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Cardiovascular clinical Flashcards

1
Q

What is transient loss of consciousness defined as?

A

A state of real or apparent loss of consciousness with loss of awareness,characterised by amnesia for the period of unconsciousness,loss of motor control,loss of responsiveness, and a short duration.

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2
Q

What are the causes of TLOC?

A
  1. Head trauma
  2. syncope
  3. Epileptic seizures
  4. TLOC mimics e.g. psychogenic, pseudo-syncope.
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3
Q

Define what syncope is.

A

Transient loss of consciousness due to cerebral hypoperfusion, characterised by rapid onset,short duration, and spontaneous complete recovery.

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4
Q

What are the three categories of syncope?

A
  1. Reflex
  2. Orthostatic
  3. Cardiac
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5
Q

What is reflex syncope

A

Neural reflexes Causes cardioinhibition through vagal stimulation.

This causes bradycardia and a decrease in CO

Depression of sympathetic activity to blood bessels cause vasodepression.

This causes vasodilation (decrease in SVR, CO, SV and eventually MAP)

This leads to systemic hypotension causing a transient period of cerebral hypoperfusion

results in syncope

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6
Q

What are the three subtypes of reflex syncope?

A
  1. Vasovagal syncope ( most common type for all syncope)
  2. situational syncope
  3. Cartoid sinus syncope.
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7
Q

How is faint activated in Vasovagal reflex syncope?

A
  1. Emotional distress

2. orthostatic stress

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8
Q

What is vasovagal reflex syncope associated with?

ii. Give examples of this.

A

Typical prodrome.

ii. Pallor
Sweating
Nausea

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9
Q

How can Vasovagal reflex syncope be averted?

A
  1. Adopting the horizontal gravity neutralisation position (lying down)
  2. crossing legs.

this increases venous return

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10
Q

VVS is associated with increased mortality true or false?

A

false

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11
Q

How do you treat VVS?

A
  1. Education
  2. reassurance
  3. avoidance triggers
  4. adequate hydration
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12
Q

How does fainting occur from a situational reflex syncope?

A
  1. cough
  2. Micturition- action of urinating
  3. swallowing
    i. e a specific trigger.
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13
Q

How do you treat SRS?

A

Treat the cause, if possible (e.g. cough)

Advise patient to lie down, if possible (e.g. during a coughing episode)

Avoid dehydration and excessive alcohol

Cardiac permanent pacing may be needed in some cases of situational syncope

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14
Q

What are the risk factors of Carotid sinus reflex syncope?

ii. how do you treat CSS?

A
  1. mechanical manipulation of the neck
  2. shaving
  3. tight collar
  4. Elderly males
  5. carotid artery atherosclerosis
  6. Injury to head or neck
  7. radiation
    ii. Cardiac permanent pacing
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15
Q

How does Postural (orthostatic) hypotension occur?

A

failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

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16
Q

What are the risk factors to orthostatic hypotension?

A 
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
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17
Q

What is a positive result for orthostatic hypotension?

ii. What needs to occur?

A

When there is a drop in:

  1. systolic pressure by 20 mmHg (with or without symptoms).
  2. diastolic blood pressure of at least 10 mm Hg (with symptoms)
    ii. A positive result is indicated by a drop, within 3 minutes of standing from lying down
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18
Q

What are the symptoms of orthostatic hypotension?

A 
Symptoms may include those of cerebral hypoperfusion
 such as: 
1. lightheadedness 
2. dizziness, 
3. blurred vision,
 4.faintness
5. falls
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19
Q

What the causes for cardiac syncope?

A
  1. Arrhythmias
  2. acute myocardial infarction
  3. structural cardiac disease e.g. aortic stenosis
  4. PE
  5. Aortic dissection

all lead to sudden drop in CO

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20
Q

What are the main factors which suggest cardiac syncope and not other forms of reflex syncope?

A
  1. Syncope during excretion or when supine
  2. structural cardiac abnormality or coronary heart disease is present
  3. A family history of sudden death at young age
  4. Sudden onset palpitations immediacy followed by syncope

Findings on ECG suggestive of arrhythmic syncope

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21
Q

What are the risk factors of atheroma?

A
  1. cigarette smoking
  2. hypertension
  3. Hyperlipidemia
  4. diabetes
  5. Age (elderly)
  6. gender (males)
  7. Genetics
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22
Q

How does the process of atherosclerosis occur?

A
  1. Primary endothelial injury
    (e. g. smoking, hypertension, hyperlipidemia)
  2. accumulation of lipids and macrophages
  3. Migration of smooth muscle cells
  4. increase in size
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23
Q

when is atherosclerosis likely to cause a critical disease?

A

It is the only artery supplying an organ or tissue (i.e. There is no collateral circulation)

The artery diameter is small (e.g coronary artery versus common iliac artery)

Overall blood flow is reduced (i.e. cardiac failure)

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24
Q

What can atherosclerosis cause?

A
  1. Stenosis
  2. Thrombosis
  3. Aneurysm
  4. Dissection
  5. Embolism
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25
Q

What are the characteristics of arterial stenosis?

A

NARROWING OF THE ARTERIAL LUMEN

REDUCED ELASTICITY

REDUCED FLOW IN SYSTOLE

TISSUE ISCHAEMIA

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26
Q

What the clinical effects of cardiac ischemia?

A

REDUCED EXERCISE TOLERANCE

ANGINA

UNSTABLE ANGINA

MYOCARDIAL INFARCTION

CARDIAC FAILURE

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27
Q

What are the clinical effect of cardiac fibrosis?

A

LOSS OF CARDIAC MYOCYTES

REPLACEMENT BY FIBROUS TISSUE

LOSS OF CONTRACTILITY

REDUCED ELASTICITY & FILLING

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28
Q

What are the clinical effects of thrombosis?

A

MYOCARDIAL INFARCTION

CEREBRAL INFARCTION

RENAL INFARCTION

INTESTINAL INFARCTION

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29
Q

Clinical examples of lipid related issues?

A
  1. Xanthomata - deposition of yellowish cholesterol-rich material that can appear anywhere in the body in various disease state
  2. Xanthelasma - yellow deposits of plaque on upper eye lids
  3. Corneal arcus - epositing of phospholipid and cholesterol in the peripheral cornea in patients over the age of 60 which appears as a hazy white, grey, or blue opaque ring
  4. milky blood /serum- Turbid, cloudy or milky serum (lipemic serum) may be produced by the presence of fatty substances (lipids) in the blood
  5. Coronary heart disease.
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30
Q

What lipid related values do we measure?

A
  1. Total cholesterol
  2. HDL cholesterol
  3. Triglycerides if requested - this is effective by prandial status
  4. LDL cholseterol if requested
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31
Q

What is the average value of LDL cholesterol in relation to total cholesterol?

A

LDL is normally 2 mmol ml lower then total cholesterol

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32
Q

What should be the value for Total Cholesterol HDL ratio?

A

If value is lower than 4.5 than good

if higher than 5 than needs to be treated.

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33
Q

Describe the types of studies used to treat diseases.

A

Case-control study: two different groups differing in outcome are identified and compared on their causal attribute

cohort study - Follows a group of people over time

randomised clinical trial- experiment in which trial participants are randomly allocated treatment

systematic review

meta-analysis

Expert opinion.

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34
Q

What is the role of statins?

A
  1. Lowers cholesterol

2. slows down atherosclerosis process

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35
Q

What is the normal BMI range?

A

18-24 kg/m2

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36
Q

What would be the BMI an overweight person.

A

Range of 25-30 kg/m2

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37
Q

What would be the BMI of an obese person?

A

30 kg/m2 or higher

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38
Q

Give examples of statins

A 
atorvastatin 
fluvastatin 
lovastatin 
pravastatin 
simvastatin 
rosuvastatin - more efficient than atorvastatin and simvastatin
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39
Q

what is familial hypercholesterolemia

ii. what should you look at?

A
  1. As common as type 1 diabetes

It causes LDL cholesterol level to be very high

ii. Ankles and knuckles

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40
Q

what is familial hypercholesterolemia

ii. what are the symptoms

A
  1. As common as type 1 diabetes

It causes LDL cholesterol level to be very high

ii. 
chest pain with activity
xanthomas 
xanthelasmas
 corneal arcus
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41
Q

Define what hypertension is.

ii. What is its clinical blood pressure?

A

A disorder in which the level of sustained arterial pressure is higher than expected for the age,sex,and race of the individual.

ii. 140/90 mm Hg or higher

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42
Q

How can you classify hypertension?

