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FINALS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the two types of acute coronary syndrome?

A

Stable and unstable angina

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2
Q

What is the definition of angina?

A

A symptom, caused by inadequate oxygenation to the myocardium

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3
Q

What is the cause of angina?

A

formation of an atherosclerotic plaque leads to obstruction of a coronary artery meaning there is less blood flow to the heart causing inadequate oxidisation

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4
Q

What is the main difference between stable and unstable angina symptoms wise?

A

Unstable angina has increasing frequency and severity of symptoms that does not get better unrest or GTN

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5
Q

What are the symptoms of stable angina?

A

Chest pain or pressure lasting several minutes
symptoms provoked by exercise or racial stress
relieved by rest or GTN spray

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6
Q

what investigations might want to perform to someone who has stable angina?

A

resting ECG shows no changes
cardiac biomarkers (tropponins) should be normal
fasting lipid profile
fasting blood glucose
and HbA1c
CXR - HF, DD
FBC - look for underlying infection or anaemia which could cause similar symptoms, or exacerbate angina

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7
Q

If someone presents to any with chest pain what investigations are necessary?

A 
order a full cardiac work up. 
FBC, - anaemia, underlying infection DD
Cardiac troponins, (+cardiac isoforms CK-MB, 
Creatinine kinase )
CRP - DD
ECG
CXR

If you suspect another couse you can perform more imaging. A CXR could rule out pulmonary oedema. CTPA for PE

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8
Q

How do you treat stable angina?

A

Improving lifestyle

control hypertension
anti platelet therapy ( aspirin, second-line= clopidogrel)

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9
Q

How do you treat unstable angina?

A

Oxygen (if decompensating), nitrates, and morphine

anti platelet therapy (aspirin, clopidogren) + consider adding anticoagulants (LMWH, Warfrin)

statins

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10
Q

There are various different cardiac markers:
Troponin
creatinine MB, CK

which is the best to look at and why?

A

High sensitivity troponin are very sensitive.

More so than creatinines:
They only last about 1 day after MI whereas troponins last around 1 week.
CK is general and can be from basically any muscle breakdown and is a good marker if renal function is good. CK MB is specific to myocyte muscle breakdown
HS troponins are high sensitivity.

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11
Q

If someone presents to you with chest pain that occurred 1h ago has now gone and the troponin levels are low does that mean that they are in the clear?

A

no

HS troponin peak after 3 h

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12
Q

a patient who had chest pain an hour ago which is now resolved,
troponin came back negative
x-ray was clear,
no clear ECG changes
is keen to be discharged, is it safe to discharge?

A

No
do serial troponin until 3hrs have passed
do serial ECG’s

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13
Q

In a heart attack what to drugs can give the pain relief?

A

Morphine

GTN

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14
Q

Under new guidelines when should you start oxygen in a chest pain patient?

A

If saturation is under 94%

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15
Q

What is the management of a patient who has a confirmed heart attack?

A

M(O)NA
PCI
Anticoagulation

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16
Q

When is PCI indicated in a heart attack?

A

Within 12 hrs from onset of symptoms and within 120 mins from diagnosis

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17
Q

If PCI isn’t indicated what else can you give?

A

Fibrinolysis treatment:

Altepase
Tenecteplase
Streptokinase

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18
Q

What are contraindications to fibrinolysis?

A

Acute pancreatitis; aneurysm; aortic dissection; arteriovenous malformation; bacterial endocarditis;

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19
Q

Who performs a PCI?

A

Interventional cardiologist

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20
Q

What other drugs/Mx should be considered in the treatment of acute coronary syndrome?

(apart from PCI/ thrombolysis)

A

Anticoagulants:

  • LMWH
  • Clopidogrel

Bisoprolol

Glycoprotein 11B/11a inhibitor – not commonly used

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21
Q

What ECG leads show changes in an anterior infarct?

A

leads V3, V4

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22
Q

What leads do you find changes in a posterior infarct?

A

V7, V8, V9 – these are V5, V6 put more laterally in the axilla, you know to do this if you see reciprocal changes V1, V2, V3

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23
Q

What leads do you find changes in an inferior infarct?

A

leads II,III,aVF

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24
Q

What leads one to find changes in a septal infarct?

A

V1, V5

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25
Q

What can the consequences of an MI?

A

Death
VSD
ventricular aneurysm occurring 4 to 6 weeks post heart attack due to a weakened myocardium

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26
Q

What is heart failure?

A

Where cardiac output does not meet the demands of the body without increasing diastolic function

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27
Q

What are the three types of heart failure based on ejection fraction?

A
  1. heart failure with reduced ejection fraction (<49%)
  2. heart failure with midrange ejection fraction ( 40-49%)
  3. heart range with normal ejection fraction (>50%)
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28
Q

Is all heart failure congested heart failure?

A

Yes

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29
Q 
A patient comes to you complaining of:
dysnopea
needing to use an extra pillow to help sleep
SOB
cough

what is the most likely diagnosis?

A

Congestive heart failure

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30
Q

What physical signs are present during congestive heart failure?

A 
Tachycardia (>120bpm)
distended neck veins+JVP
s3 gallop
hepatomegaly
chest crackles
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31
Q

What investigations are used to diagnose congestive heart failure?

A

Chest x-ray
transthoracic echo
ECG

FBC - anaemia = poor prognosis
serum lipids
iron studies - ? iron overload cardiomyopathy
HbA1c
urea and electrolytes (including creatinine) - renal function, renal disease can cause HF and be caused by HF
TSH - can cause HF

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32
Q

What findings would you see on test x-ray for congestive heart failure?

A

Cardiomegaly
Pulmonary congestion (kerlay B lines)
pleural effusion

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33
Q

What ECG changes can you find with congestive heart failure?

A

Prolonged QRS (above 120)

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34
Q

What is the management of heart failure?

A 
ACEi or ARB (if ACEi intolerant)
B blockers
Loop diuretics (frusemide) + other diuretics

digoxin can be used

if underlying cause treat that

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35
Q

How does hypertension cause heart failure?

A

High blood pressure causes the left ventricle to hypertrophy.
This is due to the pressure overload which occurs in the heart.
The heart chamber becomes smaller due to the hypertrophy, and there is less cardiac output.
Thus causing heart failure.

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36
Q

How do cardiac myopathies cause heart failure?

A

The heart muscle becomes enlarged, thick or rigid or in some cases scarred.
This abnormal heart muscle causes the heart to enlarge – cardiomyopathy. And also causes cardiac dysfunction.
The cardiac output is reduced either due to reduced space in the ventricles or because the heart loses contractility.
Thus causing heart failure

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37
Q

How does valvular disease cause heart failure?

A

The inappropriate function of the valve will cause heart failure because of either:
1. increased pressure
2. increase volume
3. both.
this will cause hypertrophy of the chamber.
The condition will deteriorate until there is insufficient cardiac output thus causing heart failure

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38
Q

How does ischaemic disease cause heart failure?

A

Ischaemic heart failure.
Thrombus detaches and migrates to vessels supplying the myocardium (coronary arteries)
this means myocardium isn’t oxygenated and cannot bleat effectively.
This will cause inadequate cardiac output and heart failure

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39
Q

What is pulmonary hypertension?

A

High blood pressure in the pulmonary arteries caused by precipitating lung disorder.

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40
Q

What is the pathology of pulmonary hypertension?

A

There is a precipitating lung disorder

there is hypoxaemia and vasoconstriction

increasing the resistance in pul. vessels.

this can lead to right-sided heart failure due to the right ventricles trying to overcome the high-pressure

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41
Q

What are the characteristic symptoms of pulmonary hypertension/cor pulmonale?

A 
Fainting
 fatigue
 and shortness of breath
 distended neck veins and JVP
 hepatomegaly
 oedema

past medical history of chronic lung conditions

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42
Q

What investigation are necessary in order to diagnose cor pulmonale?

A

lung CT and echocardiogram

chest x-rays, CTPA, spirometry and lung function tests can all be useful in finding lung pathology

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43
Q

What is the management of pulmonary hypertension

A

Treating the underlying condition
treating the caused heart failure
oxygen therapy is usually required

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44
Q

What is the definition of a cardiomyopathy?

A

Inappropriate ventricular hypertrophy or dilatation caused by mechanical or electrical dysfunction
can be primary or secondary

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45
Q

What is a primary cardiomyopathy?

