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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is ischaemic heart disease?

A

When coronary arteries are blocked by athersclerosis.

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2
Q

What conditions can ischaemic heart disease cause?

A

Stable angina, unstable angina, NSTEMI and STEMI.

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3
Q

What are the three main features of stable angina?

A
  1. Central crushing chest pain radiating to neck/jaw.
  2. Brought on with exertion.
  3. Relieved with 5 minutes rest or GTN spray.
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4
Q

What is acute coronary syndrome?

A

An umbrella term for unstable angina, NSTEMI and STEMI.

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5
Q

Name and define the four types of angina.

A
  1. Stable - relieved with rest/GTN spray.
  2. Unstable - pain at rest, not relieved with rest/GTN spray.
  3. Prinzmetal’s - Coronary vasospasm (cocaine users).
  4. Decubitus - Induced lying flat.
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6
Q

What are the three non-modifiable risk factors for ischaemic heart disease.

A

Age, family history, male.

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7
Q

What are the 6 modifiable risk factors for ischaemic heart disease?

A

Smoking, alcohol, poor diet, low exercise, obesity, stress.

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8
Q

What is the primary prevention of IHD?

A

Qrisk score which calculates the risk of an MI in the next 10y, if above 10% start on statins.

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9
Q

What is the secondary prevention of IHD?

A

For patients who have had angina, MI, stroke and TIA:
Four A’s - Aspirin, atorvastatin, atenolol, ACE-i.

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10
Q

What is the grace score and it’s use?

A

Predictor of mortality from MI in next 6m to 3y in patients with ACS - guides treatment.

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11
Q

What is the pathophysiology of ischaemic heart disease?

A

Atherosclerosis formation - fatty streak and fibrous cap rupture.

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12
Q

What is the first line diagnosis of stable angina?

A

ECG - resting is normal as it is exercise induced.

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13
Q

What is the gold standard method to diagnose stable angina?

A

CT angiogram - shows atherosclerotic arteries.

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14
Q

How occluded are the coronary arteries in stable angina?

A

70-80% occluded.

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15
Q

What is the treatment for acute symptomatic stable angina?

A

GTN sublingual spray.

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16
Q

What is the long term treatment for stable angina?

A

Lifestyle modifying - lose weight, stop smoking, stop drinking, healthier diet, exercise.

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17
Q

What is the first line treatment for stable angina?

A

Medications.

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18
Q

What is the first line medication for stable angina?

A

CCB or beta blockers.

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19
Q

What is the second line medication for stable angina? Which type of the medications?

A

CCB and beta blockers.
-CCB have to be non-rate limiting to prevent bradycardia.

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20
Q

What is the third line medication for stable angina?

A

CCB, beta blockers and another (nitrates/ivabrodine).

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21
Q

What are other medications that may be used to treat stable angina?

A

ACE-i, statins, aspirin, hypertension treatment.

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22
Q

How is stable angina treated is medications are unsuccessful?

A

Surgery: PCI (stent) or CABG (bypass graft).

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23
Q

Is there infarction in unstable angina?

A

No, only ischaemia.

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24
Q

What are the features on an ECG of unstable angina?

A

Normal (may show ST depression/T wave inversion).

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25
Q

What are the levels of troponins and creatine kinase in unstable angina?

A

Normal levels.

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26
Q

How occluded are the coronary arteries in NSTEMI?

A

Major occlusion.

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27
Q

Is there infarction in NSTEMI?

A

Yes.

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28
Q

What are the ECG features of NSTEMI?

A

ST depression, T wave inversion and pathological Q waves.

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29
Q

What are the troponin and creatine kinase levels in NSTEMI?

A

Both elevated.

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30
Q

How occluded are the coronary arteries in STEMI?

A

Total occlusion.

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31
Q

Is there infarction in STEMI?

A

Yes - Transmural infarction.

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32
Q

What are the ECG features of STEMI?

A

ST elevation and Q waves, new LBBB.

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33
Q

What are the troponin and creatine kinase levels in STEMI?

A

Both elevated.

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34
Q

What are the symptoms of acute coronary syndrome?

A

Central crushing chest pain that radiates to the arm/jaw with N+V, sweating, SOB, palpitations and impending doom.

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35
Q

What are the three main ways acute coronary syndrome are diagnosed?

A
  1. ECG
  2. Biomarkers
  3. CT angiography
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36
Q

What is the main medication treatment for acute coronary syndrome?

A

BANS:

-Dual antiplatelet (aspirin + clopidogrel), GTN spray and simvastatin.

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37
Q

What is the treatment for unstable angina/NSTEMI?

A

BMOAN:

-Beta blockers, morphine, oxygen, aspirin and GTN spray.

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38
Q

What is the treatment for STEMI?

A

If less than 2h - PCI.
More than 2h - Thrombolysis with alteplase.
-CABG.

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39
Q

How is acute coronary syndrome prevented long term?

A

6A’S:
-Aspirin, another antiplatelet (clopidogrel), atorvastatin, ACE-i, atenolol, aldosterone antagonist.
Lifestyle:
-Stop smoking, reduce alcohol, better diet.

