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Phase 2A > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is atherosclerosis?

A

The build up of plaque (made up of fats, cholesterol, cellular waste products, calcium and fibrin) in and on the artery walls which results in thickening or hardening of the arteries.

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2
Q

What are 7 major risk factors for atherosclerosis?

A
  • Age
  • Tobacco smoking
  • High serum cholesterol
  • Obesity
  • Diabetes
  • Hypertension
  • Family history
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3
Q

What is a neointima?

A

A new or thickened layer of arterial intima formed in atherosclerosis by migration and proliferation of cells from the media.

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4
Q

What are 6 inflammatory cytokines found in plaques?

A

IL-1, IL-6, IL-8, IFN-y, TGF-b, MCP-1

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5
Q

What is the structure of an atherosclerotic plaque?

A
  • Lipids (incl. cholesterol)
  • Necrotic core (dead cells)
  • Connective tissue
  • Fibrous cap
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6
Q

What are the steps of atherosclerosis?

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within the intima.
  3. Migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation and degradation of the extracellular matrix
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7
Q

What is a fatty streak?

A

The earliest lesion of atherosclerosis which consists of aggregations of lipid-laden macrophages and T-lymphocytes within the intimal layer of the vessel wall.

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8
Q

What are the constituents of intermdiate atherosclerotic lesions?

A
  • Lipid laden macrophages (foam cells)
  • Vascular smooth muscle cells
  • T lymphocytes
  • Adhesion and aggregation of platelets to vessel wall
  • Isolated pools of extracellular lipid
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9
Q

What are the characteristics of fibrous plaques or advanced lesions?

A
  • Impedes blood flow
  • Prone to rupture
  • Covered by dense fibrous cap made of extracellular matrix
    proteins including collagen (strength) and
    elastin (flexibility) laid down by smooth muscle cells that
    overly lipid core and necrotic debris
  • May be calcified
  • Contains: smooth muscle cells,
    macrophages and foam cells and T
    lymphocytes
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10
Q

What occurs when the atherotic plaque ruptures?

A

Plaques constantly grow and recede and if there is increased enzyme activity it can reach the fibrous cap and cause rupture so the basement membrane, collagen, and necrotic tissue are exposed to blood and a thrombus forms resulting in partial or complete vessel occlusion.

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11
Q

What is plaque erosion?

A

Second most prevalent cause of coronary thrombosis.
- Usually occurs in early lesions with a small lipid core and thickened fibrous cap
- Results in a ‘white thrombus’ formed of platelets and fibrinogen rather than a red thrombus of RBCs and fibrin

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12
Q

What is the difference between plaque erosion and rupture?

A

Plaque rupture is the disruption of a fibrous cap over a lipid core, erosion is the superficial disruption of a fibromuscular plaque without a core.

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13
Q

Where does atherosclerosis occur?

A

Within peripheral and coronary arteries with focal distribution along the length of the artery.

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14
Q

What is acute coronary syndrome?

A

A spectrum of acute myocardial ischaemia and/or infarction (unstable angina, STEMI, NSTEMI)

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15
Q

Define unstable angina

A

Myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis.

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16
Q

What are 5 risk factors for acute coronary syndrome?

A
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Metabolic syndrome (abdominal obesity, hypertension, impaired fasting glucose, high triglyceride levels, and low HDL cholesterol levels)
  • Renal impairment
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17
Q

What are 5 key symptoms of unstable angina?

A
  • chest pain
  • excessive sweating
  • epigastric pain
  • dyspnoea
  • syncope (fainting)
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18
Q

What is the first line investigation for acute coronary syndrome?

A

ECG

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19
Q

What is the first line treatment for ACS?

A

Aspirin 300mg

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20
Q

What is the key presentation for STEMI?

A

New or increased and persistent ST-segment elevation in at least 2 contiguous leads (leads connecting to adjoining areas of tissue)

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21
Q

What is the acute management for STEMI?

A

MONA

Morphine
Oxygen (if sats <94%)
Nitrates
Aspirin

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22
Q

What is the key presentation for NSTEMI?

A

elevated troponin levels

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23
Q

What are the possible mechanisms leading to a NSTEMI?

A
  • Plaque rupture with superimposed non-occlusive thrombus or embolic events leading to coronary vascular obstruction
  • Dynamic obstruction, such as in vasospasm
  • Progressive luminal narrowing (i.e., chronic arterial narrowing from restenosis)
  • Inflammatory mechanisms (i.e., vasculitis)
  • Extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia, or hypoxia).
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24
Q

What are myocardial infarction complications?

A

Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler syndrome (autoimmune pericarditis)
Embolism
Recurrence regurgitation

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25
Q

What is troponin?

A

A protein complex which regulates actin-myosin contraction and acts as a highly sensitive marker for cardiac muscle injury.

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26
Q

What does elevated troponin indicate?

A

Higher risk of mortality in patients with suspected ACS

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27
Q

What is the effect of aspirin?

A

Irreversibly binds to and inactivates cyclo-oxygenase 1 (COX-1), which normally produces prostaglandins and thromboxanes which promote inflammation and clotting. This produces an inhibitory effect on platelet aggregation and so helps to reduce risk of blood clots and myocardial infarction.

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28
Q

What is the effect of P2Y12 inhibitors?

A

They bind antagonistically to the platelet P2Y12 receptor and prevent the binding of ADP which attenuates platelet aggregation and reaction of platelets to thrombus stimuli such as thrombin.