A

A condition confined to the heart muscle which can be genetic, mixed, acquired

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46
Q

What is a secondary cardiomyopathy?

A

Myocardial involvement occurring as part of the systemic or multiorgan disorder

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47
Q

What are the three common cardiomyopathies?

A

Idiopathic
myocarditis
alcoholic

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48
Q

What are genetic cardiomyopathy examples?

A

Duchenne’s muscular dystrophy

genetic haemochromatosis

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49
Q

What are infective cardiomyopathy examples?

A

Can be viral (coxackies!), bacterial (GAS) or parasytic

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50
Q

What are autoimmune cardiomyopathy examples?

A

SLE
giant cell vasculitis/ myocarditis
sarcoidosis

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51
Q

What are toxic cardiomyopathy examples?

A

Alcohol
cocaine
methamphetamines
iron overload

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52
Q

What nutritional deficiencies can cause cardiomyopathy?

A

ZInc
copper
thamaline

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53
Q

What drugs can cause cardiomyopathy?

A

Antipsychotics - clozapine olanzapine risperidone

chloroquine

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54
Q

What endocrine causes of cardiomyopathy?

A 
Hypo and hyperthyroidism
 Cushing's
 Addison's
 pheochromocytoma
 acromegaly
 diabetes
 pre-partum
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55
Q

Which electrolyte abnormalities can cause cardiomyopathy?

A

Hypocalcaemia

hypophosphataemia

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56
Q

What investigations are used to diagnose cardiomyopathy?

what do they show?

A

Chest x-ray - and large top shadow
echocardiogram - ventricular dilation and reduced stroke volume with lower ejection fraction
ECG - non specific findings
Biopsy - underlying cause (infection, iron build up, antibodies)

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57
Q

What is the treatment of cardiomyopathy?

A

Treating any underlying cause

heart failure management

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58
Q

What is the pathophysiology of mitral regurgitation?

A

Blood leaks backwards into the left atrium when the ventricle contracts

this reduces cardiac output and increases the amount of blood remaining in the atrium

this causes there to be a delegation of the Chambers and increases left ventricular diastolic function

these changes are in order to try and maintain cardiac output

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59
Q

What causes for mitral regurgitation?

A

rheumatic fever
infective endocarditis
acute dilatation of the left ventricle from myocarditis or ischaemia (post MI)

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60
Q

What is the purpose of an echocardiogram?

A

Let’s at structural and valvular abnormalities
assesses pressure within the ventricles
looks at flow of blood

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61
Q

While investigations are required in mitral regurgitation?

A

ECG

echocardiogram

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62
Q

What is the management of mitral regurgitation

A

if they are asymptomatic and left ventricular injection function (LVEF) >60
= ACEi and B Blockers
if LVEF is <60
= surgery
if symptomatic and LVEF > 30
= surgery + ACEi and B Blockers + Diuretic
if symptomatic ND LVEF < 30
= same as with >30 but with additional surgical measures

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63
Q

What type of surgery is used in mitral regurgitation?

A

percutaneous mitral valve leaflet repair

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64
Q

What is the pathophysiology of mitral stenosis?

A

and event occurs/congenital

leading to the fusion of the leaflets of the valves.

This restricts blood flow increasing the left arterial pressure causing pulmonary congestion and increasing its blood pressure.

restricted orifices of the valve limit the filling of ventricle/

there is limited cardiac output

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65
Q

What investigations will you use for mitral stenosis?

A

Echocardiogram.
ECG.
chest x-ray

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66
Q

What would an echocardiogram show in mitral stenosis?

A

Hockey stick shaped mitral deformity

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67
Q

What Myerson ECG showed in mitral stenosis?

A

Rhythm disturbances such as atrial fibrillation

left atrial enlargement and right ventricular hypertrophy

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68
Q

what finding would you see on chest X ray for Mitral stenosis?

A

Mainly ordered as a baseline test

can show enlarged left atrium giving a double right heart border and a prominent pulmonary artery plus other signs of pulmonary congestion

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69
Q

What’s the treatment of mitral stenosis?

A

If asymptomatic do not treat.

a symptomatic treatment with diuretics and surgery

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70
Q

In what exceptions to an asymptomatic patient would you treat mitral stenosis?

A

If pregnant

if severe and asymptomatic
- there is either a small valve area or a large pressure gradient

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71
Q

What is the main cause of mitral stenosis?

A

Rheumatic fever

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72
Q

What causes mitral prolapse?

A

Unknown thought to have some genetic link

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73
Q

What investigation is indicated for mitral prolapse?

A

Echocardiogram - shows leaf prolapse

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74
Q

What is the management of mitral prolapse?

A

If asymptomatic:

  • reassure
  • start on aspirin or warfarin (second line)

if symptomatic:

  • halter/ ambulatory monitoring indicates management plan
  • aspirin or warfarin (second line) if halter positive also give beta-blockers

if severe asymptomatic or symptomatic:
- valve repair plus aspirin or warfarin (second line)

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75
Q

What other two types of aortic regurgitation?

A

Acute

Chronic

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76
Q

What is the pathophysiology of acute aortic regurgitation?

A

Blood passes back through they’ll take valve causing a sharp increase in end-diastolic pressure in the left ventricle

heart begins to compensate with an increased heart rate and contractility to keep up with the increased preload

at one point this will fail and stroke volume is maintained

acute aortic regurgitation’s medical emergency causes sharp increase in left arterial pressure, pulmonary oedema and cardiogenic shock

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77
Q

What is the pathophysiology of chronic aortic regurgitation?

A

there is regurgitation back into the left ventricle

increasing left ventricular volume and pressure

causing hypertrophy and dilation to maintain stroke volume and reduce the now raised and diastolic volume

however due to the compensatory methods developed in the chronic process the end-diastolic pressure is normal

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78
Q

what investigations are indicated in aortic regurgitation?

A

ECG
Echo +Dopper
x-ray

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79
Q

What ECG changes would show on aortic regurgitation?

A

S T wave changes

left axis deviation or conduction abnormalities

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80
Q

What is the management of acute aortic regurgitation?

A

IV Inotropes - dopamine
IV vasodilators - nitroprusside
urgent valve replacement

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81
Q

What is the management of mild chronic aortic regurgitation?

A

If mild and asymptomatic:
reassurance.

if mild and symptomatic:
see if there is an underlying cause and treat that.

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82
Q

What is the management of mild chronic aortic regurgitation?

A

if severe and asymptomatic with ejection fraction >50%:
assess whether or not it is the compensating with exercise tolerance test:
if they manage to exercise tolerance test starts on vasodilator therapy - nifedepine

if they are in fact decompensated assess for surgery.

if the ejection fraction is < 50% or symptomatic:
assess for surgery immediately.

is unsuitable for surgery use:

  • vasodilators (nifedipine)
  • ACE inhibitors
  • transcaheter approach
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83
Q

what is the pathophysiology of aortic stenosis?

A

Calcification of the leaflets leads to abnormal blood flow across the valves

the turbulent flow damages the endothelium initiating an inflammatory response further calcifying the valves (like atherosclerosis).

this causes a pressure overload and hypertrophy of the left ventricle which compensates for a while but eventually will fail causing heart failure

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84
Q

How does rheumatic fever cause aortic stenosis?

A

There is an autoimmune inflammatory response triggered by streptococcal infection

from molecular mimicry

both the infection and the immune system to target the valvular endothelium causing damage and stenosis

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85
Q

What are risk factors to aortic stenosis?

A

Cardiovascular risk factors ( including diabetes)

majority caused by a congenital bicuspid valve- found commonly in co-optation of the water and Turners syndrome

rheumatic fever

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86
Q

What would an ECG show in aortic stenosis?

A

Left ventricular hypertrophy
absent Q waves
atrioventricular block
or bundle branch block

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87
Q

What investigations would you perform for aortic stenosis?

A

Echo and Doppler
ECG

consider an MRI and cardiac catheterisation (shows elevated pressure gradient)

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88
Q

What is the treatment for an unstable patient with aortic stenosis?

A

Vasodilator or beta-blockers or balloon valvuloplasty until patient is stable enough for surgery

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89
Q

What is the treatment for a stable but symtpmatic patient with aortic stenosis

A

If low risk:
aortic valve replacement
if they are intermediate risk management is saying that they might need a TAVR

is high risk they need an aortic valve replacement and a TAVR

any risk then needs long-term infective endocarditis prophylaxis and long-term anticoagulation

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90
Q

What is the treatment for a stable and asymptotic patient with aortic stenosis

A

The clinical follow-up and an echo every 1 to 2 years unless they are severe in which case surgery is needed

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91
Q

What is the pathophysiology of tricuspid stenosis?

