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Phase 2a Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is Atherosclerosis

A

A degenerative condition of arteries characterised by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis.

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2
Q

What are 7 risk factors for atherosclerosis

A

Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history

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3
Q

What 4 components is an atherosclerotic plaque composed of

A

Lipid
Necrotic core
Connective tissue
Fibrous cap

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4
Q

What are 4 major cell types involved in atherogenesis

A

endothelium, macrophages, smooth muscle cells and platelets.

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5
Q

What are the 4 steps in the process of atherosclerosis

A

Fatty streaks
Intermediate lesions
Fibrous plaques of advanced lesions
Plaque rupture

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6
Q

What are features of fatty streaks

A

Earliest lesion of atherosclerosis
Appears at a very early age (<10 years)
Consists of aggregations of lipid-laden macrophages (foam cells) and T lymphocytes within the intimal layer of the vessel wall

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7
Q

What are intermediate lesions of atherosclerosis

A

Composed layers of vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall.

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8
Q

What are features of fibrous plaques of advanced lesions

A

Impedes blood flow
Prone to rupture
Contains smooth muscle cells, macrophages and foam cells and T lymphocytes

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9
Q

What is involved in plaque rapture of atherosclerosis

A

Fibrous cap has to be resorbed and redeposited in order to be maintained – if balance shifts, cap becomes weak and then the plaque ruptures
Thrombus formation and vessel occlusion

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10
Q

What is involved in the initiation of atherosclerosis

A

Endothelial dysfunction and injury around sites of damage, with subsequent lipid accumulation at sites of impaired endothelial barrier.
Local cellular proliferation and incorporation of oxidised lipoproteins occurs.
Mural thrombi (thrombi adhered to vessel wall) heal the vessel and repeat of cycle.

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11
Q

What is involved in the adaptation of an atherosclerotic plaque

A

As plaque progresses to 50% of lumen size, vessel can no longer compensate by re-modelling.
Becomes narrowed – drives cell turnover within the plaque.
New matrix surfaces and degradation of matrix.
May progress to unstable plaque

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12
Q

What is involved in the clinical stage of atherosclerosis

A

Plaque continues to encroach upon the lumen and runs the risk of haemorrhage.
T cell accumulation is stimulated.
Inflammatory reaction against the plaque contents

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13
Q

What is the clinical manifestation of atherosclerosis

A

Atherosclerosis is usually asymptomatic until the artery is so narrowed that the organs and tissues no longer receive an adequate blood supply.

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14
Q

What is the clinical manifestation of atherosclerosis of the coronary arteries

A

chest pain/ pressure (angina)

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15
Q

What is the clinical manifestation of atherosclerosis of the brain arteries

A

transient ischaemic attack (TIA): weak arms and legs, slurred speech, temporary vision loss, drooping face muscles.

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16
Q

What is the clinical manifestation of atherosclerosis of the peripheral arteries

A

peripheral artery disease: leg pain when walking

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17
Q

What is the clinical manifestation of atherosclerosis of the renal arteries

A

high blood pressure or kidney failure.

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18
Q

What are 4 management options for atherosclerosis

A

Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel/ ticagrelor – inhibits the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
PCI – percutaneous coronary intervention

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19
Q

What is restenosis and how to prevent it

A

a major limitation of treatment
The recurrence of abnormal narrowing of an artery or valve after corrective surgery.
Drug eluting stents improve duration of stents – anti-proliferative and inhibits healing.

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20
Q

How are chest x-rays used to investigate heart disease

A

Provides just a snapshot of the heart and little detail but can be an important source of information.
An enlarged heart suggests congestive heart failure
Signs of pulmonary oedema suggested decompensated heart failure
A globular heart may indicate pericardial effusion
Metal wires and valves will show up, evidencing previous cardiothoracic surgery

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21
Q

How is echocardiography used to investigate heart disease

A

Ultrasound is used to give real-time images of the moving heart. This can be transthoracic (TTC) or transoesophageal (TOE), at rest, during exercise or after infusion of a pharmacological stressor.
If the patient is too unwell to be moved, an echo machine can be brought to them and continuous TOE imaging may be used as a guide during surgery.

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22
Q

How are cardiac CT scans used to investigate heart disease

A

This can provide detailed information about cardiac structure and function. CT angiography permits contrast-enhanced imaging of coronary arteries during a single breath hold with very low radiation doses.
It can diagnose significant stenosis in coronary artery disease with an accuracy of 89%.
CT coronary angiography has a negative predictive value of >99%, which makes it an effective non-invasive alternative to routine transcatheter coronary angiography to rule out CAD.

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23
Q

How are cardiac MRIs used to investigate heart disease

A

A radiation-free method of characterising cardiac structure and function including viability myocardium.
By varying the settings, different defects can be found. MR is the first-choice imaging method to look at diseases that directly affect the myocardium.

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24
Q

How is nuclear imaging used to investigate heart disease

A

Perfusion is assessed at rest and with exercise or pharmacologically-induced stress.
This test is particularly useful for assessing whether myocardium distal to a blockage is viable and so whether stenting or CABG will be of value.

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25
Q

What 4 abnormalities can ECGs identify

A

Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Electrolyte disturbances

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26
Q

What does the p-wave represent

A

atrial depolarisation

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27
Q

What does the QRS complex represent

A

ventricular depolarisation

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28
Q

What does the T-wave represent

A

ventricular repolarisation

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29
Q

What does the PR interval represent

A

atrial depolarisation and delay in AV junction (delay allows time for the atria to contract before the ventricles contract).

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30
Q

What is the standard calibration of an ECG

A

25 mm/s
0.1mV/mm

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31
Q

What are bipolar leads

A

leads with a positive and negative electrode

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32
Q

What are unipolar leads

A

only a positive electrode and a virtual reference point with zero electrical potential

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33
Q

how many electrodes are used in a 12 lead ECG

A

10
( 6 chest and 4 limb)

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34
Q

What is Einthovens triangle.

A

The map of limb lead placement
lead 1,2,3 are limb to limb
lead aVF,VL,VR are centre of the triangle to limb

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35
Q

What is the ECG appearance for right atrial enlargement

A

tall (>2.5mm) p- wave
(p pulmonale)

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36
Q

What is the ECG appearance for left atrial enlargement

A

notched (M-shaped) p- wave
(P mitrale)

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37
Q

What is the ECG appearance for first degree heart block

A

Long PR interval

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38
Q

What depth of S wave is considered pathological

A

30mm

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39
Q

What features of the Q wave are considered pathological

A

> 2mm deep and >1mm wide
25% amplitude of the subsequent R wave

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40
Q

What is the QRS axis

A

This represents the overall direction of the heart’s electrical activity, and abnormalities of the QRS axis hint at ventricular enlargement or conduction blocks.

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41
Q

What the normal appearance of the ST segment

A

flat (isoelectric)

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42
Q

What change in the ST segment is considered pathological

A

elevation or depression by 1mm or more can be pathological.

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43
Q

What is the normal amplitude of the T wave

A

Should be at least 1/8 but less than 2/3 of the amplitude of R

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44
Q

What features of the T wave can be considered pathological

A

Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted
Amplitude exceeding 10mm

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45
Q

What is the normal appearance of the QT interval

A

isoelectric
QT interval decreases when heart rate increases
Regular interval is 0.35-0.45s

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46
Q

What would be considered pathological about the QT interval

A

more than half of the interval between adjacent R wave

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47
Q

What are U waves

A

Small, round, symmetrical and positive in lead II, with amplitude <2mm (regular)
U wave should be same direction as T wave

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48
Q

How do you calculate heart rate for regular rhythms

A

count the number of small boxes between QRS complexes and divide by 1500 for BPM

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49
Q

How do you calculate heart rate for irregular rhythms

A

count the number of beats present over 10 seconds then multiply by 6

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50
Q

What is the quadrant approach for QRS axis

A

For the QRS complex in aVF and lead 1
positive+ positive = normal axis
positive + negative = right axis deviation
negative + positive = left axis deviation
negative + negative = indeterminate axis

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51
Q

What is the appearance of sinus tachycardia on ECG

A

All impulses are initiated in the sinoatrial node hence all QRSs are preceded by a normal P wave with a normal PR interval.
Tachycardia means rate >100bpm

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52
Q

What is sinus bradycardia

A

Sinus rhythm at a rate <60bpm

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53
Q

What are 8 causes of sinus bradycardia

A

Physical fitness
Vasovagal attacks
Sick sinus syndrome
Drugs (β-blockers, digoxin, amiodarone)
Hypothyroidism
Hypothermia
Raised intracranial pressure
Cholestasis

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54
Q

What are 6 causes of Atrial fibrilation

A

IHD, thyrotoxicosis, hypertension, obesity, heart failure, alcohol

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55
Q

What are 5 conditions that cause ST elavation

A

Normal variant, acute MI, Prinzmetal’s angina, acute pericarditis, left ventricular aneurysm

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56
Q

What are 6 conditions that cause ST depression

A

Normal variant, digitoxin toxicity, ischaemic, angina, NSTEMI, acute posterior MI

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57
Q

What 3 things could cause T inversion in leads v1-v3

A

normal, right bundle branch block, RV strain

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58
Q

What 4 things could cause T inversion in leads V2-V5

A

anterior ischaemia, HCM, subarachnoid haemorrhage, lithium

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59
Q

What 3 conditions could cause T inversion in leads V4-V6 and aVL

A

lateral ischaemia, LVH, left bundle branch block

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60
Q

What is the ECG presentation of Myocardial infarction in the first hours

A

the T wave may become peaked and ST segments may begin to rise

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61
Q

What is the ECG presentation for Myocardial infarction within 24 hours

A

T wave inverts. ST elevation rarely persists, unless a left ventricular aneurysm develops. T-wave inversion may or may not persist.