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29
Q

Give 3 examples of P2Y12 inhibitors

A

Clopidogrel, Prasugrel, Ticagrelor

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30
Q

What is the effect of GPIIb/IIIa antagonists?

A

They bind to GPIIb/IIIA receptors on the platelet plasma membrane preventing the binding fibrinogen and von Willebrand factor. This inhibits the aggregation of platelets and formation of thrombi.

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31
Q

Give 3 examples of GPIIb/IIIa antagonists

A

Abciximab, Eptifibatide, Tirofiban

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32
Q

What is PCI?

A

Percutaneous coronary intervention describes the combination of coronary angioplasty with stenting.

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33
Q

What is CABG?

A

Coronary artery bypass graft. A piece of a vein from the leg or artery from the chest is used to create an alternative route for blood flow between the aorta and coronary artery’s when the normal route is blocked.

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34
Q

What is the cause of angina?

A

Mismatch of oxygen demand and supply.

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35
Q

What are the risk factors of IHD?

A
  • age
  • smoking
  • family history
  • diabetes mellitus
  • hyperlipidaemia
  • hypertension
  • kidney disease
  • physical inactivity
  • male
  • stress
  • obesity
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36
Q

What factors exacerbate IHD?

A

Affecting supply:
- anaemia
- hypoxaemia
- polycythemia
- hypothermia
- hypovolaemia
- hypervolaemia

Affecting demand:
- tachyarrthythmia
- valvular heart disease
- hypertension
- hypertrophic cardiomyopathy

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37
Q

What 4 environmental factors exacerbate IHD?

A
  • cold
  • emotional stress
  • exercise
  • heavy meals
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38
Q

What are differential diagnoses for chest pain?

A
  • myocardial ischaemia
  • pericarditis/myocarditis
  • pulmonary embolism/pleurisy
  • chest infection/pleurisy
  • gastro-oesophageal
  • musculoskeletal pain
  • psychological
  • dissection of the aorta
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39
Q

What is pericarditis?

A

Inflammation of the pericardium

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40
Q

What are the 6 categories for causes of pericarditis?

A

Viral (coxsackie virus is most common)
Bacterial (TB)
Autoimmune (SLE, Sjorgens Syndrome, RA)
Neoplastic (metastatic lung, breast)
Metabolic
Traumatic and iatrogenic

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41
Q

What are the risk factors for pericarditis?

A
  • male
  • age 20-50
  • transmural myocardial infarction
  • cardiac surgery
  • neoplasm
  • viral and bacterial infection
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42
Q

What are the key presentations of pericarditis?

A
  • severe, pleuritic, rapid onset chest pain
  • pericardial rub
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43
Q

What is the first investigation for pericarditis?

A

ECG

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44
Q

What is the management of pericarditis?

A
  • sedentary activity until resolution of symptoms and ECG/CRP
  • High dose NSAID or Aspirin
  • Colchicine (to prevent constrictive pericarditis)
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45
Q

What pathology can be identified using ECG?

A
  • arrhythmias
  • myocardial ischaemia and infarction
  • pericarditis
  • chamber hypertrophy
  • electrolyte disturbances (i.e. hyperkalaemia, hypokalaemia)
  • drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
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46
Q

What is the normal intrinsic rate of the SA node?

A

60-100bpm

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47
Q

What is the normal instrinsic rate of the AV node?

A

40-60 bpm

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48
Q

What is the normal intrinsic rate of the ventricular cells?

A

20-45 bpm

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49
Q

What is the passage of electrical conduction through the heart?

A

Sinoatrial node –> AV node –> Bundle of His –> Bundle branches –> Purkinje fibres

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50
Q

What are the significances of the letters in the PQRST sequence?

A

P wave = Atrial depolarisation
PR interval – time taken for electrical activity to move between the atria and the ventricles (120-200ms)
QRS sequence = Atrial repolarisation (not visible) and Ventricular depolarisation
ST segment – time between depolarisation and repolarisation of the ventricles (ventricular contraction)
T wave = Ventricular repolarisation

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51
Q

What are unipolar and bipolar leads?

A

unipolar leads = one point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart
- Measures the potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative)
- Sometimes known as augmented leads

bipolar leads = two different points on the body
- Measure the potential difference (voltage) between two electrodes
- One positive and one negative electrode

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52
Q

What is the normal length of the PR interval?

A

120-200 ms (3-5 little squares)

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53
Q

What is the normal width of the QRS complex?

A

No more than 110ms (<3 little squares)

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54
Q

In which leads should the QRS interval be dominantly upright?

A

Leads I and II

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55
Q

In which leads must the P and T waves be upright?

A

Leads I, II, V2-V6

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56
Q

What psychosocial factors affect CHD?

A
  1. behaviour patterns
  2. depression/anxiety
  3. social support
  4. work
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57
Q

Which ECG leads produce an inferior view of the heart?

A

Leads II, III, aVF

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58
Q

Which leads produce a lateral view of the heart?

A

I, aVL, aVR, V5, V6

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59
Q

Which leads produce an anterior view of the heart?

A

V3, V4

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60
Q

What is the most common congenital heart problem?

A

ventricular septal defect

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61
Q

Which leads produce a septal view of the heart?

A

V1, V2

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62
Q

What is Prinzmetal’s angina?

A

Mismatch in blood supply and demand to heart muscle due to coronary vasospasm (atherogenesis) –> seen in cocaine users
* ECG shows ST elevation

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63
Q

What is Eisenmenger’s syndrome?

