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Phase 2a > Cardio > Flashcards

Cardio Flashcards

1
Q

Average blood pressure?

A

120/80 mmHg

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2
Q

Differential diagnosis of chest pain?

A
  • Angina
  • ACS
  • Pulmonary embolism
  • Pericarditis
  • GORD
  • Aortic dissection
  • MI
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3
Q

Conditions associated with peripheral chest pain?

A
  • Pulmonary infarct
  • Pneumonia
  • Pneumothorax
  • Herpes zoster
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4
Q

Assessment of chest pain?

A

SOCRATES

Site

Onset

Character

Radiating

Associated symptoms

Timing

Exacerbating and relieving factors

Severity

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5
Q

Examples of chest pain characteristics

A

Constricting, sharp, dull, crushing, prolonged

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6
Q

Common symptoms of cardiovascular disease?

A
  • Chest pain
  • Dyspnoea
  • Palpitations
  • Syncope
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7
Q

What is pleural pain?

A

Pain made worse by inspiration which suggests inflammation in the pleural cavity or pericardium or infarction

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8
Q

Syncope?

A

Temporary impairment of consciousness due to inadequate cerebral blood flow

  • if associated with limb weakness and dysarthria - could be a problem with the CNS
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9
Q

What is a sinus rhythm?

A

Any cardiac rhythm where depolarisation begins at the SA node - if the P wave is visible

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10
Q

How to calculate heart rate using an ECG?

A

300/ no. of big squares if regular and if irregular then its no. of QRS comples x 6

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11
Q

Order of analysing an ECG?

A

Rate

Rhythm

Axis deviation

P wave

PR segment

QRS complex

ST-segment

T wave

J point

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12
Q

Bradycardia and tachycardia ECG heart rate?

A

less than 60 for bradycardia and more than 100 for tachycardia

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13
Q

Rhythm: 100% irregular?

A

VF or AF

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14
Q

Rhythm: regular lengthening then shortening with respiration?

A

Sinus arrhythmia

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15
Q

ECG pattern of A fib?

A

No P wave and irregularly irregular

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16
Q

ECG pattern of A flut?

A

Sawtooth pattern of atrial depolarization

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17
Q

ECG showing slow ventricular depolarisation?

A

QRS complex greater than 3 little boxes (wide)

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18
Q

Normal cardiac axis range?

A

-30º to +90º

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19
Q

If lead 1 is positive and lead 2 is negative, what is the axis deviation?

A

Left axis deviation

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20
Q

What is the cardiac axis?

A

The overall direction of ventricular depolarisation on the ventricle plane measured from a 0 reference point

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21
Q

Inferior leads?

A

II, III and aVF

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22
Q

Septal leads?

A

V1 and V2

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23
Q

Anterior leads?

A

V3 and V4

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24
Q

Lateral leads?

A

I, aVL, V5 and V6

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25
Q

How above and below the isoelectric line should the ST segment be to be pathogenic?

A

>1mm above and >0.5mm below

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26
Q

What is the corrected QT interval and how do you calculate it?

A

Estimates QT interval at a standard heart rate of 60 beats per min

QT/ square root of R-R

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27
Q

Normal PR segment Range?

A

0.12 - 0.2 seconds

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28
Q

What does the PR segment show?

A

How fast AV conduction is

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29
Q

What is P mitrale an indication of?

A

Left atrial hypertrophy

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30
Q

What is P pulmonale an indication of?

A

Right atrial hypertrophy

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31
Q

What is the difference in appearance of the p wave between P mitrale and P pulomale?

A

Mitrale - bunny ears (bifid)

Pulmonale - Tall as 2.5mm

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32
Q

Difference between STEMI and NSTEMI?

A

STEMI

  • common cause of MI
  • Complete blockage of heart blood supply

NSTEMI

  • Narrowing of blood supply to the heart and not as fatal
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33
Q

1st degree heart block on an ECG?

A

PR consistently wide (0.22 seconds) - no missed beats

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34
Q

What are the 2 types of 2nd degree Heart block?

A

Mobitz I - PR interval keeps getting wider and wider until QRS complex disappears then the pattern starts again

Mobitz II - 2:1 heartblock - P - QRS - P – P -QRS

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35
Q

3rd degree heartblock on an ECG?

A

P wave and QRS complex are independent of each other so it means that the atria and ventricles are contracting when they feel like it

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36
Q
A
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37
Q

ECG abnormalities associated with MI?

A
  • Peak P wave and ST elevation
  • Initially tall T wave which then becomes inverted
  • Pathological Q wave
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38
Q

ECG pattern showing Pulmonary embolism?

A

SI QII TIII

  • Deep pathological and inverted
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39
Q

ECG showing Increased Calcium?

A

Short QT interval

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40
Q

ECG showing low Calcium?

A

Long QT interval

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41
Q

ECG showing raised potassium?

A

Peak T wave + No P wave + wide QRS

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42
Q

ECG showing Low potassium?

A

Flat T wave + Peak P wave + Big U wave

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43
Q

ECG showing LBBB?

A

Roll safe bunny ears

V1 - rS

V6 - bunny ears

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44
Q

ECG showing RBBB?

A

V1 rSR - M shape

V6 - slurred S

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45
Q

What is meant by a low voltage QRS complex?

A

<5mm in limb leads and <10mm in precordial leads

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46
Q

What factors can result in a low voltage QRS complex?

A
  • Obesity
  • COPD
  • Hypothyroidism
  • PE
  • BBB
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47
Q

What is Bifascicular block?

A

RBBB + LB hemiblock = left axis deviation - one of the 2 fasciles are involved

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48
Q

What is trifascicular block?

A

RBBB + LB hemiblock + 1st degree HB caused by ventricular hypertrophy

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49
Q

What can Chest X-rays be used to identify?

A
  • Cardiomegaly
  • Pericardial effusions
  • Dissection or dilatation of the aorta
  • Calcification (pericardium or valves)
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50
Q

What is a cardiac CT used for?

A

Aorta and coronary artery disease/ Calcification and Stenosis

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51
Q

What are Echoes used for?

A

Use ultrasound to look at different structures of the heart

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52
Q

What is cardiac catheterisation used for?

A
  • Angiograph
  • Blood samples
  • Measure intracardiac pressure
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53
Q

What is cardiac MR used for?

A

Anatomy and function of the myocardium

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54
Q

What is cardiac nuclear imaging used for?

A

Using radiotracers to measure perfusion at rest, exercise or pharmacologically induced stress after MI

  • With a bit of stress is there still perfusion after MI or is it completely blocked
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55
Q

What is electrocardiography?

A

Strap someone to an ECG while rest, exercise or pharmacologically induced stress to increase myocardial O2 demand and looking at any changes in electrical activity of the herat

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56
Q

What is the tilt test used for?

A

Diagnose vasovagal syncope by replicating the action of standing to see if they pass out and quickly recover

  • looking out of bradycardia and hypotension
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57
Q

How does a dopplar ultrasound work?

A

High frequency ultrasound waves bounce off red blood cells so can be used to measure blood flow through veins and arteries and pressure of blood moving through a valve

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58
Q

2 different types of echo?

A

Tranoesophageal

Transthoracic

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59
Q

What are some complications of cardiac catheterisation?

A

Tamponade

Loss of peripheral pulse

Contrast reaction

Haemorrhage

infection

Angina

Arrhythmia

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60
Q

What is ischaemic heart disease (IHD)?

A

Imbalance between supply of O2 and demand of O2 to cardiac muscle

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61
Q

Most common cause of IHD?

A

Coronary atheroma

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62
Q

Aside from coronary atheroma, what are some other causes of IHD?

A
  • spasms
  • Thrombosis
  • Artritis
  • Thyrotoxicosis
  • Myocardial hypertrophy
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63
Q

Non-modifiable risk factors of MI?

A
  • Age
  • Gender
  • Family history
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64
Q

Modifiable risk factors of IHD?