A

In regards to cause - primary/essential (unknown cause) and secondary (known)

In regards to consequence - benign and malignant( acute severe).

white-coat hypertension - elevated clinical pressure but normal ABPM( <135/85)

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43
Q

What occurs in malignant hypertension?

ii. what can it cause?

A

Severe hypertension

Bilateral retinal haemorrhages and exudates

papilloedema (may not be present)

ii. AKI

heart failure

encephalopathy

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44
Q

What are the characterstics of primary hypertension?

A 
No obvious cause
Genetic factors (twin studies)
Salt intake -25% salt sensitive
Protein intake  
Renin - Angiotensin system
Sympathetic activity  (as BP = TPR x CO)
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45
Q

What underlying diseases could be the cause for secondary hypertension?

A

Renal disease (any renal disease) - reduced renal blood flow causes excess renin release and salt and water overload

Endocrine disease

Aortic disease

Renal artery stenosis

Drug therapy (cortizol steroids have an increase in BP)

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46
Q

What can benign hypetenson cause?

A

Serious life threatening morbidity.

eventually leading to :
Left ventricular hypertrophy Congestive cardiac failure Increases atheroma Increases aneurysm rupture - aortic dissection, Berry aneurysms
Renal disease

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47
Q

What can left ventricular hypertrophy cause?

A 
INCREASED LV LOAD
POOR PERFUSION 
INTERSTITIAL FIBROSIS
MICRO-INFARCTS
DIASTOLIC DYSFUNCTION

sudden cardiac death!

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48
Q

The greater the diastolic pressure in benign hypertension the greater the risk of ?

A

Strokes and Myocardial infarction

Every 10mmHg of diastolic pressure above 85 doubles risk of MI

Every 8mmHg of diastolic pressure above 85 doubles risk of stroke

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49
Q

What is the diastolic pressure of malignant hypertension?

A

> 130-140 mm Hg

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50
Q

What are the symptoms of malignant hypertension?

A

Causes cerebral oedema - seen as papilloedema (swelling of optic disc)

Acute renal failure

Acute heart failure

Headache and cerebral haemorrhage

Blood vessels show fibrinoid necrosis and endarteritis proliferans of their walls

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51
Q

What is pregancy associated hypertension known as?

ii. what are its symptoms?
iii. What are its causes?

A

Pre- eclampsia

ii. Increased maternal and fetal morbidity and mortality

Hypertension secondary to silent renal or systemic disease

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52
Q

Describe what Stage 1 hypertension is.

A

When clinical BP is higher or 140/90 mmHg

and at home BP is 135/85 mmHg

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53
Q

Describe what stage 2 hypertension is

A

Clinical blood pressure is 160/100 mmHg or higher

When resting BP is 150/95 mmHg or higher.

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54
Q

Describe what severe hypertension is.

A

when clinical Blood pressure 180/110 mmHg or higher.

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55
Q

Describe the effect of hypertension on elastic arteries.

ii. What does this have on the peripheral vascular resistance?

A

Internal lamina thickening, smooth muscle,hypertrophy and fibrosis.

Therefore lumen narrows and decreases endothelial function causing a decrease in compliance.

ii. Increases it thereby again increasing blood pressure

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56
Q

Describe the effect of hypertension on smaller arteries.

A

Hyaline sclerosis occurs narrowing the lumen.

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57
Q

Atherosclerosis is accelerated under hypertension true or false?

A

true

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58
Q

What are the risk factors which lead to an increase in atheroma?

A

Hypercholesterolaemia

diabetes

smoking

impaired glucose tolerance

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59
Q

What happens with decreased vascular compliance which is secondary to atherosclerosis?

A

Makes systolic Blood pressure become disproportionately greater than diastolic.

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60
Q

Give examples of cerebal complications caused by hypertension.

A

Transient ischemic attack

Cerebal infarction

Intracerebal haemorrhage- caused by extravasation (leakage of fluid from its vessel) of blood from micro aneurysms along walls of small intracerebral arterioles.

subarachnoid haemorrhage - due to degeneration of internal elastic membrane at apex of bifurcation which itself is caused
by haemodynamic stress.

Dementia

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61
Q

Carotid artery bifurcation is particularly vulnerable to atherosclerosis true or false?

A

true

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62
Q

What is the carotid bifurcation?

A

Where the common carotid artery terminates and where the external and internal carotid artery form.

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63
Q

What aortic related issues does hypertension cause?

A

aortic aneurysm - a sac like dilation of weakened aortic wall

aortic dissection- where blood enters the wall of aorta through a small tear in the tunica intima. Creates a large amount of stress causing two layers which compromises blood flow.

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64
Q

where is the main effect of hypertension on the kidneys?

A

Renal arteries and glomeruli.

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65
Q

How do you diagnose Hypertension?

A

Confirm diagnosis: ABPM or home BP monitoring and also clinic BP. ABPM preferred over HOME BPM

just go straight to management if clinical BPM >180/110

Look for end organ damage:

  1. Urine analysis -Proteinuria and microalbumuria.
  2. ECG or ECHO for LVH
  3. Fundoscopy

Pregnancy - dip stick

Bloods: FBC , U&E, glucose and cholesterol

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66
Q

What are the causes for peripheral arterial occlusive disease?

A
  1. Atherosclerotic or inflammatory process causing stenosis.

2. Thrombus formation.

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67
Q

What is accelerated (malignant) hypertension?

ii. what ethnic group is it most common in?

A

Refers to accelerated microvascular damage. small arteries and arterioles show fibrinoid necrosis.

ii. afrocaribbean

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68
Q

What are the risk factors of hypertension?

A

Race - Afrocaribbean more likely

Gender - greater in men

Age- if you old uh oh

Enviroment

Obesity

Diabetes

Too much salt in diet

Stress

Abnormalities in nervous,circulatory and renal systems

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69
Q

What are the risk factors of CVD?

A

Age

positive family history

Smoking

diabetes

Male

Afrocaribbean

Hypercholesterolaemia

obesity

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70
Q

What are the signs and symptoms of Hypertension?

A

Mainly asymptomatic - except for malignant hypertentsion

Signs:

renal damage

Radiofemoral delay

weak femoral pulses

renal bruits

cushings syndrome

End-organ damage: LVH , retinopathy and proteinuria

for malignant hypertension:

headaches and visual disturbances

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71
Q

Why when taking blood pressure should the arm be elevated to heart level?

A

If arm is below then there is an overestimate of systolic and diastolic values

while vice versa if arm is raised.

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72
Q

If the fourth kortikoff sound is heard what might this suggest?

A

Left ventricular stress- caused by hypertension

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73
Q

what Might carotid bruits suggest?

A

Indicator of secondary hypertension and organ damage.

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74
Q

What does hypertension cause in the eyes?

A

hypertensive retinopathy - retinal vascular damage. If untreated has high mortality rate.

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75
Q

What are the three types of hypertensive retinopathy?

A

Mild- Generalised arteriolar narrowing and silver wall wiring (arteriolar wall opacity)

Moderate- retinal haemorrhage (dots,blots or flamed shaped)

accerlerated- visual loss

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76
Q

What are the gradings for hypertensive retinopathy?

A

Grade 1- arteriolar narrowing

Grade 2- Increased generalised narrowing

Grade 3- haemorrhages

Grade 4- papilledema

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77
Q

What are the two types retinal vein thrombosis?

A

central vein occlusion

branch vein occlusion

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78
Q

No salt added diet leads to blood pressure dropping below 2-4 mm Hg true or false?

A

true

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79
Q

How do you manage hypertension

A

Treat underlying causes: stop smoking and drinking. Reduce salt intake

Drugs:

A: ACE inhibitor (lisinopril) or ARB (candesartan) if ACE not tolerated

C: calcium channel blocker e.g. nifedipine

D: Thiazide diuretic

Step 1: ACE/ARB if <55year or give C or D if >55/black

Step 2 A+ C or A+D

Step 3 A+C +D

All start at stage 2 or above only stage 1 if:

	Diabetes. 
	Renal disease. 
	End organ damage. 
	Established cardiovascular disease. 
	10 year cardiovascular risk > 20%.

beta blockers: usually not first line for hypertension but considered in young people who:

Intolerant to ACE/ARB

pregnant

or there is an increase in sympathetic drive (sweating)

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80
Q

Give examples of causes of secondary hypertension.