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40
Q

What are six complications of acute coronary syndrome?

A

DREAD:
Death, rupture, edema (HF), arrhythmia/aneurysm, Dressler’s syndrome.

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41
Q

What is heart failure?

A

Heart failure is the inability for the heart to deliver blood thus oxygen at a satisfactory rate for the body’s metabolic requirements.

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42
Q

What is the most common cause of heart failure?

A

IHD.

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43
Q

What are four other causes of heart failure?

A

Cardiomyopathy, valve disease, cor pulmonale, anything with increased cardiac work (obesity, htn, pregnancy, arrhythmias).

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44
Q

What are the five risk factors for heart failure?

A

Age (65+), smoking, obesity, previous MI, male.

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45
Q

What is the pathophysiology of heart failure?

A

Decreased CO - RAAS/SNS activated to compensate, this works initially but then fails and heart isn’t as well adapted leading to a fluid overload.

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46
Q

What is congestive HF?

A

HF affecting left and right circuits.

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47
Q

What is the difference between acute and chronic heart failure?

A

Acute - New onset or chronic HF deterioration.
Chronic - Develops slowly.

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48
Q

What is the difference between systolic and diastolic heart failure?

A

Diastolic - Filling issues
Systolic - Pumping issues

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49
Q

What is the ejection fraction in systolic and diastolic heart failure?

A

Diastolic - >50% (normal).
Systolic - <40% (reduced).

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50
Q

Which three things cause diastolic heart failure?

A

Cardiomyopathy, LVH, aortic stenosis.

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51
Q

What causes systolic heart failure?

A

IHD, MI and cardiomyopathy.

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52
Q

What does LHS HF cause?

A

Pulmonary vessel backlog - pulmonary oedema.

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53
Q

What does RHS HF cause?

A

Systemic venous backlog - peripheral oedema.

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54
Q

What is a way to remember the main symptoms of HF?

A

SOFAPC:

-SOB, orthopnea, fatigue, ankle swelling, pulmonary oedema, cold peripheries.

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55
Q

What are three extra symptoms of HF?

A

Increased JVP, tachycardia, end respiratory crackles.

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56
Q

Which four things are used to diagnose HF?

A

Bloods, ECG, CXR, ECHO.

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57
Q

What are the bloods for HF?

A

BNP is elevated (released from ventricles under mechanical stress).

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58
Q

What are the features of a heart failure ECG?

A

Shows underlying causes (e.g LVH, ischaemia).

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59
Q

What are the features of heart failure on a CXR?

A

ABCDE:

A - Alveolar oedema
B - B-lines
C - Cardiomegaly
D - Dilated upper lobe vessels
E - Effusion (pleural)

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60
Q

How is acute heart failure treated?

A

OMFG:
Oxygen, morphine, furosemide, GTN spray.

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61
Q

What are the three methods to treat chronic heart failure?

A

Lifestyle changes, medications and surgery.

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62
Q

What are the first line medications for heart failure?

A

ACE-I and beta blockers.

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63
Q

What is the second line medication for heart failure?

A

ARB, nitrates and furosemide.

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64
Q

What is the third line medication for heart failure?

A

Cardiac resynchronisation or digoxin.

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65
Q

What is a last resort to treat heart failure?

A

Heart transplant.

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66
Q

How is heart failure treated in young patients?

A

Heart transplant.

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67
Q

What is hypertension?

A

Abnormally high blood pressure.

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68
Q

What is stage 1 hypertension?

A

140/90 or ABPM >135/85.

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69
Q

What is stage 2 hypertension?

A

160/100 or ABPM >150/95.

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70
Q

What is malignant hypertension?

A

> 180/110.
Extremely high blood pressure which causes organ damage.

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71
Q

What is the primary cause of hypertension?

A

Idiopathic - 95% of cases.

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72
Q

What are four secondary causes of hypertension?

A

5% of cases - ROPE:

Renal disease (CKD/AKI), Obesity, Pregnancy, Endocrine (Conn’s, Cushing’s, pheochromocytoma).

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73
Q

What are nine risk factors for hypertension?

A

Age, black ethnicity, less exercise, obesity, smoking, diabetes, stress, increased salt intake, FHx.

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74
Q

What are the symptoms of hypertension?

A

Asymptomatic - found on screening.

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75
Q

Which organs can malignant hypertension affect and what can this cause?

A

Head (stroke), eye (retinal haemorrhage), heart (HF, aortic dissection) and kidneys (AKI).

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76
Q

How is hypertension diagnosed?

A

If a patient comes to clinic with a stage 1 reading, ABPM to confirm and Qrisk.
Assess organ damage (eye, urinalysis and ECHO/ECG - heart).

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77
Q

What is the first line treatment for hypertension?

A

ACE-i

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78
Q

What is the second line treatment for hypertension?

A

ACE-i and CCB

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79
Q

What is the third line treatment for hypertension?

A

ACE-i, CCB and diuretic

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80
Q

What is the fourth line treatment for hypertension?