A

High pressure pulmonary flow with a VSD so that pressure in the RV is greater and deoxygenated blood enters LV so patient becomes cyanotic (blue) and has clubbing of fingers.

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64
Q

What are the clinical signs for VSD?

A

Large defect: small breathless skinny baby, increased resp rate, tachycardia, big heart
Small defect: loud systolic murmur, thrill (buzzing sensation), well grown, normal heart rate and size

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65
Q

What are the clinical signs of ASD?

A
  • pulmonary flow murmur
  • fixed split second heart sound (delayed closure of PV because more blood has to get out)
  • big pulmonary arteries on CXR
  • big heart on CXR
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66
Q

What is AVSD?

A

Atrio-ventricular septal defects - strong association with Down’s syndrome
= hole at the centre of the heart which involves the ventricular septum, the atrial septum, the mitral and tricuspid valves

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67
Q

What is the tetralogy of Fallot?

A

A combination of 4 congenital heart defects which usually result in a lack of oxygen-rich blood reaching the body.
- pulmonary stenosis
- ventricular septal defect
- dextroposition (heart on the right, apex to the left)
- right ventricular hypertrophy

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68
Q

What is the key issue in tetralogy of Fallot?

A

Anterior dislocation of the septum below the pulmonary outflow - this results in the other issues.

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69
Q

What is a ‘Fallot spell’

A

Stenosis of the RV outflow leads to higher pressure in the RV than the LV this causes deoyxgenated blood to enter the right ventricle and makes patient look blue.

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70
Q

What is complete transition of the great arteries (TGA)?

A

When the aorta comes off the right ventricle and the pulmonary trunk off the left ventricle.

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71
Q

What is coarctation of the aorta?

A

Narrowing of the aorta just after the arch with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body. This occurs as a result of an excessive sclerosing /obliterating process that normally closes the ductus arteriosus, extending into the aortic wall.

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72
Q

What is endocardial fibroelastosis?

A

Secondary endocardial fibroelastosis is a frequent complication of congenital aortic stenosis and coarctation. Profound dense collagen and elastic tissues deposited on the endocardial aspect of the left ventricle produces progressive stiffening of the heart and cardiac failure.

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73
Q

What is cor pulmonale?

A

Right ventricular hypertrophy and dilatation due to pulmonary hypertension.

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74
Q

What are the symptoms of a patent ductus arteriosus?

A

Blood is shunted from aorta to pulmonary trunk which creates risk of pulmonary overload and Eisenmenger’s.
Symptoms: dyspnoea, failure to thrive, machine-like murmur

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75
Q

What is the definition of heart failure?

A

The inability of the heart to deliver oxygenated blood to tissues at sufficient rate for the tissue’s metabolic requirements.

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76
Q

What are the causes of heart failure?

A

Most common: Ischaemic heart disease

  • cardiomyopathy
  • vascular disease
  • cor pulmonale
  • anything which increases cardiac strain (obesity, pregnancy, arrhythmias, hypertension, hyperthyroidism)
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77
Q

What are the risk factors for heart failure?

A

Age (65+ yrs)
Smoking
Obesity
Previous MI
Male
african descent

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78
Q

What is the pathophysiology of heart failure?

A
  1. Weakened cardiac muscles result in decreased cardiac output
  2. This activates the compensatory mechanisms of RAAS and SNS which temporarily increase BP as a result of increased aldosterone, ADH and adrenaline/NAd
  3. Soon compensation fails and heart undergoes cardiac remodelling in response to compensation and cardiac output decreases causing multi-systemic effects.
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79
Q

What are the key manifestations of heart failure?

A

Shortness of breath, ankle swelling, fatigue

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80
Q

What is the key blood marker in heart failure diagnosis?

A

Brain natriuretic peptide (BNP) (released from ventricles in response to increased mechanical stress) - the higher the BNP, the more severe the HF

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81
Q

What are the XR findings in heart failure?

A

Alveolar oedema
Kerley B Lines
Cardiomegaly
Dilation of UPPER lobe vessels
Effusions

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82
Q

What is the most common cause of heart failure

A

Ischaemia

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83
Q

What is the management for heart failure?

A
  • lifestyle changes
  • ACE-i + B-blocker
    + spironolactone + furosemide
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84
Q

What is the definition of hypertension?

A

Blood pressure ≥140/90mmHg

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85
Q

What are the initiating factors for hypertension? (8)

A

DRIED ICE
- Disturbance of autoregulation
- Renal sodium retention
- Insulin resistance/hyperinsulinaemia
- Excess sodium intake
- Dysregulation of RAAS with elevated plasma renin activity
- Increased sympathetic drive
- Cell membrane transporter changes
- Endothelial dysfunction

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86
Q

Which medications increase blood pressure?

A
  • NSAIDs
  • SNRIs (serotonin and norepinephrine reuptake inhibitors)
  • Corticosteroids
  • Oral contraceptives (oestrogen containing)
  • Stimulants
  • Anti-anxiety drugs
  • Anti-TNFs
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87
Q

What are the risk factors for hypertension?

A
  • age >65yrs
  • moderate/high alcohol intake
  • sedentary lifestyle
  • FH of hypertension of CAD
  • obesity
  • metabolic syndrome
  • diabetes mellitus
  • black ancestry
  • hyperuricemia
  • obstructive sleep apnoea

** Smoking is NOT a risk factor

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88
Q

what is the equation for BP?

