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Phase 2a > Cardiovascular Conditions > Flashcards

Cardiovascular Conditions Flashcards

1
Q

Describe stable angina

A

Narrowing of the coronary arteries results in insufficient blood flow to the myocardium.

During time of high demand (exercise), unable to meet demand = symptoms.

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2
Q

Name 3 reasons why stable angina occurs

A
  1. Impairment of blood flow by proximal arterial stenosis
  2. Increased distal resistance e.g. left ventricular hypertrophy
  3. Reduced oxygen-carrying capacity of blood e.g. anaemia
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3
Q

Define coronary flow reserve

A

A ratio of the maximal flow down a coronary vessel to the resting flow.

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4
Q

Name 5 non modifiable risk factors of cardiovascular

A
  1. Older age (1)
  2. Male
  3. Ethnic background
  4. Family history (2)
  5. Kidney disease
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5
Q

Name 7 risk factors of cardiovascular disease

A
  1. Smoking (1)
  2. High blood level of non-lipoprotein cholesterol
  3. Lack of physical activity
  4. Unhealthy diet
  5. Alcohol intake above recommended levels
  6. Obesity/overweight
  7. Stress
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6
Q

In CVD how should pain be describe

A

OPQRST

Onset
Position
Quality - character
Relationship
Radiation
Relieving or aggravating factors
Severity
Timing
Treatment

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7
Q

Name the GS investigations for stable angina

A

CT coronary angiography

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8
Q

Describe RAMP as a management for stable angina

A

RAMP

Refer to cardiology
Advice about the diagnosis, management and when to call an ambulance.
Medical treatment.
Procedural or surgical interventions.

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9
Q

Describe the medication pathway for stable angina

A
  1. Immediate symptom relief
    - GTN spray
  2. Long term symptomatic relief
    - Beta blocker
    - Calcium channel blockers
    - Long-term acting nitrates
  3. Secondary prevention (4As)
    Aspirin - 75mg once daily
    Atorvastatin - 80mg once daily
    ACE inhibitor
    Already on beta blocker
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10
Q

Describe the surgical interventions for stable angina

A

PCI with coronary angioplasty

Coronary artery bypass graft (CABG)

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11
Q

Describe the clinical features of stable angina

A

Central chest pain
Tightness of exertion
Pain - radiates to one or both arms, neck or jaw.

Dyspnoea
Sweating
Nausea

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12
Q

What is the cause of stable angina

A

Atherosclerosis - leads to narrowing of coronary arteries that results in ischaemia

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13
Q

In stable angina what would an ECG show

A

Normal or ST depression

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14
Q

What must stable angina be relived by

A

Rest or a dose of subinguinal GTN

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15
Q

Name 5 differential diagnosis for stable angina

A

Unstable angina
ACS
Peptic ulcer
Oesophageal spasm
Reflux
Oesophagitis

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16
Q

Define unstable angina

A

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

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17
Q

When would angina be classed as unstable angina

A

Prolonged > 20 minutes

New onset of severe angina

Angina that is increasing in frequency

Longer duration

Lower in threshold

Angina that occurs after a recent myocardial infarction

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18
Q

Name the 3 types of acute coronary syndromes

A
  1. ST elevation myocardial infarction = STEMI
  2. Non-St elevation myocardial infarction = NSTEMI
  3. Unstable angina
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19
Q

Name the clinical features of acute coronary syndromes

A

Central constricting chest pain, associated with
- Nausea and vomiting
- Sweating and clamminess
- Feelings of impending doom
- Shortness of breath
- Palpitations
- Pain radiating to the jaw or arms

Longer than 20 minutes

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20
Q

What type of patient may have a silent MI

A

Diabetic patients

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21
Q

Describe an ECG of a STEMI

A

ST segment elevation in lead consistent with area of ischemia.

New left bundle branch block.

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22
Q

Describe the ECG and troponin levels of an NSTEMI

A

ST segment depression in a specific region (possible T wave inversion or pathological waves).

Pathological Q waves may be a late sign.

Raised troponin

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23
Q

Describe the ECG and troponin levels of unstable angina

A

ECG - may be normal or show ST-depression, transient ST-segment elevation or T wave inversion

Normal troponin

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24
Q

Left coronary artery

Which ECG leads show this area?
What is the view of the heart?

A

I, aVL, V3-6

Anterolateral

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25
Q

LAD

What ECG leads show this area?

What area of the heart is this?

A

V1-4

Anterior

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26
Q

Circumflex

What ECG leads show this area?

What heart area is this?

A

I, aVL, V5-6

Lateral

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27
Q

Right coronary artery

Which leads show this area?

What heart area is this?

A

II, III, aVF

Inferior

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28
Q

Describe the treatment of an acute STEMI which presents within 12 hours of onset

A
  1. Within 12 hours + can be done in 2 hours = PCI + prasugrel + aspirin
  2. PCI not possible + presenting in 12 hours = Fibrinolysis + ticagrelor + aspirin. ECG 60-90 mins after fibrinolysis
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29
Q

Describe the BATMAN approach to a STEMI

A
  • B – Beta blocker unless contraindicated.
  • A – Aspirin 300mg stat dose.
  • T – Ticagrelor 180mg stat dose – clopidogrel 300mg is an alternative.
  • M – Morphine – titrated to control pain.
  • A – Anticoagulant – low molecular weight heparin (LMWH).
  • N – Nitrates (e.g. GTN) to relieve coronary artery spasm.
  • Give oxygen only if their oxygen saturations are dropping, < 95%.
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30
Q

Describe the treatment for an NSTEMI

A

GRACE score to assess for PCI

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31
Q

Describe the treatment for unstable angina

A

Acute management - antiplatelet and anticoagulation therapy

Long term - reduce risk factors

Treatment the same as NSTEMI

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32
Q

Describe Dressler’s syndrome

A

Post-myocardial syndrome

Occurs 2-3 weeks after MI

Causes by localised immune response causing pericarditis

NSAIDs - in severe cases steroids

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33
Q

Describe the complications of an acute coronary syndrome

A

DREAD

Death
Rupture of heart septum or papillary muscles
oEdema - heart failure
Arrythmias and Aneurysm

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34
Q

Define Heart Failure

A

Inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissue, despite normal or increase cardiac filling pressures.

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35
Q

Name 5 symptoms of heart failure

A

Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight

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36
Q

Name 7 signs of heart failure

A

Tachycardia
Displaced apex beat
Raised JVP
Added heart sounds and murmurs
Hepatomegaly
Peripheral and sacral oedema
Ascites

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37
Q

What is the 1st line investigation in heart failure

A

NT pro-BNP

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38
Q

Describe the ECG of a patient who has heart failure

A

Usually, abnormal
- Arrythmias
- Ischemic ST- and T- wave changes

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39
Q

Describe the management of heart failure (HFrEF)

A

Mainly in HFREF

ACEi + BB

MRA if symptoms persist

Diuretics for fluid retention

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40
Q

Describe right sided heart failure

A

Occurs due to left-sided heart failure

  • Results in increased fluid pressure transferred into the lungs
  • Results in damage to heart’s right side
  • Right side loses pumping power - blood backs up into the veins
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41
Q

Name the two types of left sided heart failure

A
  1. Systolic failure HFrEF - heart failure with reduced ejection
  2. Diastolic failure HFpEF - heart failure with preserved ejection
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42
Q

Describe HFrEF

A

Left ventricle loses ability to contract normally

Reduced ejection

EF < 40%

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43
Q

Describe HFpEF

A

Ventricle loses ability to relax - muscle becomes stuff

Heart cannot properly fill with blood during rest period

EF greater than or equal to 50%

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44
Q

Describe hypertensive heart failure

A

Heart is unable to pump blood properly due to high blood pressure.

Heart walls can become thickened and/or stiff and the blood vessels become narrow and constrict

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45
Q

Describe cor pulmonale heart failure

A

Right sided heart failure secondary to a pulmonary condition

Lung disorder produces pulmonary hypertension

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46
Q

Define abdominal aortic aneurysm

A

Permanent pathological dilation of the aorta with diameter >1.5x the expected anterior posterior diameter, given the patients sex and size.

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47
Q

Describe the aetiology of an AAA

A

Threshold 3cm or more

> 90% of aneurysms originate below the renal arteries

Cause unknown?

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48
Q

What are the clinical features of a ruptured AAA

A

New abdominal pain

And/or
- Back pain
- Cardiovascular collapse
- Loss of consciousness

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49
Q

What are the clinical features of an unruptured AAA

A

Asymptomatic

Minority of patients present with
- Abdominal, back and groin pain

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50
Q

What are the 2 main presentations of AAA

A

Ruptured
Unruptured

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51
Q

Describe the 1st line investigations of an AAA

A

Aortic ultrasound

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52
Q

What is the 2nd line investigation in an AAA (unruptured)

A

CTA or magnetic resonance angiography

  • Used for anatomical mapping to assist with operative planning
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53
Q

Describe the management of an AAA

A

Ruptured or symptomatic AAA
- Urgent surgical repair

Unruptured (asymptomatic) if detected on incidental finding
- Surveillance
- No surgery until risk of rupture exceeds risk

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54
Q

Define aortic dissection

A

When a separation has occurred in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media

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55
Q

Describe the aetiology of an aortic dissection

A

Most commonly occurs with a discrete intimal tear but can occur without one.