A

ACE-i, CCB, diuretic and 4th drug (b-blocker or spironolactone).

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81
Q

What is the first line treatment for hypertension in black patients?

A

CCB

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82
Q

What are four complications of hypertension?

A

HF, IHD, CKD and stroke.

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83
Q

What is an aortic aneurysm?

A

A weakness in the wall of the aorta that has swollen out and has a chance of rupturing.

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84
Q

Where are the most common sites for aortic aneurysms?

A

Most common in abdominal aorta.
Less common thoracic aorta which includes the ascending, descending and the aortic arch.

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85
Q

Where is the typical site of AAA?

A

Infrarenal abdominal.

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86
Q

What is a false aneurysm?

A

When the intima and media ruptures so the adventitia bulges out which is often caused by trauma.

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87
Q

What are the seven risk factors for AAA?

A

Male, age, smoking, family history, hypertension, CVD, connective tissue disorders.

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88
Q

What are the typical symptoms of an AAA?

A

Typically asymptomatic until rupture.

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89
Q

What are the signs/symptoms of AAA when ruptured?

A

Sudden epigastric pain that radiates to the flank.
Hypotension, tachycardia, vomiting/coughing up blood and cardiac tamponade.

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90
Q

How is an AAA diagnosed?

A

Imaging - USS, EHCO, CT/MRI angiogram.

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91
Q

How is a non-ruptured AAA treated?

A

If small, manage conservatively and monitor.
If large or expanding rapidly, repair via surgery (TEVAR/open).

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92
Q

How is a ruptured AAA treated?

A

Emergency - Stabilise with ABCDE, fluids and transfusions.
Surgery - Replace walls with graft.

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93
Q

What is an aortic dissection?

A

A tear in the intima resulting in blood dissecting through the media and separating the layers apart.
Surgical emergency.

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94
Q

What causes an aortic dissection?

A

Mechanical wall stress.

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95
Q

Who is aortic dissection most common in?

A

Men aged 50-70.

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96
Q

What are six main risk factors for aortic dissection?

A

Hypertension, connective tissue disorders, FHx, AAA, trauma, smoking.

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97
Q

Which four conditions can increase the risk of aortic dissection?

A

CABG, aortic valve replacement, bicuspid aortic valve, coarctation of the aorta.

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98
Q

What are the main two locations for an aortic dissection?

A

A - Ascending aorta before brachiocephalic artery.
B - Descending aorta after left subclavian artery.

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99
Q

Explain the pathophysiology of aortic dissection.

A

Blood dissects media and intima and pools in the false lumen.
Decreased perfusion to organs.

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100
Q

What is the two main symptoms of aortic dissection?

A

Sudden onset ripping/tearing chest pain which may radiate to the back.
Syncope.

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101
Q

What are the three signs of aortic dissection?

A

Difference in blood pressure between arms, diastolic murmur, hypotension.

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102
Q

What is used to diagnose of aortic dissection?

A

CXR and ECG to rule out other things such as MI.
CT/MRI angiogram.

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103
Q

How is aortic dissection treated?

A

Surgical emergency, can be open or TEVAR depending on the location.

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104
Q

What are the five complications of aortic dissection?

A

MI, stroke, cardiac tamponade, aortic valve regurgitation, death.

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105
Q

What is a DVT?

A

Deep vein thrombus in a deep vein.

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106
Q

What are the locations of DVT?

A

Calf - Less threatening.
Thigh - Life threatening.

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107
Q

What is a PE?

A

When a DVT embolises and lodges in the pulmonary circulation.

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107
Q

What is a PE?

A

When a DVT embolises and lodges in the pulmonary circulation.

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108
Q

What are the risk factors for DVT?

A

Virchow’s triad:
-Hypercoagulability - Pregnancy, obesity, sepsis, malignancy.
-Venous stasis - Immobility, AF.
-Endothelial injury - Smoking, trauma, surgery.

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109
Q

How does a DVT present?

A

Unilateral swollen calf with engorged leg veins which is warm with oedema.

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110
Q

How does a DVT with complete occlusion present?

A

Blue leg with tenderness.

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111
Q

How is a DVT diagnosed?

A

Doppler USS of leg, and measure D-dimer.
D-dimer is sensitive (95%), but not specific.
Perform a Wells score.

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112
Q

How is a DVT treated?

A

Medications - DOACs (apixaban), warfarin, LMWH.
Surgery if iliofemoral (catheter thrombolysis).

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113
Q

What is a life threatening complication of DVT?

A

Pulmonary embolism.

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114
Q

What is peripheral vascular disease?

A

Atherosclerosis of the lower limb arteries which can cause claudication and limb ischaemia.

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115
Q

What are the risk factors for PVD?

A

Same for CVD - Smoking, htn, age, obesity, CKD, T2DM, alcohol, stress.

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116
Q

What is the pathophysiology of PVD progression?

A

Intermittent claudication - Atherosclerotic partial lumen occlusion, pain on exertion.
Critical limb ischaemia - Large occlusion, perfusion is inadequate for metabolic demand.
Acute limb ischaemia - Total occlusion of artery due to thrombus formation.