A

Hyperaldosteronism

Renovascular disease e.g. (atheromatous renal artery stenosis and fibro-muscular hyperplasia)

Paranchymal renal disease

Coarctation of the aorta

Phaechromocytoma

Cushing’s syndrome

Drugs

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81
Q

What are the presenting features of secondary hypertension?

A

Onset if younger then 35 and especially if younger than 20

Sudden loss of good blood pressure control.

Resistance to adequate drug treatment.

systolic BP greater than 200 mm Hg and diastolic greater than 120 mm Hg

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82
Q

What is ALT?

A

alanine transaminase. It is an enzyme found mostly in the liver. When liver cells are damaged, they release ALT into the bloodstream.

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83
Q

Why is swimming good?

A

Doesn’t cause osteoarthritis.

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84
Q

What is a fundoscopy?

A

An exam that uses a magnifying lens and a light to check the fundus of the eye (back of the inside of the eye, including the retina and optic nerve).

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85
Q

What would be shown on an ECG with LVH?

A

Large QRS wave.

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86
Q

Does diuretic drugs increase uric acid?

A

yes so don’t use it with gout.

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87
Q

Describe the diastolic pressures pattern.

A

Rises till age of 50 and then falls.

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88
Q

Describe the systolic pressure pattern.

ii. What does this do to pulse pressure?

A

Keeps increasing.

ii. Increases causing syncope more likely to occur. As drugs will treat how systole pressure but will lower already low diastolic BP in elderly.

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89
Q

How do you calculate CV risk ?

A

Use Assign score.

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90
Q

What does an abdominal bruit suggest?

A

Renal failure.

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91
Q

What is a bruit?

A

A sound heard over an artery or vascular channel, reflecting turbulence of flow. Most commonly, a bruit is caused by abnormal narrowing of an artery.

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92
Q

Fasting glucose level ?

A

00 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it’s 126 mg/dL (7 mmol/L) or higher on two separate tests, the the patient has diabetes.

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93
Q

Fasting glucose test is used for what?

A

To detect for diabetes see patients normal blood sugar level

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94
Q

What does ankle swelling suggest?

A
  1. Right sidedHeart failure
  2. Nephrotic syndrome
  3. Calcium channel blockers (drugs)
  4. Hypothyroidism
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95
Q

What enzyme do statins inhibit?

A

Hmg Coa reductase

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96
Q

What must you say to a patient when prescribing ace inhibitor and ARBs?

A
  1. Never take them if they have diarrhoea and vomiting as it causes acute renal failure.
  2. They’re renal function needs to monitored at least annually. 7-10 days after if stop using them
  3. Be aware of dry cough
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97
Q

What is normal eGFR value?

A

60 or more.

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98
Q

What do Aceinhibitors end in?

ii. Beta blockers
iii. ARBs

(rule of thumb not all of them)

A

i. -pril
ii. -lol
iii. -artan

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99
Q

What is papillodema?

A

Is inflammation of the optic disc

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100
Q

What is hypertensive retinopathy associated with?

A

Generalised or local narrowing of retinal arterioles.

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101
Q

What might acute or severe hypertension cause?

A

Retinal arterioles may leak or become occluded. This causes:

  1. extravascular oedema
  2. Intra- retinal haemorrhages
  3. Nerve fibre layer infarcts
  4. retinal microaneurysms
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102
Q

What is papilloedema associated with?

A

flame haemorrhages

venous congestion

vascular exudates

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103
Q

Give examples of drugs which cause hypertension.

A

Alcohol

Caffeine

Nasal sprays and remedies

NSAIDS

Erythropoietin.

Corticosteroids

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104
Q

How would you test for chronic kidney diesease?

A

Estimate Glomerulus filtrate rate.

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105
Q

How would you test for cushings syndrome?

A

24 hour free cortisol and creatinine.

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106
Q

How would you test for coarctation of aorta?

A

BP in both arms plus one leg ; echo

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107
Q

How would you carry out urinalysis?

ii Can you give examples of how to make sure the procedure is carried out properly?

A

dipstick test.

ii. Must be analysed within an hour

keep reagent strips in original container don’t refrigerate

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108
Q

What would a positive result of protein and blood in urine dipstick test suggest?

ii. what is the proteinuria value which is deemed to significant?
iii. What happens if glycosuria is present?

A

Renal disease or target organ damage.

ii. 150mg/24 hours.
iii. suggests diabetes.

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109
Q

What is hypokalemia?

ii. what does it suggest?

A

Mean low serum potassium - levels less than 3.5 mmol/L

ii. highly suggestive of primary aldosteronism. Even if patient is on diuretic

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110
Q

What is hyperuricaemia?

ii. what does it suggest?

A

Is an usually high level of uric acid in the blood due to reduced excretion or increased cell turnover.

ii. risk of gout in those who use diuretics.

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111
Q

What happens if urea and creatine levels are increased?

A

Suggest underlying renal damage or disease.

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112
Q

What is microalbuminuria?

A

abnormal urinary excretion of albumin between 30-300mg/24 hour and is found in 8-15% of patients with hypertension.

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113
Q

What does anaemia suggest?

A

Renal impairment can be associated with anaemia which can be caused by hypertension. Or that the hypertension is secondary.

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114
Q

What does a raised mean corpuscular volume suggest

A

covert high alcohol intake, a major cause of secondary hypertension.

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115
Q

Describe what happens to people with ischaemic heart disease?

A

Stable accumulation of flow restriction
angina

unstable clinical syndromes
heart attack
NSTEMI
STEMI

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116
Q

What is common symptom of IHD?

ii what is the normal clinical diagnosis?

A

Chest pain

ii. Angina

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117
Q

What is common symptom of IHD?

ii what is the normal clinical diagnosis?

A

Chest pain

ii. Angina

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118
Q

What different diagnosis can you get on the GI tract which seems like chest pain but isn’t?

A

Reflux, burning, acid, waterbrash, provoked by food
Peptic ulcer pain. Epigastric, boring, point of finger gesture, relief by antacids / food
Oesophageal spasm
Biliary colic

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119
Q

What differential diagnosis can you get with MSK which seems like chest pain but isn’t?

A

Injury, location, tender, prolonged, exac. by moving area,

Nerve root pain, character, prolonged

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120
Q

What are the differential diagnosis of pericarditis which appears like chest pain?

A

Central, posture related

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121
Q

What is pleuritic pain described as?

A

Focal, exacerbated by breathing, sharp, catching

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122
Q

Give examples of emergency differential diagnosis for chest pain

A

Myocardial infarction
Severe, associated autonomic upset, angor animi
Ongoing pain, despite >10mg Morphine

Pulmonary embolus
Breathlessness, dull (maybe pleuritic)

Dissection of aorta
Tearing, excruciating, severe then eases

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123
Q

What is angor animi?

A

Angor animi is a symptom defined as a patient’s perception that they are in fact dying.

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124
Q

What are the pros of perfusion imaging?

A

Non invasive
Pharmacological stress in less mobile patients
More precision than ETT
Risk stratification

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125
Q

What are the cons of perfusion imaging?

A

Radiation

False positives and negatives

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126
Q

What are the pros and cons of CT angiography?

A

Non-invasive
Anatomical data and risk stratification

cons
Radiation
Less precise than angiography, particularly when calcium present
Cost

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127
Q

What are the pros and cons of an angiography?

A 
Pros
“Gold standard”
Anatomical and risk stratification
Follow-on angioplasty
Cons
Risk 1:1000 death, stroke
Radiation
Contrast: renal dysfunction, rash, nausea
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128
Q

What are the complications of a Coronary artery bypass surgery (CABG)?

A 
Death 1-2%
Stroke 2-3%
MI 3%
Atrial fibrillation
Infection
Cognitive impairment
Sternal malunion
Renal failure
Failure to recover
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129
Q

What are the complications of Percutaneous coronary interventions?

A 
Death 0.8%
Stroke 0.6%
MI 1-2%
Renal failure
Bleeding
Vascular complications
Stent thrombosis
Stent restenosis
Emergency CABG may be required.
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130
Q

What is the PCI technique?

A 
Vascular access
Anti-platelet drugs, anticoagulation
Catheter to ostium of coronary
Guidewire down vessel
Balloons threaded over wire
Stent(s) implanted
Balloon, catheter, wires removed
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131
Q

What symptoms/factors should be presented in a patient in order for a angiography to be used?

A 
Suitability for revascularisation
Multi-vessel disease, diffuse or focal
Left main disease 
Diabetes
Co-morbidities
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132
Q

What is the ideal choice of preference if someone is having a STEMI?

A

PCI

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133
Q

What is a STEMI?