A

There is a produced orifice size causing reduced and turbulent blood flow during diastole to the right ventricle.

this causes are to be elevated right atrial pressure.

there is pulmonary congestion and reduced cardiac output with atrial enlargement and hypertrophied this can precipitate atrial fibrillation

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92
Q

How does rheumatic fever because tricuspid stenosis?

A

There is an antibody cross sensitivity between group a strep and the host tissue

and inflammatory response targeting mainly the leaflets causes fibrin deposition

this leads to fusion

and the chord tendinae are shortened

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93
Q

What are the causes of tricuspid stenosis?

A

Rheumatic fever/ rheumatic heart disease- as a late complication

rarely:
coronary heart disease and infective endocarditis and carcinoid syndrome heart disease

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94
Q

What investigations are necessary for tricuspid stenosis?

A 
ECG
 chest x-ray
 echo
 Doppler
 liver function test
 full blood count
 blood cultures
 24-hour excretion of urinary 5-HIAA (carcinoid)
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95
Q

What is the management of tricuspid stenosis if congenitally acquired?

A

Surgery and pre-op alprostadil

a post up anti platelet

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96
Q

What is the management of tricuspid stenosis in rheumatic fever?

A

Fluid and sodium restriction
loop diuretics
surgery if severe enough

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97
Q

What is the management of tricuspid stenosis in carcinoid heart disease?

A

Fluid and sodium restriction
loop diuretics
somatostatin analogues
valve replacement

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98
Q

How do somatostatin analogues work?

A

suppression of the secretions of the pituitary, pancreas, stomach, and gut; interference with growth factors; and direct antiproliferative effects on some tissues

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99
Q

What is tricuspid regurgitation?

A

Blood throwing back through the tricuspid valve causes elevation in right ventricular pressure

this causes right ventricular enlargement

eventually there is a reduced cardiac output

eventually also affects the atrium causing atrial distension and heart failure

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100
Q

What are the causes of tricuspid regurgitation?

A

Congenital

secondary causes are rheumatic fever, infective endocarditis and carcinoid

can also be caused by rheumatoid arthritis

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101
Q

How would you treat congenital tricuspid regurgitation?

A

Unless the surveyor and symptomatic manage heart failure symptoms, if severe symptomatic requires replacement

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102
Q

How would you manage secondary tricuspid regurgitation?

A

Treat any underlying cause and heart failure symptom management

if severe surgery

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103
Q

What is pulmonary stenosis?

A

The narrowing of the pulmonary valve causes an increase in right ventricular strain

Due to its congenital nature myocardium undergoes hyperplasia however if not congenital there is hypertrophy of the heart

eventually the pressure buildup will become severe and cause pulmonary congestion causing heart failure

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104
Q

What are the causes of pulmonary stenosis?

A

Congenital is most common: associated with noone’s and William’s

secondary causes are carcinoid, infective endocarditis, myocardial tumours

basically only one where rheumatic fever doesn’t affect the valve

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105
Q

What is the murmur associated with tricuspid regurgitation?

A

It is a high pitched, holosystolic murmur.

it is best heard at the left lower sternal border and it radiates to the right lower sternal border

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106
Q

What is the murmur associated with pulmonary stenosis?

A

midsystolic high-pitched crescendo-decrescendo murmur heard

best at the pulmonic listening post and radiating slightly toward the neck, (the murmur of pulmonic stenosis does not radiate as widely as that of aortic stenosis)

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107
Q

What would an ECG show for pulmonary stenosis

A

Right axis deviation with peaked P waves

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108
Q

What is the management of mild pulmonary stenosis?

A

Observation

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109
Q

What is the management of moderate pulmonary stenosis?

A

Surgery

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110
Q

What is the management of severe pulmonary stenosis?

A

Usually present at birth

give supplemental O2 with alprostadil and then surgery

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111
Q

What is pulmonary regurgitation

A

Helps equalise the pressure of the right ventricle and the pulmonary artery causing pulmonary congestion this can lead to pulmonary hypertension and heart failure

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112
Q

what the causes of pulmonary regurgitation?

A

congenital cases are rare to is usually in conjunction with another valve disease (occurs secondary to it) such as mitral stenosis, or infective endocarditis or rheumatic heart disease or in Marfan syndrome

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113
Q

What is the murmur of pulmonary regurgitation?

A

Pulmonic regurgitation produces a soft, high-pitched, early diastolic decrescendo murmur heard best at the pulmonic listening post (left upper sternal border)

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114
Q

What is infective endocarditis?

A

An episode of bacteraemia leading to the colonisation of an area of the heart causing vegetation

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115
Q

what is the pathophysiology of invective Endocarditis?

A

Underlying risk factors cause turbulent blood flow across the endothelium causing damage to it usually of the valvular surfaces of the heart.

Pay platelets and fibrin adhere to the underlying collagen of the endothelium taking a pro-thrombotic milau.

An episode of bacteraemia leads to the colonisation of the thrombus.

The colonisation causes further inflammatory response precipitating further fibrin and platelet buildup making a vegetation.

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116
Q

What are the causes of infective endocarditis?

A

Classically caused by Staphylococcus aureus

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117
Q

patient who has a prosthetic heart valve presents to you with fevers, chills, night sweats, myalgia, fever, weight loss and anorexia, weakness, arthralgia, headaches, shortness of breath

what are you concerned about?

A

Infective endocarditis

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118
Q

what are the risk factors for infective endocarditis?

A

Prior history of infective endocarditis
presence or prosthetic valve
post heart transplant patients

recent history of IV drug use
dental work
in hospital stay
catheters

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119
Q

How would you diagnose infective endocarditis?

A

You have to follow the Duke criteria in which he must have:

  • two major criteria
  • one major and three minor criteria
  • five minor criteria
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120
Q

What are the major criteria for infective endocarditis?

A

An echo showing the vegetations or access
positive blood cultures
a new valvular regurgitation mamma
coxiella brunette inflection

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121
Q

What are the minor criteria for infective endocarditis?

A

Predisposing heart condition or IV drug use
a fever of 38°C or over
M belie to organs or brain haemorrhages
glomeruli nephritis, also notes, rust spots, rheumatoid factor
positive blood cultures that do not meet specific criteria

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122
Q

How would you manage bacterial endocarditis?

A

first ABCD approach

If a patient presents with decompensated heart failure diuretics and prompt surgery is needed

blood cultures echo and broad-spectrum antibiotics started

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123
Q

What is the antibiotic of choice used if staphylococcus is on blood culture?

A

Beta-lactam (vancomycin)

Methillin resistant ad trimethoprim and clindamycin

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124
Q

what is rheumatic fever?

A

An autoimmune disease resulting from infection from group a Streptococcus causing molecular mimicry.

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125
Q

What is the pathophysiology of rheumatic fever?

A

There is antibody attachment and basement membrane to the valve endothelium duty molecular mimicry.

There is up-regulation and adhesion of T cells.

These T cells then infiltrate and cause Neo- vascularisation and further recruitment of T cells damaging the endothelium.

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126
Q

How would you define primary rheumatic fever?

A

A patient without prior episodes of rheumatic fever and no evidence of rheumatic heart disease

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127
Q

How would you describe recurrent rheumatic fever?

A

A patient with documented rheumatic fever in the past but without evidence of established rheumatic heart sees

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128
Q

What is the Jones criteria?

A

The diagnostic criteria for rheumatic fever

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129
Q

What are the major criteria of the Jones criteria/ symptoms of rheumatic fever?

A 
Pancarditis
 poly arthritis
Sydenham Chorea
 subcutaneous nodules
 erythema marginatum (pink rings on the torso and inner surfaces of the limbs which come and go for as long as several months.)
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130
Q

What are the minor criteria of the Jones criteria/ symptoms of rheumatic fever?

A 
Fever
 arthralgia
 prolonged PR interval
 increased ESR or CRP
 leucocytosis
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131
Q

What is required to diagnose rheumatic fever?

A

recent group A streptococcal infection with at least 2 major manifestations or 1 major plus 2 minor manifestations present.

or..