A

Hyperlipidaemia

DM

Smoking

Excessive alcohol

High cholesterol and fat

Psychosocial

Increased coagulation factors

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65
Q

What is the QRISK2?

A

Assessment tool used in primary care to estimate the likelihood of a patient having a cardiovascular event in the next 10 years taking into account factors such as :

  • Age, Gender, Smoking, DM, BMI, Cholesterol levels and others
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66
Q

Angina Pectoris?

A

Descriptive term for chest pain that arises from the heart as a result of myocardial ischaemia

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67
Q

Debicutus Angina?

A

Angina when laying down

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68
Q

Nocturnal angina?

A

Angina when sleeping

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69
Q

Variant/ Prinzmetal angina?

A

Angina due to coronary artery spasms

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70
Q

Unstable angina?

A

Critical angina with recent-onset and increasing in severity

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71
Q

Crescendo angina?

A

Critical ischaemia but not infarction

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72
Q

Coronary syndrome X angina?

A

+ve symptoms, +ve exercise test but normal coronary arteries on angiogram - functional abnormalities of coronary micro vascularization

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73
Q

Environmental Exacerbating factors for angina?

A

Cold

Heavy meal

Emotional stress

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74
Q

Exacerbating factors for angina?

A

SUPPLY: Anaemia, Hypoxia, Hypothermia, Hyper/hypovolaemia and polycythemia

DEMAND: Hypertension, tachycardia, VHD, Hyperthyroidism, Hypertrophic cardiomyopathy

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75
Q

What percentage of stenosis causes problems?

A

70%

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76
Q

OHM’s law?

A

Change in pressure = Flow x Resistance

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77
Q

What does posuelle’s law show us?

A

The greater the resistance the greater the pressure will be

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78
Q

Clinical features of angina?

A

Central crushing chest pain + breathlessness

  • radiates to the arms and neck and is relieved by GTN spray
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79
Q

What investigations would be done to diagnose angina?

A
  • Cardiac catheterisation to look at the state of coronary arteries
  • ECG - ST depression and T wave flat or inverted
  • Perfusion image testing/ pharmacological stress test for those who can’t exercise
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80
Q

Management of angina?

A

Immediate/ symptomatic treatment - GTN spray

Prophylactic treatment - Beta blocker, CCB, Nitrates, ACEi (ivabradine last resort)

Secondary prevention - Antithrombin and antiplatelet ( aspirin, clopidogrel) and lipid-lowering (stains) exercise, no smoking, diet

Revascularisation - PCI + CABG

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81
Q

PCI?

A

stent, balloon with antiproliferative drugs + dual platelet therapy (aspirin and cliopidogrel) as a method of revascularisation

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82
Q

CABG

A

Coronary artery bypass grafting - L or R internal mammary artery joins the aorta to the other side of the blockage of a coronary artery

Saphenous vein joins AA to right coronary artery

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83
Q

ACS?

A

Acute coronary syndromes are a group of unstable coronary artery diseases due to rupture of atherosclerotic plaque (formation of clot of platelets - vasoconstriction - the release of serotonin and thromboxane A2 )

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84
Q

How would you differentiate between NSTEMI and Angina?

A

NSTEMI would have elevated levels of troponin and creatine kinase

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85
Q

Clinical features of ACS?

A

Unbelievable chest pain at rest

Minimal exertion pain

Syncope

Arrhythmia

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86
Q

Treatment of NSTEMI and Unstable angina?

A

Antiplatelet, Antithrombins, Anti-ischaemia, Plaque stabilisers

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87
Q

Examples of antiplatelet drugs?

A

Aspirin

Clopidogrel - Prasugrel - Ticugrelor

GPIIb/IIIa - e.g. abciximab (ab-six-see-mab)

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88
Q

Mechanism of action of Clopidogrel?

A

Irreversibly binds to the P2Y12 ADP receptors of platelets and prevents platelet aggregation

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89
Q

Examples of antithrombins?

A

Heparin

Enoxaparin - LMWH

Synthetic Pentasaccharides FONDAPARINUX

Bivalirudin - Binds and inhibits clot bound thrombus

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90
Q

Examples of anti-ischaemic drugs?

A

Nitrates

Beta Blockers

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91
Q

Examples of Plaque stabilisers?

A

Statins

ACEi

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92
Q

2 different types of risk stratifications used to predict the risk of STEMI/death in patients with UA and STEMI and used to provide a basis for therapeutic decision making?

A

GRACE - global registry of acute coronary events

TIMI - Thrombolysis in myocardial infarction

  • both look at a range of factors to estimate risk of STEMI/death and to help choose the most appropriate combination of treatment
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93
Q

Risk stratification low?

A

Cardiac stress test followed by Exercise ECG

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94
Q

Risk stratification high?

A

PCI/ CABG

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95
Q

What is the most common cause of death in developed countries?

A

STEMI - rupture of atherosclerotic plaque - thrombosis and complete occlusion of a coronary artery

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96
Q

Clinical features of STEMI?

A

Chest pain radiating down arms, neck and jaw

Sweating

Breathless

Vomiting

Some can be silent

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97
Q

Investigations of MI?

A
  • ECG - ST elevation, Tall T wave followed by inversion, pathological Q wave
  • Cardiac markers - Creatine kinase, Troponin T and I
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98
Q

Emergency treatment of STEMI?

A

IV, Bloods, O2, GTN, Antiemetics and Morphine, Aspirin, Clopidogrel

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99
Q
A
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100
Q

Management of uncomplicated STEMI?

A

ECG

Secondary prevention - antiplatlets, statin, BB, ACEi and modification of CAD risk factor

Submaximal exercise

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101
Q

Methods of limiting the size of infarction?

A

PCI

Fibrinolytic agents - activate plasminogen to plasmin

Beta blockers - metoprolol

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102
Q

Examples of fibrinolytic agents?

A

Reteplase or Tenecteplase

Streptokinase - cheap but can develop antibodies against it

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103
Q

MI <90 mins management?

A

Reperfusion - angioplasty + dual antiplatelet therapy

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104
Q

MI >90 mins management?

A

Thrombolysis - reteplase or tenecteplase

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105
Q

Complications of MI?

A

Pericarditis (sharp chest pain and pericardial rub)

Atrial or ventricular arrhythmias

Heart block

Heart failure

Embolism

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106
Q

Post MI, what would be an indication to prescribe aldosterone antagonist?

A

Heart failure or if the ejection fraction <40%

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107
Q

What is heart failure?

A

Structural or functional abnormalities of the heart meaning it can’t pump or maintain sufficient cardiac output to meet the demands of the body

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108
Q

3 main causes of heart failure?

A

IHD, Dilated cardiomyopathy, Hypertension

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109
Q

Incidence of Heart failure?

A

10% of >65 year olds

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110
Q

Pathophysiology of heart failure?

A

HF causes compensatory mechanisms to be overwhelmed and become pathological as heart failure develops

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111
Q

Compensatory mechanism of HF?

A
  1. Activation of the sympathetic nervous system
  2. RAAS
  3. Natriuretic peptide
  4. Ventricular dilatation
  5. Ventricular remodelling
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112
Q

How does the overactivation of the sympathetic nervous system lead to heart failure?

A

vasoconstriction:

Venous - good as it increases venous return and so preload - grater stroke volume and force of contraction

Arteriolar constriction - increase afterload - so greater pressure that the heart has to work against to pump blood out of the body

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113
Q

How does the overactivation of the RAAS system lead to HF?

A

Due to decrease CO - RAAS causing retention of sodium and water - increase venous return and BP

  • Too much salt and water resulting in peripheral and pulmonary oedema + dyspnoea
  • Causes arteriolar constriction - increases afterload
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114
Q

What is the relationship between natriuretic peptide and HF?

A

Elevated Natureitic peptide is an indicator of heart failure - the aim is to lower blood pressure due to diuretic, natriuretic and hypotensive properties

Pro-BNP

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115
Q

Where are natureitic peptides formed?