Acute = process is less than 14 days old

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56
Q

Describe the clinical features of an aortic dissection

A

Abrupt onset of chest, back or abdominal pain.
- Severe intensity
- Ripping or tearing

Other features
- Syncope
- Heart/renal failure
- Mesenteric or limb ischemia

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57
Q

Describe the GS investigation for an aortic dissection

A

CT angiogram

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58
Q

Describe the CXR of aortic dissection

A

Widened mediastinum
Double/irregular aortic contour

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59
Q

What are the two clinical diagnosis for aortic dissection

A

Stanford type A and B

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60
Q

Define Stanford type A - aortic dissection

A

Involvement of the ascending aorta and/or arch.

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61
Q

Define Stanford type B - Aortic dissection

A

Dissections of the descending aorta

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62
Q

Describe the management of an aortic dissection

A

Oxygen/advanced life support protocol

Haemodynamic support without delay if suspected

Type A - urgent surgical repair
Type B - managed medically to control HR and BP

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63
Q

Name a complication of an aortic dissection

A

Aortic rupture

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64
Q

Name 4 supraventricular tachycardias

A
  1. Atrial Fibrillation
  2. Atrial Flutter
  3. AVRT
  4. AVNRT
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65
Q

Define atrial fibrillation

A

Uncoordinated atrial electrical activity and consequently ineffective atrial contraction.

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66
Q

Describe the pathophysiology of supraventricular tachycardias

A

Atrial ectopics from the pulmonary veins trigger micro re-entry circuits in the atria causing chaotic electrical activity

Activity is intermittently conducted through the AVN which gives rise to the characteristic irregularly irregular ventricular state

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67
Q

Describe the clinical features of AF

A

Irregularly irregular pulse
with or without any one of:
- Palpitations
- Dyspnoea
- Chest pain
- Fatigue
- Dizziness
- Polyuria
- Syncope

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68
Q

What is the good standard investigation for atrial fibrillation

A

12-lead ECG

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69
Q

Describe the ECG of acute AF

A

Irregular R-R intervals - where AV conduction is not impaired

Absence of distinct repeating P waves.

Irregular atrial activation.

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70
Q

Describe the ECG of chronic fibrilation

A

Absent P waves

Presence of fibrillatory waves and irregular QRS complex.

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71
Q

What are the 3 categories of AF

A
  1. Paroxysmal
  2. Persistent
  3. Permanent
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72
Q

Describe the GS management of acute AF

A

DIC cardioversion

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73
Q

Define an atrial flutter

A

Macro re-entrant atrial tachycardia with atrial rates usually 250-320bpm

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74
Q

What are the clinical features of atrial flutter

A

Palpitations
Fatigue or light headiness
Syncope
Chest pain

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75
Q

Describe the ECG of atrial flutter

A

Saw-tooth pattern between QRS complexes

Typically 2:1 AV block

Characteristics ventricular rate is 150 bpm

May fluctuate between atrial flutter and atrial fibrillation.

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76
Q

What is the management of atrial flutter

A

Haemodynamically unstable
- Emergency electrical cardioversion

Same as AF

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77
Q

Name 3 Ventricular Tachycardias

A
  1. Ventricular ectopic
  2. Prolonged QT syndrome
  3. Torsades de Pointes
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78
Q

Define ventricular ectopics

A

Extra heart beat originating in the ventricles

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79
Q

How common are ventricular ectopics

A

Very common - often benign

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80
Q

Name the common causes of ventricular ectopics

A

Usually no clinical significance

Caffeine
Alcohol
Tiredness
Hormonal changes

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81
Q

Name 4 more serious causes of ventricular ectopics

A
  1. Infection
  2. Muscle disease
  3. Channel ion disease
  4. Electrolyte imbalance
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82
Q

Name 5 clinical features of ventricular ectopics

A
  1. Largely asymptomatic
  2. Fluttering chest
  3. Dizziness
  4. Syncope
  5. Pre-syncope
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83
Q

What would you seen on an ECG of ventricular ectopics

A

Diagnosed by accident
‘Missed beat’
R on T phenomenon

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84
Q

What investigations can be used for ventricular ectopics

A

1st line - ECG
ECHO
Exercise test
MRI scan
24-hour ECG reading

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85
Q

What managment can be given for ventricular ectopics

A

Beta blocker
Calcium channel blocker

Electrophysiology study - ablation

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86
Q

Define prolonged QT syndrome

A

Characterised by prolonged QT interval on an ECG

> 450 ms in males
460 ms in females

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87
Q

Name the risk factors for prolonged QT syndrome

A

Gene mutations
Drugs
Hypokalaemia/magnesium/calcinemia
Bradyarrhythmia’s
Central nervous system lesions

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88
Q

Name the clinical features of a prolonged QT syndrome

A

Dizziness
Syncope
Arrhythmic symptoms postnatal
Palpitations
Angina
Fatigue

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89
Q

What investigations would be carried out for prolonged QT syndrome

A

ECG
Serum
- potassium
- magnesium
- calcium

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90
Q

What is the differential diagnosis for prolonged QT syndrome

A
  • Acquired structural heart disease
  • Neurocardiogenic (vasovagal) syncope
  • Neurological syncope
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91
Q

What is the management of prolonged QT syndrome

A

Usually, identifiable reversible cause

Primary treatment
- lifestyle
- beta-blocker therapy
- implantation of cardioverter-defib

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92
Q

Define Torsades de Pointes

A

Polymorphic VT with a characteristic twisting morphology occurring in the s+etting of a QT interval prolongation

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93
Q

What is Torsades de Pointes usually caused by

A

Drug induced

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94
Q

What are the key features of Torsades de Pointes

A

Episodes are usually self limiting

Frequently recurrent

Can cause impairment or loss of consciousness

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95
Q

What would be seen on an ECG of Torsades de Pointes

A

Long QT syndrome

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96
Q

What are the 2nd line investigations for Torsades de Pointes

A

Transthoracic echocardiogram
Electrolytes
Troponin I

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97
Q

What is the gold standard management of Torsades de Pointes

A

IV magnesium sulfate

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98
Q

What are the two types of conduction blocks

A

Heart Block
- 1st degree
- 2nd degree (Mobitz I and II)
- 3rd Degree

Bundle Branch Block - left and right

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99
Q

Define a heart block

A

Block is cardiac electrical disorder - impaired (delayed or absent) conduction from the atria to the ventricles

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100
Q

Describe a 1st degree heart block

A

Occurs when there is delayed AV conduction through the AV node

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101
Q

Describe a 2nd degree heart block

A

Some of the atrial impulses do not make it through the Av node to the ventricles

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102
Q

Describe a Mobitz type 1 heart block

A

Atrial impulses become gradually weaker - fails to stimulate contraction

PR gradually lengthens

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103
Q

Describe Mobitz type 2 heart block

A

Intermittent failure of interruption of AV block

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104
Q

Describe a 2:1 heart block

A

2 P waves for every QRS complex

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105
Q

Describe a 3rd degree heart block

A

Complete heart block - no communication between atria and ventricles due to complete failure of conduction

No observable relationship between P and QRS waves

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106
Q

Describe the clinical features of conduction block

A

Signs
- HR < 40 bpm
- Syncope

Symptoms
- Chest pain
- Palpitations
- Nausea and vomiting
- High BP
- Fatigue

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107
Q

Describe an ECG of 1st degree heart block

A

Can have 1:1 P and QRS wave

But have longer P-R interval > 0.2 seconds

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108
Q

Describe a 3rd degree heart block ECG

A

No relationship between P and QRS wave

Present P wave but not associated with QRS complex

PR interval absent

QRS complex narrow and broad

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109
Q

What is the management for stable heart block (1st degree conduction block, Mobitz type 1)

A

Observe

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110
Q

What is the management for unstable heart block (Mobitz type 2, complete heart block or previous asystole)

A

1st line - Atropine 400mcg IV

If no improvement
- Repeated Atropine up to 6 doses
- Other inotropes
- Transcutaneous cardiac pacing

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111
Q

What is the management for patients with high risk of asystole (Mobitz type 2, complete heart block or previous asystole).

