Cardiovascular Flashcards

1
Q

How long should the PR interval be and where is it between?

A

0.12-0.2 seconds (start of p wave to start of r wave)

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2
Q

How long should QRS be?

A

0.08-0.12 seconds

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3
Q

How long should QT be and where is it between?

A

0.35-0.45 seconds (start of QRS to end of T)

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4
Q

Which leads provide a view of the anterior and septal heart (LAD)

A

V1-4

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5
Q

Which leads provide a view of the lateral heart (Cx)

A

V5,6 + aVL, aVR + lead 1

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6
Q

Which lead provides an inferior view of the heart (RCA)

A

Lead 2, 3 + aVF

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7
Q

How long is a little square

A

0.04 seconds

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8
Q

How many milivolts is a little square

A

0.1mv

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9
Q

How long and many milivolts is a big square

A

0.2 seconds
0.5 mv

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10
Q

What does S1 sound represent

A

Mitral/ tricuspid valve closing

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11
Q

What does S2 sound represent

A

Aortic/ pulmonary valve close

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12
Q

What does S3 sound represent

A

Rapid ventricular filling - cordae tendonae twang like string as they reach their full length, opening the valve quickly (before S2). either…
1. strong healthy heart
2. heart failure/ mitral regurg

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13
Q

What does S4 sound represent

A

Turbulent flow of blood into vent due to uncomplient stiff ventricles (before S1)

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14
Q

What is cardiovascular disease

A

The development of athersclerotic arteries

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15
Q

What two affects on arteries does atherosclerosis have?

A
  • stenosis (narrowing)
  • Stiffening –> hypertension
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16
Q

What are the three major risk factors for atherosclerosis?

A
  • Old age
  • Family history
  • Hypertension
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17
Q

What are some other risk factors for atherosclerosis (7)?

A
  • Hyperlipidaemia
  • Male
  • Obesity
  • Lack of exercise
  • Diabetes
  • Smoking
  • Alcohol consumption
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18
Q

Complications of atherosclerosis

A
  • Stroke
  • IHD
  • TIAs
  • Peripheral ischemia
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19
Q

What tool can calculate the risk of stroke or MI in next 10 years, what does it ask about?

A

QRISK
Age, Gender, Family history, BP …etc

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20
Q

What 4 drugs can be used as secondary prevention of athersclerosis?

A
  • Aspirin (antiplatelet)
  • Atorvastatin
  • Atenolol (beta blocker)
  • ACE inhibitors (e.g. ramipril)
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21
Q

3 side effects of statins

A
  • Myopathy
  • Type 2 diabetes (less fat for energy)
  • Hemorrhagic stroke (rare)
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22
Q

What is ACS

A

Reduction of blood flow through the coronary arteries –> reduced O2 to myocardium

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23
Q

What are the 3 types of ACS

A
  • Unstable angina
  • NSTEMI
  • STEMI
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24
Q

What is the difference between stable and unstable angina?

A

Unstable = symptoms present at rest

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25
Q

Symptoms of angina (5)

A
  • Central crushing chest pain/ tightness
  • Nausea
  • Fatigue
  • Sweating
  • Dyspnoea
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26
Q

Diagnosis of Angina (2)

A
  • ECG
  • Coronary artery CT angiogram
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27
Q

What would an ecg show in angina (stable Vs unstable)

A

Stable = normal when resting but may show changes when exercising
Unstable = abnormal during a resting attack

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28
Q

What changes may be seen in an angina ECG (3)

A
  • ST depression
  • Inverted T wave
  • T wave tall
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29
Q

Causes of angina (2)

A
  • Atherosclerotic coronary heart disease
  • Prinzmetal’s angina (artery spasm)
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30
Q

What are 3 non invasive treatments for stable angina?

A
  • Lifestyle changes
  • Glyceryl trinitrate (GTN) spray
  • Other medications
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31
Q

What other medications are given for angina itself

A
  • Beta blocker
  • CCB
  • other - ivabradine, long acting nitrates
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32
Q

Medications for secondary prevention of CVD in angina (3)

A
  • Aspirin
  • Atorvastatin
  • ACE - inhibitor
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33
Q

What is a contrindication for beta blockers

A

asthma

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34
Q

What is a contraindication for CCBs in angina

A

Heart failure

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35
Q

What 2 invasive procedures can be carried out for angina

A
  • Percutaneous coronary intervention
  • CABG
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36
Q

What 2 vessels are often used in CABG

A
  • Internal mamory artery
  • Great saphenous vein (leg)
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37
Q

What can be used to guide Tx in angina

A

Grace score (predicts chance of MI)

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38
Q

How is NSTEMI diagnosed

A

Troponin blood levels (due to death of heart tissue)

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39
Q

How is STEMI diagnosed

A

ECG - ST elevation in 2 or more leads

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40
Q

How is NSTEMI/ unstable angina treated initially (5)

A
  • Morphine
  • Oxygen (If low sats <94%)
  • Nitrates
  • Aspirin/ anticoagulant
  • Clopidogrel/ other anti-platelet
    MONAC
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41
Q

What will be carried out after initial treatment of NSTEMI/ unstable angina

A

Angiogram if high risk GRACE score –> PCI

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42
Q

How is STEMI treated

A
  • MONAC
  • then agiogram + PCI
    … if not available –> thrombolysis
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43
Q

Preventative treatment after MI (3)

A
  • Aspirin
  • Atorvastatin
  • ACE - inhibitor
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44
Q

What is the difference between STEMI / NSTEMI in terms of heart tissue

A

STEMI = transmural - more tissue affected and disrupts electrical conduction more

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45
Q

Complications of MI

A
  • Heart failure - tissue death (valve, muscle…)
  • Dressler syndrome - pericarditis due to immune responce to tissue death
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46
Q

Who is at risk of ‘silent’ MI

A
  • Diabetics - diabetic neuropathy
  • Females more at risk
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47
Q

What is heart failure

A

Inability for heart to deliver oxygenated blood to tissues at the required rate

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48
Q

What is the most common cause of heart failure?