Rheumatic chorea: can be diagnosed without the presence of other features (which is described as ‘lone chorea’) and without evidence of preceding streptococcal infection. It can occur up to 6 months after the initial infection.

or…

Chronic rheumatic heart disease: established mitral valve disease or mixed mitral/aortic valve disease, presenting for the first time (in the absence of any symptoms suggestive of acute rheumatic fever).

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132
Q

What is the management of rheumatic fever?

A

Benzylpenicillin intramuscularly plus treating any complications

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133
Q

How would you treat arthritis caused by rheumatic fever?

A

Salycylate therapy/NSAID

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134
Q

How would you treat HF caused by rheumatic fever?

A 
Diuretic
   furosemide or spironolactone
\+/-
 ace inhibitor
\+/-
 glucocorticoids if there is pericardial effusion
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135
Q

How would you treat chorea caused by rheumatic fever?

A

Anticonvulsants such as carbamazepine or valproic acid

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136
Q

What is pericarditis?

A

Inflammation of the pericardium

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137
Q

Describe the pericardium?

A

A two layer fibrinous sack covering the hearts surface.

It has a micro villous surface secreting pericardial fluid and is a highly innovative structure (phrenic nerve)

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138
Q

What is the function of the pericardial?

A

To protect, restrict, determine cardiac filling, limit cardiac dilatation and balances the ventricles

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139
Q

What are the common causes of pericarditis?

A

90% are idiopathic recorded viral infections most common viruses are:
Coxsackie virus
mumps
EBV

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140
Q

Apart from viral causes what else can cause pericarditis?

A 
Pathogenic:
Pneumococcus
meningococcus
Ghonnococcus and chlamydia
candida
systemic diseases:
SLE
rheumatoid arthritis
sclerosis
IBD

other:
three days post MRI, radiotherapy, and cardiac surgery

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141
Q

A patient presents with :
chest pain which is worse on inspiration
has had a low grade fever
and been feeling generally under the weather

examination:
you hear high-pitched and squeaky sound heard of the left sternal edge

what is the diagnosis?

A

Pericarditis

Can also present with R sided heart failure which indicates constructive pericarditis!!!

142
Q

What investigations would you run for someone with pericarditis?

A 
ECG
 pericardial fluid culture and blood culture
 inflammatory markers
 for blood count
 urea
 chest x-ray
 echocardiogram
143
Q

What changes would you find on ECG for pericarditis?

A

ST segment elevation and PR depression

also serum proponent could be mildly elevated

144
Q

Why might you perform a chest x-ray or echo for pericarditis?

A

To check if there is a pericardial effusion and assess severity it

pericardial effusion sound in 60% of cases

145
Q

Do you admit someone suffering from pericarditis to hospital ?

A

Yes
if there’s any presentation suggesting an underlying aetiology

or

predictor of poor prognosis:

  • fever
  • subacute onset
  • symptoms of large pericardial effusion and cardiac tamponade
  • failure to respond to 7 days of NSAIDs
146
Q

what is the first-line management of pericarditis?

A

If idiopathic or viral use NSAIDs plus gastric protection for seven days and colchicine for three months afterwards to prevent re-occurrence and exercise restriction

if bacterial then systemic antibiotics plus the basic therapy

if there is a symptomatic or purulent effusion or cardiac tamponade then perform pericardial centrepieces

147
Q

what would be the second line management of pericarditis?

A

Idiopathic or viral ad corticosteroids instead of NSAID and PPI but the rest is the same

148
Q

what are the nine underlying causes of hypertension?

A

disturbance of the auto regulation reflects causing an increase in vascular resistance to match cardiac output

excess sodium intake

renal sodium retention

this regulated our AAS

increased sympathetic drive

endothelial dysfunction

increase peripheral resistance

hyper insulinaemia

cell membrane transporter dysfunction

149
Q

What is a presentation of hypertension?

A

Usually presents a symptomatically.

in more advanced undiagnosed cases you can get some symptoms:

  • headaches
  • visual changes (retinopathy)
  • dysnopea (from congestive hf)
  • chest pain
  • sensory or motor deficit (cerebrovascular disease)
150
Q

What are risk factors of hypertension?

A 
Obesity
 inactive lifestyle
 alcohol use
 metabolic syndromes
 over 60
 families Hx
 sleep apnoea
151
Q

After the initial diagnosis of hypertension what investigations need to be performed and why?

A

ECG - checking for left-ventricular hypertrophy from cardiac failure
fasting metabolic panel and EGFR- renal disease
lipid panel
full blood count - anaemia can be complication
thyroid function test

152
Q

what is the diagnostic criteria of hypertension?

A

he patient should be seated quietly for at least 5

Two or more measurements should be made on two or more occasions and the average recorded.

153
Q

What values are pre-hypertension?

A

120-130/80-89

154
Q

What values are hypertension stage I?

A

140-159/90-99

155
Q

What values are hypertension stage II?

A

160+/100+

156
Q

What values of a hypertensive crisis?

A

180+/110+

157
Q

What is the treatment of an adult with hypertension who is younger than 55 or type II diabetic?

A

step 1: ACE inhibitor (or ARB)
step 2: add a calcium channel blocker or thiazide like diuretic
step 3: all three
step 4: add low-dose spironolactone or an alpha blocker or beta-blocker, resistant hypertension should be confirmed with ambulatory monitoring.

158
Q

What is the treatment of an adult with hypertension who is over 55 or a black patient of African/Caribbean descent?

A

step 1: CCB
step 2: add an ACEi or thiazide like diuretic
step 3: all three
step 4: add low-dose spironolactone or an alpha blocker or beta-blocker, resistant hypertension should be confirmed with ambulatory monitoring.

159
Q

What are treatment aims for hypertension?

A

To get the blood pressure below 140/90 unless they are over 80 or particularly frail then 150/90

160
Q

In hypertension when would you want to measure both standing and sitting blood pressure?

A

Resistant hypertension
anyone with type II diabetes
anyone with symptoms of postural hypotension
anyone over 80

161
Q

An example of an ace inhibitor?

A

Ramipril

162
Q

What are side effects of ramipril/acei?

A 
Dizziness
 headache
 hypotension
 cough
 rash
 angioedema
163
Q

Give an example of an ARB?

A

candesartan

164
Q

What are side effects of candesartan/arbs?

A 
Abdominal pain
 back pain
 hypotension
 hyperkalaemia
 renal impairment
165
Q

What are side effects of CCB’s?

A 
Peripheral oedema
 flushing
 palpitations
 abdominal pain
 muscle cramps
 rash
166
Q

Give an example of a CCB?

A

Amlodipine

167
Q

Give an example of Thiazide like diuretic and where thiazide like diuretics work?

A

Hydrochlorothiazide

Distal convoluted tubule

168
Q

what are side effects of Thiazide like diuretics?

A 
Alkalosis
 hypokalaemia
 diarrhoea
 nausea
 postural hypotension
169
Q

Gave an example of a beta-blocker?

A

metoprolol

170
Q

Give side effects of metoprolol?

A 
cough
 erectile dysfunction
 dry eye
 fatigue
 peripheral coldness
 constipation
171
Q

When is nifedipine contraindicated absolutely?

A

Malignant hypertension - in the acute Mx

as causes BP to drop too suddenly and can cause MI

172
Q

what is the pathophysiology of atherosclerosis?

A
  1. Through a variety of mechanisms there is endothelial damage (we are taking in arteries)
  2. this increases the permeability of cells
  3. LDL can now pass through the intimal layer triggering white blood cells to (monocytes) morph into macrophages
  4. the macrophages release free radicals which oxygenate the LDL
  5. oxygenated LDL further up regulates the white blood cell response causing more macrophages
  6. macrophages engulfed the oxidised LDL particles and form foam cells
  7. foam cells eventually die and propagate inflammation forming a fatty streak. the immune inflammatory response also causes smooth muscle proliferation and migration from the tunica media into the internal layer in response to cytokines
  8. smooth muscle cells form the plaques for breast capsule and endothelial layers then cover the plaque
  9. over time there is calcification of the plaque and crystallisation hardening the blood vessel
  10. now higher pressure and turbulent blood flow which passes onto the plaque damages the endothelium
  11. causing clots to form forming a thrombus which can detach and cause embolus.
173
Q

what causes peripheral vascular disease

A 
Atherosclerosis
 aortic co-arctation
 arterial embolism 
 venous thrombosis
 temporal arteritis
174
Q

What is peripheral vascular disease?