A

Temporary transvenous cardiac pacing

Permeant implantable pacemaker

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112
Q

What are the possible reasons for a left bundle branch block

A

Always pathological

May be due to conduction system degeneration or myocardial pathologies

May occur after a procedure

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113
Q

What are the possible reasons for right bundle branch block

A

Can be physiological or the result of damage to the right bundle branch

E.g.
PE
IHD
ASD
VSD

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114
Q

Describe a bundle branch block

A

Depolarisation only occurs down one side

Abnormally depolarises the septum from one side to the other

Other ventricle wall is depolarised but occurs much slower and less efficient

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115
Q

What are the clinical features of a bundle branch block

A

Usually - asymptomatic
- syncope

RBBB - splitting of the second heart sound

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116
Q

Describe an ECG of a left bundle branch block

A

W in V1 - deep downwards defection
M in V6 - broad notched or ‘M’ wave

WiLLiaM

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117
Q

Describe the ECG of a right bundle branch block

A

M in V1 - RSR wave
W in V6 - QRS wave

MaRRoW

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118
Q

What are the physiological mechanisms involved in the development of hypertension

A

Cardiac output
Peripheral resistance
RAAS
Autonomic nervous system

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119
Q

Define hypertension

A

> (or equal to) 140/90 mmHg

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120
Q

Are hypertension values always the same

A

Depends on clinical setting

Low/high CVD risk

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121
Q

Describe the management of hypertension

A

Lifelong
- BP response
- Medication
- Lifestyle changes

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122
Q

When is hypertension a clinical emergency

A

Evidence of immediate damage
- Papilledema
- Acute kidney injury
- Acute stroke
- Acute coronary syndrome
- Aortic dissection

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123
Q

Define bleeding time

A

Clinical lab test performed to evaluate platelet function.

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124
Q

Describe the pathophysiology of a DVT

A

Fibrin driven

Venous circulation = low pressure = fibrin rich

Blood does not go back to the heart = swelling

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125
Q

What is the main risk factor for a DVT

A

Virchow’s Triangle

Immobilisation
- Long haul flights
- Surgery
- Trauma

Endothelium
- Injury - physical, chemical

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126
Q

What are the clinical features of a DVT

A

Unilateral nature of swelling and assessing risk factors

  • Leg pain
  • Swelling
  • Tenderness
  • Warmth
  • Redness
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127
Q

What is the GS investigations for a DVT

A

Doppler ultrasound

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128
Q

Describe the general management of a DVT

A

Medication- main = anticoagulant
- Heparin or LMWH
- Warfarin
- DOAC

  • Compression stocking
  • Underlying cause
  • Recannalisation
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129
Q

What is the prevention of a DVT

A

Mechanical
- Hydration
- Early mobilisation
- Compression stocking
- Foot pumps

Chemical
LMW Heparin

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130
Q

What are the complications of a DVT

A

Phlegmasia Alba Dolens/Phlegmasia Cerulae Dolens

Pulmonary Embolism

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131
Q

Define a pulmonary embolism

A

Life-threatening condition resulting from dislodged thrombi occluding the pulmonary vasculature

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132
Q

Why does a pulmonary embolism occur

A

Potentially fatal complication of a DVT

51% DVT develop into PE

Consequence of thrombus formation within a deep vein of the body - normally lower extremities

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133
Q

What are the symptoms of a pulmonary embolism

A

Symptoms
- Breathlessness
- Pleuritic chest pain

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134
Q

Name 3 signs of PE

A
  • Tachycardia
  • Tachypnoea
  • Pleural rub
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135
Q

What is the GS investigation for a pulmonary embolism

A

CTPA

Computerised tomography pulmonary angiography

Detailed visualisation of pulmonary vessels and emboli

Includes radiation

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136
Q

Describe the investigation route of PE

A
  1. Wells score
  2. If high risk of PE = D-dimer
  3. D-dimer raised = CTPA
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137
Q

What is the GS investigation in PE if a CTPA is contraindicated

A

V/Q scan

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138
Q

Define peripheral artery vascular disease

A

Narrowing or occlusion of the peripheral arteries affecting the blood supply to the lower limbs

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139
Q

Name 6 reasons for why arterial vascular disease occurs

A
  1. Atherosclerosis
  2. Inflammatory
  3. Vasospastic
  4. Compression
  5. Traumatic
  6. Pro-thrombotic conditions
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140
Q

Describe acute ischaemia in artery vascular disease

A

6Ps

Pain
Pulselessness
Pallor
Perishingly cold
Paralysis
Pins and needles

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141
Q

Describe chronic ischemia in artery vascular disease

A

Caused by atherosclerosis

Rest pain

Buerger’s test

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142
Q

Describe the GS investigation for artery vascular disease

A

ABPI

Ankle Brachial

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143
Q

Describe the management of artery vascular disease

A

Risk factor modification
- Antiplatelets
- Statin
- Stop smoking
- BP
- DM

Exercise programme

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144
Q

What are invasive treatments for arterial vascular disease

A

Carotid endarterectomy

Stenoses
Short occlusion
DEB/DES
Bypass surgery

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145
Q

What classification is used to diagnose venous vascular disease

A

CEAP Classification

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146
Q

What clinical assessments for venous peripheral disease

A

Tap test - Schwartz
Trendelenburg test
Torniquet test
Perthes test

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147
Q

What investigations are used for venous vascular disease

A

Duplex - gold standard
MRV - Pelvic
Venography

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148
Q

What is the management for superficial venous disease

A

Lifestyle
Compression
Sclerotherapy
Endo-venous treatments
Surgical stripping

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149
Q

What is the management for deep venous disease

A

Lifestyle
Compression
Stents
Valves

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150
Q

Define Pericarditis

A

Acute inflammation of pericardium with or without effusion

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151
Q

What are the causes of pericarditis

A

Viral (most common)
Purulent bacterial
Tuberculosis
Dressler’s syndrome

Majority = idiopathic

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152
Q

What are the risk factors of pericarditis

A

Male sex
Age 20-50 yrs - most common 41-60
Transmural myocardial infarction
Cardiac surgery
Neoplasm
Viral and bacterial infections
Uraemia or on dialysis
Systemic autoimmune disorders

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153
Q

Describe the clinical features of pericarditis

A

Sharp pleuritic chest pain - worse on inspiration and lying down + relieved by sitting forwards

Dyspnoea
Cough
Hiccups
Fever
Tachycardia

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154
Q

Describe the chest pain in pericarditis

A

Severe
Sharp and pleuritic
Rapid onset
Left anterior chest or epigastrium
Radiates to the arm
Relieved by sitting forward, exacerbated by lying down

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155
Q

Describe the clinical examination of pericarditis

A

Clinical examination
- pericardial rub
- sinus tachycardia
- fever
- signs of effusion

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156
Q

What would an ECG of pericarditis look like

A

Saddle shaped
PR depression

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157
Q

How is a clinical diagnosis made in pericarditis

A

Made with 2 of 4 of them:
- Chest pain
- Friction rub
- ECG changes
- Pericardial effusion

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158
Q

What is the management of pericarditis

A

Sedentary lifestyle
NSAIDs
Colchicine

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159
Q

Describe a pericardial effusion

A

Present when the fluid in the pericardial space exceeds its physiological amount <50mL.

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160
Q

How can a pericardial effusion be classified

A

Onset
Distribution
Haemodynamic impact
Composition
Size based

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161
Q

What are the GS investigation for a pericardial effusion

A

transthoracic echocardiograph

Assess size
Assess the effect on heart function

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162
Q

Describe an ECG of pericardial effusion

A

Low voltage QRS complex

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163
Q

Describe the signs of pericardial effusion

A

Soft and distant heart sounds
Muffled apex beat
Raised (JVP) jugular venous pressure
Dyspnoea

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164
Q

What is a complication for pericardial effusion

A

Cardiac tamponade

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165
Q

Describe a cardiac tamponade

A

Compromised ventricular filling due to pericardial effusion

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166
Q

Define infective endocarditis

A

Infection of heart valve/s or other endocardial lined structures within the heart

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167
Q

What increases the risk of infective endocarditis

A

Have abnormal heart valve, regurgitant or prosthetic valves

Introduce infectious material into the blood stream or directly onto the heart during surgery

Have had a previous IE

IVDU

Poor dental hygiene

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168
Q

When should infective endocarditis be suspected

A
  1. New regurgitant heart murmur
  2. Embolic events of unknown origin
  3. Sepsis of unknown origin
  4. Fever (most frequent sign)
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169
Q

What are some peripheral signs of infective endocarditis

A

Splinter haemorrhages
Osler’s nodes
Janeway lesions
Retinal infarcts

Finger clubbing

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170
Q

Name the 2nd investigation used for infective endocarditis

A

Blood cultures - 3 different sites over 24 hours

Raised ESR, CRP

CXR - cardiomegaly

ECG - prolonged PR interval

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171
Q

What is the criteria used to test for infective endocarditis

A

Modified Dukes Criteria

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172
Q

What are the criteria for the Modified Dukes Criteria

A

Definite IE - 2 major, 1 major + 1 minor, 5 minor

Possible IE - 1 major + 1 minor, 3 minors

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173
Q

Describe the GS investigation in infective endocarditis

A

ECHO

  • TTE (transthoracic)
  • TEE (transoesophageal) - more sensitive
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174
Q

Describe the management in infective endocarditis caused by staphylococcus

A

Flucloxacillin + rifampicin + gentamicin

Prolonged cause - 2 weeks IV followed by oral

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175
Q

When would operations be chosen in infective endocarditis

A

Infection cannot be cured with antibiotics

Complications

Remove infected device/replace valve after infection cured

Remove large vegetation before they embolise

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176
Q

What are the differential diagnosis for infective endocarditis

A

Lymphoma
Pulmonary embolism
Deep vein thrombosis
Drug fever
TB
Meningitis

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177
Q

Name 4 valvular heart diseases

A
  1. Aortic stenosis
  2. Mitral regurgitation
  3. Aortic regurgitation
  4. Mitral stenosis
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178
Q

Define aortic stenosis

A

Obstruction of blood flow across the aortic valve due to aortic valve fibrosis and calcification

Blood flow out of left atrium

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179
Q

What type of problem is aortic stenosis

A

Pressure problem

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180
Q

What are the 3 types of aortic stenosis

A
  1. Supravalvular
  2. Subvalvular
  3. Valvular
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181
Q

Describe the pathophysiology of aortic stenosis

A

Pressure gradient develops between L. Ventricle and aorta = increased afterload.