A

Ischemic heart disease - MI

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49
Q

What are some other causes of heart failure (4)?

A
  • Cardiomyopathy
  • Valvular disease
  • Hypertension/ cor pulmonale
  • Arhythmias
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50
Q

Risk factors for heart failure (6)

A
  • Age (65+)
  • Smoking
  • Obesity
  • Previous MI
  • Male
  • Genetics/ family history
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51
Q

Pathophysiology of heart failure

A

Decreased cardiac output for whatever reason –> increased SNS and RAAS –> heart works harder, remodels and fails

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52
Q

What 3 hormonal mechanisms initially compensate for the effects of heart failure

A
  • RAAS
  • ADH
  • Adrenaline/ NAd
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53
Q

What is conjestive heart failure?

A

Heart failure in left and right side

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54
Q

What is reduced ejection fraction heart failure

A

The heart is pumping a smaller fraction of blood into the body with each stroke (can indicate worse prognosis)

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55
Q

Is reduced or preserved ejection fraction heart failure systolic or diastolic failure

A

Reduced = systolic
Preserved = diastolic

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56
Q

How is heart failure time classified

A

Chronic
Acute - life threatning

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57
Q

What is normal ejection fraction of the heart?

A

50-70%

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58
Q

What is classed as reduced ejection fraction heart failure?

A

<40%

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59
Q

Which sided heart failure results in pulmonary and which systemic oedema?

A

Left = pulmonary oedema
Right = systemic oedema

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60
Q

3 cardianal signs of heart failure

A
  • Breathlessness
  • Peripheral oedema
  • Faitigue
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61
Q

What are some other signs of heart failure (5)

A
  • Orthopnoea (breathless when lying)
  • Paroxysmal nocturnal dysponea
  • Increased jugular pressure
  • Bibasal crackles (pul oedema)
  • Tachy/ hypotensive
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62
Q

What is paroxysmal nocturnal dysponea?

A

Waking at night with severe shortness of breath

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63
Q

What 3 mechanisms cause paroxysmal nocturnal dysponea?

A
  • Lying flat –> fluid settles on large area of lungs –> can’t breathe
  • Repiratory center in pons less active when asleep
  • Less adrenaline during sleep
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64
Q

How does the NY heart association classify heart heart failure

A
  • 1 - no limit on exercise
  • 2 - slight limit on exercise
  • 3 - marked limit on exercise
  • 4 - symptoms even at rest
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65
Q

Heart failure diagnostic tests (4)

A
  • Blood test for B-type natriuretic peptide
  • Echo
  • Chest X-ray
  • ECG
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66
Q

Why is B-type natiuretic peptide released in heart failure?

A

Stressed ventricular myocytes
Higher BNP levels = worse heart failure

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67
Q

What is indicitive of heart failure on CXR (5)

A
  • Alveolar bat wing oedema (fluid around heart)
  • Kerley B-lines
  • Cardiomegaly
  • Dilated upper lobe vessels
  • Pleural Effusion (fluid in pleural space)

ABCDE

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68
Q

How is heart failure treated (3 steps)

A
  • Lifestyle changes
  • Medications
  • Surgery for underlying cause/ heart transplant
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69
Q

What 4 medications and what order are used in heart failure

A
  1. ACE inhibitors + Beta blockers
  2. Aldosterone antagonists - spironolactone
  3. Loop diuretics - furosemide

ABAL

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70
Q

What is an abdominal aortic aneurism

A

Permanent dilation of the aorta of more than 50%

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71
Q

Risk factors for AAA

A
  • Connective tissue disorders - marfans/ EDS
  • Smoking
  • Obesity
  • Hypertension
  • Elderly
  • Atherosclerotic RFs
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72
Q

What point in the aorta do AAA usually occur below?

A

Renal arteries

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73
Q

Which layers of the aorta are affected in an AAA

A

All 3 layersm - intima, media and adventitia

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74
Q

How dilated must the aorta be to be considered an aneurysm

A

3 cm

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75
Q

What are the signs/ symptoms of AAA

A

None until rupture then…
* sudden epigastric pain raidiating to flank
* Pulsatile mass in abdomen
* Tachy + hypo

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76
Q

How is an AAA diagnosed

A

Abdominal ultrasound

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77
Q

How is AAA treated

A
  • Lifestyle changes
  • Surgery if bad enough
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78
Q

What are the two types of surgery for AAA

A
  • EVAR (endovascular repair) - stent graft put throught femoral artery
  • Open surgery
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79
Q

How dilated must an AAA be for surgery

A

> 5.5cm or increasing at 1cm/year

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80
Q

How is a ruptured AAA treated?

A
  • ABCDE - emergency
  • Fluids + transfusion if needed (be carfeul not to displace clots)
  • Surgical repair urgently or after angiogram
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81
Q

What percent of AAA rupture anteriorly and what percent retroperitoneal

A
  • 20% anteriorly - into peritoneal cavity (worse)
  • 80% retroperitoneal
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82
Q

Why is atherosclerosis so much less common in venous circulation?

A
  • No smooth muscle cells
  • Much lower pressures
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83
Q

What is an aortic dissection?

A

Tear in the intima of the aorta which allows blood to dissect between the intima and media

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84
Q

What are 5 risk factors for aortic dissection?

A
  • Hypertension
  • Atherosclerosis
  • Connective tissue disorders
  • Trauma
  • Smoking
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85
Q

What are the two most common locations for dissection to occur?

A
  • Sinotubular junction - just after root of aorta, near valve
  • Just distal to left subclavian artery origin
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86
Q

How does the stanford classification classify 2 types of dissection?