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117
Q

At what stage of PVD is there pain at rest?

A

Critical limb ischaemia.

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118
Q

What are three complicatons of acute limb ischaemia?

A

Irreversible nerve and muscle damage, skin changes (gangrene).

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119
Q

When is the pain of critical limb ischaemia the worst?

A

At night when gravity doesn’t pull blood to the feet.

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120
Q

What are the symptoms of acute/critical limb ischaemia?

A

6Ps: Pulselessness, pallor, pain, paralysis, paresthesia, perishing cold.

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121
Q

What are the five signs of PVD?

A

Skin changes on leg - colour and ulceration.
Lack of lower leg pulse.
Reduced skin temperature and sensation.

122
Q

What is the Buerger test and what is it used for?

A

Used to diagnose PVD.
Elevate legs to 45 degrees for 1min, will cause pallor due to low blood flow then dark red legs due to reactive hyperaemia.

123
Q

How is PVD diagnosed?

A

Ankle-brachial pressure index (ABPI). Measures ankle systolic BP against arm systolic BP. Lower = worse.
-USS to assess the degree of stenosis.
-CT or MRI angiography.

124
Q

What is the normal range for ABPI?

A

0.9-1.3.

125
Q

What is the ABPI range for mild PVD?

A

0.6-0.9.

126
Q

What is the ABPI range for moderate to severe PVD?

A

0.3-0.6.

127
Q

What is the ABPI range for severe PVD?

A

Less than 0.3.

128
Q

What is the treatment for intermittent claudication?

A

Lifestyle management and exercise.
-Medical (statin, antiplatelet)
-Surgery.

129
Q

What is the treatment for critical limb ischaemia?

A

Analgesia and revascularisation. Angioplasty, bypass surgery, endarterectomy.

130
Q

What is the treatment for acute limb ischaemia?

A

Thrombolysis, thrombectomy, bypass surgery.

131
Q

What is a major complication of PVD?

A

Leg amputation.

132
Q

What is pericarditis?

A

Inflammation of the pericardium.
Can be acute or chronic.
Can be with or without effusion.

133
Q

Who is pericarditis most common in?

A

Young adults who have had a previous viral infection.

134
Q

What are the six causes of pericarditis?

A

Idiopathic.
Viral (coxsackie).
Bacterial (TB).
Autoimmune (SLE, RA).
Dressler’s syndrome.
Cancer (lung/breast).

135
Q

What is the most common cause of pericarditis?

A

Viral - coxsackie virus.

136
Q

What is the pathophysiology of pericarditis?

A

The pericardial layers can rub together and cause further inflammation.
Can remain dry or become effusive.

137
Q

What is the presenting symptom of pericarditis?

A

Severe sharp pleuritic chest pain with referral to left shoulder tip that is relieved by sitting forward and worse when lying flat.

138
Q

What are three other symptoms of pericarditis?

A

SOB, fever, cough.

139
Q

How is pericarditis diagnosed?

A

ECG, CXR, bloods, pericardial friction rub.

140
Q

What are the features on an ECG of pericarditis?

A

Widespread saddle shaped ST elevation and PR depression.

141
Q

What does elevated troponin levels in pericarditis suggest?

A

Myopericarditis - extended inflammation to myocardium.

142
Q

What is the treatment for pericarditis?

A

Mostly self-limiting.
Treat with NSAIDs and colchicine.
Treat underlying cause (TB - Abx).

143
Q

What are three complications of pericarditis?

A

Pericardial effusion, cardiac tamponade, myocarditis.

144
Q

What is cardiac tamponade?

A

Accumulation of fluid in pericardial space which usually accompanies pericarditis.

145
Q

How is cardiac tamponade caused?

A

Typically pericarditis.

146
Q

Why is cardiac tamponade dangerous?

A

There is a large accumulation of fluid in the pericardial space which squeezes the heart and leads to impaired diastole and reduced ejection during systole.

147
Q

What are the signs/symptoms cardiac tamponade?

A

Beck’s triad: Hypotension, increased JVP, muffled heart sounds.
Pulsus paradoxus: Systolic BP drops by >10mmHg on inspiration.

148
Q

How is cardiac tamponade diagnosed?

A

Usually ECHO (GS).
CXR, ECG.

149
Q

How is cardiac tamponade treated?

A

Treat underlying cause.
Urgent pericardiocentesis.

150
Q

What is infective endocarditis?

A

Infection of the endocardium (inner lining of the heart).

151
Q

Which valve does infective endocarditis typically affect?

A

Mitral valve but in IVDU the tricuspid valve.

152
Q

When would IE be suspected?

A

If a patient presents with fever and a new murmur.

153
Q

What causes infective endocarditis?

A

Typically bacteria:
-Staph aureus - mc.
-Strep viridans - mouth/oral surgery, IVDU.
-Staph epidermidis - prosthetic valves.

154
Q

What are the four risk factors for infective endocarditis?