LV function initially maintained by compensatory pressure hypertrophy.

Compensatory mechanisms exhausted = Lv function declines.

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182
Q

What are the 2 causes of aortic stenosis

A
  1. Congenital
  2. Acquired
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183
Q

Name the 4 strong risk factors associated with aortic stenosis

A

Age > 60 years
Congenitally bicuspid aortic valve
Rheumatic heart disease
Chronic kidney disease

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184
Q

Describe the clinical features of aortic stenosis

A

Syncope
Angina
Dyspnoea
Sudden death

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185
Q

What investigations are used for aortic stenosis

A

ECHO - quantitative doppler echocardiography

Measures
- L, ventricular size and function
- Doppler derived gradient and valve area

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186
Q

Describe the medical management for aortic stenosis

A

Limited as AS is mechanical problem

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187
Q

Describe the surgical management for aortic stenosis

A

1st line - as AS is a medical problem

Aortic valve replacement
Transcatheter aortic valve implantation

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188
Q

Define mitral regurgitation

A

Backflow of the blood from the LV to the LA during systole

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189
Q

What type of problem is mitral regurgitation

A

Volume problem

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190
Q

What is the compensatory mechanism of mitral regurgitation

A

Left atrial enlargement, LVH and increased contractility

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191
Q

Describe the main causes of mitral regurgitation

A

Primary - disease of leaflets e.g. rheumatic fever, infective endocarditis

Secondary - dilated cardiomyopathy. Normal valve architecture but impaired due to abnormal LV/LA dilated cardiomyopathy

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192
Q

Describe the clinical features of the murmur of mitral regurgitation

A

Auscultation - pansystolic murmur at the apex radiating to the axilla

Loudest over the mitral area

Loudest on expiration in the left lateral decubitus position

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193
Q

Describe the GS investigations for mitral regurgitation

A

Echocardiogram

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194
Q

Define aortic regurgitation

A

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

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195
Q

What type of problem is aortic regurgitation

A

Combined pressure AND volume overload

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196
Q

What are the compensatory mechanisms of aortic regurgitation

A

LV dilation
LVH
Progressive dilation leads to heart failure

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197
Q

What are the clinical features of chronic aortic regurgitation

A

Asymptomatic for years

Initial symptoms
- Palpitations
- Pounding heart when lying on the left side
- Dyspnoea

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198
Q

Describe the 2 key investigations of aortic regurgitation

A

Echocardiogram

CXR

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199
Q

Describe the general management of aortic regurgitation

A

Surgical treatment SAVR

Serial echocardiogram

Vasodilators

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200
Q

Define mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole

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201
Q

What is the predominant cause of mitral stenosis

A

Rhematic heart disease

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202
Q

What are the clinical features of mitral stenosis

A

Progressive dyspnoea (LA dilation)
Increased transmitral pressures
RHF symptoms
Haemoptysis

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203
Q

What are the GS investigations of mitral stenosis

A

Echocardiograph

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204
Q

Describe the management of mitral stenosis

A

Serial echocardiography

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205
Q

Define shock

A

Life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to and consequently oxygen utilised by cells

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206
Q

What does shock describe

A

Pathophysiological state with many different causes

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207
Q

How is shock characterised

A

By the release of cytokines and other inflammatory response syndrome mediated by tissue hypoxia

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208
Q

Name 3 potential causes of shock

A
  1. Decreased blood perfusion of tissues
  2. Inadequate blood oxygen saturation
  3. Increased oxygen demand from tissues
209
Q

Define hypovolemic shock

A

Loss of blood or plasma cause inadequate tissue perfusion.

210
Q

Describe the pathophysiology of hypovolaemic shock

A

Loss of blood volumes is detected by low-pressure stretch receptors in the atria and arterial baroreceptors in the aorta and carotid artery

211
Q

When does hypovolemic shock occur

A

After haemorrhage

Systolic BP decrease after 30-40% of blood volume is lost

212
Q

What is the management for hypovolemic shock

A

Stop bleeding - replace blood if required

Warm all fluids

If needed - give fresh frozen plasma and platelets early

213
Q

Define anaphylactic shock

A

Sudden onset of life-threatening airway and/or breathing and/or circulation problems (with or without skin changes) after exposure to a trigger (allergen).

214
Q

What is the management of anaphylactic shock

A

Diagnosis is clinical

Treat with IM adrenaline and secure airways

215
Q

Define septic shock

A

Life threatening organ dysfunction caused by dysregulated host response to infection

216
Q

What is the score tool used in septic shock

A

National Early Warning Score 2 (NEWS2)

217
Q

What is the management for septic shock

A

Within 1 hour of being recognised

  • Take 2 sets of blood cultures
  • Measure serum lactate on a blood gas
  • Assess the patents hourly urine output
  • Give IV broad spectrum antibiotics (after taking blood cultures)
  • IV fluids if any sign of circulatory insufficiency
  • Oxygen if required
218
Q

Define cardiogenic shock

A

Characterised by low CO state of circulatory failure that results in end-organ hypoperfusion and tissue hypoxia

219
Q

Define neurogenic shock

A

Characterised by organ tissue hypoperfusion resulting from the disruption of normal sympathetic control over vascular tones due to damage of the nervous system

220
Q

When does neurogenic shock often arise from

A

Spinal cord (T6)

221
Q

What is the 1st line management for neurogenic shock

A
  1. IV fluid
222
Q

Define hypertrophic cardiomyopathy

A

Left ventricle muscle becomes thickened

223
Q

Define dilated cardiomyopathy

A

Heart muscle becomes thin and dilated.

May be genetic or secondary to another condition

224
Q

Define restrictive cardiomyopathy

A

Heart becomes rigid and stiff with impairment ventricular filling during diastole

225
Q

What are the signs of hypertrophic cardiomyopathy

A

Ejection systolic murmur at low left sternal border

4th heart sound

Thrill at lower sternal border

226
Q

What is the GS the investigation of hypertrophic cardiomyopathy

A

Echocardiography - establish diagnosis

227
Q

What is the management of hypertrophic cardiomyopathy

A

Depends on severity of symptoms
- Beta blockers
- Surgical myectomy
- Alcohol septal ablation
- Implantable cardioverter defib
- Lifestyle factors

228
Q

In hypertrophic cardiomyopathy what medication is avoided

A

ACE inhibitors and nitrates

229
Q

Define rheumatic fever

A

Autoimmune disease mostly occurs following a group A streptococcal throat infection

230
Q

What systems can rheumatic fever affect

A

Multiple systems
- Joints
- Heart - only affects here can lead to permanent damage
- Brain
- Skin

231
Q

What are the 5 major manifestations of rheumatic fever

A

Carditis (most common)
Arthritis (most common)
Chorea
Erythema marginatum
Subcutaneous nodules

232
Q

What is the diagnosis test for rheumatic fever

A

No single test to diagnose.