A

BP = CO x TPR

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89
Q

What factors affect blood pressure?

A
  • Preload
  • Contractility
  • Vessel hypertrophy
  • Peripheral constriction
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90
Q

What are the common symptoms of hypertension?

A

Most often symptomless.
- headache
- visual changes
- dyspnoea
- chest pain
- sensory of motor deficit

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91
Q

What is the gold standard screening for hypertension?

A

ECG

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92
Q

What is the management for hypertension?

A
  • Lifestyle modification and monitoring (increase exercise, reduce sodium intake, lose weight)

Medical treatment thresholds: low CDV risk = 160/100mmHg, high CDV risk = 140/90mmHg
- calcium channel blockers, ACEis, ARBs, diuretics, B-blockers

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93
Q

What is aortic stenosis?

A

Narrowing of the aortic valve.

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94
Q

What are the causes of aortic stenosis?

A

Congenital: can occur with unicuspid, bicuspid, tricuspid valve and is commonly associated aortic coarctation, dissection or aneurysm

Acquired: degenerative calcification, rheumatic heart disease, rare causes (infectious vegetations, Paget disease, Rheumatoid arthritis)

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95
Q

What is the pathophysiology of aortic stenosis?

A

Development of a pressure gradient between the left ventricle and aorta (increased afterload).
LV function intially maintained by compensatory pressure hypertrophy but when compensatory mechanism exhausted, LV function declines.

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96
Q

What are the key presentations of aortic stenosis?

A
  • Dyspnoea (50%) - on exertion due to heart failure
  • Angina (35%) - increased myocardial oxygen demand, demand/supply mismatch
  • Syncope (15%) - exertional
  • Sudden death (<2%)
97
Q

What are the physical signs of aortic stenosis?

A
  • slow rising carotid pulse + decreased pulse amplitude
  • Heart sounds- soft or absent second heart sound, S4 gallop due to LVH.
  • Ejection systolic murmur- crescendo-decrescendo character.
98
Q

What is the first line investigation for aortic stenosis?

A

Echocardiography (LV size and function most important)

99
Q

How is aortic stenosis managed/treated?

A
  • good dental hygiene/care
  • medicines have limited role as problem is mechanical
  • aortic valve replacement surgery
  • transcatheter aortic valve implantation (TAVI)
100
Q

What are the indications for intervention for aortic stenosis?

A

Any symptomatic patient with severe AS.
Any patient with decreasing EF (ejection fraction).
Any patient undergoing CABG with moderate or severe AS
Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS

101
Q

What are the risk factors for aortic stenosis?

A
  • age >60yrs
  • congenitally bicuspid aortic valve
  • rheumatic heart disease
  • chronic kidney disease (up to 55% of patients on dialysis have aortic valve calcification)
102
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole.
Mild MR is seen in 80% of normal individuals.

103
Q

What are the causes of mitral regurgitation?

A
  • Myxomatous degeneration
  • Ischaemic MR
  • Rheumatic heart disease
  • Infective endocarditis
  • Cardiac trauma
104
Q

What is the pathophysiology of MR?

A

Symptoms are caused by pure volume overload of the heart.
- compensatory mechanisms: left atrial enlargement, lVH and increased contractility
- progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension
- progressive left ventricular volume overload leads to dilatation and progressive heart failure

105
Q

What are the clinical manifestations of MR?

A
  • pansystolic murmur at the apex radiating to the axilla
  • Exertion dyspnoea
  • heart failure
106
Q

How is mitral regurgitation diagnosed?

A

ECG (LA enlargement , AF, LVH with severe MR)
also: CXR, echocardiogram

107
Q

What is the management for MR?

A
  • rate control medication for AF (B-blockers, CCBs, digoxin)
  • anti-COAGs in AF and flutter
  • nitrates/diuretics in acute MR
  • chronic HF Rx if chronic MR with CCF
  • reparative surgery is indicated with any symptoms at rest or on exercise
108
Q

What is normally the length of the compensatory phase in mitral regurgitation?

A

10-15 years

109
Q

What is aortic regurgitation?

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.

110
Q

What are the causes of aortic regurgitation?

A

Bicuspid aortic valves, rheumatic heart disease, infective endocarditis

111
Q

What is the pathophysiology of aortic regurgitation?

A

Asymptomatic until the 4th or 5th decade with gradual progression.
Combined pressure and volume overload.
Compensatory mechanisms (LV dilation, LVH, progressive dilation leads to heart failure)

112
Q

What are the clinical manifestations of AR?

A
  • Wide pulse pressure
  • palpitations
  • Hyperdynamic and displaced apical impulse
    On auscultation:
  • Diastolic blowing murmur at the left sternal border
  • Austin flint murmur (apex): regurgitant jet impinges on anterior MVL (mitral valve leaflet) causing it to vibrate
  • Systolic ejection murmur (due to increased flow across the aortic valve)
113
Q

What is the gold standard investigation for AR?

A

Echocardiogram (evaluation of AV and aortic root with measurements of LV dimensions and function)

114
Q

What is the management for aortic regurgitation?

A
  • consider IE prophylaxis
  • medical: vasodilators (ACEIs indicated in CCF or HTN)
  • surgical treatment if any symptoms at rest or on exercise
115
Q

Define mitral stenosis

A

The obstruction of inflow that prevents proper filling during diastole

116
Q

What are the causes of MS?