A
  1. Male, elderly with prosthetic valves.
  2. Young, IV drug user.
  3. Young with congenital heart defect.
  4. Rheumatic heart disease.
155
Q

What is the pathophysiology of infective endocarditis?

A

Damaged endocardium has platelet deposition, bacteria adheres here and causes vegetations.
Typically occurs around valves

156
Q

What are the symptoms of infective endocarditis?

A

Vague - fever.

157
Q

What are five signs in infective endocarditis?

A
  1. Valve regurgitation.
  2. Osler nodes (finger nodules).
  3. Janeway lesions (painful hand marks).
  4. Splinter haemorrhages (on fingernails).
  5. Roth spots (retinal haemorrhages).
158
Q

What is the diagnostic criteria of infective endocarditis?

A

Made using Duke’s criteria (2 major or 1 major and 2 minor):
-ECHO (GS) and blood cultures.
1. Major = 2 +ve blood cultures, ECHO vegetations.
2. Minor = IVDU, immune signs, 1+ve blood culture, pyrexia.

159
Q

How is infective endocarditis treated?

A

Depends on the bacteria:
-S. Aureus = Vancomycin and rifampicin.
-S. viridans = Benzylpenicillin and gentamycin.

Surgery - Remove valve if incompetent and replace with prosthetic.

160
Q

What are four complications of infective endocarditis?

A

Heart failure, aortic root abscesses, septic emboli and sepsis.

161
Q

What is stenosis in valve disease?

A

Narrowing of a valve.

162
Q

What is regurgitation in valve disease?

A

Leaky, insufficient valve.

163
Q

What are the main four valve diseases?

A

Mitral stenosis and regurgitation.
Aortic stenosis and regurgitation.

164
Q

What does mitral stenosis do to the heart?

A

Causes left atrial hypertrophy.

165
Q

What does aortic stenosis do to the heart?

A

Causes left ventricular hypertrophy.

166
Q

What does mitral regurgitation do to the heart?

A

Left atrial dilation.

167
Q

What does aortic regurgitation do to the heart?

A

Left ventricular dilation.

168
Q

What is mitral stenosis?

A

Narrow mitral valve which makes it more difficult for the left atrium to push blood to the ventricle and causes left atrial hypertrophy.

169
Q

What are the main causes of mitral stenosis?

A

Rheumatic fever and infective endocarditis.

170
Q

Which murmur does mitral stenosis cause?

A

Low pitched mid diastolic murmur.

171
Q

When is mitral stenosis heard loudest?

A

At the apex beat on expiration.

172
Q

Which two things is mitral stenosis associated with?

A

Malar flush and atrial fibrillation.

173
Q

How are valve diseases diagnosed?

A

Gold standard is ECHO.
Others are CXR and ECG.

174
Q

How are valve diseases treated?

A

Monitoring, drugs and valve replacements (can be open or like PCI).

175
Q

What is mitral regurgitation?

A

Incompetent mitral valve which allows blood to leak back into left atrium causing left atrial dilation.

176
Q

What can mitral regurgitation cause and why?

A

Congestive heart failure as leaking valve causes a reduced ejection fraction and a backlog of blood.

177
Q

What five things cause mitral regurgitation?

A

Idiopathic, IHD, IE, RHD and connective tissue disorders.

178
Q

What is the murmur for mitral regurgitation?

A

Pan-systolic high pitched whistling murmur.

179
Q

Where is the mitral regurgitation murmur best heard? Where does it radiate and what else may be heard?

A

At the apex, it radiates to the axilla and an S3 sound may be heard.

180
Q

What is aortic stenosis?

A

Narrowing of the aortic valve which results in left ventricular hypertrophy.

181
Q

What is the most common valve disorder?

A

Aortic stenosis.

182
Q

What causes aortic stenosis?

A

Idiopathic age related calcification.
RHD.

183
Q

What is the murmur for aortic stenosis?

A

Ejection systolic high-pitched crescendo decrescendo character.

184
Q

What are three other signs of aortic stenosis?

A
  1. Slow rising pulse and narrow PP.
  2. Murmur radiates to carotids.
  3. Exertional syncope
185
Q

How is an at risk patient with aortic stenosis treated?

A

TAVI (transcutaneous aortic valve implant).

186
Q

What is aortic regurgitation?

A

A leaky, insufficient aortic valve.

187
Q

What does aortic regurgitation result in and why?

A

Heart failure due to back pressure of blood waiting to get through to the left side of the heart.

188
Q

What is the murmur for aortic regurgitation?

A

Early diastolic soft blowing murmur.

189
Q

What causes aortic regurgitation?

A

Idiopathic age related weakness.
Connective tissue disorders.

190
Q

What are four signs of aortic regurgitation?

A

Austin Flint murmur - Mid diastolic low pitched rumble.
Corrigan pulse - Collapsing pulse, rapidly appearing and disappearing pulse.
Quincke sign - Nail bed pulses when pressed.
De Musset sign - Visible nodding of head in time with arterial pulsation.

191
Q

What is a bundle branch block?