Jones Test
- Evidence of a strep A infection
+
2 major criteria
OR
One major criteria and 2 minor criteria

233
Q

What is the management of rheumatic fever

A
  • Initial management
  • Antibiotic therapy
  • Diazepam
  • Long term penicillin
234
Q

Name 5 structural heart defects which results in narrowing

A
  1. Tetralogy of Fallot
  2. Ventricular Septal Defect
  3. Atrial Septal Defect
  4. Atrio-ventricular septal defects (AVSD)
  5. Patent Ductus Arteriosus
235
Q

Define tetralogy of fallot

A

Ventricular septal defect with over-riding aorta and right ventricular outflow tract obstruction and resulting RV hypertrophy

236
Q

Describe the pathophysiology of tetralogy of fallot

A

Stenosis of the heart RV outflow leads to the RV being at higher pressure than the left

Result = blue blood passes from the RV to LV

Patients = Blue

237
Q

What are the 4 classical findings of tetralogy of fallot

A
  1. A mal-alignment ventricular septal defect
  2. Aorta over-riding VSD
  3. Right ventricular outflow tract obstruction
  4. Secondary right ventricular hypertrophy
238
Q

How is tetralogy of fallot diagnosed

A

Echocardiography

239
Q

What are the 6T’s used to recall the differential diagnosis of cyanotic lesions

A

Tetralogy of fallot
Transposition of great arteries
Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid valve abnormalities
Tons of others

240
Q

What is the management of tetralogy of fallot

A

Surgical repair
- Complete intracardiac repair

241
Q

Define ventricular septal defect

A

Congenital or acquired defects in the inter-ventricular septum that allow shunting of blood

242
Q

Describe the pathophysiology of ventricular septal defect

A

Hold between high pressure LV and low pressure RV

243
Q

What are the investigations of ventricular septal defects

A
  1. Echo
    Chest x-ray
    ECG
  2. Cardiac MRI
    Cardiac CT scan
    Cardiac catheterisation
244
Q

What is the management of a large ventricular septal defect

A

Complete repair
PA band

245
Q

What is the management of a small ventricular septal defect

A

No form of management needed

Small risk of infection

246
Q

Describe Eisenmenger syndrome

A

High pressure pulmonary blood flow

Damages pulmonary vasculature

Resistance to blood flow through lungs increases

RV pressure increases

Shunt direction reverses

Patient = Blue

247
Q

What is a possible complication of congenital heart conditions

A

Eisenmenger syndrome

248
Q

Define atrial septal defect

A

Abnormal connection between two atria
- primum
- secundum
- sinus venosus

249
Q

Describe the pathophysiology of atrial septal defect

A

Slightly higher pressure in the LA than RA

Shunt L to R

= Not blue

Increased flow into right heart and lungs

Extra volume to the lungs

250
Q

What are the clinical features of an atrial septal defect

A

Pulmonary flow murmur

Fixed split second heart sound

Big pulmonary arteries on CXR

Big heart on chest x-ray

251
Q

What is the management of atrial septal defect

A

Surgical
Percutaneous - keyhole technique

252
Q

Describe AVSD

A

Hole in very centre of the heart

Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves

Can be complete or partial

253
Q

What is the management of AVSD

A

Medical treatment
- Diuretics and vasodilators to reduce preload and afterload
- Increase calories

Surgical treatment

254
Q

What are the clinical features of patent ductus arteriosus

A

Continuous ‘machinery’ murmurs
If large - big heart, breathless
Eisenmenger’s syndrome

255
Q

Describe the management of patent ductus arteriosus

A

Surgical or percutaneous

256
Q

Define coarctation

A

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

257
Q

Describe the clinical features of coarctation

A

Right arm hypertension

Bruits over the scapula and back from collateral vessels

Murmurs

258
Q

What is the management of coarctation

A

Surgical vs. percutaneous repair

Subclavian flap repair
End to end repair

259
Q

What is the clinical blood pressure reading and ambulatory/home BP reading of stage 1 hypertension

A

Clinical

> (or equal to) 140/90 mmHg

Ambulatory/home BP

> (or equal to) 135/85 mmHg

260
Q

What is the clinical blood pressure reading and ambulatory/home BP reading of stage 2 hypertension

A

Clinical

> (or equal to) 160/100 mmHg

Ambulatory/home BP

> (or equal to) 150/95 mmHg

261
Q

What is the clinical blood pressure reading of stage 3 hypertension

A

> (or equal to) 180/120 mmHg

262
Q

What is the aims of clinical BP and ambulatory/home BP in < 80

A

Clinical

< 140/90 mmHg

Ambulatory/home

< 135/85 mmHg

263
Q

What is the aims of clinical BP and ambulatory/home BP in > 80 (or equal to)

A

Clinical

< 150/90 mmHg

Ambulatory/home

< 145/85 mmHg

264
Q

Name differential diagnosis of ACS

A

Other ACS
Pericarditis
Aortic dissection
PE
Aortic stenosis
Hypertrophic cardiomyopathy

265
Q

Define an NSTEMI

A

Partial occlusion of major artery or complete occlusion of minor

266
Q

Describe the clinical features of ACS

A

Sudden onset of crushing chest pain
Radiating to L arm or jaw
Longer than 20 mins
Diaphoresis
Nausea
SOB

267
Q

What is the GS investigation of NSTEMI

A

Troponin + ECG

268
Q

What is a 2nd investigation in NSTEMI

A

Coronary angiogram

If clinically unstable
Within 24 hours

269
Q

What is given after an NSTEMI

A

Dual therapy

Antiplatelet (aspirin) + clopidogrel (P2Y12 receptor inhibitor)

270
Q

What is the immediate treatment of an NSTEMI

A

Antiplatelet - 300mg aspirin
Analgesia
GTN or IV opioids
Initial anti-thrombin therapy
Oxygen

271
Q

What is troponin a marker for

A

Myocardial damage

272
Q

Define STEMI

A

Complete occlusion of major coronary artery

Full thickness damage of heart

273
Q

What is the 1st line management of a STEMI

A

MONA

Morphine
Oxygen
Nitrates
Aspirin 300mg

274
Q

What is the GS management of STEMI

A

PCI in 2 hours

275
Q

ECG - A STEMI of the l. anterior descending artery would show as…

A

ST elevation in V1-V3

276
Q

ECG - A STEMI of r. coronary artery would show as…

A

ST changes in inferior leads II, III, aVF

277
Q

ECG - A STEMI of l. circumflex artery would show as…

A

ST elevation in lateral leads I, aVL, V5-6

278
Q

Define prinz metal angina

A

Clinical condition characterised by chest discomfort or pain with rest with transient ECG changes in ST segment, with prompt response to nitrates

279
Q

Describe the clinical features of prinz metal angina

A

Chest pain at rest 5-15 minutes

Midnight to early morning

Pain decreases with short acting nitrates

280
Q

Who is prinz metal angina seen in

A

Younger patients with less CVD risk scores

281
Q

What are not risk factors for prinz metal angina

A

Smoking and inflammation by CRP

Other risk factors are same as CVD

282
Q

What is GS investigation for prinz metal angina

A

Evidence of coronary spasm during coronary angiogram

283
Q

Name the ECG changes seen in prinz metal angina

A

ST segment elevation or depression

284
Q

What is 1st line management in prinz metal angina

A

Calcium antagonist due to vasospastic angina

285
Q

Name 2nd line management in prinz metal angina

A

Smoking cessation

Avoiding medication or drugs that can induce

286
Q

Name 6 differential diagnosis of prinz metal angina

A

Acute pericarditis
Anxiety
Aortic dissection
MI
GORD
Unstable angina

287
Q

Describe the pathophysiology of prinz metal angina

A

Spasm in coronary arteries = decrease in blood supply to the myocardium generating symptoms like chest pain

288
Q

Name the risk factors of heart failure

A

HTN
Diabetes
Obesity
Sleep apnoea
CKD
Thyroid disorders
Anaemia
AF
Lifestyle habits

289
Q

What is heart failure based upon

A

L. ventricular ejection fraction

290
Q

Describe the 2nd line investigation in heart failure

A

If NT-pro BNP > 400

= Transthoracic echocardiography

291
Q

Name some signs which would be shown on a clinical exam of heart failure

A

Displaced apex beat - left ventricular dilation

Dullness on percussion = pleural effusion

292
Q

What is the treatment of heart failure mainly for

A

HFrEF

293
Q

Describe the management for HFpEF

A

Manage co-morbidities

294
Q

Name 7 differential diagnosis of heart failure

A

AKI
ARDs
Pneumonia
COPD
Cirrhosis
MI
Cardiomyopathy

295
Q

Based on frank starling law what does heart failure result in

A

= optimal myocardial contracility

CO = SV x HR

Co = reduced
HR = reduced
Preload = reduced
Contracility = reduced

Afterload = increased

296
Q

Name the causes of Heart failure

A

HIGH VIS

Hypertension
Infection/immune
Genetic
Heart attack

Volume overload (organ failure)
Infiltration
Structural

297
Q

What are the 2 most common reasons for heart failure

A

Hypertension
Heart attack - ischaemic heart disease

298
Q

Describe BNP

A

Increases when myocardial stress - correlates with severity of disease

299
Q

Describe NT-pro BNP

A

Helps with diagnosis + informs type and urgency of further investigations

300
Q

Describe the ECG of heart failure

A

Left tachycardia
AF
L. axis deviation - L. ventricular hypertrophy
P wave abnormalities
Prolonged PR interval
Wide QRS complex

301
Q

Describe the chest xray in heart failure

A

ABCDE

Alveolar oedema
Kerley B lines
Cardiomegaly - thoracic ratio > 50%
Dilated upper lobe vessels
Effusions e.g. pleural effusions

302
Q

Describe the classes of heart failure

A

1 - asymptomatic
2 - slight limitation = mild
3 - marked limitation
4 - inability to carry out normal activity

303
Q

Name what infections/immune conditions could cause heart failure

A

HIV (viral)
Bacterial (sepsis)
Autoimmune (lupus, rheumatoid arthiritis)