A

ST elevated myocardial infarction

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134
Q

What do people complain of if they have intermitten claudication?

A

Patients with intermittent claudication complain of exertional discomfort, most commonly in the calf, which is relieved by rest.

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135
Q

what is Spironolactone used for?

A

Essential hypertension (high blood pressure with an unknown cause)

Hypokalemia (potassium deficiency)

Edema (fluid retention)

Severe heart failure

136
Q

What is a DVT?

A

Deep Venous Thrombosis. Formation of thrombi within the lumen of the vessels that make up the deep venous system

137
Q

What is a pulmonary embolism?

A

Pulmonary Embolism. A thrombus (clot) that has embolised (travelled) and lodged in the pulmonary circulation

138
Q

What does Distal vein thrombosis refer to?

A

refers to DVT of the calves

139
Q

What does does proximal vein thrombosis refer to?

A

Refers to DVT of the popliteal or the femoral vein. They are closer to the heart then distal ones.

140
Q

DVT can be asymptomatic true or false?

A

true.

141
Q

What are the three factors which allow for formation of a DVT?

A
  1. Circulatory stasis ( example: Left ventricular dysfunction, immobility or paralysis, varicose veins, venous obstruction)
  2. Hypercoagulate state (caused by :malignancy, pregnancy, inflammatory bowel disease, sepsis)
  3. Endothelial injury (caused by : venous injury, venous valvular disease, trauma, indwelling catheter).
142
Q

What are the the risk factors of VTE?

i. Exposing risk factors
ii. predisposing risk factors?

A 
i. Surgery
Trauma
Acute medical illness
Acute heart failure*
Acute respiratory failure
Central venous catheterisation 
Cancer
inflammatory diseases
ii.
Surgery
Trauma
Acute medical illness
Acute heart failure*
Acute respiratory failure
Central venous catheterisation 
cancer (both types of risk factors)
inflammatory diseases (both types of risk factors)
143
Q

What are the symptoms of DVT?

A

Painful and swollen limb with redness and heat. Tenderness along vein. Sub acute development

144
Q

What are the symptoms of PE?

A

Sudden SOB with Pleuritic Pain +/- Collapse +/- Haemoptysis. Hypoxia and tachycardia on Obs. BP may be low.

145
Q

How do you test for VTE?

A

D- Dimer test- 1 Fibrin D-dimer is produced whenever fibrin (a protein that is the chief component of a blood clot), is being actively degraded somewhere within the vascular system

146
Q

What would you do if patient has high risk of DVT or PE?

A

Scan.

147
Q

What would you do if low risk probability of DVT or ?

A

D-dimer test.

148
Q

What are the causes of post thrombotic syndrome?

A

DVT-induced damage to valves in the deep veins and valvular reflux leading to venous hypertension. Typically occurs after 5 years of idiopathic DVT?

149
Q

What are the symptoms Post thrombotic syndrome?

A 
Pain
Oedema
Hyperpigmentation
Eczema
Varicose collateral veins 
Venous ulceration
150
Q

How would you manage DVT?

A

Oral Anticoagulation

There is a small subset of patients where Thrombolysis can be considered but this is only in highly specialist centres

151
Q

How would you manage PE?

A

PE – High Risk = Thrombolysis then oral anticoagulation
Intermediate or Low Risk = Oral Anticoagulation
Again highly specialist centres may consider some Intermediate Risk patients for Thrombolysis.

152
Q

What is the definition of stroke?

A

Acute onset of focal neurological symptoms and signs due to disruption of blood supply

153
Q

What are the two main types of strokes?

A
  1. Ischaemic (80-85%)

2. Hemorrhagic (15-20%)

154
Q

What are the causes for hemorrhagic stroke?

A

Raised blood pressure

Weakened blood vessel wall due to
- structural abnormalities like aneurysm,
arteriovenous malformation(AVM)
- inflammation of vessel wall(vasculitis)

155
Q

What are the causes of ischaemic stroke?

A

Thrombotic- clot blocking artery at the site of occlusion

Embolic- clot blocking artery has travelled to artery it occludes from somewhere more proximal in the arteries or the heart

Hypoperfusion- due to reduced flow of blood due to stenosed artery rather than occlusion of artery

156
Q

Give examples of non modifiable risk factors?

A 
Age
Family history of stroke
Gender
Race
Previous stroke
157
Q

Give examples of modifiable risk factors?

A

Hypertension - 10 mm Hg reduction in SBP reduces risk of Stroke by 20%
Hyperlipidaemia
Smoking- doubles risk of ischaemic stroke.
Prior history of TIA especially if recent and recurrent
Atrial fibrillation
Diabetes
Congestive heart failure
Alcohol excess
Obesity
Physical inactivity

158
Q

What Diet could be used to treat hypertension?

A

DASH diet- stands for Diet approaches to stop hypertension.

159
Q

How do you differentiate between haemorrhagic and ischaemic stroke?

A

Brain imaging. e.g CT Brain or MRI

160
Q

How does cardioembolism occur

ii. Where is it normally found
iii. what is the main cause?

A

embolism from a clot formed in the heart

ii. (usually left atrium)
iii. atrial fibrillation

161
Q

How does atheroembolism occur?

A

embolism from a thrombus forming on a atherosclerotic plaque- platelet rich clots

162
Q

What test would you carry out to differentiate between the two types of embolitic strokes?

A

Atheroembolism- carotid scanning, CT/MR angiography of aortic arch

Cardioembolism- Echocardiogram

163
Q

How can you treat an ischaemic stroke?

A

Thrombolysis- upto 4.5 hrs from onset of symptoms

Thrombectomy- upto 6 hrs from symptom onset, usually after having started thrombolysis

BOTH HEAVILY TIME DEPENDENT AS BRAIN TISSUE DIES RAPIDLY.

164
Q

How would you carry out medical management with a stroke caused by atheroembolic or thrombus?

A

Antiplatelets(Aspirin 75 mg +Dipyridamole MR 200 mg twice daily/Clopidogrel 75 mg daily)

Statins to treat high lipids

Diabetes management

165
Q

How would you carry out medical management with a stroke caused by atrial fibrillation?

A

Anticoagulate as soon as possible if less than 48 hours

e.g. Warfarin (Vitamin K antagonist) or NOACS however NOAC only used with non valvular AF

Cardiovert as well

166
Q

Using hypertensives is a good way to manage stroke prevention true or false?

A

True.

167
Q

Give examples of surgical management.

A

Haematoma evacuation

Relief of raised intracranial pressure Obstructive hydrocephalus Large total MCA infarctions

Carotid endarterectomy

168
Q

What is a TIA?

A

Known as transient ischaemic attacks, which have Temporary neurological symptoms due to occlusion of artery stopping flow of blood.

169
Q

Why are they temporary?

A

because arteries are capable of dissolving small clots.

170
Q

What are the symptoms of chronic venous disease?

A

very variable though 40% present with varicose veins.

  1. bleeding
  2. thrombophletis
  3. chronic venous insufficiency
  4. ulcerations
171
Q

What investigations can be used for chronic venous disease?

A

Duplex scan

State of the deep veins (occlusions or incompetence)

Saphenofemoral or saphenopopliteal incompetence?

172
Q

Give examples of complications to interventions of chronic venous disease?

A 
Thrombophlebitis
Skin staining
Local ulceration
Wound infection (~10%)
Nerve damage
‘Recurrence’
173
Q

What is an oedema?

A

Accumulation of fluid in interstitial space

174
Q

What are the causes of oedema?

A
  1. Raised capillary pressure - caused by :

arteriolar dilatation

Left ventricular failure - pulmonary oedema

Right ventricular failure - peripheral oedema (ankle, sacral)

Prolonged standing - swollen ankles

  1. Reduced plasma osmotic pressure

Normal [plasma protein]p = 65-80 g/l
Oedema if < ~ 30 g/l

malnutrition

protein malabsorption

excessive renal excretion of protein

hepatic failure

  1. Lymphatic insufficiency

Lymph node damage

Filariasis - elephantiasis

4.Changes in capillary permeability

inflammation

histamine increases leakage of protein

175
Q

What would clinical investigations show for pulmonary oedema?

i. Auscultations
ii. Chest X ray

A

i. Clinically there may be crepitations in auscultation of lung bases
ii. Chest X-ray shows haziness in perihilar region

176
Q

Symptoms of pitting oedema?

A

swelling in Ankles

swelling in Sacrum

177
Q

What is heart failure?

A

HF is a complex clinical syndrome resulting from structural or functional impairment of ventricular filling (mainly left) or ejection of blood

178
Q

What are the causes of heart failure?