A
  • Atria
  • Ventricles (brain)
  • Vascular endothelium
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116
Q

How does ventricular dilatation lead to heart failure?

A

Normally FS mechanism - When you have decreased ejection fraction the heart works to increase preload and so the force of contraction

pathological - Increase venous return so increased volume size but the force of contraction isn’t increasing causing the ventricle to become dilated (plateau on a graph)

=

peripheral and pulmonary oedema and increased tension

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117
Q

How does ventricular remodelling lead to heart failure?

A

Hypertrophy leads to loss of myocytes and increases scar tissue - becomes non-compliant

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118
Q

What can cause ventricular remodelling?

A
  • Multifactorial
  • Apoptosis of myocytes
  • Changes in cardiac gene expression
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119
Q

Most common type of heart failure?

A

Left sided heart failure

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120
Q

What differences would you see between LV systolic dysfunction and RV systolic dysfunction?

A

Left - IHD, Hypertension, Pulmonary hypertension

Right - secondary to LVSD because it has to work harder since the left is moving mad - peripheral oedema and abdominal pain due to hepatic congestion

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121
Q

Symptoms of heart failure?

A

External dyspnoea

Orthopnoea

Paroxysmal nocturnal dyspnoea

Fatigue

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122
Q

Signs of heart failure?

A
  • Tachycardia
  • Elevated JVP
  • Cardiomegaly
  • Extra heart sounds
  • Lung crackles
  • Pleural effusions
  • Ascites
  • Ankle oedema
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123
Q

Investigations used to diagnoses HF?

A

CXR

ECG

BLOODS

ECHO

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124
Q

What factors will you be looking ar in terms of blood to diagnose HF?

A

Anaemia, Liver biochem, U+E, TFT, BNP or pro-BNP

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125
Q

How is heart failure managed?

A

Drugs - ACEi or AG2A, Vasodilators, BB, Diuretics, Digoxin - increases the force of contraction but slows down rate, Inotropes

Surgery - revascularisation, cardiac resynchronisation therapy, transplant

General - Education, exercise, diet, smoking

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126
Q

Some clinical features of acute HF?

A

Pulmonary oedema

hypertension

Cardiogenic shock

High output cardiac failure

Right heart failure

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127
Q

What is systemic hypertension?

A

Chronic high blood pressure

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128
Q

Difference between essential and secondary hypertension?

A

Essential - No known identifiable cause as it is multifactorial (lifestyle factors) - treatment is usually modifying lifestyle

secondary - caused by another known identifiable disease that sometimes could be treated e.g CKD, Diabetic nephropathy, Endocrine (adrenals), correction of aorta, Drugs (oestrogen-containing oral contraceptives, steroids, NSAIDS, vasopressin)

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129
Q

Clinical features of hypertension?

A
  • can be asymptomatic
  • Fibroid necrosis - END ORGAN DAMAGE:
  • Kidneys - haematuria, proteinuria and KD
  • Brain - cerebral abscess, haemorrhage
  • Retina - flame-shaped haemorrhage, Cotton wool spots, hard exudate and papilloedema
  • Cardio - Acute HF and aortic dissection
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130
Q

Examination of Hypertension?

A
  • Chronic BP
  • Signs relating to the cause
  • End organ effects
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131
Q

Grading or severity of retinal abnormalities?

A

1. Turosity and reflectiveness of retinal arteries (bending due to atherosclerosis)

2. (1 +) arteriovenous nipping - when an arteriole crosses a vein causing it to be compressed and bulge

3. (2+) flame-shaped haemorrhages and cotton spots

4. (3+) papilloedema - swelling of the optic disc

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132
Q

What is classed as high blood pressure?

A

140/90

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133
Q

Stage 1 hypertension BP?

A

CBP >140/90 and AMBP or HBP - >135/85

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134
Q

When would you offer treatment to a stage 1 hypertensive?

A
  • Over 80 years old
  • 1 of the following risk factors:

End organ damage

CVD

REnal disease

DM

Qrisk2 >20%

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135
Q

Stage 2 hypertensive?

A

CBP >160/100 or AMBP/HBP >150/95

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136
Q

Stage 3 hypertensive BP?

A

>180/110

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137
Q

What are the 2 key players in hypertension?

A

RAAS system and the sympathetic nervous system

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138
Q

Why would Caucasians be given ACEi instead of CCB to treat hypertension?

A

Caucasians have higher levels of renin than other ethnicities

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139
Q

Group A hypertensives examples and MOA?

A

ACEi - Ramipril, Enalapril

Inhibit A1 to A2 and inhibit the breakdown of bradykinin to inactive peptides

ACE enzyme also associated with perfusion and filtration of kidneys so when inhibited the kidneys become affected

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140
Q

CI of ACEi?

A

Renal artery stenosis

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141
Q

Side effects of ACEi?

A

Decreased A2 - First does hypotension, Acute renal failure, Tetragenic effects on pregnancy

Increased Bradykinin - Dry cough, urticaria, anaphylactoid rash due to decreased leukocytes

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142
Q

Group B hypertensives examples and MOA?

A

ARB - For patients who can’t tolerate ACEi - Valsartan, Losartan, Irbesartan

Angiotensin 2 receptor antagonists prevent it causing an increase in peripheral resistance and cardiac output

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143
Q

CI of ARB?

A

Pregnancy

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144
Q

Side effects of ARB?

A

Symptomatic hypotension (dehydration or volume depletion)

Increase potassium

potential renal dysfunction

Angio-oedema

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145
Q

Group C hypertensives examples and MOA?

A

CCB - Dihydropyridine, Phenylalkylamine and Benzothiazempines

Block L type calcium channels so that smooth muscle can relax

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146
Q

MOA of dihydropyridines and examples?

A

AMLODIPINE, NIFEDIPINE, FELODIPINE, LACIDIPINE

  • Affect vascular smooth muscle and cause peripheral arterial vasodilation
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147
Q

MOA of phenylakylamines and example?

A

VERAPAMIL

  • Decrease heart rate and force of contraction (chronotropic and ionotropic)
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148
Q

MOA of benzothiazepines and example?

A

DILTIAZEM

  • Affects both heart and peripheral (HR and FC) and peripheral vasodilation
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149
Q

What are the side effects of CCB?

A

Flushing

Ankle swelling

Headache and palpitations (brain thinks low blood volume so increases HR and BP)

Bradycardia

AV block

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150
Q

Group D hypertensives examples?

A

DIURETICS - Increase water and sodium excretion by blocking reabsorption of ions

LOOP - FUROSEMIDE (Na/Cl/K ascending loop of henle)

THIAZIDE - HYDRCHOLORTHIAZIDE (Na/Cl but increase calcium)

K+ SPARRING/ ALDOSTERONE ANTAGONIST - SPIRONOLACTONE (Na)

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151
Q

Side effects of diuretics?

A

Hypovolaemia, hypotension and loss of electrolytes

Build up of uric acid

erectile dysfunction

impaired glucose tolerance

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152
Q

MOA beta blockers?

A

They inhibit noradrenaline receptors and so decrease the effect of the sympathetic nervous system

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153
Q

When are beta blockers contraindicated?

A

Asthma, COPD, PVD

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154
Q

Give an example of an Alpha receptor blocker?

A

DOXASOZIN

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155
Q

Give an example of a central acting antihypertensive?

A

MOXONIDINE AND METHYLDOPA

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156
Q

Give an example of a renin inhibitor?

A

Aliskiren

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157
Q

In an emergency, why would you give the BB and CCB orally rather than IV or sublingual?

A

It would decrease the BP too much and too fast and the patient is at risk of cerebral infarction

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158
Q

What is a cardiac arrhythmia?

A

Abnormal cardiac rhythm

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159
Q

What is a sinus rhythm?