304
Q

Name the genetic features which could result in heart failure

A

Hypertrophic obstructive cardiomyopathy
Dilated cardiomyopathy

305
Q

Name the infiltration that could cause heart failure

A

Sarcoidosis
Amyloidosis
Haemochromatosis

306
Q

Name the structural that could cause heart failure

A

Valve disease
Septal defects

307
Q

Define ejection fraction

A

% of blood pumped with each beat

308
Q

What is the normal ejection fraction

A

55-60%

309
Q

Describe ischaemic heart failure

A

One or more frequent causes
Obstructive plaques
Determines reduced coronary blood flow

310
Q

Describe myopathic heart failure

A

Dilated = heart enlarged + weakened = harder to pump blood

Hypertrophic = heart abnormally thick = harder to pump blood

311
Q

Describe hypertensive heart failure

A

Increase BP = unable to pump blood correctly

Heart walls = thicken + stiffen + blood vessels become narrow and constrict

312
Q

Name the different forms of heart failure

A

Right sided
Left sided
Ischaemic
Myopathic
Hypertension
Cor-pulmonale

313
Q

Name the key differences in AAA between genders

A

Men 4-6x more likely than women

Female more likely to rupture

Mortality = higher in women operatively

314
Q

What is a complication of an AAA

A

Endoleak

315
Q

Name 5 differential diagnosis of AAA

A

Renal colic
Diverticulosis
Bowel ischaemia
Ovarian torsion
Peptic ulcer

316
Q

Name 3 differential diagnosis of aortic dissection

A

MI
Aortic aneurysm
Cardiac tamponade

317
Q

Name the risk factors for aortic dissection

A

Marfan syndrome
Ehler’s Danlos syndrome
Bicuspid aortic valve
Cortication
Smoking
Family history

318
Q

Name the 2nd line management in acute AF

A

If DC cardioversion unsuccessful

Flecainide or amiodarone

319
Q

What should be given > 48 hours before cardioversion

A

BB or rate limiting CCB

320
Q

Describe the 1st line management in chronic AF

A

Rate control - BB, rate limiting CCB or diltiazem

Failure = digoxin

Then consider amiodarone

321
Q

What is given for a month post cardioversion

A

Anticoagulants

322
Q

Name the risk factors of supraventricular tachycardias

A

Age
HTN
HF
DM
Obesity
Coronary artery disease
Other cardiac conditions

323
Q

Name the differential diagnosis of supraventricular tachycardias

A

Other supraventricular tachycardias

324
Q

What tools are used in AF

A

CHA2DS2VASC tool

ORBIT score

325
Q

Define AVRT (atrioventricular re-entrant tachycardia)

A

Occurs when myocardial fibres connect the atrium to ipsilateral ventricles across mitral or tricuspid annulus, pre-existing ventricles

326
Q

Name the clinical features of AVRT

A

Dizziness
Syncope
Chest pain
SOB
Palpitations

327
Q

Name the risk factors of AVRT

A

Ebstein’s anatomy
Hypertrophic cardiomyopathy
Mitral valve prolapse
Ventricular septal defects

328
Q

What is the ECG of AVRT

A

Narrow QRS complex - due to conduction solely by AV node

329
Q

What is the GS investigation of AVRT

A

12-lead ECG

330
Q

What is a 2nd investigation of supraventricular tachycardias

A

ECHO

331
Q

What is the management of AVRT if symptomatic

A

Catheter ablation

332
Q

What is another name for AVRT

A

Wolff-Parkinson White syndrome

333
Q

Define AVNRT (atrioventricular nodal re-entrant tachycardia)

A

Caused by re-entry within the AV node while some fibres are still refractor

Impulse will only be the excitable pathway

334
Q

Name the clinical features of AVNRT

A

Dizziness
Syncope
SOB
Palpitations
Polyuria
HR 140-280 bpm

335
Q

Name 2 risk factors of AVNRT

A

Coronary artery disease
Heart failure

336
Q

What is the GS investigation of AVNRT

A

12-lead ECG

337
Q

Describe the ECG of AVNRT

A

Ventricular rhythm 150-250bpm

P wave not visible - hidden by QRS complex

OR

P wave may be visible before or after QRS complex

Depends on the pathway

338
Q

Describe the ECG of the slow-fast pathway in AVNRT

A

P wave sometimes seen after QRS.

Pseudo S lead II

Pseudo R lead V1

339
Q

Describe the ECG of fast-slow pathway in AVNRT

A

P-wave before QRS or P wave on ST-T segment

340
Q

What is the 1st line management of symptomatic AVNRT

A

Catheter ablation

341
Q

What is the 2nd line management of symptomatic AVNRT

A

If catheter ablation not possible

BB, diltiazem, verapamil

342
Q

Describe the epidemiology of AVNRT

A

1/4 of population has 2 pathways that input

One slower and one rapid

343
Q

Describe the pathophysiology of ventricular ectopics

A

Electrical impulse starts from the ventricles before electrical impulse can be made by the atrium

344
Q

Name the differential diagnosis for ventricular ectopics

A

LBBB

345
Q

What does prolonged QT syndrome increase the risk of

A

Syncope
Ventricular arrythmias (torsades de pointes)
Sudden cardiac death

346
Q

Name 4 clinical features of torsades de pointes

A

Tachycardia
Hypotension
Syncope
Dizziness

347
Q

Name the risk factors for torsades de pointes

A

Coronary artery disease
MI
Hypertrophic cardiomyopathy
Electrolyte imbalance

348
Q

What is the 2nd line medical management of torsades de pointes

A

Beta blocker
Atrial pacing
Anti-arrythmia drugs

349
Q

Name 3 differential diagnosis of torsades de pointes

A

Ventricular tachycardia
Ventricular fibrillation
Drug-toxicity

350
Q

Describe the complications of Torsades de pointes

A

If not controlled can lead to ventricular fibrillation

Sometimes death

351
Q

Name the causes of 1st degree conduction block

A

Hypokalaemia
Myocarditis
Inferior MI
AV blocking drugs e.g. BB, CCB, digoxin

352
Q

Name the differential diagnosis of conduction blocks

A

Congenital heart block
Sinoatrial exit block
1st degree AV block
MI
Medication toxicity

353
Q

What is does a 1st degree conduction block increase the risk of

A

AF

354
Q

Name the causes of Mobitz type 1 (2nd degree)

A

Av blocking drugs
Inferior MI
Fit athletes due to vagal toning

355
Q

Describe the ECG of Mobitz type 1

A

PR lengthens before a QRS complex is dropped

356
Q

Name the causes of Mobitz type 2

A

Anterior MI
Mitral valve surgery
SLE
Lyme disease
Rheumatic fever

357
Q

Describe the ECG of Mobitz type 2

A

Normal PR interval with intermittently dropped QRS

QRS broad - if conduction failure located in bundle of his

358
Q

What is there a risk of in Mobitz type 2 and 3rd degree complete block

A

Asystole

359
Q

What is a complication of 3rd degree conduction block

A

Sudden cardiac death

360
Q

Define RBBB

A

Right bundle no longer conducts - do not contract at the same time

Left 1st then right

361
Q

Define LBBB

A

Left bundle no longer conducts - does not contract at the same time

Right 1st then left

362
Q

Name 4 risk factors of LBBB

A

Younger children/adults < 35
Hypertension
Coronary artery disease
Left ventricular hypertrophy

363
Q

How are bundle branch blocks diagnosed

A

ECG

364
Q

Define hypertension

A

Persistently elevated arterial blood pressure

365
Q

Name the red flags of hypertension

A

Headache
Visual disturbances
Seizures
N&V
Chest pain

366
Q

Describe hypertension in genders

A

Women < 65 BP less than men

Women 65-74 = BP higher than men

367
Q

Name risk factors of hypertension

A

Sex
Black African/Black Caribbean
Increased age
Lifestyle factors

368
Q

Name secondary causes of hypertension

A

Kidney disease (most common)
Cushing’s syndrome
Hypo/hyperthyroidism
Combined oral contraceptive pill
Renal cell carcinoma
Acromegaly

369
Q

What is the single biggest risk factors of CVD

A

HTN

370
Q

What are the possible causes of hypertension

A

Primary (90%)
Secondary
White coast syndrome

371
Q

Name 2 2nd investigations of a DVT

A

D-dimer

Wells score

372
Q

What is the GS management of DVT

A

Anticoagulant

373
Q

Name the risk factors of DVT

A

Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen
Malignancy

374
Q

Name 3 differential diagnosis of DVT

A

Cellulitis
Lymphedema
Asymmetrical oedema due to cardiac or renal failure

375
Q

What type of respiratory failure can PE cause

A

Type 1

376
Q

Describe the management of an unstable PE

A

Iv tissue plasminogen activator

Catheter direct thrombolysis

Open pulmonary embolectomy

377
Q

What is used to assess risk of PE/DVT

A

Wells Score

378
Q

Describe the 1st line management of a stable PE

A

DOACs e.g. apixaban or rivaroxaban

379
Q

Describe the 2nd line management of stable PE

A

LMWH followed by warfarin

380
Q

Name the differential diagnosis of PE

A

Heart attacks
Heart failure
Pericarditis
Cardiac tamponade
Pneumonia
Pneumothorax