A

Peripheral vascular disease (PVD) is a slow and progressive circulation disorder.

Narrowing, blockage, or spasms in a blood vessel can cause PVD.

PVD may affect any blood vessel outside of the heart including the arteries, veins, or lymphatic vessels.

175
Q

What is the definition of claudication?

A

Inadequate blood flow during exercise causing fatigue discomfort or pain

trouble when walking
may have ulcers
muscular pain

176
Q

What is the definition of critical limb ischaemia?

A

Compromise of blood flow to the extremity causing limb pain at rest

pain is muscular
patients often having also gangrene and ulcers which do not heal
trouble when walking

177
Q

What is acute limb ischaemia ?

A 
A sudden disease in which limb perfusion is decreased that threatens limbic viability causing the six Ps
 pain
 paralysis
 paraesthesia
 pulseless nurse
 parlour
 perishing with cold
178
Q

What staging is used for peripheral vascular disease?

and what is each stage?

A

Fontaine staging

  1. asymptomatic
    2a. mild claudication
    2b. moderate to severe claudication
  2. ischaemia rest pain
  3. ulceration or gangrene
179
Q

What is the presentation of peripheral vascular disease?

A

Usually is asymptomatic

however may present with intermittent claudication symptoms

males may present with erectile dysfunction

symptoms are usually worse on one side and the other

180
Q

What are some red flags in peripheral vascular disease?

A

Pain in larger muscles of the upper leg (indicates narrowing of the femoral artery)

diminished pulses or absent pulses (indicating acute limb ischaemia)

+ paralysis, paraesthesia, pallor, and perishing with cold

181
Q

What is the first line test in peripheral vascular disease?

A

An ankle brachial index

or

toe brachial index

182
Q

Describe the test ankle brachial index?

what result would be significant?

A

The ratio of the blood pressure at the ankle compared to the arm whilst resting done using a Blood pressure monitor

and ABI= 0.90 is positive

183
Q

What follow-up tests might you want to do if a patient with peripheral vascular disease has an ABI of over 0.9?

A

A Doppler ultrasound

CT angiography or MR angiography

184
Q

What is a screening process for peripheral vascular disease?

A

An ABI will be done for anyone at risk
the criteria are:
- 65 or over
- 50 to 64 with risk factors or family history
- under 50 with diabetes mellitus and one other risk factor
- known atherosclerotic disease in another vessel bad

185
Q

What is the toe brachial index test and when is it used?

A

it is used when you suspect lower extremity PAD or

in patients with:
long-standing diabetes
or who are very elderly

due to the vessels in ankle not being compressible

186
Q

What is the management of acute ischaemic event in peripheral vascular disease?

A

Assess whether or not the limits viable

if the limb is still viable= endovascular revascularisation and intra-arterial thrombolysis or surgical revascularisation

if the limb isn’t viable than amputation is required

in both cases a follow-up of:

  • antiplatelet (aspirin or clopidogrel)
  • analgesia
  • anticoagulation (Heparin)
187
Q

what is the ongoing management of peripheral vascular disease?

A

If not life limiting = antiplatelet therapy

if life limiting = antiplatelet therapy plus Cilostazol or Naftidrofuryl, used to help vasodilate

188
Q

what is aortic dissection?

A

An intimal tear extending into the medial layer of the aortic wall

189
Q

What is the pathophysiology of aortic dissection?

A

The intimal tear extends into the medial layer of the aortic wall

blood then passes through the media causing damage

this causes the deception to propagate down words (or upwards) through the medial layer creating a false lumen

190
Q

What are the risk factors for aortic dissection?

A
  • Hypertension
  • atherosclerotic disease
  • aortic aneurysm
  • bicuspid aortic valve ( weakened aortic wall)
  • co-optation of the aorta ( long-standing hypertension)
  • marphans syndrome ( weakened aortic wall)
  • Ehlers danlos syndrome ( weakened aortic wall)
  • smoking
  • family history
191
Q

what is the presentation of aortic dissection?

A

Severe chest pain drugs were described as a ripping pain
acute onset
gradually extending pain
syncope

192
Q

What signs might you find on aortic dissection?

A

A different blood pressure and left and right arm
a weakened pulse
diastolic murmur ‘crescendo’
hypotension

193
Q

What is a first line investigation in aortic dissection?

A

CT angiography including abdomen and pelvis

194
Q

What investigations might you want to perform to exclude differential diagnosis of aortic dissection?

A

ECG - MI
cardiac enzymes
chest x-ray - pulmonary causes

195
Q

After performing a CT angiography in someone presenting with aortic dissection what other investigations would you want to do?

A

Type and cross for surgery
lactate levels indicating mild perfusion
full blood count to assess level haemorrhage

196
Q

What is the management of an aortic dissection?

A

ABCDE approach until confirmed

once confirmed I the beta-blocker blockade keeping the heart rate below 60 bpm (labetalol)

give opioids

if blockade isn’t enough give vasodilator’s (nitroprusside or 2nd line diltazapam)

surgery

197
Q

If you managed to treat an aortic dissection what is the ongoing management?

A

Managing hypertension using beta-blockers with or without ACE inhibitors

if both BB and ACEi not enough

then adding thiazide diuretics and/or calcium channel blockers

198
Q

What other causes of an aortic aneurysm?

A

Diminished arterial wall integrity

atherosclerosis

199
Q

What are the three types of AAA?

A
  1. Congenital
  2. infectious
  3. inflammation causing abnormal accumulation of macrophages and cytokines
200
Q

What are congenital conditions which predispose to AAA?

A

Marfan’s syndrome
bicuspid valves

have accelerated medial degeneration - diminished arterial wall integrity

201
Q

What is the most important risk factor in aortic aneurysm?

A

cigarette smoking

202
Q

What is the presentation of an abdominal aneurysm?

A

Some patients may feel a palpable pulsating abdominal mass

most patients are symptomatic and it is found on accident

203
Q

What is the first line test for abdominal aneurysm?

A

Abdominal ultrasound

204
Q

When does an abdominal aneurysm becomes symptomatic?

what are the symptoms?

A

When it has ruptured or it is very large

pain and ripping sensation
low blood pressure symptoms
and signs of shock

or chest pain, SOB, low bp etc

205
Q

What is the management of an asymptomatic aortic aneurysm?

A

If it is small=
surveillance and aggressive risk factor management

if it is large=
elective surgery with pre-op antibiotics and aspirin and ongoing hypertension management from diagnosis

206
Q

What is the management of a symptomatic aortic aneurysm?

A

If it is ruptured=
ABCD, intubation with bag and mask central venous catheter arterial catheter and urinary catheter withholding fluids giving a target systolic blood pressure of 50 to 70 using IV beta-blockers then surgery

if it hasn’t ruptured=
surgery as soon as possible was pre-and post low-dose aspirin hypertension management as well as antibiotic therapy

207
Q

what is shock?

A

Hypoperfusion on a cellular level or increased demand without adequate physical response.

hypo perfusion doesn’t allow for normal metabolic functions and triggers a systemic stress response

once the system is overwhelmed organ failure begins

208
Q

What is the pathophysiology of shock?

A
  1. There is inadequate perfusion causing cell hypoxaemia and an energy deficit
  2. this causes lactic acid accumulation and a falling pH from anaerobic metabolism and also causes more anaerobic metabolism
  3. a fall in pHcauses metabolic acidosis which causes laser construction resulting in peripheral pooling of blood
  4. there is sound membrane dysfunction causing a release of digestive enzymes from intracellular lysosomes causing an influx of potassium influx of sodium and water
  5. this causes toxic substances to enter the circulation damaging the capillary endothelium
  6. this results in destruction dysfunction and cell death of multiorgan system
209
Q

What are the different causes of shock?

A

Hypovolaemic

  • diarrhoea and vomiting
  • low albumin
  • haemorrhage

Cardiogenic

  • myocardial infarction
  • arrhythmias
  • substance misuse

Obstructive

  • tension pneumothorax (causes an increase in inrathoracic pressure with is harder to pump against)
  • cardiac tamponade (fills pericardium causing restriction on myocardium)

Anaphylactic
- causes vasodilation and an increase in leaky vessels causing decrease in albumin

Neurogenic
- disturbances of the sympathetic nervous system cause peripheral vasodilation

210
Q

What is the initial investigations of shock?