A

Rheumatic heart disease (77-99%)
Infective endocarditis
Mitral annular calcification

117
Q

What is the pathophysiology of MS?

A

LA dilation leading to pulmonary congestion (reduced emptying).
increased transmitral pressures lead to left atrial enlargement and atrial fibrillation.

118
Q

What are the clinical manifestations of MS?

A
  • progressive dyspnoea
  • prominant “a” wave in jugular venous pulsation
  • signs of right-sided heart failure (advanced disease)
  • mitral facies
  • diastolic murmur on auscultation
119
Q

What are the investigations for mitral stenosis?

A

1st line: ECG
Gold standard: Echo (assesses mitral valve mobility, gradient and mitral valve area)
other : CXR (LA enlargement and pulmonary congestion)

120
Q

What is the management for mitral stenosis?

A
  • Medicine cannot prevent progression but BBs, CCBs and digoxin are used to control HR and prolong diastole for improved diastolic filling.
  • Diuretics are also used to treat fluid overload
  • Percutaneous mitral balloon valvotomy, if not possible MV replacement considered (any symptomatic patient with symptoms at rest, or on daily activity-level exertion)
  • IE prophylaxis
121
Q

What is infective endocarditis?

A
  • Infection of the heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc.)
  • Alongside the infection it causes infectious emboli to travel through the bloodstream.
122
Q

What are the types of infective endocarditis?

A
  • Left-sided native IE (mitral or aortic)
  • Left-sided prosthetic IE
  • Right-sided IE
  • Device related IE (pacemakers, defibrillators..)
  • Prosthetic
123
Q

What are the causes of infective endocarditis?

A
  • Abnormal valves; regurgitant or prosthetic valves are most likely to get infected
  • Infectious material introduced to bloodstream or directly onto the heart during surgery
  • Previous infective endocarditis
124
Q

What are the risk factors for IE?

A
  • age
  • IV drug abuse
  • congenital heart disease
  • prosthetic heart valves
125
Q

What is the pathophysiology of IE?

A

IE typically develops on the valvular surfaces of the heart which are subject to turbulent blood flow causing endothelial damage. This results in the adherence of platelets and fibrin to the collagen surface creating a pro-thrombotic environment.
Bacteraemia leads to colonisation of the thrombus and perpetuates further fibrin deposition and platelet aggregation, so a mature infected vegetation develops.

126
Q

What are the key presentation for IE?

A

dependent on site, organism, etc.
- signs of systemic infection (fever, sweating)
- embolisation (stroke, PE, bone infections, kidney dysfunction, MI)
- valve dysfunction (heart failure, arrhythmia)

127
Q

Signs of IE?

A
  • Petechiae, splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth spots
128
Q

What is the 1st line investigation for IE?

A

Trans-thoracic echocardiogram (TTE)

129
Q

What is the treatment for IE?

A
  • Antibiotics/antimicrobials
  • Cardiac surgery to remove infectious material and /or repair the damage (if the infection is not cured with antibiotics)
  • Treatment of other complications
130
Q

What is defined as tachycardia?

A

heart rate >100 bpm

131
Q

What are 5 examples of tachycardia?

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardia
  • Ventricular tachycardia
  • Ventricular fibrillation
132
Q

What is the definition of bradycardia?

A

Heart rate <60 bpm

133
Q

What is Mobitz type I?

A

PR interval gradually increases until AV node fails completely and no QRS wave is seen.
Then starts all over again and PR gradually lengthens.

134
Q

What is Mobitz type II?

A

Sudden unpredictable loss of AV conduction and loss of QRS. Due to loss of conduction in Bundle of His and Purkinje fibres.

135
Q

How does hyperkalaemia present on ECG?

A

Tall T waves, flattening of P waves, broadening of QRS…eventually ‘sine wave pattern’

136
Q

How does hypokalaemia present on ECG?

A

Flattening of T wave, QT prolongation

137
Q

How does Hypercalcaemia present on ECG?

A

QT shortening

138
Q

How does hypocalcaemia present on ECG?

A

QT prolongation

139
Q

How does first degree AV block present on ECG?

A

PR interval > 0.2s
Can be a sign of CAD, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance but does not usually require treatment

140
Q

How does second degree heart block present on ECG?

A

Intermittent absence of QRS complexes - indication that there is a blockage somewhere between the AV node and the ventricles.
3 types:
- Mobitz type 2
- Mobitz type 1 (Wenckebach)
- 2:1 and 3:1 conduction

141
Q

How does 3rd degree (complete) heart block present on ECG?

A

Atrial contraction is normal but no beats are conducted to the ventricles. The ventricles are still excited by their own internal ‘ectopic pacemaker’ system so both P waves and QRS complexes are seen on ECG but with no relationship between them. QRS is generally broad (160ms)

142
Q

What is 2:1 and 3:1 conduction?

A

One normal cycle followed by one cycle with an absent QRS (2:1) or one normal cycle, then 2 cycles without a QRS (3:1)

143
Q

What are ectopic beats?

A

Non-sustained beats arising from ectopic regions of atria or ventricles.

144
Q

What is heart failure?

A

Inability of the heart to deliver oxygenated blood to tissues at sufficient rate for the tissue’s metabolic requirements, despite normal or increased cardiac filling pressures.

145
Q

What is the most common cause of heart failure?

A

Ischaemic heart disease

146
Q

What are other causes of HF?