381
Q

What is a PE most commonly due to

A

Thrombus formation in the deep veins of the lower extremities

382
Q

What is a complication of a PE aggressively treated

A

R. heart failure

383
Q

What is the main management of arterial vascular disease

A

Anti-coagulants

384
Q

Name the risk factors of peripheral artery disease

A

Atherosclerosis
Smoking
Age
Diabetes
Sex

385
Q

Describe intermittent claudication in peripheral artery disease

A

Muscle pain occurs during activity and subsides with rest

386
Q

What is a complication of peripheral artery disease

A

Acute limb ischaemia

387
Q

Describe the Buerger’s test

A
  1. Patient lies supine (on back) lift patients legs angle of 45 degrees for 1-2 minutes, Look for pallor
  2. Sit patient with legs hanging off the side. Blood goes back assisted by gravity. In peripheral artery disease - blue then dark red (rubor)
388
Q

What is the Buerger’s test used to assess

A

Peripheral artery disease

389
Q

What does a Buerger’s angle of 30 degrees mean

A

Legs go pale when lifted to 30 degrees

390
Q

What is the GS investigation in pericarditis

A

ECG

391
Q

Name the 2nd line investigation in pericarditis

A

CXR - cardiomegaly (if effusion)

Raised inflammatory markers

392
Q

Why so colchicine prescribed in pericarditis

A

For 3 weeks

Binds to neutrophil to prevent them migrating to areas of uric accumulation = reduced inflammation and pain

393
Q

Name the differential diagnosis of pericarditis and pericardial effusion

A

ACS
Pneumonia
PE
GORD

394
Q

Describe the pathophysiology of pericarditis

A

Acute inflammation of pericardium - fibrous reaction - exudate and adhesions within the pericardial sac

395
Q

Name the risk factors of pericardial effusion

A

Older age
Hypertension
DM
Coronary artery disease
AF

396
Q

What can be used to find the underlying cause of pericardial effusion

A

Fluid analysis

397
Q

Describe the main management of pericardial effusion

A

Most resolve spontaneously

Treat underlying cause if needed

398
Q

When does pericardial effusion occur

A

Following acute pericarditis

399
Q

What is the clinical presentation of cardiac tamponade

A

Buck’s triad
- raised JVP
- Muffled heart sounds
- low bp

400
Q

What is a risk factor of cardiac tamponade

A

Pericardial effusion

401
Q

What is the GS investigation of cardiac tamponade

A

ECHO

402
Q

What does an ECHO of cardiac tamponade show

A

Late diastolic collapse of r. atrium

403
Q

Name 2 second line investigations of cardiac tamponade

A

CXR
ECG

404
Q

What does a CXR of cardiac tamponade show

A

Large globular heart

405
Q

What does an ECG of cardiac tamponade show

A

Low voltage QRS complex

406
Q

What is the management of cardiac tamponade

A

Urgent drainage - pericardiocentesis

407
Q

What can cardiac tamponade be caused by

A

Any disorder that results in pericardial effusion

408
Q

What is a complication of cardiac tamponade

A

Can be fatal if not treated quickly

409
Q

Describe the pathophysiology of cardiac tamponade

A

Increased intra-pericardial pressure = restricted cardiac filling = decreased cardiac output

410
Q

What is the management of infective endocarditis of an unknown cause/1st line

A

FAG

Flucloxacillin + gentamicin + ampicillin

411
Q

What is the management of infective endocarditis caused by MRSA

A

Vancomycin + rifampicin + gentamicin

412
Q

What is the management of infective endocarditis caused by not staphylococcus

A

Benzylpenicillin + gentamicin

413
Q

What is the most likely cause of infective endocarditis in IVDU

A

Staph aureus

414
Q

What is the most likely cause of infective endocarditis in poor dental hygiene/developing countries

A

Strep viridians

415
Q

What is the most likely cause of infective endocarditis in prosthetic valve surgery

A

Staphylococcus epidermis

416
Q

Define rheumatic heart disease

A

Autoimmune disease mostly occurring post strep A throat infection

417
Q

What are the 5 major manifestations of rheumatic heart disease

A

Carditis
Arthritis
Chorea
Erythema marginatum
Subcutaneous nodules

418
Q

What are the major criteria for rheumatic heart disease

A

5 major manifestations

Carditis
Arthritis
Chorea
Erythema marginatum
Subcutaneous nodules

419
Q

What does rheumatic heart disease follow

A

Initial infection typically manifests as pharyngitis

420
Q

Name the risk factors for rheumatic heart disease

A

Female
Immunocompromised
Genetic
Untreated group A strep
Low socioeconomic status
Overcrowding

421
Q

What is the criteria of rheumatic fever

A

Jones criteria

422
Q

Describe Jones Criteria

A

Must be evidence of a recent group A strep infection + 2 major criteria or 1 major + 2 minor criteria

423
Q

What can be used to test for rheumatic fever

A

Microbiology - throat culture

Rapid antigen group A strep

Anti-strep serology

424
Q

What inflammatory markers would be high in rheumatic fever

A

CRP
ESR
WCC

425
Q

Describe the 1st line conservative management for rheumatic fever

A

Bed rest until CRP has returned to normal range

426
Q

Describe the 1st line medical management for rheumatic fever

A

IV benzylpenicillin single dose + oral penicillin for at least 10 days

Add aspirin - limit inflammatory response

427
Q

Name 3 differential diagnosis for rheumatic fever

A

Septic arthritis
Juvenile arthiritis
Post-infectious reactive arthropathy

428
Q

Describe the affect on systems by rheumatic fever

A

Affects multiple systems

Joints, heart (only affects here can lead to permeant damage), brain, skin

429
Q

What hypersensitivity reaction is rheumatic fever

A

Type 2

430
Q

Describe the medical management of mitral stenosis

A

Mechanical problem, medical therapy does not prevent progression

431
Q

Define mitral stenosis

A

Narrowing of the mitral valve, which results in decreased filling of the left ventricle during systole and increased left atrial (due to incompetent left atrial emptying)

432
Q

What are the signs of mitral stenosis

A

Mitral facies

Vasoconstriction results in pinkish - purple patches on checks

433
Q

Describe the murmur of mitral stenosis

A

Low-pitched rumbling

Mid-diastolic murmur

434
Q

Name 2 other investigations of mitral stenosis

A

CXR - LA enlargement

ECG

435
Q

What is the surgical treatment of mitral stenosis

A

Percutaneous mitral balloon valvotomy

436
Q

What type of problem is mitral stenosis

A

Mechanical problem

437
Q

Name 5 differential diagnosis of valvular diseases

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Congestive HFrEF
Coronary artery disease
Pulmonary hypertension

438
Q

Name 2 clinical features of mitral regurgitation

A

Exertion dyspnoea
Heart failure

439
Q

Name 3 risk factors for mitral regurgitation

A

Mitral valve prolapse
Rheumatic heart disease
Infective endocarditis history

440
Q

What is the surgical management of mitral regurgitation

A

Mechanical tissue mitral valve

Transcatheter edge to edge repair

441
Q

Describe the murmur of aortic stenosis

A

Crescendo decrescendo

Ejection systolic murmur

Heard loudest over the aortic area

442
Q

How do you remember valvular diseases

A

PASS PAID

ASMR ARMS

443
Q

What amount of normal valve space is left in aortic stenosis

A

1/4

444
Q

Describe the signs of aortic stenosis

A

Slow rising pulse with narrow pulse pressure

Radiates to carotid arteries

Loudest on expiration and when patient sits forwards

445
Q

What would be shown on a CXR of mitral regurgitation

A

LA enlargement

446
Q

Name the signs of aortic regurgitation

A

Corrigan’s sign

De Musset’s sign

Quinche’s sign

Traube’s sign

Muller’s sign

447
Q

Define De Musset’s sign

A

Aortic regurgitation

Head tremor, in synchrony with the beating of the heart

448
Q

Define Corrigan sign

A

Aortic regurgitation

Bounding pulse in large arteries - subsequently increases

449
Q

Define Quincke’s sign

A

Aortic regurgitation

Visualisation of capillary pulsations upon light compression applied to tip of fingernail bed

450
Q

Define Traube’s sign

A

Aortic regurgitation

Double sound or murmur heard in auscultations over artery

Particular over femoral head

451
Q

Define Muller’s sign

A

Aortic regurgitation

Pustulation’s or bobbing of uvula that occurs during diastole

452
Q

Describe the risk factors of aortic regurgitation

A

Bicuspid aortic valve
Rheumatic fever
Endocarditis
Marfan syndrome
Related connective tissue disorders

453
Q

Describe the aortic regurgitation murmur

A

Decrescendo early diastolic murmur

Heart loudest at the left sternal edge

Austin flint murmur

Collapsing pulse

454
Q

What type of event is aortic regurgitation

A

Medical emergency

Sudden onset of pulmonary oedema + hypertension or cardiogenic shock

455
Q

Describe aortic regurgitation pathophysiology

A

Leakage of blood flow in LV during diastole due to infective coaptation of aortic cusps - LV dilation, LVH, progressive dilation = HF

456
Q

Name 3 risk factors of mitral stenosis

A

Rheumatic heart disease = most common

Risk - streptococcal infection

Female

457
Q

What is the 2nd line management in neurogenic shock

A

If option 1 does not work
Vasopressors and inotropes
Adrenaline
Initial immobilisation of cervical spine.

