
  • Rheumatic heart disease
255
Q

Which valves are most commonly affected in IE, in the general population and IVDUs?

A
  • Typical: mitral valve
  • IVDUs: Tricuspid valve
256
Q

What are the two most common bacteria to cause IE?

A
  • Staph aureus (IVDU, T2DM, surgery)
  • Srep viridans (poor dental hygeine)
257
Q

Describe Strep Viridans and what cardiac condition it causes

A
  • Infective endocarditis
  • Gram +ve
  • Alpha-haemolytic, optochin resistant strp
  • Assocaited with poor dental hygeine
258
Q

Describe the pathology of IE

A
  • Abnormal/damaged endocardium have increased platelet deposition
  • Bacteria adheres → causes vegetations
  • Typically around valves
  • Causes regurgitation → therefore aortic + mitral insufficiency → increased risk of heart failure
259
Q

What are the symptoms and signs of infective endocarditis?

A

Symptoms:
* vague; fever, non-specific

Signs: (JOS PR)
* Janeway lesions (painless spots on hands)
* Olser nodes (finger nodules)
* Splinter haemorrhages (finger nail-bed)
* Petechiae
* Roth spots (retinal haemorrhages)

Septic emboli (MI, stroke, PVD)

260
Q

What is the gold standard Ix for IE?

A

Transoesophageal echocardiogram (TOE ECHO)

261
Q

First line Ix for IE

A
  • Transthoracic echo (TTE) - 60% sensitive - but not invasive
  • Blood cultures (3 sites over 24 hours)
  • ESR/CRP (raised) + neutrophillia
  • ECG (Prolonged PR intervals)
262
Q

What is the Duke Criteria used for? What makes a diagnosis?

A

Diagnosis of infective endocarditis (IE)
Definite IE = 2 major or 1 major + 3 minor

Major criteria (pathogen grown in blood culture, TOE Echo shows vegetation)

263
Q

Treatment for IE (both bacteria)

A

IV antibiotics/antimicrobials for approx. 6 weeks

  • Staphylcoccus aureus → vancomycin + rifampicin (if MRSA)
  • Streptococcus viridans → benzylpenicillin + gentamycin

Surgery → remove valve if incompetent + replace with prosthetic

264
Q

Complications of IE

A
  • Acute heart failure
  • Systemic embolisation (including stroke)
  • Acute kidney injury
  • SEPSIS

Kyla's Phase 2a Flashcards (10 decks)

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