A

Coronary Heart Disease (± MI)
Hypertension (~80%)/ Diabetes
Dilated Cardiomyopathy Primary/~30% hereditary, secondary eg EtOH, adriamycin etc)

Valve disease

Tachycardic arrhythmias (poorly controlled AF)

~40% have (predominantly) HEFpEF (Heart failure with Preserved Ejection Fraction)

(typically elderly, hypertensive/diabetic ♀)

179
Q

What are the two types of heart failure?

A

Diastolic and systolic.

180
Q

What are the symptoms of heart failure?

A
  1. Shortness of breath
  2. Difficulty breathing at night when recumbent:
    i. Orthopnoea
    ii. Paroxysmal nocturnal dyspnoea
  3. Reduced exercise tolerance
  4. Fatigue
  5. Tiredness
  6. Ankle swelling
181
Q

What would you find on physical examination in relation to heart failure?

A

Neck exam
Elevated jugular venous pressure

Auscultation of the lungs
Rales or crackles

Auscultation of the heart 2,3,4
Third or fourth heart sound (S3 or S4) sometimes called a gallop rhythm
Murmur

Oedema in dependent areas2
Sacrum
Feet/ankles/lower legs

182
Q

What can ECG identify for HF?

A

Arrhythmias (irregular heart rhythms)
Past myocardial infarction (MI)
Left ventricular hypertrophy

183
Q

What can chest X-Ray identify for HF?

A

Size and shape of the cardiac silhouette

Evidence of fluid accumulation in the lungs

184
Q

How is BNP useful for testing for HF?

A

If it is elevated and patient has S.O.B then suggests Heart failure is present.

185
Q

What is a BNP?

A

a protein that is made by your heart and blood vessels. Think of as a cardiac hormone.

186
Q

What is a transthoracic echocardiogram?

A

ultrasound of the heart obtained by placing the transducer on the chest wall. Images of the heart are obtained and can provide information on chamber size, wall thickness and chamber function.

187
Q

What is an ejection fraction?

A

EF is the percentage of blood that is pumped out of the heart during each beat

188
Q

What are the ranges for healthy ejection fraction

A

A normal EF is ≥50%

189
Q

What is heart failure called when EF is normal?

A

Heart failure in the setting of a normal EF is known as heart failure with preserved ejection fraction (HFpEF)

190
Q

What is heart failure called when EF is reduced?

A

Heart failure with an EF ≤40% is known as heart failure with reduced ejection fraction (HFrEF)

191
Q

What is the patho-physiological differences between HFrEF and HFpEF

A

In HFrEF the LV is unable to eject an adequate amount of blood during systole

In HFpEF less blood is able to fill the LV in diastole, due to myocardial stiffness. Thus the LV has less blood to eject during systole

192
Q

What is the difference between STEMI and NSTEMI?

A

A STEMI or ST-elevation myocardial infarction is caused by a sudden complete (100 percent) blockage of a heart artery (coronary artery). A non-STEMI is usually caused by a severely narrowed artery but the artery is usually not completely blocked.

193
Q

When would you no longer be able to use PCI?

A

after 2 hours

194
Q

Where is the normal apex beat found?

A

Normal 5th intercostal space/mid clavicle line.

195
Q

What might a displaced apex beat suggest?

A

LVH- pressure overload

196
Q

What does a tapping apex suggest?

A

Mitral stenosis

197
Q

What does a parasternal heave suggest?

A

Right ventricular overload.

198
Q

What is a cardiac murmur?

A

Audible turbulence of blood flow

innocent and pathological.

199
Q

Where are the valves found?

A

A-2nd-3rd right inter space

P- 2nd 3rd left interspace

T- left sternal border

M- apex

200
Q

What does the 1st heart sound mean?

A

Mitral and tricuspid valve closing

start of systole

201
Q

What does the 2nd heart sound mean?

A

Aortic and pulmonary valves closing

start of diastole

202
Q

What type of systolic murmurs are there?

A

Pansystolic

Ejection systolic

203
Q

What type of diastolic murmurs are there?

A

Early diastolic

Mid diastolic

204
Q

How do you grade murmurs?

A

Six point scale

 I.    Very quiet 
II.    Quiet - easy to hear
III.    Loud
IV. 	Loud with a thrill
V. 	Very loud with a thrill
VI. 	Loud  - audible without a 				 
        stethoscope
205
Q

What are the differences between left and right sided murmurs?

A

Right sided louder with inspiration

Left sided louder with expiration.

206
Q

Name 5 conditions which give common murmurs?

A

innocent murmur

mitral regurgitation

aortic stenosis

aortic regurgitation

Mitral stenosis

207
Q

What is an innocent murmur?

A

soft sound

position is dependent

Often early systolic sound

208
Q

All diastolic murmurs are pathological true or false?

A

true

209
Q

What is valve stenosis?

A

Valves do not open properly

210
Q

What is valve regurgitation

A

Valves do not close properly

211
Q

coronary angiography is always advised along with valve replacement true or false

A

true.

212
Q

What is a raised JVP?

A

Greater than 4cm

213
Q

What do you do with persistent AF and its after 48 hours?

A

Rate control and anti coagulate

214
Q

What does troponin in the blood suggest?

A

Myocardial Infarction

215
Q

How do you class rheumatic disease?

A

JONES class

J- joints
O- MyOcarditis
N- Nodules
E- erythema marginatum
S- Sydenham chorea
216
Q

How do you examine mitral stenosis?

A

Use bell of stethoscope and make patient move left.

217
Q

What is angina pectoris?

A

chest pain which may spread to jaws and arms

it is symptomatic reversible myocardial ischaemia

218
Q

What are the main causes of angina?

A
  1. Atheroma (main)
  2. Anaemia
  3. coronary artery spasm
  4. Tachyarrhythmias
  5. Hypertrophic cardiomyopathy
219
Q

What are the signs and symptoms of Angina?

A

Main three features

  1. Constricting discomfort to the chest, jaw,neck,shoulders or arms
  2. Symptoms are brought on by exertion
  3. symptoms relieved by rest or GTN within 5 mins

Other precipitants which bring on syptoms include:

  1. cold weather
  2. emotion
  3. heavy meals - cardiac work load increases

Other symptoms include:

  1. Dyspnoea
  2. Nausea
  3. sweatiness
  4. faintness
220
Q

What are the main types of angina pectoris?

A

Stable angina - Induced by effort relieved by stress

unstable angina - Angina of increasing frequency or severity occurs on minimal exertion or at rest - associated with very high risk of MI

Decubitus angina - precipitated by lying flat

Variant angina - caused by coronary artery spasm (only one which causes ST elevation)

221
Q

How do you diagnose Angina?

A

ECG - usually normal (may shows ST depression or flat/inverted T waves)

or show signs of past MI

Blood tests: FBC ,U&E, TFTs , Lipids , HbA1C

can consider echo or CXR

Testing for Ischaemic heart disease can be taken after:

Angiography - use cardiac CT with Contrast or transcatheter angiography

222
Q

How do you manage Angina?

A
  1. address exacerbating factors (e.g. anaemia, tachycardia)
  2. Prevention of cardiovascular disease:

Stop smoking

exercise

optimise hypertension

diabetes control

manage hyperlipidaemia

take aspirin

  1. Symptom Relief: GTN spray - stable angina pain should go after 5 mins of use
  2. First Line prophylaxis :

Beta blockers and or Calcium channel blockers( calcium antagonists)

E.g. Atenolol - beta blocker
amlodipine - this is an example of a dihydropyridine calcium antagonist ( don’t mix non dihydropyridine and beta blocker)

  1. Second line prophylaxis: only used if BB and CBB are in contraindication
    i. Long acting nitrates ( isosorbide mononitrate) - venodilator - lowers BP and gives headaches
    ii. Nicorandil - K+ channel activator gives Mouth/GI ulcers
    iii. Ivabradine - reduces heart rate only in sinus rhythm
    iv. Ranolazine : inhibits late Na+ current. effective against refractory angina
  2. Revascularisation (PCI)
223
Q

When do you dial 999 when using GTN relief for angina?

A

If chest pain has still not gone after 5 mins on the second dosage

224
Q

What is acute coronary syndromes (ACS)?

A

A collection of diseases sharing the same pathology

These include:

  1. Unstable angina
  2. STEMI (ST elevated myocardial infarction)
  3. NSTEMI (Non ST elevated myocardial infarction)
225
Q

What does Myocardial infarction mean?