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62
Q

What are 3 potential ECG findings for pulmonary embolism

A

sinus tachycardia, RBBB, right ventricular strain pattern

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63
Q

What is Echocardiography

A

A non-invasive technique that uses the differing ability of various structures within the heart to reflect ultrasound waves.

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64
Q

What is M-mode echocardiography

A

(motion mode): a single-dimension image

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65
Q

What is two-dimensional echocardiography

A

(real time): a 2D, fan-shaped image of a segment of the heart is produced on the screen. It is good for visualising conditions such as congenital heart disease, LV aneurysm, mural thrombus, LA myxoma, septal defects.

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66
Q

What is colour flow echocardiography

A

different coloured jets illustrate flow and gradients across valves and septal defects.

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67
Q

What is tissue doppler imaging

A

this employs Doppler ultrasound to measure the velocity of myocardial segments over the cardiac cycle. Particularly useful for assessing longitudinal motion, helping the diagnosis of systolic and diastolic heart failure.

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68
Q

What is transoesophageal echocardiography

A

more sensitive than transthoracic echocardiography as the transducer is nearer to the heart. Useful for diagnosing aortic dissections, assessing prosthetic valves, finding cardiac source of emboli.

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69
Q

What is stress echocardiography

A

evaluates ventricular function, ejection fraction, myocardial thickening, and to characterise valvular lesions.

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70
Q

What are 7 uses of echocardiography

A

Quantification of global LV function
Estimating right heart haemodynamics
Valve disease
Congenital heart disease
Endocarditis
Pericardial effusion
Hypertrophic cardiomyopathy

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71
Q

What is white coat hypertension

A

an elevated clinic pressure, but normal Ambulatory Blood Pressure Monitoring (ABPM)

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72
Q

What is hypertension

A

Chronic elevation of blood pressure in the arteries. WHO classification: >140/90mmHg.

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73
Q

What is the threshold for malignant hypertension

A

> 160/110mmHg

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74
Q

Why is hypertension important to diagnose and manage

A

Hypertension is the chief risk factor for cardiovascular mortality, causing 50% of all vascular deaths.

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75
Q

What is the pathophysiology behind hypertension

A

Altered renin-angiotensin system elevates BP by impairing sympathetic output, increasing mineralocorticoid secretion and direct vaso-constriction.
This is balanced by atrial natriuretic factor.
Changes to auto-regulation produce an increase in peripheral resistance, which would normally allow increased BP, diuresis and restoration of normal pressure and volume
Hypertension alters blood vessel walls whereby the lumen size is decreased as the wall thickness increases.

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76
Q

What is malignant hypertension

A

a rapid rise in BP leading to vascular damage. Pathological hallmark is fibrinoid necrosis.

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77
Q

What is primary hypertension

A

90% of cases of hypertension are primary, and aetiology is unknown.

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78
Q

What are 4 causes of secondary hypertension

A

Endocrine disease
Renal disease
Exogenous agents (drugs)
Lifestyle

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79
Q

What are the signs and symptoms of hypertension

A

Usually asymptomatic
Malignant hypertension;
Bilateral renal haemorrhages
Papilledema
Headache and visual disturbance
Look for end-organ damage e.g. retinopathy

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80
Q

What are the tests for hypertension

A

First line= clinical BP
stage 1= >140/90
Stage 2= >160/90
stage 3= >180/120
gold standard= Ambulatory BP

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81
Q

What is cor pulmonale

A

Right ventricular hypertrophy and dilatation due to pulmonary hypertension.

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82
Q

What is cor pulmonale caused by

A

Caused by primary pulmonary hypertension
Can also be caused by emboli, cystic fibrosis or chronic bronchitis

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83
Q

What is the threshold and treatment goal for hypertension

A

Treat all patients with a BP 160/100mmHg
Treatment goal <140/90mmHg – reduce blood pressure SLOWLY

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84
Q

What are the lifestyle changes for hypertension

A

Stop smoking
Low-fat diet
Reduce alcohol and salt intake
Increase exercise
Reduce weight if obese

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85
Q

What is the drug therapy for hypertension

A

Monotherapy = Ca2+ channel antagonist
Combination Rx = ACE-I (or ARB) + Ca2+ channel antagonist or diuretic.

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86
Q

What is the group name and action of calcium antagonists

A

dihydropidines - inhibit the opening of voltage-gated calcium channels in vascular smooth muscle, reduced calcium entry and thereby calcium available for muscle contraction.

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87
Q

What is the action of ACE inhibitors and 2 examples

A

prevent generation of angiotensin II from angiotensin I.
Ramipril and captopril

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88
Q

What is the action of angiotensin receptor blockers and 2 examples

A

block the action of angiotensin II at peripheral angiotensin II receptors. Used if ACEi intolerant.
Losartan, Azilsartan

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89
Q

What is the action of thiazide diuretics and an example

A

inhibit sodium reabsorption by the DCT, reducing the ECF volume, which is elevated in hypertension.
Bendroflumethiazide

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90
Q

What is Angina pectoris

A

Recurrent transient episodes of chest pain due to myocardial ischaemia

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91
Q

What are 4 types of angina

A

Stable angina: induced by effort, relieved by rest. Good prognosis.
Unstable angina: angina of increasing frequency or severity – occurs on minimal exertion or at rest. Associated with high risk of MI.
Decubitus angina: precipitated by lying flat.
Prinzmetal angina: caused by coronary artery spasm (rare).

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92
Q

What is the pathology of angina

A

Myocardial ischaemia occurs whenever myocardial oxygen demand outstrips supply
A significant fixed stenosis of a coronary artery impairs coronary blood flow when myocardial oxygen demand increases e.g. during exercise

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93
Q

4 causes of angina

A

Atheroma!!!

Rarer;
Anaemia
Coronary artery spasm
Tachyarrhythmias

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94
Q

What are 10 risk factors for angina

A

Gender
Family history
Personal history
Age
Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Sedentary lifestyle
Stress

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95
Q

what are the 3 angina clinical presentations

A

Constricting/heavy discomfort to the chest, jaw, neck, shoulders or arms
Symptoms brought on by exertion
Symptoms relieved within 5min by rest or GTN spray.

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96
Q

What are 5 symptoms of angina

A

Dyspnoea
Nausea
Sweatiness
Faintness
Crushing chest pain

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97
Q

What are 7 differential diagnoses for angina

A

Pericarditis/ myocarditis
Pulmonary embolism
Chest infection
Dissection of the aorta
Gastro-oesophageal reflux/spasm/ulceration
Psychological
Musculo-skeletal

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98
Q

What is the ECG presentation for angina

A

Often normal – there are no direct markers of angina
Signs of IHD – T-wave inversion, BBB

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99
Q

What is the management for angina

A

Address exacerbating factors: anaemia, tachycardia, thyrotoxicosis.
Symptom relief: glyceryl trinitrate (GTN) spray. Ambulance required if pain doesn’t subside 5 minutes after second dose.

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100
Q

What is the primary prevention for angina

A

Reducing the risk of CAD and complications
Risk factor modification

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101
Q

What are 4 lifestyle changes for angina

A

Stop smoking
Exercise
Dietary advice
Optimise hypertension and diabetes control

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102
Q

What are 3 pharmacological interventions for angina

A

75mg aspirin daily
Consider ACE inhibitors (if diabetic)
Address hyperlipidaemia (high cholesterol)

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103
Q

What are the physical interventions used for angina

A

Percutaneous Coronary Intervention (PCI) and sometimes surgery

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104
Q

What is the action of beta blockers in angina and an example

A

antagonise sympathetic nervous activation and therefore reduce work of heart and O2 demand. bisoprolol

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105
Q

What is the action of nitrates in angina and an example

A

dilate systemic veins (venodilators) to reduce preload on the heart: Frank-S mechanism ‘reduce work of heart and O2 demand’.
Isosorbide mononitrate

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106
Q

What is the action of calcium channel antagonists in angina and an example

A

dilate systemic arteries (arterodilators) to reduce afterload on the heart. Reduced energy then required to produce same CO. Amlodipine

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107
Q

What is the action of statins for angina

A

reduce anginal events, reduce LDL-cholesterol.

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108
Q

What is the method of Percutaneous coronary intervention (PCI-stenting)

A

A balloon is inflated inside the stenosed vessel, opening the lumen. A stent is then inserted to reduce the risk of re-stenosis.

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109
Q

What is CABG surgery

A

Coronary artery bypass graft

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110
Q

What are Acute coronary syndromes

A

Acute coronary syndromes include unstable angina and myocardial infarctions. These share a common underlying pathology – plaque rupture, thrombosis, and inflammation.