A

Type A - proximal to origin of left subclavian (more common)
Type B - distal to left subclavian

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87
Q

Where can blood in the false lumen flow to?

A
  • Back up the aorta into the pericardial space
  • Puncture out of artery into media stinum
  • Puncture back into the lumen
  • Down the aorta and compress branching arteries
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88
Q

What are the signs/ symptoms of aortic dissection

A
  • Sudden onset tearing chest pain
  • Tachy/ hypo
  • Aortic regurg murmur
  • Weak radial pulse
  • Cardiac tamponade - blood collects around pericardium
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89
Q

How is aortic dissection diagnosed?

A
  • Ultrasound - can be transoesophageal
  • CT angiogram
  • Chest x-ray
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90
Q

How would an aortic dissection present in a chest x-ray

A

Widened media stinum > 8cm

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91
Q

How is aortic dissection treated?

A
  • Surgery
  • Medication if less severe
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92
Q

What two types of surgery treat aortic dissection?

A
  • Open surgical repair
  • EVSR - endovascular repair
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93
Q

What medications are used to treat less serious aortic dissections

A
  • Beta blockers - to treat hypertension e.g. esmolol
  • Vasodilators - e.g. sodium nitroprusside
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94
Q

What is hypertension and what are the required readings for diagnosis?

A

High blood pressure
140/90 in clinic or…
135/85 home readings

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95
Q

What percentage of cases is primary/ essential hypertension?

A

95%

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96
Q

What can cause secondary hypertension (4)

A
  • Renal disease (most common) e.g. CKD
  • Obesity
  • Pregnancy
  • Endocrine e.g. hyperaldosteronism

ROPE

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97
Q

What are 6 risk factors for hypertension

A
  • Older age
  • Ethnicity - black
  • Overweight
  • Sedentary
  • High salt intake
  • Family history
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98
Q

What are the stages of hypertension?

A
  1. 140/90 or 135/85 (home)
  2. 160/100 or 150/95 (home)
  3. 180/120
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99
Q

What are signs/ symptoms of severe hypertension?

A
  • Headache
  • Blurred vision
  • Heart failure
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100
Q

How is hypertension diagnosed?

A

Reading of 140/90 recorded in clinic –> 24 hour ambulatory BP device (above 135/85 = diagnostic)

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101
Q

What hypertension treatment is started for those under 55 or with diabetes?

A

ACE inhibitor

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102
Q

What hypertension treatment is started for those over 55 or black

A

Calcium channel blocker

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103
Q

What drugs are used next in the treatment of hypertension?

A
  • Add one of CCB or ACE inhibitor
  • Add thioside like diuretic
  • Add beta blocker/ K+ sparing diuretic depending on K+ blood levels
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104
Q

What drug can be used in replacement of ACE inhibitor

A

Angiotensin 2 receptor blocker

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105
Q

This flashcard is an overview of hypertension treatment… draw out the pathway if you like for treatment

A
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106
Q

What is an example of ACE-i and dose used for hypertension

A

Ramipril - up to 1.25-10 mg per day

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107
Q

What is an example of a CCB and the dose for hypertension

A

Amlodipine - 5-10mg

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108
Q

What are 2 examples of Thiazide like diuretic and dose for hypertension

A
  • Indapamide - more potent
  • Bendroflumothiazide - less potent
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109
Q

What is an example of a beta blocker and dose for hypertension

A

Bisoprolol - 5-20mg

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110
Q

What is an example of a K+ sparing diuretic and dose for hypertension

A

Spironolactone - 25mg

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111
Q

What is an example of an Angiotensin 2 receptor blocker and dose for hypertension

A

Candesartan - 8-32mg

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112
Q

Why might ARB be used instead of ACE-i

A

ACE-i can cause a dry cough

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113
Q

How do ACE-i cause a dry cough?

A

ACE breaks down bradykinin –> bradykinin contracts airway smooth muscle

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114
Q

What are 4 complications of hypertension?

A
  • Heart failure
  • CKD
  • IHD
  • Cerebrovascular accident
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115
Q

What are the treatment targets for hypertension?

A

<140/90 if under 80

<150/90 if over 80 (prevent falls)

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116
Q

What other test are important to do in those with hypertension?

A

Assess end organ damage:
* Fundoscopy (look for papilloedema)
* Urine dipstick (creatinine, albumnin)
* ECG

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117
Q

What is a deep vein thrombosis?

A

A clot that forms in a deep vein (can be anywhere in the body)

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118
Q

Where are DVTs most common and which vessels are often affected?

A

Below the calf (anterior and posterior tibial veins)

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119
Q

What is a pulmonary embolism?

A

A foreign body that mobilises and blocks a pulmonary artery (usually the result of a DVT that mobilises)

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120
Q

What are the three factors in virchows triad and what might cause them?

A

Venous stasis (immobility)
Endothelial injury (smoking, trauma/injury)
Hypercoagulability (sepsis, pregnancy, the pill)

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121
Q

What does a PE result in? (2)

A
  • Cor pulmonale
  • VQ mismatch
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122
Q

Signs/ symptoms of PE (7)

A
  • Cough + haemoptysis
  • Shortness of breath
  • Sudden pleuritic chest pain
  • Evidence of DVT
  • Tachycardic
  • Hypoxic
  • Tachypnea
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123
Q

What score can acess the likelihood of having a PE

A

Wells score

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124
Q

What Wells score is suggestive of a PE?

A

4<

(evidence of DVT = 3; tachycardic = 1.5)

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125
Q

How is a pulmonary embolism diagnosed?

A
  • D-dimer (suggests PE)
  • CT pulmonary angiogram (diagnostic)
  • ECG - S1Q3T3 and RBBB (suggestive - occurs with cor pulmonale)
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126
Q

What is a D-dimer test?