A

When there is a conduction block in the right or left (LBBB and RBBB).

192
Q

What is the way to remember bundle branch blocks on ECG?

A

WiLLiaM MaRRoW:

LBBB is WiLLiaM (W in V1, M in V6).
RBBB is MaRRoW (M in V1, W in V6).

193
Q

What does LBBB and RBBB mean in reference to the heart beating?

A

L - LV activated later than RV.
R - RV activated later than LV.

194
Q

What is AV block?

A

Partial or complete interruption of impulse transmission from the atria to the ventricles.

195
Q

What are the types of AV blocks?

A

First degree, second degree, third degree.

196
Q

How is a first degree AV block diagnosed?

A

PR interval is prolonged (200ms+) and every P wave is followed by a QRS.

197
Q

What are the symptoms and treatment of first degree AV block?

A

Asymptomatic and no treatment.

198
Q

What causes first degree heart block?

A

Usually drugs - Bb, CCB, digoxin.

199
Q

What is a second degree AV block?

A

When some P waves are conducted and some aren’t.

200
Q

What are the types of second degree AV blocks?

A

Mobitz I and Mobitz II.

201
Q

What is second degree Mobitz I AV block?

A

PR prolongation until a QRS is dropped. The PR interval progressively elongates.

202
Q

What are the symptoms and treatment of second degree Mobitz I AV block?

A

No treatment unless symptomatic.
Sx - syncope and Tx is a pacemaker.

203
Q

What causes second degree heart block?

A

Drugs, MI, RHD.

204
Q

What is second degree Mobitz II AV block?

A

PR interval consistently prolonged with a randomly dropped QRS.

205
Q

What are the symptoms and treatment of Mobitz II AV block?

A

Syncope, SOB, chest pain.
Treatment with a pacemaker.

206
Q

What is a third degree AV block?

A

Complete heart block, the atria and ventricles beat independently to each other.

207
Q

What sustains the ventricular rhythm in third degree AV block?

A

Ventricular escape rhythm (20-40).

208
Q

What causes third degree AV block?

A

MI, hypertension, structural heart disease.

209
Q

How is third degree AV block treated?

A

IV atropine and a permanent pacemaker.

210
Q

What is the most common arrhythmia?

A

Atrial fibrillation.

211
Q

What is atrial fibrillation?

A

An irregularly irregular atrial rhythm that causes palpatations.

212
Q

What are the causes of atrial fibrillation?

A

SMITH:
Sepsis, mitral valve pathology, IHD/idiopathic, thyrotoxicosis, hypertension.

213
Q

What are the risk factors for atrial fibrillation?

A

Being over 60y, T2DM, hypertension, valve defects, MI history.

214
Q

What is the pathophysiology of atrial fibrillation?

A

Uncoordinated, rapid and irregular contraction of the atria due to disorganised electrical activity. Separate from the SA node.

215
Q

What is atrial fibrillation associated with?

A

Tachycardia, HF, risk of stroke.

216
Q

What are the three types of atrial fibrillation?

A

Paroxysmal, persistent and permanent.

217
Q

What are the four symptoms of atrial fibrillation?

A

Palpitations, SOB, chest pain, syncope.

218
Q

What are three signs of atrial fibrillation?

A

Irregularly irregular pulse, hypotension, thromboemboli.

219
Q

How is atrial fibrillation diagnosed?

A

ECG (diagnostic).

220
Q

What are the ECG features of atrial fibrillation?

A

Absent P waves, fibrillary squiggles and normal QRS waves (variable RR wave).

221
Q

What is the general treatment for atrial fibrillation?

A

Rate control, rhythm control and anticoagulation.

222
Q

Why are anticoagulants used in atrial fibrillation? Which anticoagulants are used?

A

To prevent thromboembolic events (stroke). Turbulent flow in the atria means stasis of blood (Virchow’s triad).
Warfarin, DOACs, LMWH.

223
Q

How is the rate controlled in atrial fibrillation?

A

Beta-blockers, CCB, digoxin.

224
Q

How is the rhythm controlled in atrial fibrillation?

A

Cardioversion (pharmacological and electrical).
-Pharmacological = Flecainide and amiodarone.
-Electrical = Defibrillation.

225
Q

What are three complications to atrial fibrillation?

A

Heart failure, ischaemic stroke, mesenteric ischaemia.

226
Q

What is atrial flutter and how is it recognised?

A

Irregularly regularly atrial rhythm. More regular than AF and less severe.
Diagnosed on ECG with a sawtooth pattern.

227
Q

What are the symptoms of atrial flutter and how is it treated?

A

SOB, palpitations.
Same treatment as AF.

228
Q

What is the long term curative treatment for Afib and atrial flutter?

A

Radiofrequency ablation.
Burns accessory pathways to prevent arrhythmias.

229
Q

What is tachycardia and bradycardia?

A

Bradycardia is <60bpm.
Tachycardia is >100bpm.

230
Q

What is long QT syndrome? Why is it dangerous?