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111
Q

What is myocardial infarction and the two types

A

myocardial cell death, releasing troponin.
Non-ST-elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)

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112
Q

What is ischaemia

A

a lack of blood supply (sometimes cell death)

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113
Q

What is the pathology of acute coronary syndromes

A

Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases. Uncommon causes include coronary vasospasm without plaque rupture, drug abuse, dissection of the coronary artery and thoracic aortic depression.

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114
Q

What are 5 features involved in the diagnosis of acute coronary syndromes

A

An increase in cardiac biomarkers (e.g. troponin)
Symptoms of ischaemia
ECG changes of new ischaemia
Development of pathological Q waves
New loss of myocardium

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115
Q

What are 5 symptoms of acute coronary syndromes

A

Acute central chest pain lasting >20min
Nausea
Sweatiness
Dyspnoea
Palpitations

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116
Q

What are silent acute coronary syndromes

A

ACS without chest pain – seen in elderly and diabetic patients.
May present with syncope, pulmonary oedema, epigastric pain an vomiting

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117
Q

What are 7 signs for Acute coronary syndromes

A

Distress
Anxiety
Pallor
Sweatiness
4th heart sound
Possibly signs of heart failure
Low grade fever

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118
Q

What are 5 differential diagnoses for Acute coronary syndromes

A

Stable angina
Pericarditis
Myocarditis
Takotsubo cardiomyopathy
Aortic dissection

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119
Q

What is the ECG appearance for STEMI

A

STEMI: tall T waves, ST elevation, or new LBBB occurs within hours. T wave inversion and pathological Q waves follow non-specific changes

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120
Q

What is the appearance on Chest X-ray for acute coronary syndrome

A

Cardiomegaly
Pulmonary oedema
Widened mediastinum

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121
Q

What is the use of troponins in investigating acute coronary syndromes

A

specific marker of myocardial necrosis
Serial troponins are required to differentiate non-ST elevated Mis from unstable angina (no troponin rise).

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122
Q

What is used for symptom control of ACS

A

Manage chest pain with PRN GTN and opiates.

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123
Q

What can be done to modify risk factors for ACS

A

Patients should be strongly advised and helped to stop smoking
Identify and treat diabetes mellitus, hypertension and hyperlipidaemia
Advise a diet high in oily fish, fruit, vegetables, fibre and low in saturated fats
Encourage daily exercise
Mental health – flag it up to a patient’s GP

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124
Q

Name 5 classes of cardioprotective medications

A

protective medications
Antiplatelets: aspirin and Clopidogrel. Clopidogrel is a P2Y12 inhibitor (dual antiplatelet therapy)
Anticoagulants e.g. fondaparinux
Inhibit both fibrin formation and platelet activation
Beta-blockade reduces myocardial oxygen demand
ACEi – patients with LV dysfunction, hypertension or diabetes
High dose statin e.g. atorvastatin

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125
Q

Which patients should be considered for revascularisation in ACS

A

STEMI patients and very high-risk NSTEMI should receive immediate angiography. Patients with multivessel disease may be considered for CABG instead of PCI.

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126
Q

What is unstable angina

A

Severe acute myocardial ischaemia without myocardial necrosis.
Almost always due to coronary artery atherosclerosis.

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127
Q

What is the pathology of unstable angina

A

Erosion of the surface of an unstable atherosclerotic plaque stimulates platelets to aggregate over the plaque
Platelet fragments may also break off and embolise down the artery
The reduction in coronary blood flow causes acute ischaemia of the affected myocardium, but not myocardial necrosis.

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128
Q

What is the presentation of unstable angina

A

Acute coronary syndrome with sudden onset of prolonged ischaemic cardiac chest pain at rest or on minimal exertion.
The ECG shows ischaemic changes, but not ST-elevation

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129
Q

What is the clinical classification of unstable angina

A

Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina
No significant rise in troponin levels.

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130
Q

What is the difference between unstable angina and NSTEMI

A

NSTEMI involves enough occlusion to cause myocardial damage and elevation in serum troponin and creatine kinase. Unstable angina does not cause myocardial damage.

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131
Q

What is Myocardial infarction

A

Full-thickness necrosis of an area of myocardium.

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132
Q

What is the chest pain associated with MI

A

Unremitting
Usually severe
Occurs at rest
Associated with sweating, breathlessness, nausea/vomiting

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133
Q

What is Subendocardial/ patchy infarction

A

involves the innermost layer and some middle parts of the myocardium, but not the epicardium. NSTEMI

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134
Q

What is transmural infarction

A

infarction of the full thickness of the myocardium

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135
Q

What is the pathology of MI

A

Results from rupture of an unstable coronary artery atherosclerotic plaque stimulates the formation of an occlusive fibrin-rich thrombus over the plaque
Complete occlusion of the coronary artery leads to full-thickness necrosis of the area of myocardium supplied by that artery.

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136
Q

What is the difference between STEMI and NSTEMI

A

NSTEMI is a retrospective diagnosis made after troponin results.
ST elevation MI and MI associated with LBBB are associated with larger infarcts unless effectively treated.

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137
Q

What is the difference between MIs and unstable angina

A

MIs have troponin rises, unstable angina does not.

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138
Q

What are the 6 steps to initial management of STEMI

A

Attach ECG monitor and record a 12-lead ECG
IV access. Bloods for FBC, U&E, glucose, lipids, troponin
History of cardiovascular disease; risk factors for IHD
Aspirin 300mg and ticagrelor 180mg
Morphine 5-10mg IV +anti-emetic
STEMI on ECG = primary PCI

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139
Q

What is the treatment of STEMI

A

Aspirin – inhibits platelet function
LMW heparin
Thrombolytic therapy

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140
Q

What are 13 complications of MI

A

Cardiac arrest
Cardiogenic shock
Left ventricular failure
Bradyarrhythmia
Tachyarrhythmia
Right ventricular failure
Pericarditis
Systemic embolism
Cardiac tamponade
Mitral regurgitation
Ventricular septal defect
Dressler’s syndrome
Left ventricular aneurysm

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141
Q

What are 2 features of right ventricular failure

A

Presents with low cardiac output
Fluid is key – avoid vasodilators and diuretics.

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142
Q

What are 2 features of pericarditis and its treatment

A

Central chest pain, relieved by sitting forwards
ECG: saddle-shaped ST elevation
Treatment: NSAIDs

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143
Q

What is the potential cause and therapy for systemic embolism

A

May arise from LV mural thrombus
After large anterior MI, consider anticoagulation with warfarin for 3 months

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144
Q

What is the presentation, investigation and treatment for cardiac tamponade

A

Presents with low cardiac output, pulsus paradoxus, muffled heart sounds
Diagnosis: echocardiogram
Treatment: pericardial aspiration, surgery

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145
Q

What is the presentation and treatment for mitral regurgitation

A

Presentation: pulmonary oedema
Treatment: consider valve replacement

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146
Q

What is Dressler’s syndrome and its treatment

A

Recurrent pericarditis, pleural effusions, fever, anaemia
Treatment: NSAIDs if severe

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147
Q

What is Cardiac failure

A

Inability of the heart to keep up with the demands on it, and the failure of the heart to pump blood with normal efficiency = cardiac output is inadequate for the body’s requirements.

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148
Q

What causes the diminishing of cardiac contraction force

A

exceeding stretch capability of sarcomeres

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149
Q

What triggers the hypertrophic response to cardiac failure

A

Angiotensin 2
ET-1 and insulin-like growth factor 1
TGF-beta

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150
Q

What is systolic failure

A

inability of the ventricle to contract normally, resulting in low cardiac output. Ejection fraction <40%.

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151
Q

What are 3 causes of systolic failure

A

IHD
MI
Cardiomyopathy

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152
Q

What is diastolic failure

A

inability of the ventricle to relax and fill normally, causing increased filling pressures. (stiff heart = left ventricle can’t fill properly with blood during diastolic phase, reducing the amount of blood pumped out to the body). Typically, ejection fraction is >50% (termed heart failure with preserved EF).

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153
Q

What are 5 causes for diastolic failure

A

Ventricular hypertrophy
Constrictive pericarditis
Tamponade
Restrictive cardiomyopathy
Obesity

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154
Q

What is the outcome of left ventricular failure

A

pulmonary congestion (heart is not able to pump efficiently so blood backs up in the veins that take blood through the lungs. Pressure in these vessels increases and fluid is pushed into the alveoli) and then overload of right side.

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155
Q

What are 9 symptoms of left ventricular failure

A

Dyspnoea
Poor exercise tolerance
Fatigue
Orthopnoea (SOB when lying flat)
Paroxysmal nocturnal dyspnoea (SOB at night, awakening from sleep)
Nocturnal cough
Wheeze
Cold peripheries
Weight loss

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156
Q

What is the outcome of right ventricular failure

A

venous hypertension (high pressure in the veins of the legs, caused by venous insufficiency where blood leaks downwards due to the effect of gravity through leaky valves) and congestion.