A

Measures a protein released when clot is fibrinolysed

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127
Q

What does S1Q3T3 refer to?

A

Large S wave in lead I
Big Q wave in lead III
Inverted T wave in lead III

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128
Q

How does the Wells score affect the investigations done for a PE

A

If 4> then D-dimer done first, if raised –> CTPA
If 4< then CTPA done

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129
Q

What is a massive PE usually defined as?

A

Systolic BP of <90

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130
Q

How is a pulmonary embolism treated?

A
  • If massive PE - thrombolysis
  • Non-massive PE - anticoagulation
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131
Q

What are 2 examples of thrombolytic drugs?

A
  • streptokinase
  • alteplase
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132
Q

What is an exmple of anticoagulants used for PE and DVT

A
  • First line = Apixaban/ Rivaroxiban
  • LMWH (If CI e.g. renal failure)
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133
Q

What class of drug are apixaban and rivaroxiban and what do they inhibit?

A

DOACs

They inhibit factor Xa

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134
Q

How do LMWH work

A

Bind to and activate antithrombin

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135
Q

What is an example of a LMWH

A

Dalteparin

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136
Q

What is a complication of untreated pulmonary embolism?

A

cor pulmonale –> increased pulmonary resistance –> increased right ventricle strain –> right ventricle hypertrophy –> RV failure

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137
Q

What are the symptoms of a deep vein thrombosis (3)

A

Unilateral leg:
* Swelling
* Redness
* Oedema

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138
Q

What does a complete occlusion of a large vein cause?

A

Clotting backs up into cappilaries causing arterial ischemia (phlegmasia cerulea dolens)

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139
Q

What are the signs/ symptoms of Phlegmasia cerulea dolens (2)

A
  • Blue leg
  • Painful
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140
Q

How is DVT investigated?

A
  • D-dimer (raised)
  • Duplex sonography - diagnostic (allows flow of blood to be seen)
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141
Q

What wells score is suggestive of DVT?

A

1<

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142
Q

How is DVT treated?

A

Same as non massive PE:
* Apixaban/ rivaroxaban = first line
* LMWH if CI (e.g. renal failure)

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143
Q

What is a differential diagnosis for DVT?

A

Cellulitis - red swollen leg

  • Confirm with D-dimer (-ve) and should have high WBC count
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144
Q

What is peripheral vascular disease?

A

Reduction of blood flow through peripheral arteries (IHD of limbs)

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145
Q

What are risk factors for PVD (8)

A

Basically atherosclerotic RFs:
* Smoking
* Age
* Hyperlipidemia
* Male
* Age
* Hypertension
* T2DM
* Obesitiy
* Ethnicity?

146
Q

What is Acute limb ischemia

A

Sudden decrease in perfusion of the limb = emergency

147
Q

What is a severe form of chronic limb ischemia?

A

Critical limb threatning ischemia

148
Q

What are the symptoms of PVD (8)

A
  • Pain
  • Pallor (pale)
  • Pulsetiless
  • Paresthesia (pins and needles)
  • Pereshingly cold
  • Paralysis
    6 Ps
    Also:
  • Ulcers;
  • Bruits (pulsatile areas due to turbulent blood flow)
149
Q

How long do nerve and muscle damage take to occur after infarction?

A
  • nerve = 6 hours
  • muscle = 6-10 hours
150
Q

What are the stages of PVD

A
  1. Assymptomatic
  2. Brought on with exercise (stable angina)
  3. Occurs at rest (unstable angina)
  4. Infarction (MI)
151
Q

How is PVD investigated?

A
  • Ankle brachial pressure index
  • Duplex ultrasound
  • CT angiogram
152
Q

What is Ankle brachial pressure index (ABPI)

A

Compares the blood pressure at ankle (anterior and posterior tibial arteries) to the brachial pressure. Ankle/brachial

153
Q

What ABPI values suggest intermittent claudication and then chronic ischemia

A

Intermittent claudication = 0.5-0.9
Chronic ischemia = <0.5

154
Q

How is intermittent claudication treated?

A
  • Adress risk factors
  • Treat HT
  • statins, antiplatelets
155
Q

How is chronic limb ischemia treated?

A

Revascularisation surgery:
* PCI
* Bypass

156
Q

How is acute limb threatening ischemia treated

A

Revascularisation quickly within 4-6 hours

157
Q

What are some complications of PVD

A
  • Amputation
  • Loss of function/ weakness
  • Rhabdomyolysis
158
Q

What are some further complications of rhabdomyolysis?

A

Release of K+ and Ca2+ into blood –> AKI + arrhythmias

159
Q

What is pericarditis?

A

Inflammation of the pericardium with or without effusion

160
Q

What are the two types of effusion that can occur in the pericardium?

A
  • Exudate
  • Hemorrhagic (blood)
161
Q

What are the causes of pericarditis (6)?

A
  • Idiopathic
  • Infectious
  • Dressler’s syndrome (after MI)
  • Autoimmune (e.g. SLE, RA, Sjogren’s)
  • Tumours (lung/ breast)
  • Drug induced
162
Q

What are the 3 layers of the pericardium?

A
  • Outer fibrous pericardium
  • Parietal serous pericardium
  • Visceral serous pericardium
    Layers can rub together in pericarditis and exacerbate inflammation
163
Q

What are the symptoms of pericarditis?

A
  • Sharp pleuritic chest pain –> left shoulder (phrenic nerve)
  • Dyspnoea
  • Pericardial friction rub on oscultation
164
Q

What position is pericardial frication rub best heard in pericarditis?

A

Leaning forward

165
Q

When is pericarditis chest pain worst?

A

Lying down

166
Q

How is pericarditis investigated?

A
  • ECG
  • Blood tests for sign of infection
  • Echo (TTE or TOE)
  • Xray (and other imaging)
167
Q

How is pericarditis reflected in an ECG?