458
Q

What are the symptoms of neurogenic shock

A

Hypotension
Bradycardia
Warm pink skin

459
Q

What are the risk factors of neurogenic shock

A

Spinal cord trauma and injury
Car accidents
Sports injuries
Nerve damage
Guillain-Barre syndrome

460
Q

Name a common cause of death after an MI

A

Cardiogenic shock

461
Q

Name the symptoms of cardiogenic shock

A

Altered mental state
Cold extremities
Peripheral cyanosis
Urine output < 30mL/hour

462
Q

Name the causes of cardiogenic shock

A

Acute MI
Mechanical deficit
Contractility defect
PE
R. ventricular failure

463
Q

Describe the diagnosis of cardiogenic shock

A

Based on diagnostic factors

Blood
ABG
Lactate

464
Q

Describe the 1st line management of cardiogenic shock

A

Restoration of coronary blood flow

Medication to manage BP

465
Q

What is the management of cardiogenic shock caused by a MI

A

Urgent coronary bypass

466
Q

What plays a vital role in the prognosis of cardiogenic shock

A

Underlying cause

467
Q

Describe the pathophysiology of cardiogenic shock

A

Progressive state of hypoperfusion (systolic < 90mmHg) lasting 30 minutes = leads to systemic hypoperfusion

CO and BP fall = increase sympathetic tone - cardiac and systemic affects

468
Q

Describe the symptoms of septic shock

A

Symptoms are variable and often non-specific

Low BP
Confusion
Nausea
Cold clammy skin

469
Q

Describe the risk factors of septic shock

A

Weakened immune system
Autoimmune condition
Cirrhosis of liver
Kidney disease
Cancer

470
Q

What are the signs of anaphylactic shock

A

Cardinal signs
Skin rash
Wheezing/inspiratory stridor

471
Q

Name the risk factors of anaphylactic shock

A

Previous anaphylactic reactions
Allergies or asthma
Previous history of anaphylaxis

472
Q

Describe the cause of hypovolaemic shock

A

Movement of fluid from the interstitium to intravascular space and mobilisation of intracellular fluid

473
Q

Name a sign of hypovolaemic shock

A

Thirst increase

474
Q

Name a 2 test result of hypovolaemic shock

A

Reduced eGFR
Lactic acidosis

475
Q

Why are fluids warmed in hypovolaemic shock

A

Risk of hypothermia - increase mortality

476
Q

What is the treatment of hypovolaemic shock due to massive haemorrhage

A

Give fresh frozen plasma and platelet early

477
Q

Name the different causes of shock

A

Distributive
Cardiogenic
Hypovolaemic
Obstructive

478
Q

What are the general symptoms of shock

A

Unwell
Fever
Chest pain
SOB
Abdominal pain

479
Q

Name the general risk factors of shock

A

Increasing age
MI
Arrythmias
Trauma
GI bleeding
Ruptured AAA
Burns/heat stroke
Pancreatitis
Sepsis

480
Q

Describe the general signs of shock

A

Tissue hypoperfusion may be present without hypotension

Arterial hypotension + organ dysfunction

481
Q

What risks is cardiomyopathy associated with

A

Heart failure
Myocardial infarction
Arrythmias
Sudden cardiac death (on exertion)

482
Q

Describe the symptoms of cardiomyopathy

A

Asymptomatic

Symptoms - may occur on exertion

Symptoms of heart failure

483
Q

Name the risk factors of hypertrophic cardiomyopathy

A

Autosomal genetic condition

Results from a defect in the genes for sarcomere family history

484
Q

Name the differential diagnosis for cardiomyopathy

A

Congestive heart failure
Cerebrovascular accident
Sudden cardiac death
Thromboembolism

485
Q

Define tetralogy of fallot

A

Ventricular septal defect overriding aorta and RV outflow tract = RV hypertrophy

486
Q

Name the risk factors of tetralogy of fallot

A

Trisomy 21, 18 or 13
DiGeorge’s syndrome - chromosome 22q11 deletion
Alagille’s syndrome
Environmental factors
Family history of congenital heart disease

487
Q

Describe the symptoms of tetralogy of fallot

A

Fallot spells - patient goes blue

Stop feeding
Stop crying

488
Q

What are the 4 clinical findings of tetralogy of fallot

A

Ventricular septal defect (VSD)
Aorta-over riding VSD
R. ventricular outflow tract obstruction
Secondary r. ventricular hypertrophy

489
Q

What is the GS investigation in tetralogy of fallot

A

Echocardiogram

490
Q

Name the 1st line management in tetralogy of fallot

A

Surgical repair

Complete intracardiac repair - before age 2

491
Q

Describe the prognosis of tetralogy of fallot post surgery

A

Often get pulmonary valve regurgitation in adult life and require re-do surgery

492
Q

Name the differential diagnosis of tetralogy of fallot

A

6T’s of cyanotic congenital heart disease

493
Q

Describe the 6Ts of cyanotic congenital heart disease

A

Tetralogy of fallot
Transposition of great arteries
Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid valve abnormalities
Tons of others

494
Q

Describe the pathophysiology of tetralogy of fallot

A

Stenosis of RV outflow leads to RV being at high pressure to left = blue blood passes from RV to LV

495
Q

Define coaraction of aorta

A

Narrowing of aorta at the site of insertion the ductus arteriosus

496
Q

Name the risk factors of ventricular septal defect

A

Family history of congenital heart disease
Down’s syndrome (trisomy 21)
Maternal alcohol consumption on during pregnancy

497
Q

Describe the clinical features of ventricular septal defect

A

Blood flows from high pressure to low = not blue

Depends if large or small

498
Q

If there is large ventricular septal defect what symptoms would this present in

A

Large - high pressure pulmonary blood flow

SOB
Poor feeding
Failure to thrive
Skinny baby

499
Q

If there is a small ventricular septal defect what symptoms would this present in

A

Small increase in pulmonary blood flow

Asymptomatic

500
Q

Describe the diagnosis in coaraction of aorta

A

Commonly only clinical sign = weak femoral pulse

Ejection systolic murmur
Unequal blood pressure between arms
Cold extremities

501
Q

Name the risk factors of coaraction of aorta

A

Male gender
Genetic conditions e.g. Turner syndrome
Family history

502
Q

Describe the clinical features of coaraction of aorta

A

Right arm hypertension
Bruits (buzzes) over scapula and back from collateral vessels
Murmur

503
Q

Describe the ECG in coaraction of aorta

A

Normal with mild coaraction

504
Q

Describe the chest x-ray in coaraction of aorta

A

Indentation of aortic shadow or signs of congestive HF

505
Q

Describe the MRI in coaraction of aorta

A

Determines nature of abnormalities

506
Q

Describe the management of severe coaraction of aorta

A

Severe urgent repair

507
Q

Describe the management of mild coaraction of aorta

A

Repair to prevent problems in long term

508
Q

Describe the surgical management in coaraction of aorta

A

Surgical (mostly children) pr percutaneous repair

509
Q

Name the differential diagnosis of coaraction of aorta

A

Aortic stenosis
Cardiomyopathies
Primary hypertension
Viral myocarditis

510
Q

Describe the different classifications of coaraction of aorta

A

Severe - complete/almost obstruction to aortic flow. Collapse with HF

Mild - hypertension. Incidental murmur

511
Q

Define ventricular septal defect

A

Congenital or acquired defects in the inter ventricular septum allowing shunting of blood

512
Q

Name the 1st line investigations of ventricular septal defect

A

ECHO
Chest x-ray
ECG

513
Q

Name the 2nd line investigations of ventricular septal defect

A

Cardiac MRI
Cardiac CT scan
Cardiac catheterisation

514
Q

Describe the management of a large ventricular septal defect

A

Fixing in infancy - PA band.
Complete repair

515
Q

Describe the management of small ventricular septal defect

A

No need for intervention

516
Q

Name the differential diagnosis for ventricular septal defect

A

Eisenmenger syndrome
Endocarditis
Embolization
Aortic insufficiency

517
Q

Describe the pathophysiology of ventricular septal defect

A

Hole between high pressure LV and low pressure RV

Can result in increased pressure in the lungs

518
Q

Name a complication of large ventricular septal defect

A

Eisenmenger syndrome

519
Q

Name a complication of small ventricular septal defect

A

Endocarditis

Phase 2a (15 decks)

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