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157
Q

What are 3 causes of right ventricular failure

A

LVF
Pulmonary stenosis
Lung disease

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158
Q

What are 6 symptoms of right ventricular failure

A

Peripheral oedema
Ascites
Nausea
Anorexia
Facial engorgement
Epistaxis

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159
Q

What is acute heart failure

A

new-onset acute or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with/without signs of peripheral hypoperfusion.

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160
Q

What is chronic heart failure

A

develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late.

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161
Q

What is low-output heart failure

A

cardiac output is low and fails to increase normally with exertion.

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162
Q

What are 3 causes of Low-output heart failure

A

Excessive preload: mitral regurgitation or fluid overload (e.g. from renal overload)
Pump failure: decreased heart rate, negatively inotropic drugs
Chronic excessive afterload: e.g. aortic stenosis, hypertension.

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163
Q

What is high-output heart failure

A

output is normally increased in the face of extremely increased needs. Failure occurs when cardiac output fails to meet these needs.

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164
Q

What are 4 causes of High-output heart failure

A

Anaemia
Pregnancy
Hyperthyroidism
Paget’s disease

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165
Q

What are the tests for heart failure

A

FBC – U&E
CXR
ECG – may indicate cause (MI, ischaemia, ventricular hypertrophy)
Echocardiography – indicates the cause and can confirm the presence or absence of LV dysfunction.
Objective evidence of cardiac dysfunction at rest

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166
Q

What are the signs of heart failure

A

Cyanosis
Decreased BP
Narrow pulse pressure
Pulsus alternans
Displaced apex (LV dilatation)
Pulmonary hypertension
Pink frothy sputum
Signs of valve diseases

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167
Q

What are the 5 differential diagnoses for heart failure

A

COPD
Emphysema
Myocardial infarction
Pulmonary embolism
Pneumonia

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168
Q

What are the 9 steps in management of acute cardiac failure

A

Sit the patient upright
High flow oxygen if low peripheral capillary oxygen saturation
Treat any arrhythmias
Investigations whilst continuing treatment
Diamorphine 1.25-5mg IV slowly (caution in liver failure and COPD)
Furosemide 40-80mg IV slowly (larger doses required in renal failure)
GTN spray 2 SL puffs
If systolic BP 100mmHg, start a nitrate transfusion
If systolic BP is <100mmHg, treat as cardiogenic shock and refer to ICU

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169
Q

What is 6 management options in chronic heart failure

A

Stop smoking, stop drinking alcohol, eat less salt, optimise weight and nutrition.
Treat the cause
Treat exacerbating factors e.g. anaemia, infection
Avoid exacerbating factors e.g. NSAIDs (fluid retention)
Annual flu vaccine, one-off pneumococcal vaccine
medications

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170
Q

What 7 medications can be used for heart failure

A

Diuretics
ACE inhibitors
ARB
β-blockers
Mineralocorticoid receptor antagonists
Digoxin
Vasodilators

171
Q

What is intractable heart failure and its management

A

failure that is resistant to further treatment -> palliative care.

172
Q

What is Valvular heart disease

A

Any disease process involving one or more of the four valves of the heart.

173
Q

What are 2 congenital valvular heart diseases

A

Congenital aortic stenosis
Congenital bicuspid valve

174
Q

What are 3 acquired Valvular heart disease

A

Degenerative calcification
Rheumatic heart disease
Rare causes

175
Q

What is mitral regurgitation

A

Backflow through the mitral valve during systole.

176
Q

Whats are the different outcomes of acute vs chronic mitral regurgitation

A

Acute – back up into the lungs
Chronic – LA dilation as it has had time to adjust

177
Q

What is the pathophysiology of mitral regurgitation

A

Pure volume overload
Compensatory mechanisms: left atrial enlargement, LVH and increased contractility
Progressive LA dilation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilatation and progressive HF

178
Q

6 Causes of mitral regurgitation

A

Rheumatic fever
Infective endocarditis
Mitral valve prolapse
Ruptured chordae tendinea
Papillary muscle dysfunction
Cardiomyopathy

179
Q

What are 4 symptoms of mitral regurgitation

A

Dyspnoea (exertion)
Pulmonary oedema
Fatigue
Palpitations

180
Q

What are 3 signs of mitral regurgitation

A

AF – displaced, hyperdynamic apex
Pansystolic murmur at apex radiating to axilla
Severity: the more severe, the larger the left ventricle

181
Q

What are 4 tests for mitral regurgitation

A

ECG; AF, P-mitrale if in sinus rhythm, LA enlargement, LV hypertrophy
CXR – large LA and LV
Mitral valve calcification
Echocardiogram

182
Q

What are 5 management options for mitral regurgitation

A

Control heart rate if fast AF (beta blockers)
Anticoagulate if there is a history of AF, embolism, prosthetic valve or additional mitral stenosis
Vasodilators – hydralazine (calcium channel blockers)
Diuretics (for fluid overload) improve symptoms
Surgery – repair/replace valve.

183
Q

What is mitral valve prolapse

A

The most common valvular abnormality. It is a condition in which the two valve flaps of the mitral valve do not close smoothly or evenly, but instead bulge upwards into the left atrium.

184
Q

What are the symptoms of mitral valve prolapse

A

Usually asymptomatic
May develop atypical chest pain, palpitations, and autonomic dysfunction symptoms

185
Q

What are the 2 signs of mitral valve prolapse

A

Mid-systolic click and/or late systolic murmur

186
Q

What are 4 complications of mitral valve prolapse

A

Mitral Regurgitation (MR)
Cerebral emboli
Arrhythmias
Sudden death

187
Q

What are 2 tests for mitral valve prolapse

A

Echocardiogram is diagnostic
ECG may show inferior T-wave inversion

188
Q

What is the treatment for mitral valve prolapse

A

β-blockers may help palpitations and chest pain. Surgery if severe MR.

189
Q

Define Mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole.
Normal mitral valve area 4-6cm2. Symptoms begin at areas less than 2cm2.

190
Q

Mitral stenosis key symptoms

A

Dyspnoea, orthopnoea, haemoptysis, RHF symptoms, palpitations

191
Q

What are 4 causes of mitral stenosis

A

Rheumatic fever
Congenital
Infective endocarditis
Malignant carcinoid

192
Q

What is 7 clinical presentations for mitral stenosis

A

Pulmonary hypertension causes dyspnoea, haemoptysis
Pressure from large left atrium on local structures causes hoarseness (recurrent laryngeal nerve)
Dysphagia
Bronchial obstruction
Fatigue
Palpitations
Chest pain

193
Q

What are 6 signs for mitral stenosis

A

Prominent ‘a’ wave in jugular venous pulsations: due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure
Mitral facies – severe MS leads to vasoconstriction: pink patches on cheeks
Malar flush on cheeks
Low-volume pulse
Low pitch rumbling at apex

194
Q

What are 3 investigations for mitral stenosis

A

ECG – may show AF and LA enlargement
CXR – LA enlargement and pulmonary congestion
Echo – assess mitral valve mobility, gradient and mitral valve area

195
Q

What are the management options for mitral stenosis

A

Atrial fibrillation – rate control is crucial
Medications
Serial echocardiography
Mitral balloon valvotomy
Mitral valve replacement

196
Q

What are the medications used in mitral stenosis management

A

Anticoagulate with warfarin
β-blockers, CCBs, digoxin – control heart rate, prolong diastole (improved diastolic filling)
Diuretics – reduce fluid overload

197
Q

What is Aortic stenosis

A

Narrowing of the aortic valve opening that restricts blood flow from the left ventricle to the aorta.
Normal aortic valve is 3-4cm2. Symptoms occur when valve area is ¼ of normal.

198
Q

What are the 3 types of Aortic stenosis

A

Supravalvular
Subvalvular
Valvular

199
Q

What is the pathophysiology of Aortic stenosis

A

A pressure gradient develops between the left ventricle and the aorta (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines

200
Q

What are 3 causes for aortic stenosis

A

Senile calcification (most common)
Congenital (bicuspid valve, Williams syndrome)
Rheumatic heart disease

201
Q

What are 6 clinical presentations for aortic stenosis

A

Angina (Chest pain)
Syncope
Breathlessness
Exertional dyspnoea
Dizziness, faints
Systemic emboli (if infective endocarditis)

202
Q

What are 3 signs for aortic stenosis

A

Slow rising carotid pulse with narrow pulse pressure
Heaving, non-displaced apex beat
Ejection systolic murmur – crescendo-decrescendo character

203
Q

What are the 5 investigations for aortic stenosis

A

Echocardiography
LVH, dilation, ejection fraction
Doppler derived gradient and valve area
Cardiac catheter can access valve gradient, LV function, CAD.
Pulsus parvus et tardus – weak and late pulse

204
Q

What are 2 differential diagnoses for aortic stenosis

A

Hypertrophic cardiomyopathy
Aortic sclerosis

205
Q

What are 4 management options for aortic stenosis

A

Poor prognosis without surgery for symptomatic patients
Valve replacement – definitive treatment
Percutaneous valvuloplasty/ replacement
TAVI – transcatheter aortic valve implantation

206
Q

What is aortic sclerosis

A

Senile degeneration of the valve. There is an ejection systolic murmur; but no carotid radiation, and normal pulse and S2 heart sound.