A

Myocardial cell death

causes release of troponin

226
Q

What are the causes of ACS?

A
  1. atherosclerotic plaque rupture and thrombosis which occlude the coronary vessels
  2. inflammation
227
Q

What are the risk factors of ACS?

A

Non modfiable
1. Age

  1. Male
  2. family history of IHD

Modifiable

  1. Smoking
  2. hypertension
  3. Diabetes
  4. Hyperlipidaemia
  5. obesity
228
Q

What are the signs and symptoms of ACS?

A

Symptoms

  1. Acute chest pain lasting >20 min - radiates to neck and arms
  2. Nausea
  3. Dyspnoea
  4. Palpitations
  5. May have silent ACS (no chest pain) - common in diabetics and elderly

Signs:

  1. Distress
  2. Anxiety
  3. Pallor
  4. sweatiness
  5. changes in BP and pulse
  6. 4th heart sound potentially
229
Q

How do you diagnose ACS?

A

General : Bloods FBC, U&E , glucose , cardiac enzyme( troponin)

STEMI:

TnT (troponin T and I)

ECG:
shows ST segment elevation

new onset Left bundle branch block (LBBB)

Might show T wave inversion or pathological Q waves

NSTEMI:

Tn (troponin T and I ) increase

ECG:

No ST segment elevation

may show ST depression

T wave inversion or even normal

Unstable Angina:

Troponin level does not rise

ECG:

T wave inversion

ST depression or even normal

230
Q

How do you manage STEMI?

A

MONA + C (clopidogrel)

  1. Morphine: 5-10 mg and anti emetic
  2. Oxygen if hypoxic
  3. Nitrate: GTN spray to manage symptom and patient has BP >90 mmHg
  4. Aspirin (unless already given)
  5. Clopidogrel/ticagrelor

PCI if :

i. patient presenting within 12 hours of symptom and available in next 90 mins
ii. ECG changes (new LBBB) or ST elevation
iii. No contraindications

otherwise thrombolysis - unless recent aggressive CPR

231
Q

How do you manage Non STEMI and unstable angina?

A

MONA + C (clopidogrel)

  1. Morphine: 5-10 mg and anti emetic
  2. Oxygen if hypoxic
  3. Nitrate: GTN spray to manage symptom and patient has BP >90 mmHg
  4. Aspirin (unless already given)
  5. clopidogrel/ ticagrelor
  6. Anticoagulation ( fondaprinux) or LMWH
  7. Oral beta locker e.g. bisoprolol
  8. PCI and angiography should be requested based on severity (GRACE score)
232
Q

How do you manage ACS in the after initial management?

A
  1. Symptom control
  2. Modify risk factors
  3. Optimise cardio protective medications - Give ACE inhibitor and Beta blocker

Aspirin for at least 12 months to decrease vascular events risk (MI and stroke)

233
Q

which is more specific for cardiac muscle damage- troponin or creatinine kinase?

A

troponin

creatinine kinase also peaks in skeletal muscle and brain

234
Q

what leads have ST elevation in an inferior STEMI?

A

II, III, aVF

235
Q

what leads have ST elevation in an anteroseptal STEMI?

A

V1-V4

236
Q

what leads have ST elevation in a lateral STEMI?

A

1, aVL, V5, V6

237
Q

What is the difference between Angina and MI?

A
  1. Duration is longer for MI ( 30 mins vs 10)
  2. Onset - Angina comes about on exertion while MI at rest
  3. MI usually more severe
  4. MI has sweating, nausea and vomiting as usual associated symptoms Angina doesn’t
238
Q

Discuss the three different isoforms of troponin.

A

Troponin C binds Calcium - Identical in heart and skeletal muscle

Troponin I in absence of Ca2+binds to actin, inhibits actin-myosin ATPase induced contraction - cardiac specific isoforms

Troponin T links troponin complex to tropomyosin, facilitates contraction - cardiac specific isoforms

239
Q

What are the complications of MIs?

A
  1. Cardiac arrest

2, Cardiogenic shock

  1. LVF
  2. Arrhythmias
  3. RVF - Low CO and raised JVP
  4. Pericarditis - relieved by sitting forward
  5. systemic embolism - presents with pulmonary oedema
  6. Mitral regurgitation
  7. Dressler’s syndrome - recurrent pericarditis , pleural effusions , fever and anaemia also raised ESR. May lean forward (autoimmune phenomenon) . Occurs 4-6 weeks after MI
  8. cardiac tamponade - presents with low CO, pulsus paradoxus, Kussmaul’s sign
240
Q

what are the types of infarct that are related to an MI?

A

Transmural - affects all of the myocardial wall - cause ST elevation and Q waves

subendocardial - necrosis <50% of the myocardial wall - cause ST depression

241
Q

What is heart failure?

A

A condition of the inability of the cardiac output to meet the physiological demands of the body.

It is caused by damage to the valves, ventricular muscle or both. This results in back pressure of blood with congestion of organs

242
Q

What are the key classifications of heart failure?

A

LVF

RVF

Systolic failure - inability of the the ventricle to contract normally

diastolic failure - inability of the ventricle to relax normally

Low output failure - cardiac output is low and fails to rise normally with exertion.

High output heart failure - rare. Output is normal or normal yet the requirement is much higher. Cardiac output fails to meet these needs

243
Q

What are the causes of Left ventricular heart failure?

A

CVS: coronary artery disease, hypertension, valve disease arrhythmia, cardiomyopathy.

Volume overload: CKD, nephrotic syndrome.

High output states: anaemia, sepsis, liver failure.

244
Q

What are the causes of Right ventricular heart failure?

A
  1. LVF
  2. Pulmonary stenosis
  3. Lung disease
245
Q

What are the signs and symptoms of LVF?

A

PULMONARY OEDEMA

  1. Dyspnoea
  2. Poor exercise tolerance
  3. Fatigue
  4. orthopnoea
  5. Paroxysmal
  6. PND
  7. nocturnal cough (+/- pink frothy sputum)
  8. wheeze

signs:

S3.

Bibasal crepitation’s.

Displaced apex beat.

246
Q

What are the signs and symptoms of RVF?

A

Peripheral oedema

ascites

nausea

anorexia

facial engorgement

Signs:

Raised JVP,
hepatomegaly,
chest vein dilation,
ascites

247
Q

What is congestive heart failure?

A

When LVF and RVF occur together and there is a combination of clinical features

248
Q

How do you classify Heart failure?

A

New york heart association:

  1. No limitation of physical activity
  2. Slight limitation of physical activity
  3. Marked limitation of physical activity
  4. Inability to carry out physical activity

Framingham criteria: either 2 or major and 0 minor or 1 major and 2 or more minor

1.Major criteria - PAINS

Paroxysmal nocturnal dyspnoea

Acute pulmonary oedema

Increased heart size and central venos pressure

Neck vein dilation

S3 gallop

  1. Minor Criteria - PAIN

Pleural effusion

Ankle oedema

Increased heart reate (>120)

Nocturnal cough

249
Q

How do you diagnose heart failure?

A

Bloods: FBC, U&E, BNP.

BNP is raised

ECG: LVH, left bundle branch, pathological Q waves, AF.

Echo: should be used if either abnormal. However it is still the gold standard

CXR: ABCDE

Alveolar oedema ( batwings)

Kerley B lines ( septal lines)

Cardiomegaly

Dilated prominent upper lobe veins

Effusion (pleural)

will also have: cuffing and fluid in fissures

250
Q

How do you manage heart failure?

A

Acute heart failure - emergency treat like emergency pulmonary oedema (ABCDE)

A- sit up and give o2

chronic heart failure - stop smoking and drinking. Eat less salt

Drugs:

Loop diuretics: relieve symptoms e.g. furosemide or bumetanide. Side effects include decrease in k+ and renal impairment

Ace inhibitor: Consider for Left ventricular systolic . Prolongs life by preventing cardiac remodelling (or use ARB)

Beta blocker: carvedilol or bisoprolol - decreases mortality. “start low go slow”

Other drugs

Digoxin: helps symptoms even in sinus rhythm

Hydralazine – isosorbide dinitrate combination. (vasodilator)

Spironolactone – if loops are not providing enough symptom relief or are complicated by hyperkalemia

Sacubitril – Valsartan.

Combination of ARB with Sacubitril, which is a drug the increases the levels of ANP/BNP.

Surgical intervention:

Cardiac resynchronisation

LV assist device

heart transplantation

251
Q

What are the two types of ejection fraction is heart failure asssociated with?