A

Waves of depolarisation that control cardiac rhythm originating from the SA node

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160
Q

What is sinus arrhythmia?

A

Fluctuations in parasympathetic tone (autonomic) resulting in phasic changes in sinus discharge

e.g. Inspiration = increase HR = Decrease parasympathetic tone

Expiration = Decrease HR = Increase parasympathetic tone

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161
Q

What is the result of sinus arrhythmia?

A

Irregular pulse

162
Q

What is sinus bradycardia?

A

Slow and regular heartbeat

163
Q

4 broad causes of sinus bradycardia?

A

Extrinsic

Intrinsic

Sick sinus syndrome

Neural mediated - vasovagal attacks

164
Q

Extrinsic causes of sinus bradycardia?

A
  • Beta blockers
  • Digoxin
  • other antiarrhythmics
165
Q

Intrinsic causes of sinus bradycardia?

A
  • ischaemia or infarction of SA node
  • Fibrosis of atria or SA node
166
Q

Sick sinus syndrome?

A

Caused by fibrosis of the SA node or depolarization from the SA node doesn’t travel out of perinodal tissue to atria

167
Q

What is heart block?

A

Slow heart rate or abnormal rhythm due to electrical conduction abnormalities

168
Q

Explain 1st degree AV heart block?

A

Delayed AV conduction

ECG: consistent prolonged PR intervals (>0.22 seconds) and heart rate maintained

169
Q

What is the difference between Mobitz 1 and Mobitz 2?

A

baso both have missing ventricular contractions - the difference is if PR interval progressively gets longer or remains constant - when some atrial conductions fail to reach the ventricles

  • Mobitz 1 - PR interval progressively gets longer then no QRS showing no conduction followed by ventricles missing a contraction
  • Mobitz 2 - PR interval constant with occasional QRS complex missing so conduction to ventricles is occasionally blocked
170
Q

Explain 3rd degree AV heart block?

A

Complete heart block - no communication between the atria and ventricles - P and QRS doing whatever they want

  • spontaneous ventricular contractions
171
Q

In 3rd-degree heart block - how different would the ECG appear if ventricular contractions originated in the bundle of his compared to the Purkinje fibres?

A

Bundles of his - Narrow QRS complexes at 50-60 bpm

Purkinje fibres - Broad QRS complexes at 40bpm

172
Q

What is supraventricular tachycardia?

A

Tachycardia that arises from the atria or AV junction

173
Q

What is sinus tachycardia?

A

Fast consistent heart beat >100bpm

  • physiological response to excitement and exercise
174
Q

2 types of atrioventricular junctional tachycardia?

A

AV nodal re-entry tachycardia

AV reciprocating tachycardia (WPW)

175
Q

What are atrioventricular junctional tachyarrhythmias?

A

Re-entry circuits resulting in 2 separate pathways of impulse conduction - often seen in younger people

176
Q

Describe AVNRT?

A
  • Bundle of fibres in the AV node
  • Each have own conduction times and refectory periods = local re-entry circuit
  • The atrial rate is stimulated by re-entrant impulses which causes an increase in ventricular contraction rate = PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
177
Q

Describe AVRT?

A
  • Accessory pathway (global re-entry) - bundle of kent - between atria and ventricles
  • P wave, Short PR interval + delta wave
  • Resting ECG of WPW - atrial depolarisation to pass to the ventricles before it gets to the AV node due to accessory pathway
178
Q

Different between orthodromic and antidromic AVRT?

A

Orthodromic follows the normal direction and so has a narrower QRS complex than antidromic

179
Q

Symptoms of atrioventricular junctional tachycardia?

A

SUDDEN

  • Rapid regular palpitations
  • Dizziness
  • Dyspnoea
  • Central chest pain
  • Nausea
180
Q

Acute management of AV junction tachycardia?

A

maintain and restore sinus rhythm if haemodynamically stable

  • Valsalva - forced exhalation against a closed airway
  • Carotid sinus massage

DRUGS: Adenosine (block AV conduction), BB, CCB

181
Q

Long term management of AV junctional tachycardia?

A

Cardiac catheter ablation - making small scars in heart tissue to prevent abnormal electrical signals moving through the heart

182
Q

General causes of atrial tachyarrhythmia?

A

Obesity

Hypertension

Age

183
Q

Endocrine causes of atrial tachyarrhythmia?

A

DM

Thyrotoxicosis

184
Q

Metabolic causes of atrial tachyarrhythmia?

A

Alcohol

Electrolyte imbalance

185
Q

What is Atrial fibrillation?

A

Irregularly irregular - missing P waves

  • AV node conducts a proportion of atrial impulses to produce an irregular ventricular response
186
Q

A complication of atrial fibrillation?

A

Thromboembolism that forms in the atria (x5 more likely to get a stroke)

187
Q

Symptoms of AF?

A

Fatigue due to decreased CO and palpitations

Can be asymptomatic

188
Q

How does the management of AF differ if you found it <48 hours or >48 hours?

A

<48 - Heparin

>48 - DC cardioversion - amiodarone - cardioversion - amiodarone

189
Q

Management of chronic Atrial fibrillation?

A

Control rate and rhythm

Rate: BB, CCB, Digoxin

Rhythm: Cardioversion, Anti-arrhythmic (amiodarone or propafenone), Catheter ablation

‘pill in pocket’ - propafenone, Flecainide, sotalol

190
Q

What indication are the indications to give a patient Rhythm controlling drugs for AF?

A

>65

Highly symptomatic

Onset AF or Heart failure

191
Q

What is the assessment for anticoagulation?

A

CHA2DS2-VaSc

C - Congestive HF

H - Hypertension

A - Age (64-74 or >74)

D- Diabetes

S - Stroke or TIA

Va - Vascular disease

S - Sex - female

also look at time and any issues with valves

192
Q

What is the difference between atrial fibrillation and atrial flutter?

A

A fib - AV node conducts a proportion of atrial impulses to the ventricles causing an irregular ventricular rhythm

A flut - AV node conducts every second flutter - atrial rate is 300bpm while ventricular rate is 150bpm

ECG difference - missing P wave and irregularly irregular compared to sawtooth

193
Q

How can you clearly identify A flut on an ECG?

A

Do ECG after giving a carotid sinus massage which impairs AV conduction

194
Q

Management of A flut?

A

DC cardioversion

Amiodarone

Catheter ablation

195
Q

Different types of ventricular tachyarrhythmias?

A

Ventricular ectopic beats

Sustained VT

Non-sustaine VT

V fib

Long QT syndrome

196
Q

What are ventricular ectopic premature beats?

A
  • Extrasystole
  • Ectopic electrical activity not conducted to ventricles through normal conducting tissue
197
Q

Clinical presentation of a patient with ventricular ectopic premature beats?

A

could be asymptomatic or have extra/missed/heavy beats

ECG - QRS complex wide and bizarre

198
Q

Management of ventricular ectopic premature beats?

A

Beta blockers

199
Q

What is the difference between sustained and non-sustained ventricular tachycardia?

A

SUSTAINED: VT lasts >30 seconds

NON-SUSTAINED: VT> 30 seconds but <5 consecutive beats and caused by heart disease

200
Q

Management of ventricular tachycardia?

A

Beta blockers

Cadioversion or intracadiovater defibrillation

201
Q

What is ventricular fibrillation?

A

Very rapid or irregular ventricular activation with no mechanical effect so no cardiac output

202
Q

Clinical presentation of ventricular fibrillation?

A

Palpitations

Syncope

Respiration ceases

CAN CAUSE CARDIAC ARREST - sudden loss of blood flow

203
Q

Management of ventricular fibrillation?

A

Defibrillation

204
Q

What is long QT syndrome

A

QT interval represents ventricular systole - ventricular depolarisation and repolarisation

  • Ventricular repolarisation is prolonged - Heart muscle takes longer than normal to recharge for next contraction = dangerous arrhythmias
205
Q

What are some causes of long QT syndrome?