A
  • hypertension
  • alcohol excess
  • cardiomyopathy (primary disease of the heart muscle)
  • valvular
  • endocardial
  • pericardial causes
147
Q

What are the risk factors for HF?

A
  • age >65 yrs
  • smoking
  • obesity
  • previous MI
  • male
  • alcohol excess
148
Q

What are the categories of the NY Heart Association Classification?

A

1 - No limitation (asymptomatic)
2 - Slight limitation (mild HF)
3 - Marked limitation (symptomatically moderate HF)
4 - Inability to carry out any physical activity without discomfort (symptomatically severe HF)

149
Q

What is the treatment for HF?

A
  • lifestyle modification (↓BMI, exercise, stop smoking and reduce alcohol)
  • ACE-i + B blocker for all patients
    + Spironolactone + furosemide
    + Consider cardiac resynchronisation therapy (improves AV coordination)
  • Surgery = consider revascularisation, valve surgery, heart transplant (last resort)
150
Q

What is the gold standard investigation for heart failure?

A

abnormal ECG (e.g. evidence of LVH)

151
Q

What are the key presentations of heart failure?

A

Non-specific signs of cardiac disease: SOB, ankle swelling, fatigue
Also: orthopnoea, oedema, 3rd + 4th heart sounds, bibasal crackles, hypotensive, tachycardia

152
Q

What causes 3rd degree (complete) heart block?

A

MI - can be transient
Chronic - often due to fibrosis around the bundle of His or BBB of both branches
Always indicates underlying disease - more often fibrosis than ischaemia.

153
Q

What is a BBB?

A

A complete or partial interruption of the electrical pathways inside the wall of the heart between the ventricles.

154
Q

What are the causes of BBB?

A
  • blood clots in the lungs
  • chronic lung disease e.g. COPD
  • cardiomyopathy
  • heart wall defects
155
Q

What happens in RBBB?

A

The R bundle is not working so the electric signals to the right ventricle are blocked and so the left ventricle contracts just before the right ventricle.

156
Q

What is the presentation of RBBB on ECG?

A

Wide QRS complexes (>120ms)
RSR ‘M’ pattern in leads V1-V3
Slurred S waves in leads I, aVL and often V5 and V6
MaRRoW

157
Q

What is the presentation of LBBB on ECG?

A

Wide QRS complexes (>120ms)
Absence of Q wave in leads I, V5 and V6
Monomorphic R wave in I, V5 and V6
ST and T wave displacement opposite to the major deflection of the QRS complex
WiLLiaM

158
Q

How can you quickly diagnose RBBB from LBBB on ECG?

A

LBBB: QRS widened and downwardly deflected in V1
RBBB: QRS widened and upwardly deflected in lead V1

159
Q

What is peripheral vascular disease?

A

A range of symptoms caused by atherosclerotic obstruction of the lower extremity arteries.

160
Q

What is the most common cause of PVD?

A

Atherosclerosis

161
Q

What are the risk factors for PVD?

A
  • Smoking
  • diabetes mellitus
  • hypertension
  • hyperlipidaemia
  • age >40yrs
  • history of CAD, CVD, sedentary lifestyle, CKD, T2DM
162
Q

What are the key presentations of PVD?

A

Most often asymptomatic, intermittent claudication, diminished/absent pulse

163
Q

What is the 1st line investigation for PVD?

A

Ankle-brachial index </= 0.90

164
Q

What is the management for PVD?

A

Intermittent claudication: RF management

Chronic limb ischaemia: revascularization surgery (PCI if small, bypass if larger)

Acute limb threatening ischaemia: surgical emergency - revascularization within 4-6 hours other very high amputation risk

165
Q

What are the 3 presentations of PVD?

A

Intermittent claudication (least severe)
Chronic critical limb ischaemia
Acute limb ischaemia

166
Q

What are the 6 Ps that indicate limb-threatening ischaemia?

A

Pulselessness, Pallor, Pain, Persisting cold, Paralysis, Paraesthesia (the more that are present, the more limb threatening)

167
Q

What is atrial fibrillation?

A

irregularly irregular atrial firing rhythm

168
Q

What are the causes of AF?

A

Heart failure, hypertension, secondary to mitral stenosis, sometimes idiopathic

169
Q

What are the risk factors for atrial fibrillation?

A

Age 60+, T2DM, hypertension, valve defects, history of MI

170
Q

What is the pathophysiology of AF?

A

Rapidly firing ectopic foci (300-600bpm firing rate) cause atrial spasm, this causes atrial blood to pool instead of pumping effectively to ventricles –> decreased CO and increased risk of thromboembolic events

171
Q

What are the key presentations of AF?

A

Palpitations, irregularly irregular pulse, thromboemboli, chest pain, syncope, hypotension

172
Q

What is the gold standard investigation for AF?

A

ECG (irregularly irregular pulse with normal QRS and no P waves)

173
Q

What is the management of acutely unstable AF?

A

DC synchronised cardioversion

174
Q

What is the management for stable, long-term AF?

A

Rate: BB/CCB + oral anticoag.
Rhythm: cardioversion (DC or pharmacological) + warfarin

Surgical: radiofrequency ablation

175
Q

What is hypertrophic cardiomyopathy?

A

Genetic disease of the cardiac sarcomere, caused by mutations in genes that encode for different components of the contractile apparatus.

176
Q

How can aortic stenosis lead to heart failure?