A

Reduced -:. Reduced cardiac output due to failure of the ventricles to properly contract.

Preserved - Thought to be associated with atrial dysfunction that results in reduced ventricular filling and therefore reduced cardiac output.

252
Q

How do you manage malignant hypertension?

A

No end organ damage: oral therapy

Signs of CCF or encelphalopathy:

Labetalol or sodium nitroprusside infusion if no LVH

Furosemide + hydralazine if LV failure

want to control the reduction of BP in days not hours

253
Q

What is Mitral regurgitation?

A

Backflow through the mitral valve during systole

254
Q

What are the causes of Mitral Regurgitation?

A
  1. Left ventricular dilation
  2. Annular calcification
  3. Rheumatic fever
  4. infective endocarditis
  5. Mitral valve prolapse
  6. ruptured chordae tendinae
  7. Papillary muscle rupture
255
Q

What are the signs and symptoms of Mitral regurgitation?

A

Symptom: Dyspnoea Fatigue Palpitations

signs:
AF

displaced hyperdynamic apex,

Pansystolic murmur at apex spreads to axilla

soft S1

Loud P2

256
Q

How do you diagnose Mitral regurgitation?

A

ECG: AF and LVH

ECHO

CXR: cardiomegaly

Cardiac catheterisation

257
Q

How do you manage Mitral regurgitation?

A
  1. Symptomatic relief: ACEi / Diuretics.
  2. If in AF
    Rate control eg digoxin.
    Anti coagulation eg Warfarin.

valve replacement

258
Q

What is Mitral stenosis?

A

Narrowing of the opening of the mitral valve

259
Q

What are the causes of mitral stenosis?

A

Rheumatic fever

congenital

Mucopolysaccharidoses

Endocardial fibroelatosis

Malignant carcinoid

prosthetic valve

260
Q

What is the normal mitral valve orifice area?

A

4-6 cm2

261
Q

What are the signs and symptoms of Mitral stenosis?

A

Symptoms usually begin when the orifice becomes <2cm 2

Dyspnoea

Haemoptysis

Dysphagia

fatigue

palpitations

sign:

Rumbling mid diastolic murmur, best heard on expiration when patient lying on their side

AF due to enlarged LA

malar flush on cheeks

tapping non displaced apex

262
Q

How do you diagnose Mitral stenosis?

A

ECG: AF, P mitrale

CXR: left atrial enlargement Pulmonary oedema Mitral valve calcification

ECHO: diagnostic

263
Q

How do you manage Mitral stenosis?

A

SOB: ACEi / diuretics.

AF: rate control and anti-coagulation.

Surgical:
o Balloon valvuloplasty.
o Valve replacement.

264
Q

What are the causes of Aortic stenosis?

A

Senile calcification (main)

congenital (bicuspid valve, Williams syndrome)

Rheumatic heart disease

265
Q

What are the signs and symptoms of Aortic stenosis?

A

Classic tirad: Angina, Syncope and heart failure

Dysopnea

dizziness

faints

signs: • Ejection systolic murmur best heard at aortic region that radiates to the carotid.

Crescendo - decrescendo murmur

Bibasal creptiations

Slow rising pulse with narrow pulse pressure

Heaving non displaced apex

LV heave

aortic thrill

266
Q

How do you diagnose aortic stenosis?

A

ECG: LVH with strain pattern, P- mitrale, LAP poor R wave progression LBBB or complete AV block

CXR: Calcified aortic valve and LVH

Echo

Doppler echo can estimate across valves

267
Q

How do you manage Aortic stenosis?

A

Generally have a poor prognosis due to progressive heart failure, so surgical intervention favored.

Surgical options:
Valve replacement.

Balloon valvuloplasty.

TAVI: trans aortic valve implantation. ( if surgically unfit)

268
Q

What are the causes of aortic regurgitation?

A

Acute: Infective endocarditis, ascending aortic, dissection

chronic: Congenital, connective tissue disorders( Marfan’s syndrome, Ehlers- Danlos) and rheumatic fever

269
Q

What are the symptoms of Aortic regurgitation?

A

Exertional dyspnoea

Orthopnoea

PND (paroxysmal night dysopnea)

Palpitations, angina, syncope

signs:

Early diastolic murmur, best heard when patient is sitting forward and expiring.

Displaced apex.

wide volume pulse.

Collapsing pulse.

Head nodding with each heart beat.

Pulsations in capillary nail beds

270
Q

How do you diagnose Aortic regurgitation?

A

ECG: LVH

CXR: Cardiomegaly : dilated ascending aorta

ECHO: diagnostic

271
Q

How do you manage Aortic regurgitation?

A

Echo every 6-12 months

Medical: control hypertension – ACEi.

Surgical: valve replacement.

Surgery indicated when LV dilation and heart failure progresses

272
Q

What is infective endocarditis?

A

Inflammation fo the endocardium and valves due to infection. Usually involves the heart valves with ‘vegetation’ of the infectious agent

273
Q

What is the pathophysiology of infective endocarditis?

A

Rare

Heart valves are targeted due to lack of blood supply meaning WCC are unable to reach them

274
Q

What are the risk factors of infective endocarditis?

A

IV drug users ( especially with tricuspid valve)

Renal failure

immunosupression

Diabetes

prosthetic valves (staph aureus and epidermis main causes)

Valve abnormality

275
Q

What are the causes of Infective endocarditis?

A

Bacteria:

Strep viridans ( most common)

Staph aureus (second most common)

Strep bovis

Enterococci and coxiella burnetii

staph epidermis

HACEK group (rare)

276
Q

What are the signs and symptoms of Infective endocarditis?

A

Fever + new murmur - is endocarditis until proven otherwise

Septic signs: Fever, rigor, malaise, anaemia, Weight loss and clubbing

Immune complex deposition: Vasculitis may affect any vessel. Roth spots and splinter haemorrhages and osler nodes

vegetation may embolise causing abscesses in organs

277
Q

How do you classify Infective endocarditis?

A

Definitive infective endocarditis: 2 major or 1 major and 3 minor or 5 minor

Major Criteria:

2 separate positive blood cultures

single positive blood culture for coxiella burnetii

Minor criteria: FIVE

Fever

IV drug use or predisposing heart condition

and

Immunological phenomena e.g. osler’s nodes or roth’s spots

Vascular phenomena: mycotic aneurysm

Echocardiograph findings

278
Q

How do you diagnose Endocarditis?

A

Classification

Bloods cultures: 3 separate cultures from 3 peripheral sites

Blood tests: Anaemia, Neutrophilila, high ESR/CRP

Urinalysis: Microscopic haematuria
CXR: cardiomegaly

1st line imaging: Trans thoracic echo.

2nd line imaging: Trans oeseophageal echo.

TOE done if prosthetic valve, vegetations or non diagnostic images on TTE.

279
Q

How do you manage infective endocarditis?

A

Native valve indolent (Subacute): Amoxicillin IV 2g 4 hourly + Gentamicin

Native valve severe sepsis (Acute): Flucloxacillin IV 2g 6 hourly (4 hourly if >85kg). DRUG USERS

Prosthetic valve or Suspected MRSA: Vancomycin IV + Gentamicin IV + when therapeutic vancomycin levels reached add Rifampicin PO 600mg bd (Very good replacement VGR)

Viridans - Benzylpenicillin IV + gentamicin IV

280
Q

What is hypertrophic cardiomyopathy (HCM)?

A

familial condition affecting the heart, characterised by unexplained hypertrophy of the wall of the left ventricle

cavity space to be lost due to obstruction from asymmetric septal hypertrophy

281
Q

Discuss the prevalence of HCM.

A

Autosomal dominant or Sporadic (mainly)

70% have mutation sarcomeres genes (Beta myosin, alpha tropomyosin and troponin T issues)

282
Q

What are the signs and symptoms of HCM?

A

Sudden death is common (most common cause for young)- athletes

Angina

dysopnea

Palpitation

Syncope (fainting)

Sign:

double-apex beat

systolic thrill at lower left sternal edge

283
Q

why are arrhythmias (particularly re-entry) common in a heart with hypertrophic cardiomyopathy?

A

scarring leads to arrhythmias due to increased automacity of surrounding tissue

284
Q

How do you diagnose HCM?

A

ECG: LVH, Progressive T-wave inversion

Echo: asymmetrical septal hypertrophy;

285
Q

How do you manage HCM?

A

Symptomatic control:

Chest pain: B Blockers / Verapamil.