207
Q

What is aortic regurgitation

A

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

208
Q

What are 3 causes of acute aortic regurgitation

A

infective endocarditis, ascending aortic dissection, chest trauma.

209
Q

What are 5 causes for aortic regurgitation

A

congenital, connective tissue disorders (Marfan’s syndrome), rheumatic fever, Takayasu arteritis, rheumatoid arthritis.

210
Q

What is the pathophysiology of aortic regurgitation

A

Combined pressure and volume overload
Compensatory mechanisms: LV dilation, LH, progressive dilation leads to heart failure

211
Q

What are 4 clinical presentations of aortic regurgitation

A

Breathlessness
Orthopnoea (breathless lying down)
Palpitations
Diastolic blowing murmur

212
Q

What are 3 investigations for aortic regurgitation

A

CXR – enlarged cardiac silhouette and aortic root enlargement
Echo – evaluation of the AV and aortic root with measurements of LV dimensions and function
Cardiac catheterisation to assess severity of lesion, anatomy of aortic root

213
Q

What are 3 management options for aortic regurgitation

A

Medical: vasodilators
Serial echocardiograms to monitor progression
Surgical treatment: definitive

214
Q

What is rheumatic fever caused by

A

Pharyngeal infection with Lancefield group Aβ-haemolytic streptococci (s.pyogenes) triggers rheumatic fever 2-4weeks later.

215
Q

What is the pathology of rheumatic fever

A

An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue and may cause permanent damage to the heart valves.

216
Q

What are 4 pieces of evidence of group A β-haemolytic streptococcal infection

A

Positive throat culture
Rapid streptococcal antigen test +ve
Elevated or rising streptococcal antibody titre
Recent scarlet fever

217
Q

What is the dukes modified criteria

A

Evidence of a recent group A β-haemolytic streptococcal infection
plus 2 major criteria or 1 major+ 2 minor

218
Q

What are the 4 major criteria for rheumatic fever

A

Carditis – tachycardia, murmurs etc.
Arthritis
Subcutaneous nodules
Erythema marginatum

219
Q

What are the 3 minor criteria for rheumatic fever

A

Fever
Raised ESR/ CRP
Arthralgia

220
Q

What are the 4 management options for rheumatic fever

A

Bed rest until CRP normal for 2 weeks
Benzylpenicllin
Analgesia for carditis/ arthritis
Immobilise joints in severe arthritis

221
Q

What is infective endocarditis

A

Infection of the heart valve/s or other endocardial lined structures within the heart e.g. septal defects, surgical patches.
It is a really bad infection that showers infectious material all around the bloodstream.

222
Q

What are 5 types of Infective endocarditis

A

Left sided native IE (mitral or aortic)
Left sided prosthetic IE
Right sided IE
Device related IE (pacemakers/ defibrillators)
Prosthetic heart

223
Q

What are 3 causes of endocarditis

A

Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected
Introduce infectious material into the blood stream or directly onto the heart during surgery (bacteria e.g. Strep.viridans, Staph. Aureus)
Have had IE previously

224
Q

What is the pathology of IE by S.aueus

A

S. aureus usually gains access to the blood from the skin via indwelling vascular lines or via intravenous drug abuse

225
Q

What is the pathology of IE by S. viridans

A

S. viridans gains access to the blood from the oropharynx following tooth brushing or dentistry

226
Q

What is the mechanism of infection in IE by enterococci

A

enterococci gain access to the bloodstream following instrumentation of the bowel or bladder

227
Q

What are the clinical presentations for IE

A

Depends on site and organism
Left-sided: fever and signs of valve damage
Right-sided: fevers, chills and prominent pulmonary symptoms due to numerous septic emboli in the lungs
Signs of systemic infection e.g. fever, sweats
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, MI
Valve dysfunction – HF, arrhythmia

228
Q

What visible clinical presentations are there for IE

A

Petechiae (skin lesions)
Splinter haemorrhages (bruised nails)
Osler’s nodes (small, tender, purple nodules on the pulp of the digits)
Janeway lesions (non-tender lesions on the fingers, palm or sole)
Roth spots on fundoscopy

229
Q

What are the 2 major Duke criteria for IE

A

Bugs grown from blood cultures
Evidence of endocarditis on echo, or new valve leak

230
Q

What are the 5 minor Duke criteria for IE

A

Predisposing factors e.g. IV drug abuse
Fever
Vascular phenomena e.g. Janeway lesions
Immune phenomena e.g. Osler’s nodes
Equivocal blood cultures

231
Q

What is the Modified Duke criteria for definitive IE

A

2 major/ 1 major + 3 minor / 5 minor

232
Q

What investigations are used for IE

A

CXR – cardiomegaly, pulmonary oedema
Regular ECGs – to look for heart block
CT – to look for emboli
Raised CRP
ECG
Echo - TOE (transoesophageal echo) – improved rate of detection of vegetations
A negative result doesn’t eliminate IE
Many blood tests require long incubation periods for the organisms to grow, so they provide very slow results

233
Q

What are the treatment options for IE

A

Antimicrobials; IV for 6 weeks
Treat complications
Surgery

234
Q

What are 5 complications of IE

A

arrhythmia, HF, heart block, embolisation, stroke rehab

235
Q

What are the surgical options for IE

A

Indications: cannot be cured with antibiotics, severe valve damage, to remove infected devices, to replace valve after infection cured, to remove large vegetations before they embolise.

236
Q

What is Congenital heart disease

A

a general term for a range of birth defects that affect the normal way the heart works.

237
Q

What are 7 structural heart defects

A

Ventricular septal defect
Atrio-ventricular septal defects
Patent ductus arteriosus
Coarctaction of the aorta
Bicuspid aortic valve and aortopathy
Pulmonary stenosis
Eisenmenger syndrome

238
Q

What is Eisenmenger syndrome

A

any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, cyanosis, reversal of flow

239
Q

What are the investigations for structural heart defects

A

Echocardiography is first line
CT and MR are used to provide precise anatomical and functional information
Exercise testing assesses functional capacity

240
Q

What is the pathophysiology of VSD

A

High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber (so, not blue)
Increased blood flow through the lungs

241
Q

What are the 2 causes of VSD

A

Congenital
Acquired: post-MI

242
Q

What is VSD

A

ventricular septal defect, Abnormal connection between the 2 ventricles (a hole)

243
Q

What are 5 symptoms of VSD

A

Severe heart failure in infancy
Very high pulmonary blood flow in infancy
Breathless
Poor feeding
Failure to thrive

244
Q

What are 6 signs for VSD

A

Small, breathless, skinny baby
Increased respiratory rate
Tachycardia
Big heart on chest X-ray
Murmur varies in intensity
Harsh pansystolic murmur heard at left sternal edge (small holes give louder murmurs)

245
Q

What are 3 complications for VSD

A

Pulmonary hypertension
Eisenmenger’s complex
Heart failure from volume overload

246
Q

What are the 7 steps to eisenmengers syndrome

A

Pulmonary hypertension from initial left to right shunt
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
De-oxygenated blood enters systemic circulation
The patient becomes blue

247
Q

What are the investigations for VSD

A

ECG: normal
CXR: normal heart size, large pulmonary arteries
Cardiac catheter: step up in O2 saturation in right ventricle

248
Q

What are the treatment options for VSD

A

Many close spontaneously
Indications for surgical closure;
Failed medical therapy
Symptomatic VSD
Shunt >3:1

249
Q

What is an ASD

A

Atrial septal defect
Abnormal connection between the two atria (a hole).

250
Q

What is the pathophysiology of an ASD

A

Slightly higher pressure in the LA than the RA
Shunt is left to right (therefore not blue)
Increased flow into right heart and lungs

251
Q

What are 6 symptoms of ASD

A

Significant increased flow through the right heart and lungs in childhood
Right heart dilatation
Shortness of breath on exertion
Increased chest infections
Chest pain
Palpitations

252
Q

What are 4 signs of ASD

A

Pulmonary flow murmur
Fixed split-second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X-ray

253
Q

What are 2 complications of atrial septal defect

A

Eisenmenger’s complex
Paradoxical emboli

254
Q

What are paradoxical emboli

A

embolisms that cross an intracardiac shunt to the other side of the circulation

255
Q

What are the treatment options for ASD

A

May close spontaneously
Close if symptomatic
Transcatheter closure is more common than surgical

256
Q

What are atrio-ventricular septal defects (AVSD)

A

A hole in the very centre of the heart.
Involves the ventricular septum, atrial septum, mitral and tricuspid valves
Can be complete or partial
AV valves – instead of two separate valves, there is one big malformed one

257
Q

What are the consequences of a complete AVSD

A

Poor feeding, poor weight gain
Torrential pulmonary blood flow
Breathless as neonate
Needs repair or PA band in infancy

258
Q

What are the features of a partial AVSD

A

Presents like a small VSD/ASD
Can present in late adulthood
May be left alone if there is no right heart dilatation

259
Q

What is a patent ductus arteriosus

A

The ductus arteriosus fails to close after birth, leaving a vessel connecting the aorta and pulmonary artery.