A

The narrowing of the aortic valve means increases the load on the left ventricle and means that it has to work harder to pump blood out of the heart. This results in left ventricular hypertrophy so the muscle is enlarged and weakened which leads to heart failure if not resolved.

177
Q

What is pulmonary embolism?

A

A life-threatening condition which occurs when a blood clot gets stuck in an artery in the lung, blocking blood flow to part of the lung. This can result in right heart failure and cardiac arrest if not treated.

178
Q

What are the risk factors for PE?

A

Increasing age
DVT
Obesity
Surgery within last 2 months
Bed rest >5 days
Previous venous thromboembolic event
FHx
Malignancy

179
Q

What is the pathophysiology of PE?

A

Most often caused as a result of DVT where the clot moves from the legs and travels up through the right side of the heat and passes into the lungs where it sticks and prevents blood flow. This obstruction increases pulmonary vascular resistance, increasing the work of the right ventricle. The right ventricle compensates by increasing the heart rate (Frank-starling mechanism) which leads to over distension of the right ventricle, increased RV end-diastolic pressure and decreased RV cardiac output. Decreased RV output leads to decreased left ventricular preload. As LV filling and cardiac output decrease, low mean arterial pressure progressed to hypotension and shock.

180
Q

What are the key presentations of PE?

A

Breathlessness
Pleuritic chest pain
sign/symptoms of DVT
tachycardia
tachypnoea
pleural rub

181
Q

What investigations are used for PE?

A

ECG (sinus tachycardia)
Blood gases (type 1 resp failure, ↓O2 and CO2)
CXR, D-dimer, CT pulmonary angiogram (CTPA) spiral CT with contrast

182
Q

What is the management for PE?

A

Supportive treatment
LMW Heparin s/c
Oral warfarin INR 2-3
DOAC (direct oral anticoag) e.g. rivaroxaban, apixaban
Treat underlying cause
In emergency scenario: catheter mechanico-chemical thrombectomy or surgical thrombo-embolectomy

183
Q

What is the Wells score?

A

A number reflecting a patient’s risk of developing DVT which is calculated by a points system according to the risk factors and symptoms the patient has.
1< likely DVT
4< likely PE

184
Q

What is rheumatic fever?

A

An autoimmune condition triggered by strep. bacteria and caused by antibodies created against the bacteria which also target tissues in the body.
It is a multisystem disorder affecting the joints, heart, skin and nervous system.

185
Q

What are the risk factors for RF?

A

Poverty
Overcrowded living conditions
FHx rheumatic fever
HLA association
Genetic susceptibility

186
Q

What is the pathophysiology of RF?

A

Caused by group A beta-haemolytic streptococci, typically S. pyogenes causing tonsillitis. The immune system creates antibodies to fight the infection and these antibodies not only target the bacteria but also match antigens on the cells of the person’s body. This results in a type 2 hypersensitivity reaction where the immune system begins attacking cells throughout the body

187
Q

What are the key presentations of RF?

A

Fever
Joint pain (migratory arthritis affecting the large joints)
Rash (erythema marginatum = pink rings on torso and proximal limbs)
SOB
Chorea (sudden, uncontrollable jerking of limbs and facial muscles)
Nodules (on surfaces of joints)
Carditis (inflammation of the heart) → tachycardia/bradycardia, murmurs, pericardial rub, heart failure

188
Q

What is the Jones criteria for RF diagnosis?

A

Jones criteria for diagnosis:
Evidence of recent strep. Infection +
Two major criteria (Joint arthritis, Organ inflammation (carditis), Nodules, Erythema marginatum rash, Sydenham chorea)
OR
One major criteria plus two minor criteria (Fever, ECG changes without carditis, Arthralgia without arthritis, Raised inflammatory markers)

189
Q

What are the investigations for RF?

A

Throat swab
ASO antibody titres (Anti-strep)
Echo, ECG + CXR

190
Q

What is the management for RF?

A

Antibiotics (penicillin V)
NSAIDs for joint pain
Aspirin and steroid for carditis
Prophylactic antibiotics
Haloperidol for chorea
Monitoring and management of complications

191
Q

What is shock?

A

life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to, and consequently oxygen utilisation by, the tissues and creates risk of organ dysfunction.

192
Q

What are the key presentations of shock?

A

Weak, rapid pulse
Confusion
Reduced GCS (glasgow coma scale)
Decreased urine output
Pale, clammy skin
Increased capillary refill time
Prolonged hypotension

193
Q

What are the 5 types of shock?

A

Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic

194
Q

What causes hypovolemic shock?

A

Blood or fluid loss.
Usually result of trauma, GI bleed, dehydration

195
Q

What is the treatment for hypovolemic shock?

A

ABCDE, give O2 and IV fluids

196
Q

What are the key symptoms of hypovolemic shock?

A

hypotension, tachycardia, pale, clammy skin, confusion

197
Q

What causes septic shock?

A

Uncontrolled bacterial infection

198
Q

What are the symptoms of septic shock?

A

pyrexic, warm peripheries, bounding pulse, tachycardia

199
Q

What is the treatment for septic shock?

A

ABCDE, broad spectrum antibiotics (broad spec e.g. piperacillin/tazobactam, ceftriaxone)

200
Q

What causes cardiogenic shock?

A

Heart pump failure usually as a result of MI, cardiac tamponade, PE

201
Q

What are the key symptoms of cardiogenic shock?