A
  • Saddle shaped ST segment
  • PR depression
168
Q

What does a blood test test for in suspected pericarditis (2 key things)

A
  • Raised WBC count (infection)
  • Erythrocyte sedimentation rate (ESR)/ C reactive protein (CRP)
169
Q

What may be seen on a chest X ray in pericarditis?

A

Increased cardiothoracic ratio > 0.5

170
Q

How is pericarditis treated (2 medicines)?

A
  • NSAIDs
  • Colchicine (anti inflammatory)
171
Q

What are some complications of pericarditis (3)?

A
  • Constrictive pericarditis
  • Myocarditis
  • Pericardial effusion –> cardiac tamponade
172
Q

Complications of pericarditis

A
  • Cardiac tamponade (due to pericardial effusion)
  • Myocarditis
  • Heart failure
173
Q

What is cardiac tamponade?

A

Pericardial effusion which causes impared ventricular filling

174
Q

What can cause cardiac tamponade?

A
  • Pericarditis
  • Aortic aneurism
  • Trauma
175
Q

What are the symptoms of cardiac tamponade?

A
  • Becks triad
  • Pulsus paradoxus
176
Q

What are the three symptoms of Beck’s triad

A
  • Hypotension
  • Raised JVP
  • Muffled heart sounds
177
Q

What is pulsus paradoxus

A

A fall of more than 10 mmHg in systolic BP on inspiration

178
Q

Investigations for cardiac tamponade

A
  • ECG - varying QRS size as heart bounces around in pericardium
  • Chest X-ray - large globular heart
  • Ultrasound - diagnostic
179
Q

How is cardiac tamponade treated?

A

Pericardiocentesis (needle aspiration of pericardial sac)

180
Q

What is infective endocarditis?

A

Infection and inflammation of endocardium (particularly affects valves)

181
Q

What is a vegetation describe how it forms?

A

Damaged endothelium –> platelet fibrin mesh forms –> pathogen attaches –> more platelets aggregate, pathogens buried

182
Q

What are the two most common bacteria that cause endocarditis?

A
  • Staph aureus (staphylococci)
  • Strep viridans (streptococci)
183
Q

What is the most common gram -ve bacteria in endocarditis?

A

HACEK organisms (anronym for group)

184
Q

What are the 2 most common fungi to cause endocarditis?

A
  • Candida
  • Aspergillus
185
Q

What are some risk factors for IE

A
  • Male
  • Elderly
  • Posthetic valve
  • IV drug users
  • Congenital heart defects
  • Rheumatic heart disease
186
Q

Which valve of heart is more commonly affected

A

Tricuspid valve

Mitral valve more common in general population, however IVDU make up a large proportion of those affected, and they have their tricuspid valve infected as inject into veins

187
Q

What can a vegetation on a valve cause?

A

Regurgitation

188
Q

What are some signs/ symptoms of IE (not hand signs or eye), (3)?

A
  • Tachycardia
  • Fever
  • New heart murmur
189
Q

What are 4 main peripheral signs of IE and 2 others

A
  • Osler nodes - finger nodules
  • Janeway lesions - painful marks on palms
  • Splinter haemorrhages - on nails
  • Roth spots - retinal haemorrhage
  • Petechiae - pinpoint round spots due to bleeding
  • Septic emboli
190
Q

What criteria guide a diagnosis of IE

A

Duke criteria

191
Q

What are the 2 major Duke criteria

A
  • 2 postitive blood cultures
  • Echo shows vegetation
192
Q

What are 5 minor Duke criteria

A
  • Immunological signs (e.g. roth spots)
  • Risk factor (e.g. IVDU)
  • Septic emboli
  • 1 positive blood culture
  • Pyrexia >38
193
Q

How many criteria are required for IE to be strongly suspected?

A
  • 2 major
  • 1 major; 3 minor
  • 5 minor
194
Q

What investigations are done for IE (3)?

A
  • ECG
  • Bloods
  • Echo
195
Q

What can blood tests show in IE (3)

A
  • High ESR/CRP
  • High WBC (neutrophillia)
  • +ve cultures
196
Q

What does an ECG somtimes show in IE

A

Prolonged PR = aortic root abscess

197
Q

How is IE treated (2)

A
  • Antibiotics/ antifungals
  • Surgery - remove/ repair valve
198
Q

What antibiotics are used for staph. aureus (2)

A
  • Vancomycin
  • Rifampicin
199
Q

What antibiotic is used for strep. viridans (2)

A
  • Benzylpenicillin
  • Gentamicin
200
Q

What are some complications of IE (4)

A
  • Heart failure
  • Septic emboli
  • Valve regurgitation
  • Aortic root abscess
201
Q

What is the most common valvular disorder?

A

Aortic stenosis

202
Q

What are the two classes of valve disorder?

A
  • Regurgitation
  • Stenosis
203
Q

What affects do regurgitation and stenosis have on the chambers?

A
  • Regurgitation = proximal chamber dilation
  • Stenosis = proximal chamber dilation + hypertrophy
204
Q

When are right and left side defects best heard?

A
  • Right = on inspiration
  • Left = on expiration
205
Q

What area is a normal mitral valve and when would symtpoms begin?

A

4-6 cm^2 = normal
<2 cm^2 = symptoimatic

206
Q

What causes mitral stenosis?

A
  • Rheumatic heart disease = most common
  • Valve calcification
  • IE
207
Q

How does rheumatic heart disease cause mitral stenosis (simple)?

A

Repeated RHD = reactive inflammation of mitral valve

208
Q

What are the signs/ symptoms of mitral stenosis (4)

A
  • Malar cheek flush
  • Dyspnoea
  • Pulmonary oedema (crckling lungs)
  • Pulmonary hypertension - high JVP, etc
209
Q

What causes malar cheek flush?