A
  • Congenital - mutation of Na/K channels
  • Electrolyte disturbances - Low K/Ca/Mg
  • Drugs - Tricyclic antidepressants
206
Q

Clinical presentation of Long QT syndrome?

A

Palpitations

Syncope

ECG - Torsade de pointes - rapid irregularly shaped QRS complexes that alternate for upright to inverted

207
Q
A
208
Q

Management of Long QT syndrome?

A

ISOPRENALINE - Non-selective beta-adrenoreceptor agonist - used for bradycardia so increases heart rate - increase HR and FOC while lowering peripheral vascular resistance

209
Q

MOA atropine?

A

Blocks muscarinic receptors so to do the opposite of parasympathetic system - used for sinus bradycardia

210
Q

Beta 2?

A

Bronchodilation and vasoconstriction

211
Q

What is cardiac arrest?

A

No effective cardiac output presented as loss of consciousness and abnormal or absent breathing

212
Q

Cardiac arrest resuscitation?

A

CPR 30:2 - Asses the rhythm

Shockable? Normal? or Asystole (flatline)?

213
Q

What is an aneurysm?

A

Abnormal dilation of an artery of >50% of its original size due to weakness in the blood vessel wall

214
Q

Where are 95% of aneurysms?

A

Below renal arteries and above the bifurcation

215
Q

Difference between a true and pseudoaneurysm?

A

True - involves all layers of the blood vessel wall due to weakness in the wall (like a balloon initially hard to inflate then it becomes easier to inflate)

Pseudo - Small hole in the wall and blood enters that hold to form a blood-filled pocket but it doesn’t involve all the layers of the wall

216
Q

What is a barry aneurysm also know as?

A

Asymmetrical/ secular

217
Q

Causes of aneurysms?

A

Atherosclerosis

Hypertension

Tertiary syphilis

Thick walls of the aorta

Infection - embolic bacteria break off and get stuck in small arteries causing the vessel walls to become weaker

Connective tissue disorders - Marfans (fibrilin) or Ehlers-Danlos (collagen proteins)

218
Q

How does atherosclerosis lead to aneurysm?

A

O2 can’t pass the thick plaque causing the cells of the wall to become ischaemic

219
Q

How does tertiary syphilis lead to an aneurysm?

A

Endarthritis obliterans which is inflammation of the intima (leading to fibrosis) which causes the lumen of Vasa Vasorum to become narrow and therefore ischaemic

220
Q

Risk factors of aneurysms?

A

Male

>60

Hypertension

Smoking

Obese

Family history

221
Q

Clinical features of aneurysms?

A

Pain - chest, left flank, lower back, groin

Hypotension

Pulsating mass with HB in that region or abdominal pulsating mass

222
Q

What investigations would be used to confirm an aneurysm?

A

Ultrasound

CT

MRI

223
Q

Complications of an aneurysm?

A

Rupture

Thrombus

Embolism

Pressure on surrounding structures

Fistulae

224
Q

At what size of an intact aneurysm would surgical intervention be required?

A

>5.5cm

225
Q

Consequences of a ruptured blood clot?

A

Occlusion

Internal bleeding - cells then become an ischaemic and hypovolaemic shock

Aortic insufficiency if the aneurysm is above the valve - its then unable to close

Irritated meninges and increased pressure due to blood build up in subarachnoid space - headache and can’t flex head forward

Bloodclot

226
Q

What is an aortic dissection?

A

Tear in the tunica intima of aorta and blood begins to flow between the intima and media separating them, creating a false lumen

227
Q

Aetiology of aortic dissection?

A

Chronic hypertension

Coarctation of aorta

Connective tissue abnormalities causing wall of aorta to be weak - Ehlers-Danlos

228
Q

Type A aortic dissection?

A

Found on the first 10cm of the aorta (ascending)

229
Q

Symptoms of aortic dissections?

A

Hemiplegia

Quadriplegia

Unequal arm pulses and weak downstream pulse

Sharp stabbing pain radiating to the back

Anuria

Hypotension and shock

230
Q

Complications of aortic dissection?

A

Pericardial tamponade

Bleeding into mediastinum

Blood re-enters true lumen

Continues to build up between intima and media until it reaches a branching point and puts pressure on it e.g. flow to arms or kidneys

231
Q

Investigations to confirm aortic dissection?

A

Wide aorta on CXR

Transoesophageal Echo - determine the true and false lumen

232
Q

Management of Aortic dissection?

A

A- Surgery

  • Remove dissected area
  • Block the entry of blood into the wall

Reconstruct wall with graft

B- Beta-blockers and nitroprusside (decrease BP)

233
Q

What is peripheral arterial disease?

A

Due to multifactorial modifiable and non-modifiable factors, atherosclerosis develops resulting in stenosis of the arteries supplying limbs

234
Q

Most identifiable clinical feature of PAD?

A

Claudication - cramping muscle pain in the legs triggered by exercise and relieved by rest

235
Q

Symptoms of PAD?

A

Cramp in calf (femoral), thigh and butt (illiac) after walking and is relieved by rest

Ischaemic limb pain - burning pain made better by raising the legs - ulceration, gangrene and foot pain at rest

236
Q

What is critical ischaemia?

A

severe obstruction of blood flow to extremities resulting in ischaemic pain in hands, legs and feet. It can wake up individuals during the night

237
Q
A
238
Q

Different types of critical ischaemia?

A

Leriche’s syndrome - Butt claudication and impotence due to build up of plaque in the iliac arteries

Buerger’s Disease - Found in young and heavy smokers

  • Thromboganitis obliterans resulting in progressive inflammation, swelling and clots in medial and small arteries and veins of the hands
239
Q

Fontaine classification of PAD?

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Ischaemic rest pain
  4. Ulceration and gangrene
240
Q

Signs of peripheral arterial disease?

A
  • Absent femoral, popliteal or foot pulse
  • Cold, white legs
  • Atrophic skin
  • Painful ulcers
  • Postural dependant colour change
  • Burgers leg - lift leg and it goes pale, the lower the angle the more severe
241
Q

Investigations used to confirm PAD?

A

Ankle-brachial pressure index - the ratio of blood pressure in the ankle BP to BP in the upper arm

Normal - 1-1.12

PAD - 0.5-0.9

Critical ischaemia - <0.5

  • screen for thrombophilia
  • Measure Haemocystein - AA found in blood and increased association with the early development of heart disease
242
Q

Why must you not only do the ankle-brachial pressure index alone to confirm diagnosis of PAD?

A

Severe atherosclerosis can give false reading of BP as they can calcify and become really hard

243
Q

Management of stable PAD?

A

Colour duplex ultrasound - non-invasive method of measuring blood flow through veins and arteries

Risk modification - lifestyle and antiplatlet

Manage claudication - exercises and vasoactive drugs

244
Q

Management of acute PAD?

A
  • Percutaneous transmural angioplasty
  • Surgical reconstruction using dacron graft
  • Amputation
245
Q

What is the pericardium?

A

Fibroelastic sac filled with a thin layer of fluid that surrounds the heart and great vessels and prevents friction between the visceral ad parietal pericardium

246
Q

Normal volume of fluid in the pericardium?

A

50mL

247
Q

What is acute pericarditis?

A

Inflammation of the pericardium characterised by sharp retrosternal chest pain made worse by inspiration and relieved by leaning forward accompanied with a fever

248
Q

Causes of acute pericarditis?

A

Hypothyroidism

Secondary viral infections

Post-MI

Uraemia - excess uria and other waste products usually removed by the kidneys

Autoimmune rheumatic disease - conditions of connective tissue

Drugs

TRauma

Infection

Malignancy

249
Q

Infections that can cause pericarditis?

A

Bacteria, TB, Funi and pneumonia

250
Q

Viruses that can cause pericarditis?

A

Coxsackie B, Echo and HIV

251
Q

What is BehÇet’s Disease?