260
Q

What are 3 clinical signs of patent ductus arteriosus

A

Continuous murmur
If large – big heart, breathless
Eisenmenger’s syndrome – cyanosis

261
Q

What is the pathophsysiology of a patent ductus arteriosus

A

Breathless, poor feeding, failure to thrive
Torrential flow from the aorta to the pulmonary arteries in infancy

262
Q

What is the treatment plan for ductus arteriosus

A

Closure is usually done surgically, under local anaesthetic. There is a low risk of complications.

263
Q

What is coarctation of the aorta

A

Congenital narrowing of the descending aorta (usually occurs just distal to the origin of the left subclavian artery – the site of insertion of the ductus arteriosus).

264
Q

What other conditions is Coarctation of the aorta
associated with

A

down’s syndrome, bicuspid aortic valve and Turner’s syndrome.

265
Q

What are 5 signs and symptoms of coarctation of the aorta

A

Radiofemoral delay
Weak femoral pulse
High blood pressure
Cold feet
Scapular bruit (buzzes over the scapulae from collateral vessels)

266
Q

What are the treatment options for coarctation of the aorta

A

Surgery
Balloon dilatation

267
Q

What is tetralogy of fallot

A

A congenital heart condition involving 4 abnormalities occurring together

268
Q

What 4 abnormalities are involved in Tetralogy of Fallot

A

Ventricular septal defect (VSD)
Pulmonary stenosis
Right ventricular hypertrophy
The aorta overrides the VSD, accepting right heart blood

269
Q

What is the pathophysiology of tetralogy of fallot

A

The stenosis of the RV outflow leads to the RV being at a higher pressure than the left
Therefore (blue) blood passes from the RV to the LV

270
Q

What is the presentation for tetralogy of fallot

A

Severity depends on degree of pulmonary stenosis
Cyanotic due to decreasing blood flow to the lungs
Hypoxic spell – child becomes restless and agitated

271
Q

What are the investigations for tetralogy of fallot

A

ECG: RV hypertrophy with RBBB.
CXR may be normal or show a boot shaped heart (hallmark of TOF)
Echo: can show the anatomy and degree of stenosis

272
Q

What is the management for tetralogy of fallot

A

Surgery is usually done before age of 1 – closure of VSD and correction of pulmonary stenosis.

273
Q

What is a cardiomyopathy

A

Refers to primary heart muscle disease – often genetic. All cardiomyopathies carry an arrhythmic risk. The heart doesn’t pump as well as it should.

274
Q

What is acute myocarditis

A

Inflammation of the myocardium - often associated with pericardial inflammation.

275
Q

What are 6 causes of acute myocarditis

A

Idiopathic (unknown)
Viral, bacterial, protozoan
Spirochaetes (Lyme disease/ syphilis)
Drugs e.g. penicillin
Toxins e.g. cocaine, lithium, alcohol, lead, arsenic
Immunological e.g. heart transplant rejection

276
Q

What are 4 symptoms and signs of acute myocarditis

A

ACS-like symptoms
Heart failure symptoms
Palpitations
Tachycardia

277
Q

What are the 3 treatment options for acute myocarditis

A

Supportive
Treat underlying cause
Treat arrhythmias and heart failure.

278
Q

What is dilated cardiomyopathy

A

A dilated, flabby heart of unknown cause.

279
Q

What are the potential causes for dilated cardiomyopathy (DCM)

A

Congenital
Most autosomal dominant, but some recessive and X-linked. Mutations in several genes are recognised – dystrophin, troponin T

280
Q

What is the pathology of DCM

A

Poorly generated contractile force leads to progressive dilation of the heart with some diffuse interstitial tissue

281
Q

What are 6 conditions associated with DCM

A

alcohol, high BP, chemotherapeutics, viral infection, autoimmune.

282
Q

What are 5 clinical presentations of DCM

A

Fatigue
Dyspnoea
Pulmonary oedema
RVF
Emboli

283
Q

What are 4 signs of DCM

A

High pulse
Low blood pressure
Hepatomegaly
Mitral or tricuspid regurgitation

284
Q

What are 4 investigations for DCM

A

Bloods: low sodium indicates a poor prognosis
CXR: cardiomegaly, pulmonary oedema
ECG: tachycardia, non-specific T-wave changes
Echo: low ejection fraction

285
Q

What are the 5 management options for DCM

A

Bed rest
Diuretics
β-blockers
Anticoagulation
Transplantation

286
Q

What is hypertrophic cardiomyopathy (HCM)

A

LV outflow tract obstruction from asymmetrical septal hypertrophy.

287
Q

What causes HCM

A

Caused by sarcomeric protein gene mutations – many recognised involving beta-myosin binding protein C, troponin T, titin.

288
Q

What are 7 signs and symptoms of HCM

A

Sudden death (troponin T)
Cardiac hypertrophy and dysrhythmia (beta-myosin)
Angina
Dypsnoea
Palpitations
Dizziness
Syncope

289
Q

What are 2 investigations for HCM

A

Echo: shows asymmetrical septal hypertrophy, small LV cavity, dilated left atrium and systolic anterior motion of the mitral valve.
ECG: progressive T-wave inversion, deep Q waves

290
Q

What are the 3 treatment methods for HCM

A

β-blockers for symptoms
Amiodarone for arrhythmias
Anticoagulate for systemic emboli.

291
Q

What is restrictive cardiomyopathy

A

Restrictive filling of the ventricles. A group of diseases in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body.

292
Q

what are 3 causes of restrictive cardiomyopathy

A

Idiopathic
Amyloidosis
Endomyocardial fibrosis

293
Q

What is 2 clinical presentations of restrictive cardiomyopathy

A

Like constrictive pericarditis
Features of RVF – hepatomegaly, oedema, ascites

294
Q

right ventricular cardiomyopathy

A

A degenerative condition with progressive dilation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement.

295
Q

What is the cause of Arrhythmia right ventricular cardiomyopathy

A

Often caused by desmosome gene mutations

296
Q

What is a channelopathy

A

Inherited arrhythmia caused by ion channel protein gene mutations.

297
Q

What are the features of channelopathies

A

Usually relate to potassium, sodium or calcium channels
Channelopathies include long QT, short QT, and Brugada syndrome (abnormal electrical activity of the heart)
Structurally normal heart
May present with recurrent syncope
Be aware of QT prolonging drugs – they can kill people with long QT syndrome

298
Q

What is Familial hypercholesteremia (FH)

A

An inherited abnormality of cholesterol metabolism (abnormal LDL protein)

299
Q

What are 6 features of Familial hypercholesteraemia

A

Leads to serious premature coronary and other vascular disease
Aortic aneurysm or dissection is often inherited
Aortovascular syndromes include Marfan, Loeys-Dietz, vascular Ehler Danlos (EDS)
Inherited Cardiovascular Conditions are usually dominantly inherited – offspring have 50% risk of inheritance
Family evaluation is essential and not in question
Genetic testing is available for many of these conditions

300
Q

What is Pericarditis

A

Inflammation of the pericardium.

301
Q

What is the aetiology of pericarditis

A

Infections are a common cause, and these may be viral, bacterial or fungal
Full-thickness acute myocardial infarction causes pericarditis overlying the infarct
Other miscellaneous causes include severe renal failure, hypothyroidism, multisystem autoimmune diseases, cardiac surgery, radiotherapy, malignant infiltration, and some drugs

302
Q

What is the presentation of pericarditis

A

Central chest pain which is worse on inspiration or lying flat and relieved by sitting forward.
A superimposed large pericardial effusion may cause breathlessness

303
Q

What are the investigations for pericarditis

A

ECG shows concave (saddle-shaped) ST segment elevation and PR depression
Blood tests: FBC, ESR, cardiac enzymes, tests related to aetiologies
Cardiomegaly on CXR may indicate pericardial effusion
CMR and CT may show localised inflammation

304
Q

What is the treatment for pericarditis

A

NSAIDs or aspirin with gastric protection

305
Q

What is constrictive pericarditis

A

The heart is encased in a rigid pericardium.

306
Q

What are 5 potential causes for constrictive pericarditis

A

pericarditis, myocardial rupture, aortic dissection, pericardium filling with pus, malignancy

307
Q

What are the clinical features of costrictive pericarditis

A

Dyspnoea, chest pain, signs of local structures being compressed
Nausea
Bronchial breathing

308
Q

What are the investigations for constrictive pericarditis

A

CXR shows an enlarged, globular heart if effusion >300mL
ECG shows low-voltage QRS complexes
Echo: an echo-free zone surrounding the heart

309
Q

What are the 3 management steps for constrictive pericarditis

A

Treat the cause
Pericardiocentesis- draining
Send pericardial fluid for culture and cytology

310
Q

What are 6 cardiac causes of arrythmias

A

: ischaemic heart disease; structural changes e.g. left atrial dilatation secondary to mitral regurgitation; cardiomyopathy; pericarditis; myocarditis; aberrant conduction pathways.

311
Q

What are 6 non-cardiac causes of arrythmias

A

caffeine, smoking, alcohol, pneumonia, drugs, metabolic imbalance.