A

Back pressure of blood into pulmonary circulation–> retention of CO2 –> CO2 is a vasodilator, red cheeks

210
Q

What condition is associated with MS and why?

A

AFib as LA hypertrophy –> electrical disruption

211
Q

When is MS murmur heard?

A

Mid diastolic, low pitched

212
Q

How does MS affect S1

A

Louder as high pressure needed to shut stiff valve

213
Q

How is MS investigated?

A
  • CXR - enlarged RA
  • ECG - AFib/ enlarged RA
  • Echo = gold standard
214
Q

How is MS treated?

A
  • Medications - for symptoms
  • Surgery
215
Q

What 2 surgerys can be done for MS?

A
  • Valve replacement
  • Percutaneous balloon valvotomy (opens valve opening)
216
Q

What causes mitral regurgitation (3)?

A
  • Myxomatous degeneration
  • Marfans/ EDS
  • IE/ RHD/ MI
217
Q

What is the main symptom of MR

A

Exertion dyspnoea

218
Q

When is a MR murmur heard?

A

Pan systolic radiating to axilla

219
Q

What extra heart sound is heard in MR

A

S3

220
Q

How does MR affect S1

A

Softer

221
Q

How is MR investigated?

A
  • ECG - LA enlargement + AFib
  • CXR - LA enlargement
  • Echo = gold standard
222
Q

How is MR treated?

A
  • Medication
  • Surgery - replacement or repair
223
Q

What is the normal area and symptomatic area of aortic valve

A

normal = 3-4 cm^2
symptomatic = 1/4 of size

224
Q

What causes AS

A
  • Calcification (age related)
  • Congenital (bicuspid valve)
225
Q

What are the signs/ symptoms of aortic stenosis (3)?

A
  • Syncope (exertional)
  • Angina
  • Dyspnoea
    SAD
226
Q

What sort of murmur is an AS murmur?

A

Ejection systolic crescendo decrescendo @right sternal border 2nd space, radiating to carotids

227
Q

What other heart sound can be heard?

A

S4

228
Q

What other features are common with AS (2)?

A
  • Narrow pulse pressure
  • Slow rising pulse
229
Q

How is aortic stenosis investigated?

A
  • ECG
  • CXR
  • Echo = gold standard (LV size + function)
230
Q

How is AS treated surgically (2)?

A
  • Healthy patient = open repair/ replacement
  • At risk patient = transoesophageal aortic valve implant (TAVI)
231
Q

What causes AR (3)

A
  • Congenital bicuspid valve
  • RHD/ IE
  • Marfans/ EDS
232
Q

What are the signs/ symptoms of AR

A
  • Wide pulse pressure
  • Collapsing pulse @carotid
233
Q

What sort of murmur is heard in AR

A

Early diastolic murmur @left sternal border 3rd space

234
Q

What is a more severe murmur heard in AR?

A

Austin flint murmur - mid diastolic murmur (blood bounces of mitral valve cusps)

235
Q

How is AR investigated?

A
  • ECG
  • CXR
  • Echo = gold standard
236
Q

How is AR treated?

A
  • Medications for symptoms
  • Surgery if severe
237
Q

What is bradycardia defined as?

A

<60

238
Q

What is tachycardia defined as?

A

> 100

239
Q

What is the pathway of electrical impulses through the heart?

A

SA node –> Bachmann’s bundle –> AV node –> Bundle of His –> Right/ left bundle –> Purkinje fibres

240
Q

What is the most common arrhythmia?

A

Atrial fibrillation

241
Q

What is the rhythm of atrial fibrillation?

A

Irregularly irregular (QRS complexes)

242
Q

What can cause AF (6)?

A
  • Heart failure
  • Htn
  • Mitral valve pathology
  • IHD / MI
  • Hyperthyroidism
  • Congenital defects
243
Q

What is happening to the electrical activity for AF to occur?

A

Completely disorganised activity around both atria, with electrical activity re-entering

244
Q

What is the difference between AFib and flutter?

A
  • AFib is more disorganised
  • AFlutter has electrical signals moving in a circle, re-entering in an organised more regular way
245
Q

What are the symptoms/ signs of AF

A
  • Irregularly irregular pulse
  • Palpitations
  • Stroke
  • Syncope
  • Hypotensive
246
Q

Investivgations for AF

A

ECG = no P wave; irregularly irregular pulse; narrow QRS

247
Q

How is AF treated?

A
  • Rate control first line…
  • … then rhythm control
    Acute attack = cardioversion
248
Q

What medication is used for rate control (3)?

A
  • Beta blockers
  • CCBs
  • Cardiac glycoside
249
Q

What beta blocker might be used?

A

Atenolol

250
Q

What are the two classes of CCBs?

A
  • Dihydropyridines - peripheral vasodilators
  • Non-dihydropyridines - affect SA + AV nodes
251
Q

Which CCB is used in AF and what class?

A

Non-dihydropyridines (diltiazem)

252
Q

What cardiac glycoside is used in AF?

A

Digoxin

253
Q

How does digoxin work?

A

Inhibit Na+/K+ ATPase pump in heart

254
Q

What medications are used for rhythm control in AF (3)?

A
  • Beta blockers
  • Dronedarone
  • Amiodarone
255
Q

What are the two types of cardioversion?

A
  • Electrical cardioversion
  • Pharmacological cardioversion
256
Q

What medication is used for pharmacological cardioversion?

A
  • 1st line = Flecanide
  • 2nd line = amiodarone
257
Q

What medication can be used to treat AF that comes in attacks?

A

Flecanide

258
Q

What medications are used in AF to prevent strokes?

A

Anticoagulants

259
Q

What anticoagulants are used in AF?

A
  • Warfarin
  • N/DOACs
260
Q

How does warfarin work?

A

Vitamin K antagonist - clotting factors 10,9,7,2

261
Q

What needs to be monitored when using warfarin?