A

Recurrent multisystemic inflammatory disease that can also cause pericarditis

252
Q

What antiarrhythmic drug has been associated with pericarditis?

A

Procainamide

253
Q

Clinical features of acute pericarditis?

A

Pericardial rub - scratchy sound as the 2 layers of the pericardium rub (1S2D) - as the patient holds their breath and leans forward

Sharp chest pain made worse by inspiration

Radiating to neck and shoulders

Low fever

254
Q

How will an ECG confirm pericarditis?

A

Saddle shaped ST elevation (concave upwards)

255
Q

Management of acute pericarditis?

A
  • NSAIDS and treatment of the underlying cause
  • Systemic corticosteroids or immunosuppressants
  • Colchicine - used to treat inflammation and pain
256
Q

Complications of acute pericarditis?

A

Chronic pericarditis

Pericardial effusion

257
Q
A
258
Q

Pericardial effusion?

A

Accumulation of fluid in the pericardial sac which can be due to pericarditis which can affect ventricular function (even hyperthyroidism)

259
Q

Pericardial tamponade?

A

Medical emergency where large amounts of fluid in the pericardial sac restrict elastic ventricular filling resulting in decreased CO

260
Q

Clinical features of Pericardial tamponade/effusion?

A

Hypotension

Kussamul signs - elevated jugular venous pressure due to limited RV filling during inspiration (pulsates)

Invariable pulsus paradox - Decrease in BP during inspiration

261
Q

Explain the invariable pulsus paradox?

A

BP decreased by 10mmHg during inspiration

  • Increase venous return to the right side of the heart
  • Increases ventricular volume but rigid pericardium
  • The decrease in CO and blood just occupies more space in the heart so less is actually able to return
262
Q

Investigations used to diagnose Pericardial effusion/ tamponade?

A

CXR - large globular heart

ECG - Low voltage complexes and sinus tachycardia

Pericardiocentesis - collect fluid

Pericardial biopsy

263
Q

Management of pericardial effusion?

A
  • can sometimes resolve on its own or you drain fluid from the pericardial sac using a needle

IF RECURRENT - EXCISION OF PERICARDIAL SEGMENT SO FLUID CAN BE ABSORBED THROUGH PLEURAL AND MEDIASTINAL LYMPHATICS

264
Q

What is constrictive pericarditis?

A

Heart becomes encased in rigid fibrotic pericardial sac which prevents adequate diastolic filling of the ventricles

265
Q

Causes of constrictive pericarditis?

A

Idiopathic or intrapericardial haemorrhage during cardiac surgery

266
Q

clinical features of constrictive pericarditis?

A
  • Similar to right side heart failure
  • Kussamail sign
  • Increase JVP
  • Pulsus paradoxus
  • Oedema
  • AF

PERICARDIAL KNOCK DUE TO RAPID VENTRICULAR FILLING

267
Q

What can constrictive pericarditis be mistaken for?

A

Restrictive cardiomyopathy - both cause haemodynamic changes due to restrictive filling

268
Q

Investigations used to diagnose constrictive pericarditis?

A

CXR - normal heart + pericardial calcification

CT/MRI - pericardial thickening and calcification

269
Q

Management of constrictive pericarditis?

A

Surgical excision of pericardium

270
Q

On which side are you more likely to have valvular heart disease?

A

Left side

271
Q

What is a murmur?

A

Sounds on auscultation caused by turbulent flow

272
Q

Causes of innocent murmurs?

A

Pregnancy

Anaemia

Thyrotoxicosis

273
Q

How is a dopplar echo useful for diagnosis VHD?

A

Measures direction and velocity of blood flow - pressure across the valve

274
Q

Treatment of VHD?

A

Valve replacement

Valve repair

Valvotomy

275
Q

Why would a patient choose a mechanical valve over a biosynthetic valve?

A

Mechanical - last longer but a greater chance of thromboembolism so lifelong anticoagulation

Biosynthetic - lasts about 10 years before it needs replacing and no need for anticoagulants

276
Q

Different types of mechanical valves?

A

Ball and chain

Single tilting disc

Double tilting disc

277
Q

Different types of biosynthetic valves?

A

Bovine - cow

Porcine - pig

Homograft - human

278
Q

Complications of mechanical valves?

A

Thromboembolism

Infective endocarditis

Haemolytic anaemia

279
Q

What is mitral stenosis?

A

Stiff mitral valve leading to obstruction of blood flow from the left atrium to the left ventricle

280
Q

a complication of mitral stenosis?

A

Pulmonary hypertension and pulmonary oedema – Right ventricular hypertrophy/ dilation = RV failure

AF

281
Q

Aetiology of mitral stenosis?

A

Rheumatic heart disease

282
Q

Symptoms of mitral stenosis?

A

exertional dyspnoea

Cough with blood

AF

RH failure - fatigue and lower limb pain

Pulmonary oedema

283
Q

Signs of mitral stenosis?

A

mitral facies

Irregular or low volume pulse - A

Auscultation - loud first heart sound followed by rumbling mid-diastolic murmur

284
Q

How would the auscultation change of a patient with mitral stenosis if they had a sinus rhythm?

A

The murmur is louder because of increased blood flow through a narrow lumen

285
Q

Mitral stenosis and loud second heart sound?

A

Pulmonary hypertension due to RV overload

  • Increased JVP and ascites
286
Q

Aim of the investigations when diagnosing mitral stenosis?

A

Estimate the severity of stenosis and look for pulmonary hypertension

287
Q

CXR mitral stenosis?

A

Pulmonary venous hypertension

calcified mitral valve

Enlarged left atrium

288
Q

ECG mitral stenosis?

A

P mitrale (bunny ears)

289
Q

What is classed as severe mitral stenosis?

A

when the remaining area for blood to pass is <1cm2

290
Q

Management of mitral stenosis?

A

mild - leave alone or treat complications so antiarrhythmics (arrhythmia), diuretics (heart failure) and anticoagulants (AF)

Percutaneous balloon valvotomy

Mitral valve replacement

291
Q

What is mitral regurgitation?

A

Leakage of blood through the mitral valve from LV to LA during ventricular contraction resulting in haemodynamic changes

292
Q

Position of all 4 valves?

A

Aortic - 2IC right

Pulmonary - 2IC left

Tricuspid - 5IC left

Mitral - 5IC left mid clavicular line

293
Q

Causes of mitral regurgitation?

A

Mitral valve prolapse

Rheumatic HD

Infective endocarditis

Calcification with age

Post MI - Papillary muscles no work

Cardiomyopathy

294
Q

Clinical features of mitral regurgitation?

A

Fatigue

Diaphoresis - Excessive sweating

Dyspnoea on exertion

Low extremity oedema

295
Q

How would the auscultation look for a patient with mitral regurgitation?

A

pansystolic murmur - eventhought the mitral valve is closed blood is still whooshing through

S1 sound weak

S3 due to rapid filling of the ventricles

Apex sounds moving towards the axilla

296
Q

ECG of a patient with mitral regurgitation?

A

AF

297
Q

Management of mitral regurgitation?

A

Diuretics and ACEi - peripheral oedema

Valve repair or replacement

Valvuloplasty

Annuloplasty - a plastic ring that supports the mitral valve

Intra-aortic balloon counterpulsation - so more blood comes out of aorta than the mitral valve

298
Q

What is meant by a prolapsed mitral valve?

A

1 or more of the mitral valve leaflets is prolapsed back into the left atrium during ventricular contraction

299
Q

Clinical features of prolapsed valve?

A

Atypical chest pain

Palpitations caused by axilla

Mid-systolic click followed by a murmur

300
Q

Investigations of prolapse valve?

A

ECHO

301
Q

Management of mitral prolapse?

A

Chest pain and palpitations - beta blockers

Mitral regurgitation and AF - Anticoagulation

302
Q

What is the difference between mitral stenosis and mitral regurgitation?