A

An inherited channelopathy disorder that affects cardiac ion channels and cardiac conduction - causing a long QT interval.
It can cause ventricular tachycardia, Torsade De Pointes and ventricular fibrillation - cardiac arrest and death.

231
Q

How is long QT syndrome diagnosed?

A

ECG - QT interval is 480ms+.

232
Q

What causes Long QT syndrome?

A

Typically inherited, drugs, hypokalaemia.

233
Q

What is Torsade De Pointes?

A

Polymorphic ventricular tachycardia, can terminate or develop into ventricular fibrillation.

234
Q

What is SVT?

A

An fast heart rate where electrical signal re-enter the atria from the ventricles. Causes tachycardia.

235
Q

What are the types of SVT?

A

AVRT (WPW).
AVNRT (AV node).
Atrial tachycardia.

236
Q

What are the symptoms of SVT?

A

Palpitations, SOB, dizziness, syncope.

237
Q

How is SVT and WPW treated acutely?

A
  1. Valsalva maneuvers.
  2. IV adenosine.
  3. Electrical cardioversion.
238
Q

How is SVT and WPW treated acutely?

A
  1. Valsalva maneuvers.
  2. IV adenosine.
  3. Electrical cardioversion.
239
Q

How is SVT and WPW treated long term?

A

Radiofrequency ablation.

240
Q

What is Wolff-Parkinson-White syndrome?

A

An inherited disorder where there is an accessory pathway for impulses to travel to the ventricles (bundle of Kent).

241
Q

What are the ECG features of WPW?

A
  1. Slurred QRS waves (delta waves).
  2. Short PR interval (<120ms).
  3. Wide QRS (>120ms).
242
Q

What is cardiomyopathy?

A

Disease of the cardiac muscle that makes it hard for the heart to pump blood.

243
Q

What are the four types of cardiomyopathy?

A

Hypertrophic, dilated, restrictive and arrhythmogenic.

244
Q

What is the most common cause of sudden death in young people?

A

Hypertrophic cardiomyopathy.

245
Q

Which cardiomyopathy is the most common?

A

Dilated cardiomyopathy.

246
Q

How are cardiomyopathies diagnosed?

A

ECHO, ECG.

247
Q

What causes hypertrophic cardiomyopathy?

A

Mainly inherited, also exercise.

248
Q

What causes dilated cardiomyopathy?

A

Inherited, IHD, alcohol.

249
Q

What is hypertrophic cardiomyopathy?

A

A thick heart muscle which isn’t compliant so there is impaired diastolic filling and decreased CO.

250
Q

What is dilated cardiomyopathy?

A

Thin cardiac muscle that contract poorly and there is decreased CO.

251
Q

What is restrictive cardiomyopathy?

A

Rigid fibrotic disease myocardium which fills poorly and contracts poorly.

252
Q

What is arrhythmogenic cardiomyopathy?

A

Fibro-fatty replacement of cardiac muscle which leads to poor contraction of the heart muscle.

253
Q

How does cardiomyopathy usually present?

A

Sudden death, palpitations, heart failure, syncope, SOB.

254
Q

How are cardiomyopathies usually treated?

A

Bb, CCB, amiodarone, consider transplant and ICD.

255
Q

What is rheumatic fever?

A

Infection that is a systemic response to beta-haemolytic group A strep (pyogenes).

256
Q

How often does rheumatic fever cause rheumatic heart disease?

A

50% of the time.

257
Q

How does rheumatic fever usually present?

A

Typically pharyngitis.

258
Q

Where is rheumatic fever most common?

A

Almost all in developing countries in young people.

259
Q

What is shock?

A

A medical emergency of hypoperfusion. There is acute circulation failure, tissue hypoxia and risk of organ dysfunction.

260
Q

What are the main six symptoms of shock?

A

Pallor, cold, sweaty, decreased urine output, confusion, palpitations.

261
Q

What are six signs of shock?

A

Weak and rapid pulse, reduced GCS, increased capillary refill time, hypotension, tachycardia, pyrexic.

262
Q

What are the five types of shock?

A

Hypovolaemic, septic, cardiogenic, anaphylactic, neurogenic.

263
Q

What is hypovolaemic shock?

A

Shock due to blood loss.

264
Q

What is septic shock?

A

Shock due to uncontrolled bacterial infection (sepsis).

265
Q

What is cardiogenic shock?

A

Shock due to cardiac pump failure.

266
Q

What is anaphylactic shock?

A

Shock due to IgE type 1 hypersensitivity against an antigen/allergen and histamine release.

267
Q

What is neurogenic shock?

A

Shock due to spinal cord trauma (disrupted SNS but intact PSNS).

268
Q

What are signs exclusive to cardiogenic shock?

A

Signs of heart failure such as oedema.

269
Q

What can cause cardiogenic shock?

A

MI, cardiac tamponade, PE, HF.

270
Q

What are signs and symptoms exclusive to anaphylactic shock?

A

Puffy face, cheek flushing and urticaria (raised itchy rash).

271
Q

What are signs of neurogenic shock and how is it treated?

A

Bradycardia and hypotension.
IV atropine to inhibit the SNS.