A

International normalised ratio (INR) - how prothrombin time compares to normal adult

262
Q

What enzyme breaks down warfarin and can be affected by diet and medications?

A

Cytochrome p450

263
Q

Which NOACS are commonly used for AF?

A
  • Apixaban/ rivaroxaban
  • Dabigatran
264
Q

How do apixaban and rivaroxaban work?

A

Xa inhibitors

265
Q

How does dabigatran work?

A

Prevents thrombin activating clotting factors

266
Q

What tool can assess whether a patient should be put on anticoagulation?

A

CHA2Ds2-VASc

267
Q

What does chadvasc stand for?

A
  • Congestive heart failure
  • Hypertension
  • Age > 75 = 2
  • Diabetes
  • Stroke (previous) = 2
  • Vascular disease
  • Age 65-74 = 1
  • Sex (female)
268
Q

What tool can assess the likelihood of a bleed?

A

HAS-BLED

269
Q

What are some complications of AF (2)

A
  • Heart failure
  • Stroke
270
Q

What is Atrial flutter?

A

The atria beating too fast but in a more regular way than AF

271
Q

How fast is atrial flutter generally?

A

250-350 bpm

272
Q

What are the symptoms of atrial flutter (3)?

A
  • Dyspnoea
  • Syncope
  • Palpitations
273
Q

What heart block often occurs with atrial flutter?

A

2:1 heart block

274
Q

What pattern does atrial flutter make on an ECG?

A

Saw tooth P wave pattern

275
Q

How is atrial flutter treated?

A

Same as AF

276
Q

How else can AFib/Flut be treated using catheter

A

Catheter ablation - burn atrial septum so electrical signals cannot pass between the atria

277
Q

What is Wolff-Parkinson white syndrome?

A

An electrical connection from the atria to ventricles that surpasses the AV node

278
Q

What is this extra connection known as in WPW?

A

Bundle of Kent

279
Q

What is atrioventricular nodal reentrant tachycardia (AVNRT)

A

When the electrical activity reenters the atria through the AV node

280
Q

What is atrioventricular reentrant tachycardia (AVRT)

A

When electrical activity reenters atria through an accessory pathway (not AV node) in WPW

281
Q

How can electrical activity also travel in WPW?

A

Enter the ventricles through the bundle of Kent, and join the impulse through the AV node. (It does not always reenter the atria)

282
Q

What are some symptoms of WPW (3)?

A
  • Palpitations
  • Dizziness
  • Dyspnoea
283
Q

Features of WPW in an ECG (3)

A
  • Wide QRS
  • Delta wave (slope up early from P wave)
  • Short PR interval
284
Q

What heart rhythm can WPW, AFib/flut, AVNRT cause?

A

Supraventricular tachycardia

285
Q

How is supraventricular tachycardia treated?

A
  1. Vagal manoeuvre
  2. Adenosine
  3. Syncronised electrical cardioversion
286
Q

What are 2 examples of vagal manoeuvres?

A
  • Valsalva manoeuvre (blowing into a tube)
  • Carotid massage
287
Q

How does vagal manoeuvres treat SVT?

A

Tricks body to think BP is too high –> body works to reduce BP by slowing heart rate

288
Q

How does adenosine work?

A

Slows electrical conduction for around 10 seconds

289
Q

How does adenosine make someone feel?

A

Like they’re dying!!!!!! hahahahahahah

290
Q

What dose of adenosine is used?

A

6mg… then… 12mg… then… repeat 12mg

291
Q

How can WPW be definitively treated?

A

Catheter ablation of bundle of Kent

292
Q

What is long QT syndrome?

A

A QT interval of >480ms

293
Q

What causes long QT interval (2)?

A
  • Congenital
  • Drugs
294
Q

What electrolyte imbalances cause long QT interval (2)?

A
  • Hypokalaemia
  • Hypocalcaemia
295
Q

What causes ventricular ectopic beats?

A

Pacemaker cells in ventricles becoming stressed and sending action potential before the AP initiating in the SA node reaches it

296
Q

What is Torsades de pointes?

A

Ventricular depolarisation that rotates around a point in the heart forming QRS with varying heights

297
Q

What causes Torsades de pointes?

A

Ventricular depolarisation at the wrong point during a T wave (often due to long QT syndrome)

298
Q

What else can happen as a result of a QRS during T wave?

A

Ventricular tachycardia

299
Q

What can ventricular tachycardia progress to?

A

VFib

300
Q

How are VFib and V tachy treated?

A

Electrical defibrillation

301
Q

What causes first degree heart block?

A

Split second delay in an impulse travelling through the AV node

302
Q

How long should PR be for 1st degree heart block?

A

> 200ms

303
Q

How is 1st degree heart block treated?

A

It isn’t!!!! gotcha

304
Q

What causes 2nd degree heart block?

A

When some P waves are conducted through AV node and others are not

305
Q

What are the two types of 2nd degree heart block?

A

Mobitz 1 and 2

306
Q

What is the difference between Mobitz 1 and 2?

A

1 = PR Prolongation until QRS dropped
2 = No PR prolongation; QRS randomly dropped

307
Q

What is a fixed ratio heart block (e.g. 2:1)?

A

Ratio of P waves to QRS - occurs in Mobitz type 1 as this has a regular dropping of QRS

308
Q

What is 3rd degree heart block?

A

Complete block in AV node

309
Q

How does the heart deal with 3rd degree heart block, what happens?

A

Atria and ventricles beat independently

310
Q

How can heart blocks be treated?

A

Pacemakers

311
Q

What medication can be used to treat (3rd) degree heart block?

A

Atropine (speeds conduction through AV node)

312
Q

What can cause heart blocks (2)?

A
  • Drugs
  • MIs
313
Q

What are bundle branch blocks?