A

Stenosis is caused by rheumatic HD and blood doesn’t move back into the atria

Regurgitation is caused by mitral valve proplase and blood moves back into the atria during ventricular contraction

303
Q

What is atrial stenosis?

A

Narrowing of the aortic valve restricting blood flow from the left ventricle to the aorta - myocardial ischaemia - angina and arrhythmia

304
Q

Causes of atrial stenosis?

A

Calcification + deterioration of the aortic valve

Calcification of congenital bicuspid valve

Rheumatic heart disease (scar tissue and valves fuse together)

305
Q

Pathophysiology of aortic stenosis?

A

Obstruction of LV emptying

Concentric hypertrophy - muscle becomes thicker

Increased myocardial O2 demand - ischaemia due to decreased CO

Angina and arrhythmia

306
Q

Symptoms of aortic stenosis?

A

Angina - chest pain, syncope and dyspnoea

307
Q

Signs of aortic stenosis?

A

Harsh systolic ejection murmur that radiates to the neck (systolic crescendo decrescendo murmur)

Plateau carotid pulse - slowly rising

S2 soft and difficult to hear

308
Q

Investigations used to diagnose aortic stenosis?

A

CXR - calcification

ECG - LV hypertrophy and LV strain

ECHO - pressure gradient across the valve

CARDIAC CATHETERISATION - rule out any coronary artery disease

309
Q

Management of aortic stenosis?

A

Aortic valve replacement

Transcatheter aortic implantation - wedge a replacement valve onto the old aortic valve and its transported to the aorta through arteries

310
Q

What is aortic regurgitation?

A

When the aortic valves don’t full close so blood moves back from the aorta to the left ventricle

311
Q

Causes of aortic regurgitation?

A

Aortic root dilation - holds the leaflets apart and they don’t close properly (dissection, aneurysm, tertiary syphilis)

Valvular damage - infective endocarditis or rheumatic fever (fibrosis so baso stuck)

312
Q

Pathophysiology of aortic regurgitation?

A

The increased volume of the LV causing it to dilate by eccentric hypertrophy causing the heart muscle to become weak

Increased pulse pressure as systolic increases and diastolic decreases

313
Q

Why do you get an increased pulse pressure with aortic regurgitation?

A

Increased systolic - Increased preload due to increased stroke volume

Decreased diastolic - Decreased aortic pressure

314
Q

Symptoms of aortic regurgitation?

A

Dyspnoea

Orthopnoea (laying down)

Fatigue

315
Q

Signs of Aortic regurgitation?

A
  • Hyperdynamic circulation (wide PP) and collapsing pulse (warhammer)
  • Early diastolic decrescendo
  • Thrusting apex beat moving laterally
316
Q

Investigations of aortic regurgitation?

A

CXR - cardiomegaly and dilation of ascending/ root of the aorta

ECG - left ventricular hypertrophy

ECHO - the severity of aortic regurgitation

CARDIAC CATETERISATION

317
Q

Management of aortic regurgitation?

A

Decrease preload/ LV workload - Vasodilators and diuretics

ACEi

Aortic valve replacement

318
Q

What causes tricuspid stenosis?

A

Rheumatic fever

319
Q

Wa=hat causes pulmonary stenosis?

A

Congenital lesion

320
Q

Signs of pulmonary stenosis?

A

RV failure

Syncope

Fatigue

321
Q

What causes tricuspid regurgitation?

A

Secondary to the dilation of the RV

322
Q

Signs of tricuspid regurgitation?

A

Pansystolic murmur

Increased JVP

Enlarge liver and pulse during systole

Peripheral oedema and ascites

323
Q

Management of Tricuspid regurgitation?

A

Diuretics

324
Q
A
325
Q

Causes of pulmonary regurgitation?

A

Pulmonary hypertension

Dilation of valve rings

Endocarditis

326
Q

What is infective endocarditis?

A

Infection of the endocardium - can be acute or insidious

327
Q

Where can infective endocarditis occur?

A
  • Valves with congenital defects or acquired defects
  • Normal valves with virulent bacteria
  • Right side valves in IVD
  • Prosthetic valves (within 60 days early) (late following septicaemia)

Associated with VSD or persistent ductus arteriosis

328
Q

Pathophysiology of infective endocarditis?

A

Mass of fibrin, platelets and infective organisms form vegetations of the edges of the valves

Virulent organisms destroy the valve = regurgitation and worsening heart failure

329
Q

Clinical features of infective endocarditis?

A

systemic features of infection

Splenomegaly

Valve destruction - heart failure and murmur

Vascular phenomena - The vegetations embolise and occlude blood vessels

Metatstatic abscess in brain, spleen and kidney

Right sided endocariditis - pneumonia and pulmonary infarction

330
Q

What immune complex depositions arise in blood?

A

Vasculitis and petechial haemorrhages

Splinter haemorrhages

Roths spots - in retina

Oslar’s nodes - tender subcutaneous nodes on fingers

Janeway lesions - on palms

Deposits in joints too!

331
Q
A
332
Q

Major complication found in >70% of patients with infective endocarditis?

A

Microscopic haematuria

333
Q

Investigations done to confirm infective endocariditis?

A
  • 6 blood cultures - 3 sets taken over 24 hours
  • TTE - vegetation and valve destruction (TOE for prosthetic)
  • SEROLOGICAL TESTING
  • CXR - heart failure
  • ECG - infection affecting conduction
  • BLOOD COUNT - Normocytic normochormatic anaemia _ leukocytosis
  • URINE STIX - Haematuria
  • SERUM IMMUNIGLOBULINS AND DECREASED COMPLEMENT
334
Q

Management of infective endocarditis?

A

DRUGS - IV antibiotics - benzylpenicillin and gentamicin

SURGERY - valve replacement

335
Q

Which groups of people are at the greatest risk pf infective endocarditis?

A

IVD, prosthetic valves and immunosuppressants

336
Q

What is rheumatic fever?

A

Autoimmune reaction of Group A streptococci causing inflammatory disease in people aged between 5-15 years old - can result in rheumatic valvular disease

337
Q

Epidemiology of rheumatic fever?

A

More common in women than men

decreased prevalence due to sanitation, antibiotics and virulence of microorganisms

338
Q

Clinical features of rheumatic fever?

A

Carditis of heart layers

Polyarthritis

Skin manifestations - erythema

Sydenham’s chorea - uncontrollable movements

339
Q

Investigations done to confirm rheumatic fever?

A

FBC - leukocytes, ESR

Diagnosis based on revised duckett Jones criteria

340
Q

Management of rheumatic fever?

A

High dose aspirin

Penicillin - long term patients with cardiac damage

341
Q

What can cause myocarditis?

A

Coxsackievirus, Diphtheria, Rheumatic fever, radiation injury and some drugs - associated with HIV

342
Q

Clinical features of myocarditis?

A
  • Fever
  • Biventricular failure
  • Cardiac arrhythmia
  • Pericarditis
343
Q

Investigations to confirm myocarditis?

A

CXR - cardiac enlargement

ECG - arrhythmias and ST changes

Serum viral titres and cardiac enzymes

344
Q

Management of myocarditis?

A

Bed rest ad treatment of heart failure

345
Q

What is shock?

A

Circulating failure resulting in inadequate organ perfusion

346
Q

Clinical presentation of shock?

A

BP <90mmHg

Low/ no urine output

MAP <65

Elevated serum lactate

347
Q

Types of shock caused by inadequate CO?

A

Hypovolaemic

Pump failure: cardiogenic or secondary to PE, Pneumothorax or tamponade

348
Q

Types of shock caused by peripheral circulation failure?

A

Baso things getting in the blood

Sepsis - vasodilation caused by infection and the release of cytokines in response to G-ve endotoxin release

Anaphylactic - severe allergic reaction - Type 1 IgE mediated hypersensitivity - mass release of histamine

Neruogenic - SCI

Endocrine failure - addisons or hypothyroidism

349
Q
A
350
Q

What drugs can cause shock?