312
Q

What are 6 clinical presentations of Cardiac arrhythmias

A

Palpitations
Chest pain
Presyncope
Syncope
Hypotension
Pulmonary oedema

313
Q

What are 5 investigations for arrhythmias

A

FBC, U&E, glucose, Ca2+, Mg2+
ECG: look for signs of IHD, AF, short PR interval, long QT interval, U waves
24h ECG monitoring
Echo: look for structural heart disease e.g. mitral stenosis
Provocation tests: exercise ECG, cardiac catheterisation

314
Q

What are the 3 types of management for arrhythmias

A

Conservatively – reducing alcohol intake
Medical management – regular tablets
Interventional management – pacemakers, ablation, implantable cardioverter defibrillators

315
Q

What is sinus tachycardia and its causes

A

conduction impulses are initiated at high frequency. Causes include infection, pain, exercise, anxiety, dehydration.

316
Q

What is focal atrial tachycardia

A

a group of atrial cells act as a pacemaker, out-pacing the SAN. P-wave morphology is different to sinus.

317
Q

What is atrial flutter

A

electrical activity circles the atria 300 times per minute, giving a sawtooth baseline. The AVN passes some of these impulses on, resulting in ventricular rates that are factors of 300.

318
Q

What is Atrioventricular re-entry tachycardia

A

an accessory pathway that allows electrical activity from the ventricles to pass to the resting atrial myocytes, creating a circuit; atria-AVN-ventricles-accessory pathway-atria.

319
Q

What is Atrioventricular nodal re-entry tachycardia

A

circuits form within the AVN, causing narrow complex tachycardias.

320
Q

What is Junctional tachycardia

A

cells in the AVN become the pacemaker, giving narrow QRS complexes as impulses reach the ventricles through the normal routes; P waves may be inverted and late.

321
Q

What is bundle branch block

A

a delay or blockage along the pathway that electrical impulses travel to make your ventricle contract

322
Q

What is Ventricular tachycardia

A

this can result from circuits, similar to atrial flutter. The QRS is broad. When a circuit is in action and its plane rotates, the ECG shows broad complex tachycardia with regularly increasing and decreasing amplitudes; this is called torsades de pointes.

323
Q

What is narrow complec tachycardia

A

ECG shows rate of >100bpm and QRS complex duration of <120ms. Narrow QRS complexes occur when the ventricles are depolarised via the normal conduction pathways.

324
Q

What is the management of narrow complex tachycardias

A

Identify and treat underlying rhythm e.g. treating sinus tachycardia secondary to dehydration with IV fluids.

325
Q

What is broad complex tachycardia

A

ECG shows rate of >100bpm and QRS complexes >120ms. If no clear QRS complexes, is it VF or asystole.

326
Q

What are the differential diagnoses for broad complex tachycardia

A

Ventricular fibrillation
Ventricular tachycardia

327
Q

What is the management for broad complex tachycardia

A

Correct electrolyte problems – low potassium, magnesium, calcium

328
Q

What are ventricular extrasystoles

A

Patients describe palpitations, a thumping sensation, or their heart missing a beat. The pulse may feel irregular if there are frequent ectopics.
The ectopics are broad QRS on ECG

329
Q

What are the 5 patterns of ectopic beats

A

single
Bigeminy – ectopic every other beat
Trigeminy – every third beat is an ectopic
Couplet – two ectopics together
Triplet – three ectopics together

330
Q

What is atrial fibrillation

A

A chaotic, irregular atrial rhythm at 300-600bpm. The AVN responds intermittently, hence an irregular ventricular rhythm.

331
Q

What are 7 causes of atrial fibrillation

A

Heart failure
Hypertension
IHD
PE
Mitral valve disease
Pneumonia
Hyperthyroidism – thyrotoxicosis

332
Q

What are 5 symptoms of atrial fibrillation

A

Asymptomatic
Chest pains
Palpitations
Dyspnoea
Faintness

333
Q

What are 2 signs of atrial fibrillation

A

Irregularly irregular pulse – the apical pulse rate is greater than the radial rate, and the 1st heart sound is of variable intensity.
Signs of LVF

334
Q

What are 3 investigations for AF

A

ECG: absent P waves, irregular rapid QRS complexes
Blood tests: U&E, cardiac enzymes, thyroid function tests
Echo: left atrial enlargement, mitral valve disease, poor LV function, other structural abnormalities.

335
Q

What is the management for acute AF

A

If the patient is stable and AF started <48h ago: rate or rhythm control may be tried: amiodarone.
if the patient is stable and AF started >48h ago: rate control with bisoprolol.
Correct electrolyte imbalances, treat associated illnesses.

336
Q

What is the management for chronic AF

A

Rate control: β-blocker or rate-limiting Ca2+ blockers are 1st choice – if this fails, add digoxin.
Rhythm control: elective DC conversion

337
Q

What is Atrial flutter

A

Organised atrial rhythm, rate 250-350bpm.
Similar to AF regarding rate and rhythm control and the need for anticoagulation.

338
Q

What is the treatment for atrial flutter

A

DC cardioversion is preferred to pharmacological cardioversion. IV amiodarone may be need if rate control is proving difficult.

339
Q

What are the 5 causes for atrial flutter

A

Obesity
Hypertension
Excess alcohol
COPD
Heart failure/ CHD

340
Q

What are 4 symptoms of atrial flutter

A

Palpitations
Breathlessness
Dizziness
Chest pain

341
Q

What is the investigation for atrial flutter

A

ECG: narrow QRS complex, F waves (no P wave)
2:1 to QRS

342
Q

What is the management of Atrial flutter

A

Amiodarone – anti-arrhythmic drug
Beta blockers - Bisoprolol
LMW Heparin
Catheter ablation

343
Q

What is heart block

A

Disrupted passage of electrical impulse through the AV node.

344
Q

What is 1st degree heart block

A

the PR interval is prolonged and unchanging; no missed beats

345
Q

What is Mobitz I 2nd degree HB

A

the PR interval becomes longer and longer until a QRS is missed, the pattern then resets. This is Wenckebach phenomenon

346
Q

What is Mobitz II 2nd degree HB

A

QRSs are regularly missed e.g. after every second p wave
This is a danger rhythm as it may progress to complete heart block

347
Q

What is are 6 causes of 1st and 2nd degree heart block

A

normal variant, athletes, sick sinus syndrome, IDH, acute myocarditis, drugs (digoxin, β-blockers)

348
Q

What is 3rd degree heart block

A

no impulses are passed from atria to ventricles so P waves and QRSs appear independently of each other

349
Q

What is the pathophysiology of 3rd degree heart block

A

As tissue distal to the AVN paces slowly, the patient becomes very bradycardic, and may develop haemodynamic compromise.

350
Q

What are 7 causes of 3rd degree heart block

A

IHD, idiopathic, congenital, aortic valve calcification, cardiac surgery/trauma, digoxin toxicity, infiltration

351
Q

What is the treatment of heart block

A

IV atropine
Permanent pacemaker

352
Q

what are features of prolonged QT syndrome

A

Can be congenital – romano-ward syndrome
Ventricular repolarisation grossly prolonged
Causes: low K+, Ca2+, acute MI, diabetes, amiodarone, amitriptyline
Signs: syncope, palpitations
If acquired give IV isoprenaline

353
Q

What are features of wolff-parkinson-white syndrome

A

An extra electrical pathway in the heart, leading to periods of tachycardia.
Due to congenital accessory conduction pathway between atria and ventricles
Resting ECG – short PR interval, wide QRS complex (due to slurred upstroke/ delta wave) and ST-T changes
Patients present with SVT
It’s a type of atrioventricular reciprocating tachycardia (AVRT)
Patients will be prone to AF (and VF)

354
Q

What is an Aortic aneurysm

A

An aortic aneurysm is an abnormal bulge that occurs in the wall of the aorta. An artery with a dilatation >50% of its original diameter has an aneurysm.

355
Q

What are true aneurysms

A

abnormal dilatations that involve all layers of arterial wall.

356
Q

What are false aneurysms

A

involve a collection of blood outside the vessel, held to the vessel by surrounding tissues

357
Q

What is the pathology of aneurysms

A

Aneurysms are dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels. Incidence rises with age, described as fusiform, saccular, dissecting and arterio-venous.

358
Q

What are 5 causes of aneurysms

A

Atheroma
Trauma
Infection
Connective tissue disorders
Inflammatory

359
Q

What are the clinical presentations of a Ruptured abdominal aortic aneurysm

A

Abdominal pain
Collapse
Shock

360
Q

What are the symptoms of unruptured AAAs

A

Often none
Abdominal/ back pain

361
Q

What are 5 complications with aneuryms

A

Rupture
Thrombosis
Embolism
Fistulae
Pressure on other structures

362
Q

What is the management for aneurysms

A

Annual check-ups and monitoring with regular ultrasound scans
Surgery
Endovascular: the graft is inserted into a blood vessel in your groin and then carefully passed up into the aorta
Open – the graft is placed in the aorta through a cut in your stomach

363
Q

What is aortic dissection

A

A tear in the wall of the aorta. Blood can flow in between the layers of the blood vessel wall (dissection). This can lead to aortic rupture or decreased blood flow to organs.
Associated with aortic aneurysms.