A

A block in one side of the bundle of His

314
Q

What causes LBBB (2)

A
  • MI
  • Valvular diseases
315
Q

What causes RBBB (3)

A
  • MI
  • Valvular diseases
  • Pulmonary embolism
316
Q

How does RBBB present in an ECG

A

MaRRoW
M shape in V1 (basically 2 R waves)
W shape in V6

317
Q

How does LBBB present in an ECG

A

WiLLiaM
W shape in v1
M shape in V6 (basically 2 R waves)

318
Q

How are bundle branch blocks treated?

A

Pacemakers

319
Q

What are the three types of cardiomyopathy?

A
  • Hypertrophic
  • Dilated
  • Restrictive
320
Q

What is hypertrophic cardiomyopathy?

A

Thickening of heart muscle, particularly in the septum

321
Q

What is dilated cardiomyopathy?

A

Heart chambers thin and stretch, growing larger (particularly ventricles)

322
Q

What is restrictive cardiomyopathy?

A

Walls of heart become stiff and rigid, don’t fill well

323
Q

What causes hypertrophic cardiomyopathy (2)?

A
  • Inherited
  • Aortic stenosis
324
Q

What mutation sometimes causes hypertrophic cardiomyopathy?

A

Autosomal dominant mutation of sarcomere proteins

325
Q

How is hypertrophic cardiomyopathy treated (3 medicines)?

A
  • BBs
  • CCBs
  • Amiodarone
326
Q

What causes dilated cardiomyopathy (2)?

A
  • Inherited
  • IHD
327
Q

How is dilated cardiomyopathy treated (2)?

A
  • BBs
  • CCBs
    etc…
328
Q

What causes restrictive cardiomyopathy (2)?

A
  • Post MI
  • Granulomatous disease (e.g. sarcoidosis)
329
Q

How is restrictive cardiomyopathy treated?

A

Transplant (or they die)

330
Q

How are cardiomyopathies diagnosed (2)?

A
  • ECG
  • Echo
331
Q

What are the symptoms of cardiomyopathies (5)?

A
  • Dyspnoea
  • Syncope
  • Heart failure
  • Palpitations
  • Chest pain
332
Q

What is shock?

A

Hypoperfusion –> Tissue hypoxia –> organ dysfunction

333
Q

What are the types of shock?

A
  • Cardiogenic
  • Septic
  • Hypovolaemic
  • Anaphylactic
  • Neurogenic
334
Q

What are the symptoms of shock (4)?

A
  • Confusion + reduced GCS
  • Weak rapid pulse
  • Pale, cold skin
  • Hypotension
335
Q

What is a complication of shock?

A

Prolonged hypotension –> organ damage

336
Q

What organs are most at risk of hypotension (4)?

A
  • Brain
  • Kidneys
  • Heart
  • Lungs
337
Q

Which type of shock is caused by bradycardia?

A

Neurogenic

338
Q

What is neurogenic shock?

A

Damage to spinal cord = disrupted SNS but intact PSNS

339
Q

How is each type of shock treated?

A

ABCDE then…
* Cardiogenic - treat underlying cause
* Septic - Antibiotics
* Hypovolaemic - fluids
* Anaphylactic - adrenaline
* Neurogenic - atropine

340
Q

How does atropine work to treat neurogenic shock?

A

Blocks vagus nerve (PSNS) –> more chance for SNS to work

341
Q

What is rheumatic fever?

A

Systemic inflammatory response following infection

342
Q

What bacteria causes rheumatic fever?

A

Strep pyogenes infection (Lancefield group A beta haemolytic streptococci)

343
Q

What percent of cases of rheumatic fever affect the heart?

A

50%

344
Q

How does strep pyogenes cause rheumatic fever?

A

Antibodies against M protein attack heart valves as similar antigens (molecular mimicry)

345
Q

What does rheumatic heart disease often cause?

A

Mitral stenosis as valve inflamed and thickens

346
Q

What are the symptoms of rheumatic fever (5)?

A
  • Arthritis erythema nodosum
  • New mitral murmur
  • Sydenham’s chorea
  • Pyrexia
  • Recent strep A infection
347
Q

How is rheumatic fever diagnosed?

A
  • CXR = cardiomegaly
  • Echo
  • Jones criteria
348
Q

What is diagnostic in the Jone’s criteria?

A

Recent strep pyogens infection + 2 major or 1 major, 2 minor

349
Q

How is rheumatic fever treated?

A

Benzylpenicillin, then phenoxymethylpenicillin

350
Q

How are Sydenham’s symptoms treated?

A

Diazepam

351
Q

What is the most common inherited heart defect?

A

Bicuspid aortic valve

352
Q

What 3 inherited conditions affect the septum?

A
  • Atrial septal defect
  • Ventricular septal defect
  • Atrioventricular septal defect
353
Q

What two conditions result from the failure of tissues to close?

A
  • Patent ductus arteriosus
  • Patent foramen ovale
354
Q

What can these septal and patent conditions cause?

A

Eisenmenger syndrome

355
Q

What is Eisenmenger syndrome?

A

Left to right shunt –> pulmonary hypertension

356
Q

What 4 things together cause tetralogy of Fallot?

A
  • VSD
  • Misplaced aorta
  • Pulmonary stenosis
  • RV hypertrophy
357
Q

How is tetralogy of Fallot treated?

A

Full surgical repair

358
Q

What is coarctation of the aorta?

A

Narrowing of the aorta just after ductus arteriosus

359
Q

What does coarctation of the aorta result in?

A

More blood to upper limbs and brain than lower body

360
Q

What is the main sign of coarctation of the aorta?

A

Hypertension in the upper body

361
Q

How is coarctation of the aorta diagnosed?

A
  • CXR
  • CT angiogram
362
Q

How is coarctation of the aorta treated?

A

Surgical repair/ stent