A 
ABCDE approach
ABG to check for acidosis
measure lactate
measure glucose
do a full blood count (Hb and WCC)
 blood cultures
 U+Es to check for renal hypo perfusion
 ECG

think Buffalo six

211
Q

What is Buffalo six?

A 
Blood cultures and septic screen - CXR, LP (inc. U+E)
 urine output - hourly
 fluid resuscitation
 Start empirical antibiotics
 measure lactate
 measure oxygen saturations
212
Q

What is the initial management of hypovolaemic shock?

A

Give lots of fluids consider blood products

give a vasopressor’s and no inotropes

213
Q

What is the initial management of septic or anaphylactic shock?

A

Give fluids and vasopressor’s consider giving inotropes

214
Q

What is the initial management of cardiogenic shock?

A

Consider giving fluids
do not give vasopressor’s
give I know troops

also consider giving loop diuretics and GTN

215
Q

What is an example of a vasopressor?

A

Adrenaline or noradrenaline

216
Q

What is an example of an inotrope?

A

digoxin

217
Q

what is an atrial septal defect

A

a congenital (usually ) small hole in the heart in the atrial septum causing a left-to-right shunt

218
Q

What types of atrial septal defect are there?

A 
by location:
- premium
- secundum
(less commonly)
- sinus venosis
- unroofed

by size:

  • small 3-6mm
  • med 6-12 mm
  • large 12 + mm
219
Q

What are risk factors for developing an atrial septal defect?

A

Being female

maternal alcohol use

220
Q

What is the presentation of an atrial septal defect?

A

Left-to-right shunt causes congestive heart failure failure to thrive arrhythmias and associated symptoms

usually they are asymptomatic

221
Q

What murmur is associated with an atrial septal defect?

A

Systolic ejection murmur

222
Q

What investigations are required to diagnose an atrial septal defect and what would they show?

A

Echocardiogram - showing defect
Doppler - showing blood flow
ECG may show tall P waves (RA enlargement) and large are waves (RV hypertrophy)
chest x-ray - may show cardiomegaly and increased pulmonary vascular margins

223
Q

What is the management of an atrial septal defect?

A

if asymptomatic or small it may close on its own

if the defect does not close on its own by 2 to 4 y+ surgery

+ profylactic antibiotics are given 1h - 6m after surgery (for IE)
amoxicillin or clindamycin

224
Q

What is a ventricular septal defect?

A

The most common congenital heart disease causing a hole in the heart in the ventricular septum

Causing a left-to-right shunt

225
Q

What are risk factors of developing ventricular septal defects?

A

Down syndrome and maternal alcohol use

rarely can occur 2 to 5 days post MRI or after penetrating trauma

226
Q

How are ventricular septal defects classified?

A

by size :

  • small: 3- mm
  • med: 3-6 mm
  • large: 6+ mm

and resulting pulmonary vascular resistance: systemic resistance

227
Q

How is pulmonary hypertension caused in ventricular septal defects in infants?

A

Pulmonary hypertension can be due to increased vascular resistance but in infancy it is mainly because of an increased blood flow to the lungs

228
Q

in which area of the heart are ventricular septal defects most common?

A

perimembrane

can also be septum or muscle

229
Q

What heart murmur is associated with ventricular septal defects?

A

pan systolic murmur that doesn’t worsen on inspiration Like in tricuspid regurgitation

230
Q

In ventricular septal defects is a large murmur better than quiet murmur?

A

No a loud murmur is good as it indicates a small defect

231
Q

What is the presentation of a ventricular septal defect

A

Usually asymptomatic

larger defects present with shortness of breath failure to thrive and recurrent chest infections

232
Q

What investigations are used in ventricular septal defect and what do they show?

A

An Echo and Doppler shows heart defect and blood flow(high velocity jet)

if symptomatic the following can be present:

CXR shows cardiomegaly and increased vascular markings

ECG may show changes depending on level of severity they are different:

  1. LV enlargement
  2. LV + LA enlargement
  3. bi ventricular enlargement
233
Q

what is management of a ventricular septal defect?

A

Small:
observation and antibiotic prophylaxis if undergoing any surgery

medium to large:
surgery at 3 to 6 months

large:
until there has been corrective closure medical therapy is also required to treat paediatric heart failure

234
Q

What is the medical management of paediatric heart failure?

A

frusemide
frusemide + captopril or enalapril
frusemide + captopril or enalapril + digoxin

+ a high calorie diet

235
Q

what is pericarditis?

A

inflammation of the pericardium

usually caused by viral infections

236
Q

What are the common viral causes of pericarditis?

A

Coxsackie virus
Echo virus 8
mumps
EBV

237
Q

What are bacterial causes of pericarditis?

A

Pneumococcus
meningococcus
Connie Caucus
chlamydia

238
Q

What non-infectious causes are there of pericarditis?

A 
SLE
rheumatoid arthritis
sclerosis
IBD
radiotherapy
cardiac surgery
1 – 3 days after NI
239
Q

What nerve innervates the pericardium?

A

Phrenic nerve

240
Q

What are symptoms of pericarditis?

A

Pleuritic chest pain
fever – indicating effective cause
myalgia

241
Q

On examination what sign may you find in pericarditis?

A

A high pitched squeaky sound heard at the left external edge this is pericardial rub

242
Q

When might pericarditis cause right-sided heart failure?

A

Constrictive pericarditis

243
Q

What investigations are required in pericarditis?

A

Any chest pain will require an ECG
pericardial fluid culture and blood culture will find infective causes
check your rear for renal failure which can cause pericarditis
chest x-ray/ echo
bloods for inflammatory markers

244
Q

What signs would you find on an ECG In pericarditis?

A

ST elevation and PR depression

245
Q

What might an x-ray or echo show in pericarditis?

A

Pericardial effusion showing a water bottle -shaped cardiac silhouette

246
Q

What is the management of pericardial effusion?

A

for any cause gives NSAIDs PPI and exercise restriction
and 3 months colchicine

second line is the addition of corticosteroids unless it is a bacterial cause in which case do a pericardectomy

plus:

pericardioscentesis is required if:
symptomatic with purulent effusion and cardiac tapenade

systemic antibiotics required for infective cause

247
Q

When would you admit hospital a patient with pericarditis?

A 
A fever over 38°
insidious or subacute onset
large pericardial effusion
cardiac tamponade
failure to respond to 7 days of NSAIDs
consider admitting if they have one of the minor factors:
pericarditis with myocarditis
immunosuppressed
traumatic cause
oral anticoagulant therapy
248
Q

What is the possible underlying mechanism for hypertension?

A

Disturbances of auto regulation reflects causing there to be a persistent increase in vascular resistance

access sodium intake

renal sodium retention

disregulated RAAS

increased sympathetic Drive

increased peripheral resistance

Endothelial dysfunction

hyperinsulinaemia

Cell membrane transporter dysfunction

249
Q

what is the presentation of hypertension?

A

It is usually asymptomatic but will have some symptoms in more advanced cases:

headaches 
visual changes 
disnopea (congestive heart failure) 
chest pain 
sensory or motor deficit (from cerebrovascular disease)
250
Q

What are the risk factors for hypertension?

A 
Obesity
sedentary lifestyle
alcohol use
metabolic syndromes
black ancestry
over 60 years old
family history
sleep apnoea
251
Q

What investigations are required in hypertension?

A

Blood pressure cuff

  • ECG
  • fasting metabolic panel with EGFR (check renal damage and associated metabolic abnormalities)
  • lipid profile and urinalysis (proteinuria and increased albumin suggests and organ damage)
  • full blood count (anaemia is suggestive of a secondary causal complication)
  • TSH
252
Q

What is the management of hypertension in an adult who is under 55 years old or has Type II diabetes?

A
  1. ACE inhibitor (ARB if ACEi is CI)
  2. add CCB or thiazide like diuretic
  3. ACE inhibitor + CCB+ thiazide like diuretic

… if resistant

+ Spironolactone or beta-blocker and consult specialist

253
Q

management of hypertension in adults who is over 55yrs of black ancestry?

A
  1. CCB
  2. add ACEi or ARB or thiazide like diuretic
  3. ACE inhibitor + CCB+ thiazide like diuretic

… if resistant

+ Spironolactone or beta-blocker and consult specialist

254
Q

what are the ranges of blood pressure for:

  1. low blood pressure
  2. normal blood pressure
  3. pre-hypertension
  4. high blood pressure
  5. hypertension stage I
  6. high blood pressure hypertension stage II
  7. high blood pressure crisis
A
  1. <90
  2. 90-120
  3. 120-139
  4. 140-159
  5. 160 <
  6. 180 <
255
Q

When do you need to measure both the standing and sitting blood pressure?