A

Anaesthetics

Antihypertensives

Cyanide poisoning

351
Q

Management of anaphylactic shock?

A

Steroid, antihistamine, Adrenaline, Salbutamol

352
Q

What is sepsis?

A

Life-threatening organ dysfunction caused by deregulated host response to infection

353
Q

Signs of septic shock?

A

Multiple organ failure

Elevated lactate despite fluid restriction

Patient needs vasopressin to sustain MAP

354
Q

Things to look out for during shock?

A

Resp rate

Urine output

Organ failure

BP

Fever and sweating

Mottled skin

355
Q

What is used to diagnose a structural heart defect during pregnancy?

A

Foetal echocardiography

356
Q

What the 4 heart defects found in tetralogy of fallot?

A
  1. Stenosis of RV outflow tract -harder for deoxygenated blood to go to the lungs due to stenosis
  2. Right ventricular hypertrophy - boot shaped CXR
  3. Ventricular septal defect - but blood move from the RV to LV so deoxygenated blood goes into circulation
  4. Aorta overrides the septal defect - so can be right on it or far left
357
Q

What is the most critical feature of tetralogy of fallot?

A

Pulmonary stenosis

The severity of obstructing influences the direction of shunting

Increased obstruction = RV to LV

358
Q

What is the most common cyanotic congenital heart defect?

A

Tetralogy of fallot

359
Q

What causes tetralogy of fallot?

A

Chromosome 22 deletion

Di George syndrome

360
Q

Clinical presentation of tetralogy of fallot?

A

Cyanosis

Clubbing - finger and toes

Decreased O2 - feeding difficulty, failure to gain weight and failure to develop normally

THESE SYMPTOMS COME IN SPELLS

361
Q

Management of cyanosis?

A

O2

Squat or raise knees to the chest - Kinks femoral arteries and increases vascular resistance - increase pressure in left ventricle so blood moves more from LV to RV

362
Q

Treatment of tetralogy of fallot?

A

Surgery in the first year of life

Close septal defect

Enlarge RV outflow tract

363
Q

Explain how abnormal embryology leads to ventricular septal defects?

A

Muscular ridges grow upwards from the apex

The membranous region grows downwards from the endocardial cushion

VSD = they don’t fuse

364
Q

What percentage of CHD are VSD?

A

20%

365
Q

What other conditions are VSD associated with?

A

Foetal alcohol syndrome and downs

366
Q

Pathophysiology of VSD?

A

Greater pressure in the LV so blood moves from LV to RV and you get increased blood flow to the lungs

367
Q

What is eisehmenger syndrome?

A

Due to VSD and greater pressure in LV - Blood moves LV to RV

Increase pressure on the delicate pulmonary vasculature and increase RV pressure

Blood now ends up moving RV to LV = deoxygenated blood moving through the body

368
Q

Clinical signs of ventricular septal defects?

A

Small, breathless, skinny

Increased resp rate

Tachycardia

Holosystolic Murmur - blood going through septum

369
Q

What are the names of the 2 atrial openings during foetal development?

A

Fossa ovale

Ostium primum

370
Q

What is an ASD?

A

When the septum remains open after birth and blood moves between the atria due ostium primum

371
Q

Clinical features of ASD?

A

Acyanotic - LA to RA

Increased O2 sats in right arm, right ventricle and pulmonary artery

Delayed pulmonary closure - splitting S2 sound

Cardiomegaly

Big pulmonary arteries

372
Q

What are AV septal defects?

A

A hole in the very centre of the heart - ASD, VSD and fusion of the mitral + tricuspid valve to from a common valve

(can be complete or partial)

373
Q

Clinical presentation of AV septal defects?

A

Poor feeding + weight loss

Breathlessness

More blood going to the lungs so the heart pumps faster to pump more blood around the body

374
Q

What is a patent ductus arteriosus?

A

Maintained open connection between the aorta and pulmonary artery so blood from the aorta goes to the lungs instead

375
Q

Clinical presentation of patent ducuts arteriosus?

A

Asymptomatic

Tired

Prone to pneumonia

Cardiomegaly

Breathless

376
Q

Management of patent ducuts arteriousus?

A

Surgery to occlude the opening

377
Q

What is coarction of the aorta?

A

Narrowing of the aorta and the site of insertion of ductus arteriosus

378
Q

What is the disadvantage of a bicuspid aortic valve?

A

Degenerate faster, stenosis and regurgitation - unable to handle the stress meant for 3 leaflet aortic valve

379
Q

Complications of pulmonary stenosis?

A

RV hypertrophy - collapse

Regurgitation

Poor pulmonary blood flow

380
Q

What is cardiomyopathy?

A

A group of diseases of the myocardium that affect the mechanical or electrical function of the heart

381
Q

Examples of mechanical cardiomyopathy?

A

Hypertrophic

Dilated

Primary restrictive

Arrhythmogenic right ventricular

382
Q

What is hypertrophic cardiomyopathy?

A

Random AF - Ventricular hypertrophy in the absence of abnormal loading conditions e.g. hypertension or vascular disease

HYPERTROPHIC AND NON-COMPLIANT VENTRICLES = Decreased ventricular filling and so decreased SV

383
Q

Causes of hypertrophic cardiomyopathy?

A

Genetics - mutations of genes that code for sarcomeric proteins

384
Q

Clinical features of hypertrophic cardiomyopathy?

A

Breathless

Angina

Syncope

Jerky carotid pulse

385
Q

The most common cause of sudden death in young adults?

A

Hypertrophic cardiomyopathy

386
Q

Management of hypertrophic cardiomyopathy?

A

Amiodarone

ICD

BB and verapamil - chest pain and dyspnoea

Decrease outflow tract gradient

387
Q

What is the difference between hypertrophic and dilated cardiomyopathy?

A

Dilated - Dilated left ventricle that contracts poorly

Hypertrophic - Both ventricles are just dilated in the absence of abnormal loading conditions

388
Q

Consequence of Dilated cardiomyopathy?

A

Shortness of breath

Embolism

Decreased ejection fraction

389
Q

What is primary restrictive cardiomyopathy?

A

Rigid myocardium restricting diastolic ventricular filling and the clinical features resemble constrictive pericarditis

390
Q

Diagnosis of primary restrictive cardiomyopathy?

A

Cardiac catheterisation - endomyocardial biopsy

391
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Right ventricular wall is replaced by progressive fibro adipose tissue resulting in tachycardia and sudden death

No treatment and poor prognosis

392
Q

Clinical features of pulmonary hypertension?

A

RVF - peripheral oedema and abdo pain due to hepatic congestion

Dyspnoea

Lethargy and fatigue

Hepatomegaly

Pleural effusion

Increased JVP

393
Q

Causes of pulmonary hypertension?

A

Increased pulmonary vascular resistance or blood flow

Secondary to lung disease or L heart disease

394
Q

What is a pulmonary embolism?

A

Thromboembolism from a DVT travels through the veins to the right side of the heart and becomes lodged in the blood vessels of the lungs

395
Q

Pathophysiology of pulmonary embolism?

A

Obstruct RV outflow - Increase PVR - RH failure

Pulmonary infarct - VQ mismatch

396
Q

Clinical features of pulmonary embolism?

A

Breathless

Chest pain

Haemoptysis

Tachypnoeic

Exudative pleural effusion

397
Q

Confirmation of DVT?

A

Hoan’s sign - Calf pain at dorsiflexion of the foot

398
Q

CXR showing PE?

A

Raised hemidiaphragm

399
Q

Scoring system tool used to investigate PE?

A

Revised geneva score

400
Q

Management of PE?

A

Thrombolysis

Surgery to remove clot

Vena cava filter

401
Q

What is the leading cause of maternal death in developed countries?

A

PE - they are given LMWH because warfarin is tertragenic

402
Q
A

Phase 2a (7 decks)

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