364
Q

What are 6 risk factors for aortic dissection

A

Ageing
Atherosclerosis
Blunt trauma to the chest
High blood pressure
Bicuspid aortic valve
Coarctation (narrowing) of the aorta

365
Q

What are 7 clinical manifestations of aortic dissection

A

Chest Pain – sharp, stabbing, tearing or ripping which radiates to the back
Anxiety and feeling of doom
Fainting or dizziness
Heavy sweating (clammy skin)
Nausea and vomiting
Pale skin (pallor)
Rapid, weak pulse

366
Q

What are 6 investigations for aortic dissection

A

Aortic angiography
Chest x-ray
Chest MRI
CT scan of chest
Echocardiogram
Transoesophageal echocardiogram (TEE)

367
Q

What is peripheral vascular disease

A

Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors. Disease in which a build-up of fatty deposits in the arteries restricts blood supply to leg muscles.

368
Q

What are 2 symptoms of peipheral vascular disease

A

Cramping pain in the calf, thigh, or buttock after walking for a given distance and relieved by rest
Ulceration, gangrene and foot pain at rest

369
Q

What are 5 signs of Peripheral vascular disease

A

Absent femoral, popliteal or foot pulses
Cold, white legs
Atrophic skin
Punched out ulcers
Buerger’s angle (angle that leg goes pale when raised off the couch).

370
Q

What are 4 investigations for Peripheral vascular disease

A

FBC – anaemia, polycythaemia
ECG – cardiac ischaemia
Ankle-brachial pressure index (ABPI)
Colour duplex USS – can show vessels and blood flow within them

371
Q

What are 4 management options for peripheral vascular disease

A

Risk factor modification – quit smoking, treat hypertension and high cholesterol
Management of claudication – supervised exercise programmes reduce symptoms by improving collateral blood flow.
Surgical reconstruction – arterial reconstruction with a bypass graft.
Amputation

372
Q

What is shock

A

Circulatory failure resulting in inadequate organ perfusion. Often defined by low BP – systolic <90mmHg, with evidence of tissue hypoperfusion.

373
Q

What is cardiogenic shock

A

a state of inadequate tissue perfusion primarily due to cardiac dysfunction.

374
Q

What are the causes of cardiogenic shock

A

Myocardial infarction
Arrhythmias
Pulmonary embolus
Tension pneumothorax
Cardiac tamponade
Myocarditis
Aortic dissection

375
Q

What are 6 clinical manifestations of cardiogenic shock

A

Agitation
Pallor
Cool peripheries
Tachycardia
Slow capillary refill
Oliguria (abnormally small amounts of urine)

376
Q

What are the 6 management steps for cardiogenic shock

A

Oxygen – titrate to maintain saturations of 94-98%
Diamorphine 1.25-5mg IV for pain and anxiety
Investigations and close monitoring
Correct arrhythmias, U&E abnormalities, or acid-base disturbance
Optimize filling pressure
Look for and treat any reversible cause

377
Q

What is cardiac tamponade

A

Compression of the heart by an accumulation of fluid in the pericardial sac.
Pericardial fluid collects -> intrapericardial pressure rises -> heart cannot fill -> pumping stops.

378
Q

What are 5 causes for cardiac tamponade

A

Trauma
Lung/breast cancer
Pericarditis
MI
Bacteria

379
Q

What are 4 signs of cardiac tamponade

A

Low BP
Muffled heart sounds (Beck’s triad)
Echocardiography may be diagnostic
CXR: globular heart – left heart border convex

380
Q

What are 3 management options for cardiac tamponade

A

Pericardiocentesis – quick relief
Give oxygen, monitor ECG, set up IV
Surgery may be required

381
Q

What is the mechanism of syncope

A

A state of consciousness is maintained by adequate cerebral blood flow. Cerebral vascular autoregulation ensures that the cerebral blood flow is kept within a narrow range, independent of the underlying systemic blood pressure. If the blood pressure drops below this range, the lack of blood causes syncope

382
Q

What are the signs that indicate a CNS cause of syncope

A

aura, headache, dysarthria and limb weakness

383
Q

What are the signs that indicate a Cardiac cause of syncope

A

chest pain, palpitations and dyspnoea

384
Q

What are 3 investigations for syncope

A

Blood pressure in supine and standing positions, on immediate standing, and after 3 minutes of standing.
Basic neurologic exam – checking for sensory, motor, speech and vision deficits
12-lead ECG

385
Q

What are 5 red flag symptoms with syncope

A

Syncope with exercise
Chest pain
Palpitations
Back pain
Haematemesis- vomit blood

386
Q

What is the management for syncope

A

Treat underlying cause

387
Q

What are antiplatelet drugs used for

A

Used in low dose for secondary prevention following MI, TIA/stroke, and for patients with angina or peripheral vascular disease

388
Q

What is the mechanism of aspirin

A

Aspirin irreversibly acetylates cyclo-oxygenase, preventing production of thromboxane A2, thereby inhibiting platelet aggregation

389
Q

What are 2 types of DOAC

A

Xa inhibitors and direct thrombin inhibitors

390
Q

What are anticoagulants used for

A

treatment of AF and clots.

391
Q

Which anticoagulant is used for mechanical valves.

A

warfarin

392
Q

What are 3 anticoagulant drugs used for acute coronary syndomes

A

LMWH, fondaparinux (Xa inhibitor) and bivalirudin (thrombin inhibitor)

393
Q

What is the mechanism of beta blockers

A

Block β-adrenoreceptors, thus antagonising the sympathetic nervous system.

394
Q

What is the action of blocking β1-receptors

A

negatively inotropic and chronotropic

395
Q

What is the action of blocking β2-receptors

A

induces peripheral vasoconstriction and bronchoconstriction

396
Q

What are β-blockers used for

A

angina, hypertension, antidysrhythmic, post MI, heart failure

397
Q

What are 3 side effects of β-blockers

A

lethargy, ED, headache

398
Q

What are ACE inhibitors used for

A

hypertension, heart failure and post MI

399
Q

What are 2 side effects of ACE inhibitors

A

dry cough and urticaria

400
Q

What are loop diuretics used for

A

heart failure, and inhibit the Na/2Cl/K co-transporter

401
Q

What are side effects of loop diuretics

A

dehydration, low Na+, K+, Ca2+

402
Q

What are Thiazides and thiazide-like diuretics used for

A

hypertension and heart failure

403
Q

What are the side effects of Thiazides and thiazide-like diuretics

A

low K+, raised Ca2+, low Mg2+, increased urate, impotence

404
Q

What is the action of potassium sparing diuretics

A

aldosterone antagonists directly block aldosterone receptors; amiloride blocks the epithelial sodium channel in the distal convoluted tubules

405
Q

What are vasodilators used for

A

heart failure, IHD and hypertension

406
Q

What is the action of nitrates

A

preferentially dilate veins and the large arteries, lower filling pressure (pre-load)

407
Q

What is the action of hydralazine

A

primarily dilates the resistance vessels, thus lowering BP (after-load)

408
Q

What is the action of calcium antagonists

A

Decrease cell entry of Ca2+ via voltage-sensitive channels in smooth muscle, thereby promoting coronary and peripheral vasodilation and reducing myocardial oxygen consumption.

409
Q

Which channel do Calcium antagonists block

A

L-type Ca2+ channels

410
Q

What are 4 side effects of calcium antagonists

A

flushes, headaches, ankle oedema, lowered LV function

411
Q

What are the features of dihydropyrdines

A

Mainly peripheral vasodilators and cause a reflex tachycardia so are often used with a β-blocker.
Used mainly in hypertension and angina
e.g. amlodipine

412
Q

What are the features of Non-dihydropyridines

A

Slow conduction at the AV and SA nodes
May be used to treat hypertension and angina and dysrhythmias
e.g. verapamil

413
Q

What is the action of digoxin

A

Blocks the Na+/K+ pump
It is used to slow the pulse in fast AF
As it is a weak +ve inotrope, its role in heart failure in sinus rhythm may be best reserved if symptomatic despite optimal ACE-i therapy

414
Q

What are 4 side effects of digoxin

A

nausea, decreased appetite, yellow vision, confusion

415
Q

What is amiodarone

A

A class III anti-arrhythmic

416
Q

What is the action of amiodarone

A

Prolongs the cardiac action potential, reducing the potential for tachyarrhythmias

417
Q

What is amiodarone used for

A

Used in both supra-ventricular and ventricular tachycardias, including during cardiac arrest.

418
Q

What are 3 side effects of amiodarone

A

thyroid disease, liver disease, pulmonary fibrosis

419
Q

murmur for Aortic stenosis

A

systolic ejection murmur, crescendo-decrescendo. S4 sound

420
Q

Aortic regurgitation murmur

A

diastolic decrescendo murmur, austin flint

421
Q

mitral stenosis murmur

A

diastolic rumble murmur

422
Q

mitral regurgitation murmur

A

pansystolic murmur, S3 sound

423
Q

ECG presentation of RBBB

A

MARROW, m shaped QRS on v1, W shaped QRS on v6

424
Q

ECG presentation of LBBB

A

WILLIAM, W shaped QRS on v1, M shaped QRS on v6

Phase 2a Medicine (10 decks)

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