272
Q

Which congenital cardiac conditions may present or worsen in adulthood?

A

Atrial septal defects, ventricular defects and coarctation of the aorta.

273
Q

What is an atrial septal defect?

A

A hole in the atrial septum, this allows blood to flow between them.

274
Q

What are the types of atrial septal defect?

A

Patent foramen ovale, ostium secundum, ostium primum.

275
Q

Explain the pathophysiology of atrial septal defect.

A

Blood shunts from the LA to RA. Eventually the flow of the right side of the heart leads to right heart failure and pulmonary hypertension.
Eventually pulmonary hypertension leads to Eisenmenger’s syndrome.

276
Q

What is Eisenmenger’s syndrome?

A

When pulmonary pressure exceeds the systemic pressure, causing the shunt to reverse and become a right-to-left shunt across the defect. This causes blood to bypass the lungs, resulting in the patient becoming cyanotic.

277
Q

How do atrial septal defects present?

A

SOB, right sided heart failure, pulmonary hypertension, stroke, AF.
If small they may be asymptomatic.

278
Q

How are atrial septal defects treated?

A

Small may spontaneously close.
Can be closed using percutaneous transvenous catheter closure or open heart surgery.

279
Q

What is a ventricular septal defect?

A

A hole in the ventricular septum.
Can be very small or large (one big ventricle).

280
Q

Explain the pathophysiology of VSDs.

A

Left-to-right shunt which causes right-sided overload, right heart failure and increased flow into the pulmonary vessels. Pulmonary hypertension may progress to a right-to-left shunt, resulting in cyanosis (Eisenmenger syndrome).

281
Q

How do VSDs present and how are they managed?

A

Asymptomatic until adulthood (murmur).
Catheter closure, open surgery or they may spontaneously close.

282
Q

What is coarctation of the aorta?

A

When the aorta narrows around the ductus arteriosus.
The severity of narrowing can range from mild to severe.

283
Q

Explain the pathophysiology of coarctation of the aorta.

A

Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the three branches of the aorta arch.
-May be before or after any of the branches.

284
Q

How does coarctation of the aorta present?

A

May be asymptomatic.
There may be higher BP in arms and upper body compared to legs (if after branches).
Underdevelopment of the legs.
Systolic murmur below left clavicle.

285
Q

How is coarctation of the aorta managed?

A

May remain symptom free and need no treatment.
Can be stented open with balloon angioplasty or open surgical repair.

286
Q

What is tetralogy of fallot?

A

A congenital condition with four coexisting pathologies:
-Ventricular septal defect.
-Overriding aorta.
-Pulmonary valve stenosis.
-Right ventricular hypertrophy.

287
Q

How are all congenital heart defects diagnosed?

A

ECHO.

288
Q

What are the risk factors of tetralogy of fallot?

A

Rubella infection, problems with mother (alcohol in pregnancy, being over 40y, diabetic).

289
Q

When does tetralogy of Fallot present?

A

Mostly on antenatal scans and newborns.

290
Q

What are the signs and symptoms of tetralogy of Fallot?

A

Cyanosis, clubbing, failure to thrive (poor feeding/weight gain), ejection systolic murmur and tet spells.

291
Q

What are Tet spells?

A

Intermittent cyanotic episodes caused by crying, waking or exertion.

292
Q

How is tetralogy of Fallot treated? What is the prognosis?

A

Open heart surgical repair (mortality is 5% and 90% of cases live into adulthood).

293
Q

What is a patent ductus arteriosus?

A

When the ductus arteriosus fails to close.

294
Q

When should the ductus arteriosus close?

A

Stops functioning within 1-3 days and should completely close within 2-3 weeks.

295
Q

What causes a patent ductus arteriosus?

A

Unclear.
May be genetic, premature babies or a rubella infection in maternity.

296
Q

How does a patent ductus arteriosus present?

A

They tend to be small and be asymptomatic until adulthood with signs of heart failure.

297
Q

Explain the pathophysiology of patent ductus arteriosus.

A

Blood flows from aorta to PA, causing a shunt and pulmonary hypertension. The increased right heart strain leads to right ventricular hypertrophy and the increased blood returning to the LV causes left ventricular hypertrophy.
-Can cause Eisenmenger syndrome.

298
Q

How does a patent ductus arteriosus present?

A

May be picked up on newborn exam with murmur that is ‘machinery’.
-SOB, failing to thrive.

299
Q

How is a patent ductus arteriosus treated?

A

If doesn’t close spontaneously, open surgery or catheter surgery to close.

300
Q

Which conditions cause Eisenmenger syndrome?

A

ASD, VSD, patent ductus arteriosus.

301
Q

What is a bicuspid aortic valve?

A

When there are only two cusps on the aortic valve instead of three.

302
Q

What is an atrioventricular septal defect?

A

A hole in the middle of the heart, so there isn’t a complete atrial or ventricular septum.

303
Q

Which condition is atrioventricular septal defect associated with?

A

Down’s syndrome.

Phase 2a (14 decks)

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