A

In anyone with :

type II diabetes
symptomatic of postural hypotension
anyone aged over 80

256
Q

What is the target blood pressure?

A

Ideally as close to normal as possible aim for under 140/90 unless they are over 80 or particularly frail in which case aims for 150/90

257
Q

what are examples of ACE inhibitors?

A

Lisinopril
enalapril
captopril

258
Q

What are side effects of ACE inhibitors?

A 
Cough
headache
dizziness and hypotension and drowsiness
rash
angioedema
259
Q

What are examples of angiotensin two receptor antagonists A.k.a. ARB’s

A

candesartan
irbesartran
losartan

260
Q

What are side effects of ARB’s?

A 
Abdominal pain
back pain
diarrhoea
hypotension
hyperkalaemia
renal impairment
261
Q

What are some examples of a calcium channel blocker?

A

Amlodipine
filodipine
nifedipine

262
Q

What are side effects of calcium channel blockers?

A 
Muscle cramps
peripheral oedema
palpitations
flashing
abdominal pain
rash
263
Q

When is nifedipine absolutely contraindicated?

A

In the management of malignant hypertension in an acute case it causes BP to drop to suddenly and can cause myocardial ischaemia so another calcium channel blocker or other antihypertensive should be used

264
Q

What are examples of thiazide like diuretics?

A

I hydrochloride
indapamide
clorthiadone

265
Q

what are side effects ofThiazide like diuretics?

A 
alkalosis - low Cl-
diarrhoea
hyperuricaemia
nausea
postural hypotension
266
Q

what are some examples of beta-blockers used for cardiac purposes?

A

metoprolol
bisopralol
cardevilol

267
Q

What are side effects of beta-blockers?

A 
Cost
erectile dysfunction
dry eye
fatigue
peripheral coldness
vascular disease
constipation
268
Q

Describe the stages of atherosclerosis?

A
  1. endothelial damage
  2. LDL moves into inntima and oxidises
  3. macrophages engulf oxygenated LDL

foam cells formed

  1. foam cells die and propagate inflammation
  2. process unregulated

fatty streak is formed

  1. smooth muscle cells form plaques fibrous capsule
  2. calcification and crystallisation occurs
269
Q

What are the causes of peripheral vascular disease?

A 
Atherosclerosis
aortic co-arctation
arterial embolism 
thrombosis
temporal arteritis
Buegers disease
270
Q

What are symptoms of claudication?

A

Fatigue discomfort or pain in the affected limb due to inadequate blood flow during exercise

271
Q

What are symptoms of critical limb ischaemia?

A

Limb pain at rest predisposition to ulcers or gangrene due to a compromise blood flow to extremities

272
Q

What is acute limb ischaemia?

A

A sudden decrease in limb perfusion that threatens limb viability

273
Q

what are symptoms of acute limb ischaemia?

A

The six p’s

 pain
paralysis
paraesthesia
pulse listeners
pallor
perishing with cold
274
Q

what are risk factors for peripheral vascular disease?

A

Smoking
diabetes
hyperlipidaemia
cardiovascular history - family or personal
cerebrovascular history - family or personal

275
Q

If patients with peripheral vascular disease also get pain in the larger muscles of the upper leg what does this indicate?

A

Narrowing of the deep femoral artery

276
Q

True or false

patients with peripheral vascular disease may have erectile dysfunction?

A

true

277
Q

True or false

peripheral vascular disease is commonly worse in one leg

A

true

278
Q

What is crucial you do during your initial examination of a patient with peripheral vascular disease

A

Check all limb pulses

279
Q

What is the first line investigation of peripheral vascular disease?

A

And ankle brachial index

280
Q

What ABI result is positive for peripheral vascular disease?

A

less/ or equal to 0.9

281
Q

A patient presents with symptoms of intermittent claudication that ABI comes back positive what next investigations could you perform?

A
  1. doppler US
  2. CT angio
  3. MR angio
282
Q

Who is eligible for screening for peripheral vascular disease?

A
  • Anyone over/ or the age of 65
  • 50 to 64-year-olds with risk factors or a family history
  • anyone younger than 50 with diabetes mellitus and one other risk factor
  • anyone with known atherosclerotic disease in another vascular bed
283
Q

What is the acute management of an acute ischaemic event in peripheral vascular disease?

A
  1. check limb viability
  2. if it is viable:
    endovascular revascularisation + intra arterial thrombolysis OR surgical apprach
  3. if it isn’t viable:
    amputation
  4. antiplatelets (clopidogrel or aspirin), analgesia, anticoagulation (heparin)
284
Q

What is the ongoing management of claudication that is not lifestyle limiting?

A

antiplatelet therapy - Clopidogrel

285
Q

What is the ongoing management of claudication that is lifestyle limiting?

A

Antiplatelet therapy – clopidogrel, symptom relief using cilosazol or naftidrofuryl +/- revasc

286
Q

what is the ongoing management of chronic severe limb ischaemia?

A

Assessor revascularisation and give antiplatelet

some patients may benefit from spinal-cord stimulation or autologous bone marrow stem cell transplantation

287
Q

What is aortic dissection?

A

And into multi extending to the medial layer of the aortic wall so the blood passes through the media due to degeneration caused by the blood pressure it’s essentially a false lumen

288
Q

What are risk factors for aortic dissection?

A 
Hypertension
atherosclerotic aortic aneurysm
bicuspid aortic valve
co-optation of the aorta
Marfan's syndrome
Ehlers danlos syndrome
smoking
family history
289
Q

what is the common presentation of aortic dissection?

A

An acute and severe chest pain that feels like ripping
different blood pressure in the left and right arm
pulse deficits or a weakened pulse
syncope and hypertension

290
Q

What are the investigations you should do for suspected aortic dissection?

A

CT angiogram ASAP
ECG can be used to exclude other myocardial causes such as MRI

chest x-ray can be used to exclude pulmonary causes but may show a widened mediastinum

FBC, Lactate (malperfusion)
type and cross for surgery

291
Q

what is your initial management for aortic dissection?

A

ABCD E – very important to give fluids noradrenaline and O2 until confirmed

once confirmed given IV beta-blocker blockade to get heart rate less than 60 bpm (labetalol or metoprolol)
opioids

if blockade is insufficient vasodilator (nitroprusside or 2ry dilaiazam)

surgery is required

292
Q

What is the ongoing management for aortic dissection?

A

Manage hypertension using metoprolol +/- enalapril

+/- beta-blocker and ace inhibitor

+/- thiazide like diuretic +/- calcium channel blocker

293
Q

What are the three types of AAA?

A
  1. Congenital: Marfan’s and bicuspid valves
  2. infectious: staphylococcus and salmonella
  3. inflammatory: abnormal accumulation of macrophages and cytokines
294
Q

Risk factors of aortic aneurysms?

A

Cigarette smoking (most important)
family history
increased age
congenital disorders such as Marfan’s syndrome

295
Q

What is the presentation of an abdominal aortic aneurysm?

A

A palpable pulsating abdominal mass but patients are usually asymptomatic and the aneurysm is found by accident

296
Q

What is the diagnostic investigation of an aortic abdominal aneurysm?

A

Ultrasound scan

297
Q

How would you manage an asymptomatic aortic abdominal aneurysm?

A

small:
surveillance and aggressive risk factor management

med/large:
elective surgery with pre-aspirin and hypertension management

298
Q

How would you manage a symptomatic aortic abdominal aneurysm?

A

Has it ruptured?

 yes:
intubation
 central venous catheter arterial catheter urinary catheter
withholding spirits
target systolic BP is 50 to 70

surgery

no:
surgery as soon as possible

299
Q

what is the definition of shock?

A

Inadequate oxygenation of organs to meet metabolic demand causing organ damage and failure

300
Q

Describe the pathophysiology of shock?

A

inadequate perfusion causes cell hypoxaemia and an energy deficit

this causes lactic acid to accumulate and the pH to fall causing metabolic acidosis
- metabolic acidosis triggers vasoconstriction leading to the peripheral pooling of blood

cell membrane disfunction occurs causing:
sodium pump disfunction - efflux of potassium, influx of sodium and water
and digestive lysosome release

capillary endothelium is damaged

organ disfunction

301
Q

how can you classify the causes of inadequate perfusion in shock?