Arrhythmia: Amiodarone / anti coagulation

286
Q

What is Dilated cardiomyopathy (DCM)

A

A dilated, flabby heart of unknown cause

287
Q

What are the associated factors of DCM?

A
  1. Alcohol
  2. congenital (x-linked)
  3. Increase BP
  4. Haemochromatosis
  5. Viral infection
  6. Autoimmune
288
Q

What are the signs and symptoms of DCM?

A

mainly shows signs/ symptoms of RVF and LVF

Fatigue

Dysopnea

Pulmonary oedema

emboli

AF

signs:
Raised pulse and JVP

displaced and diffuse apex

s3 gallop

oedema, jaundice, hepatomegaly ascites

289
Q

How do you diagnose DCM?

A

Blood: BNP (cardiac failure)

CXR: cardiomegaly, pulmonary oedema

ECG: tachycardia, non specific T-wave changes, Poor R-wave progession

Echo: globally dilated hypokinetic heart

290
Q

How do you manage DCM?

A

Heart failure – ACEi Diuretics, B blockers etc.

Palpitations: digoxin, anti-coagulation, ICD.

Surgical:
Heart transplant.

291
Q

What is restrictive cardiomyopathy?

A

the heart becomes stiff but not hypertrophied, which results in the heart resisting normal filling with blood.

292
Q

What are the causes of restrictive cardiomyopathy?

A

Idiopathic

amyloidosis

sarcoidosis

haemochromatosis

293
Q

What are the signs and symptoms of restrictive cardiomyopathy?

A

SOB.

Peripheral oedema.

Hepatomegaly.

Raised JVP

294
Q

What is arrhythmic right ventricular cardiomyopathy?

A

Is a type of cardiomyopathy in which the myocytes become replaced with fibrous and fatty tissue.

It is an autosomal dominant condition associated with mutations in the ryanodine receptors.

295
Q

What are the signs and symptoms of arrhythmic right ventricular cardiomyopathy?

A

• Primarily presents with ventricular arrhythmias, which can cause:
o Dizziness.
o Palpitations.
o Sudden cardiac death

296
Q

How do you manage arrhythmic right ventricular cardiomyopathy

A

Management is rhythm control with either:
B blockers / amiodarone.

ICD.

297
Q

What is myocarditis?

A

Inflammation of the myocardium often associated with myopericarditis

298
Q

What are the causes of myocarditis?

A
  1. Idiopathic
  2. Viral: Enteroviruses, EBV, influenza, coxsackie A and B, Hepatitis
  3. Bacterial: Staph, strep, clostridia, TB and Mycoplasma
  4. Drugs: Trastuzumab
  5. immunological: SLE, Sarcoid
299
Q

What are the signs and symptoms of myocarditis?

A

mainly in young adults

ACS- like symptoms

heart failure symptoms

palpitations, Tachycardia soft S1 and S4 gallop

300
Q

How do you diagnose Myocarditis?

A

ECG: ST changes, T-wave inversion,atrial arrthymias

Bloods: Troponin, CRP and ESR may be raised

viral serology: swabs

301
Q

How do you manage Myocarditis?

A

treat underlying cause

supportive management: avoid exercise as this can precipitate arrhythmias

302
Q

what is cardiac myxoma?

A

rare benign cardiac tumour usually sporadic

303
Q

What is acute pericarditis?

A

Inflammation of the pericardium

304
Q

What are the causes of acute pericarditis?

A
  1. idiopathic or secondary to:
    i. viruses: Coxsackie, EBV,CMV
    ii. Bacteria: TB (most common cause worldwide),Lyme disease, Q fever
    iii. Drugs
    iv. Surgery, trauma
    v. Autoimmune: dressler’s syndrome
305
Q

What are the signs and symptoms of acute pericarditis?

A

Fever is common - (infection)

Central chest pain- worse lying down or on inspiration. Made better by leaning forward

Pericardial friction rub and pericardial effusion or cardiac tamponade

306
Q

How do you diagnose acute pericarditis?

A

ECG: concave (saddle-seat) ST segment elevation and PR depression

Blood: FBC,ESR,U&E , troponin may be raised

CXR; cardiomegaly - pericardial effusion

ECHO: if pericardial effusion is suspected

307
Q

How do you manage Acute pericarditis?

A

Analgesia.

Treat the underlying cause.

308
Q

What is pericardial effusion?

A

Accumulation of fluid in the pericardial sac

309
Q

What are the causes of pericardial effusion

A

Pericarditis (i.e. same causes)

310
Q

What are the signs and symptoms of pericardial effusion?

A

Dysopnea

Chest pain

raised JVP, bronchial breath at left base (ewart’s sign: compressed lower lobe)

muffled heart sound

hiccups - phrenic nerves compressed

311
Q

How do you diagnose pericardial effusion?

A

CXR: Large globular heart

ECG: low voltage QRS complexes

Echo: diagnostic

312
Q

How do you manage pericardial effusion?

A

Treat the cause

Pericardiocentesis: either therapeutic (tamponade) or diagnostic (bacterial)

313
Q

What is cardiac tamponade?

A

Pericardial effusion that raises intrapericardial pressure reducing ventricular filling = lowers cardiac output

314
Q

What can cardiac tamponade lead to?

A

cardiac arrest

315
Q

What are the signs and symtpoms of cardiac tamponade?

A

SOB, fatigue, palpitations, pericarditis.

raised pulse and JVP

Lowered BP

Pulsus paradoxus (large decrease in systolic pressure during inspiration. )

kussmaul’s sign (JVP rising with inspiration)

316
Q

How do you diagnose Cardiac tamponade?

A

Beck’s triad : falling BP, rising JVP, muffled heart sounds

CXR/ ECG: as per Pericardial effusion

ECHO: diagnostic

317
Q

How do you manage cardiac tamponade?

A

drainage (pericardiocentesis)

318
Q

what is coarction of the aorta?

A

a congenital defect where there is vasoconstriction just below the subclavian artery

319
Q

what is transposition of the great arteries?

A

a congenital defect where the aorta and pulmonary trunk are switched,
so deoxygenated blood gets taken to systemic circulation and oygenated blood gets taken to the lungs
(2 completely separate circuits)

320
Q

What is an atrial septal defect?

A

Hole connects the atria

321
Q

What are the main two defects of an ASD?

A

Ostium secundum: 80% of cases asymptomatic till adulthood when left to right shunt forms

Ostium primum: associated with AV valve anomaly. Symptomatic in childhood. associated with downs syndrome

322
Q

What are the signs and symptoms of ASD?

A

Chest pain

palpitations

dysopnea

arrythmias

raised JVP

pulmonary systolic murmur

323
Q

How do you diagnose ASD?

A

ECG: RBBB with LAD (primum defect)

RBBB with RAD (secundum defect)

324
Q

How do you treat ASD?

A

usually close spontaneously

if not primum defects close in childhood

transcatheter closure more common than surgical

325
Q

What is ventricular septal defect (VSD)?

A

Hole connects the ventricles

326
Q

What are the causes of VSD?

A

congenital

acquired (post MI)

327
Q

What are the signs and symptoms of VSD?

A

heart failure in infant or remain asymptomatic

signs:

Harsh pansystolic murmur heard at the left sternal edge

systolic thrill+/- left parasternal heave

328
Q

How do you diagnose VSD?

A

ECG: normal or LAD (left axis deviation), RVH or LVH

CXR: normal hear size or cardiomegaly

cardiac catheter: step up in o2 saturation in right ventricle

329
Q

How do you treat VSD?

A

close spontaneously

failed medical therapy or Symptomatic VSD - surgical closure

330
Q

What is Eisenmenger’s complex?

A

occurs in ASD and VSD

initial left to right shunt leads to pulmonary hypertension which increases right heart pressure is greater than left causing a reversal in shunt.

causes cyanosis

331
Q

What is a High LDL/HDL ratio a good indication of?

ii. what can increase HDL?

A

high risk of cardiovascular disease

ii. fibrate therapy

332
Q

when are there micro and macroscopic changes of an acute MI become visible?

A

12-24 hours

333
Q

what are the three Ps of vasovagal syndrome?

A

Posture -

Provoking factors - she was in a warm, crowded environment

Prodromal symptoms - she complained of dizziness before the collapse

334
Q

what is dextrocardia?

A

a congenital defect where the apex and ventricles points to the right side rather than left

335
Q

what are the 4 conditions associated with tetralogy of fallot?

A

Pulmonary stenosis
right ventricular hypertrophy
ventricular septal defect
overriding aorta

My Cardiovascular (8 decks)

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