A

Signs of heart failure (oedema), ↑JVP, S4

202
Q

What is the treatment for cardiogenic shock?

A

ABCDE + treat underlying cause

203
Q

What causes anaphylactic shock?

A

IgE mediated Type 1 hypersensitivity reaction to allergen, histamine release → causes excess vasodilation and bronchoconstriction

204
Q

What are the key symptoms of anaphylactic shock?

A

hypotension, tachycardia, urticaria, puffy face, flushed cheek

205
Q

What is the treatment for anaphylactic shock?

A

ABCDE + IM adrenaline

206
Q

What causes neurogenic shock?

A

spinal cord trauma e.g. RTA, disrupted SNS but intact PSNS

207
Q

What are the key symptoms of neurogenic shock?

A

hypotension
bradycardia
confusion
hypothermia

208
Q

What is the treatment for neurogenic shock?

A

ABCDE + IV atropine (blocks vagal tone, allows more PSNS inhibition, more chance for SNS to work)

209
Q

What is cardiomyopathy?

A

disease of the myocardium

210
Q

What are the 3 types of cardiomyopathy?

A

Hypertrophic, Dilated, Restrictive

211
Q

What causes hypertrophic cardiomyopathy?

A

Autosomal dominant mutation of sarcomere protein (troponin T, myosin B) (+exercise +aortic stenosis) results in a thick non-compliant heart –> impaired diastolic filling –> ↓CO

212
Q

What are the symptoms of hypertrophic cardiomyopathy?

A

can present as sudden death, otherwise chest pain, palpitations, SOB, syncope

213
Q

What are the investigations for hypertrophic cardiomyopathy?

A

confirm w/ abnormal ECG, ECHO (GS) + genetic testing

214
Q

What are the treatments for hypertrophic cardiomyopathy?

A

BBs, CCBs, amiodarone (anti-arrhythmic)

215
Q

What causes dilated cardiomyopathy?

A

Autosomal dominant mutation of cytoskeleton gene (+IHD +alcohol) leads to thin cardiac walls which contract poorly –>↓CO

216
Q

What are the symptoms of dilated cardiomyopathy?

A

SOB, heart failure, atrial fibrillation, thromboemboli

217
Q

What is used to diagnose dilated cardiomyopathy?

A

ECG, ECHO

218
Q

What is the treatment for dilated cardiomyopathy?

A

treat underlying conditions e.g. AF, heart failure

219
Q

What causes restrictive cardiomyopathy?

A

Granulomatous disease (sarcoidosis, amyloidosis), idiopathic, post-MI fibrosis
- Leads to rigid fibrotic myocardium, fills and contracts poorly → ↓CO

220
Q

What are the symptoms of restrictive cardiomyopathy?

A

severe; dyspnoea, S3 +S4 sounds, oedema, congestive HF, narrow PP

221
Q

What are the diagnostic tests for restrictive cardiomyopathy?

A

ECG, ECHO, cardiac catheterisation (definitive)

222
Q

What is the treatment for restrictive cardiomyopathy?

A

none, consider transplant (Px typically die within 1yr)

223
Q

Where is BNP secreted from?

A

B-type natriuretic peptide is mainly secreted by the ventricular myocardium in response to strain

224
Q

What is raised BNP an indicator of?

A

Heart failure most commonly
Can also indicated myocardial ischemia or valvular disease

225
Q

What are teh effects of BNP?

A

Vasodilation
Diuretic and natriuretic
Suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

226
Q

What creates the first heart sound (S1)?

A

Closing of the atrioventricular valves (tricuspid + mitral) at the start of the systolic contraction of the ventricles

227
Q

What creates the second heart sound (S2)?

A

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

228
Q

What creates the third heart sound (S3)?

A

rapid ventricular filling which causes the chordae tendinae to pull their full length and twang like a guitar string (can be normal in young people due to good heart function but in older patients can indicates heart failure)

229
Q

What causes the 4th heart sound (S4)?

A

Heard directly before S1 and is always abnormal - indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant ventricle.

230
Q

Where is the stethoscope placed to listen for pulmonary murmurs?

A

2nd intercostal space left sternal border

231
Q

Where is the stethoscope placed to listen for aortic murmurs?

A

2nd intercostal right sternal border

232
Q

Where is the stethoscope placed to listen for tricuspid murmurs?

A

5th intercostal space left sternal border

233
Q

Where is the stethoscope placed to listen for mitral mumurs?

A

5th intercostal space mid clavilcular line (apex area)

234
Q

What is Erb’s point?

A

The best place to listen for S1/S2, located in the third intercostal space on the left sternal border.

235
Q

What are the heart sounds?

A

S1 = mitral + tricuspid close
S2 = aortic + pulmonary close
S3 = shows rapid ventricular filling in early diastole (normal in young/pregnant, abnormal in mitral regurg + heart failure)
S4 = pathological “gallop” - due to blood forced into stiff hypertrophic ventricle (LVH + aortic stenosis)

236
Q

What is the CHA2-DS2-VASc scoring system?

A

Tool used to assess starting anticoagulation in patients with stroke risk due to atrial fibrillation

237
Q

What is the ABCD2 screening tool used for?

A

Estimation of stroke risk after a suspected TIA

238
Q

What is the HAS-BLED screening tool used for?

A

Estimates risk of bleeding in patients on anticoagulation

239
Q

What is Well’s criteria used for?

A

estimates risk of pulmonary embolism in clinical presentation

Phase 2A (18 decks)

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