A

fluids
cariogenic
distributive/ neurogenic
obstructive

302
Q

What are fluid causes of shock?

A

Haemorrhage
low albumin
Burns
diabetic ketoacidosis

303
Q

What are the distributive/ neurogenic causes of shock?

A

Failure of vasoregulation causing hypo perfusion
sepsis
anaphylactic
brainstem or spinal injury

304
Q

What cardiogenic causes of shock?

A

Heart failure
MI
arrhythmias
toxic substances
rapid access rise in blood pressure
nonadherence insult fluid balance or medication
infection (infective endocarditis pneumonia sepsis)
acute mechanical causes such as myocardial rupture and chest trauma

305
Q

What important investigations are needed in sepsis?

A

ABG – check for acidosis
lactate – indicates hypoperfusion and pre-terminal events
glucose - is this because of hypoglycaemia such as DKA
FBC - check for blood loss and check for infection markers
U+E – is a matter of hypo perfusion
coagulation studies – coagulopathy is associated with mortality
blood cultures and swabs as well as a chest x-ray may be needed

306
Q

Describe the first line management of sepsis?

A

is an ABCDE approach

A) Support their way and intubate if necessary (if GCS is less than eight)

B) aim for 94 to 98% oxygen or 88 to 92% oxygen if they are entitled to respiratory failure do not over oxygenate this increases mortality

C) give circulatory support

D) check their GCS

E) check body temperature and either warm or cool as appropriate

307
Q

What are indications for invasive ventilation in sepsis/ any ABCDE approach?

between CPAP and BiPAP which is better?

A 
Pneumothorax
confusion and agitation
severe hypoxaemia
recent facial or upper respiratory trauma
vomiting
copious respiratory secretions

give CPAP ideally

308
Q

In hypovolaemic shock what circulatory support is appropriate?

A

Lots of fluids IV

some vasopressors may be useful (adrenaline)

309
Q

In septic or anaphylactic shock what circulatory support is appropriate?

A

Give fluids and vasopressor’s consider inotropes (digoxin)

310
Q

In cardiogenic shock what circulatory support is appropriate?

A

Consider fluids and give inotropes

311
Q

What is the most common arrhythmia?

A

Atrial fibrillation

312
Q

What are the causes of atrial fibrillation?

A 
Pulmonary embolism
ischaemia
respiratory disease
atrial enlargement
thyroid disease
ethanol
sleep
ageing
313
Q

What other characteristic ECG findings of atrial fibrillation?

A

Absence of P waves with irregularly irregular beats and very narrow QRS complexes

314
Q

How would you class atrial fibrillation?

A

Based on duration:

first episode
recurrent ? (more than two episodes)
paroxysmal ? (less than seven days)
persistent (more than seven days)
long-standing persistent (more than one year)
permanent (more than one year with unsuccessful rhythm control or not attempted because to elderly)

315
Q

What risk is associated with atrial fibrillation how do you measure this risk?

A

thromboembolism

assess anticoagulation need using CHADS-VAC

316
Q

How do you manage atrial fibrillation?

A

Rate or rhythm control to try and get back into sinus rhythm
drugs ie amiodarone
DC cardioversion
ablation therapy

317
Q

What is atrial flutter?

A

The regular narrow complex tachycardia caused by a re-entry circuit

318
Q

What of the classic easy defining of atrial flutter?

A

sawtooth flutter P waves at around 300 bpm

319
Q

what characteristic ECG findings are therefore 1st° heart block?

A

Fixed prolonged PR interval greater than 200 ms

320
Q

What is the alternative name for 2nd° heart block type I?

A

Mobitz type 1 - wechneback phenomenon

321
Q

What is the classic ECG findings 2nd° heart block for type I?

A

Progressively prolonged PR interval until the atrial impulse is not conducted and the QRS complex is dropped

322
Q

What is the classic ECG findings 2nd° heart block for type II?

A

Consistent PR interval duration with intermittently dropped QRS complexes usually in a repeating cycle such as 2:1, 3:1

323
Q

what is the classic ECG finding For third-degree heart block?

A

Completely disorganised P waves and QRS complexes

324
Q

What is third-degree heart block?

A

Complete failure of the conduction system between the atria and ventricles

325
Q

How do you manage atrial flutter?

A

Rate control using the jocks in beta-blockers and calcium channel blockers
rhythm control using DC cardio version and ablation

+ anticoagulants if needed

326
Q

what are premature atrial complexes?

A

Extra beats originating from the SAN

327
Q

What are premature junctional complexes?

A

Extra beats occurring from the AV node causing a negative P wave on ECG

328
Q

what is paroxysmal supra ventricular tachycardia?

A

Caused by separate re-entry circuits which cause a sudden onset which is initiated by premature beat and which stop abruptly but may re-occur

329
Q

What are the two types of paroxysmal supra ventricular tachycardia?

A

AV nodal re-entry tachycardia

Atrioventricular re-entry tachycardia

330
Q

How can you manage a AVNRT?

A

Vagal manoeuvres and AB blocking drugs (beta-blockers, ccb)

331
Q

what is an example of AVRT?

A

Wolff Parkinson White syndrome

332
Q

What is a characteristic finding of a Wolff Parkinson White syndrome on ECG?

A

Delta wave

irregular rythma

short pr <120ms

slurring of QRS complex prolonging to >100ms

333
Q

what is the risk of Wolff Parkinson White syndrome?

A

ventricular fibrillation

The rapid accessory pathway can often bypass AV node causing the heart rate to reach 200 bpm

334
Q

What are junctional escape beats?

A

When the AV node becomes a backup pacemaker (40-60bpm) if the heart rate is slow enough or the essay and fails

335
Q

What is an accelerated junctional rhythm?

A

when the AVN fires at 60 to 99 bpmOccurring when there is ischaemic inflammation drugs and some electrolyte disturbances

336
Q

What is non-paroxysmal junctional tachy arrhythmia?

A

an accelerated junctional cardio

337
Q

What are premature ventricular complexes?

A

Commonest ventricular arrhythmia caused by ectopic pulses from the ventricular myocardium

338
Q

who typically has premature ventricular complexes?

A

healthy individuals but can indicate an underlying heart sees they are also associated with amlodipine antidepressants the jocks in and recreational drugs

339
Q

What is aberrant ventricular conduction?

A

The temporary alteration of the QRS complex under normal conditions

340
Q

what are ventricular or Ido-ventricular benign sustained arrhythmias?

A

Occurs when the lower pacemaker takes over

usually caused by third-degree AV block or drug induced AV block

can be caused by sinus arrest Sino atrial node block or hyperkalaemia

341
Q

What drugs can cause AV block?

A

Beta-blockers
calcium channel blockers
digoxin

342
Q

What are pan systolic benign sustained arrhythmias?

A

Occur when an ectopic focus fires independently from the basic rhythm causing a parallel beat and are usually caused by coronary artery disease

343
Q

What are the characteristic ECG findings of ventricular tachycardia?

A

A regular broad QRS complex with a rate over 100 bpm occurring with more/equal to 3pcvs

344
Q

What other three types of morphologic classification of ventricular tachycardia?

A

monomorphic
polymorphic
v rare = torsade de pointes

345
Q

What typically causes ventricular tachycardia ?

A

A re-entry circuit
underlying heart disease
electrolyte disturbances - mainly potassium
drug toxicity with TCA or antiarrhythmic’s

346
Q

What is the management of ventricular tachycardia?

A

The patient is often haemodynamically unstable after ABCD they require urgent treatment by DC cardioversion definitive treatment is ablation

347
Q

what underlying Heart conditions can cause ventricular tachycardia?

A

Long QT syndrome is
regardless in Rome
hypertrophic cardiomyopathy or die related cardiomyopathy
coronary artery disease

348
Q

What is ventricular fibrillation?

A

Disorganised and chaotic heart with them but there is ineffective action of ventricles and can cause cardiac arrest it is usually fatal if not treated

349
Q

what is a precursor to ventricular fibrillation?

A

Ventricular tachycardia

350
Q

what are the characteristic findings of ventricular fibrillation?

A

Chaotic irregular deflections of varying amplitude.

No identifiable P waves, QRS complexes, or T waves.

Rate 150 to 500 per minute.

351
Q

What is the management of ventricular fibrillation?

A

Immediate CPR and different relation ideally biphasic

FINALS (24 decks)

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