Cardiology Flashcards

1
Q

What is acute coronary syndrome?

A

[1] unstable angina

[2] NSTEMI and STEMI - non ST elevated MI and ST elevated MI

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2
Q

Pathiophysiology of an MI

A

occurs when there is insufficient blood supply to the heart (or none at all)- can cause muscle damage
is a medical emergency

This is usually due to coronary artery disease, atherosclerotic plaques in the coronary arteries cause progressive narrowing of the lumen, and symptoms occur when blood flow does not provide adequate amounts of oxygen to the myocardium when oxygen demand increases.

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3
Q

symptoms

A
crushing chest pain - may radiate to neck jaw back
patient appears pale, sweaty and grey
Nausea and vomiting
systolic BP less than 90
Shortness of breath
may present with arrhithymas and syncope
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4
Q

what is levines sign?

A

clenched fist held over the chest to describe ischemic chest pain

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5
Q

List as many risk factors…

A
FH of MI
Age 
Men - 2-3x more common
lack of exercise
high fatty diet
high cholesterol
hypertension 
hyperlipidemia 
diabetes 
smoking
alcohol
high levels of coagulation factors
stress at work
elevated CRP
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6
Q

what would be visible on an ECG

A

tall tented t waves first
tgeb ST elevated
T flattening inversion
broad q WAVES

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7
Q

additional test results

A

elevated troponin

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8
Q

how would you manage this patient?

A

GTN spray 2.5-5mg
coronary angioplasty
thrombolytics

R eassurance
O xygen
M orphine 
A nticoagulants 
N itrates 
Clopedigrel 
Emoxiprin
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9
Q

what can you give if HR is fast and what is value for it

A

HR >100bpm
metropolol
but not if hypotensive, bradycardiac, asthmatic or has HF

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10
Q

when would you consider IV insulin infusion

A

if glucose is >11mmol

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11
Q

prevention measure

A
lifestyle factors- altering diet, losing weight, doing exercise
statin 
beta blocker 
ACEi 
antiplatelet medications -clopidogrel
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12
Q

when can they drive and return to work

A

1 and 2 month respectively

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13
Q

what is dressler syndrome?

how can it be treated

A

POST MI syndrome using 2-10 weeks later
recurrent fever , chest pain and effusion
due to autoantibodies to the heart muscle
NSAIDs and steriods

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14
Q

what percentage have no pain? what percentage of deaths in the UK?

A

20%

30%

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15
Q

Hypertension…

what is it?

A

a long term condition, also known as high blood pressure, it is a major risk factor for CVD
arterial BP is elevated

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16
Q
risk factors for hypertension? (6)
including conditions (5)
A
include 
high salt intake
fatty diet
lack of exercise 
alcohol
smoking 
age 
can be caused by other conditions such as 
pregnancy 
cushing syndrome
conns syndrome
coarctation of the aorta
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17
Q

diagnosis occurs how?

A

BP checks
usually an incidential finding
can check protein in urine - Albumin:creatinine ratio
confirm with 2-3 measurements
ambulatory BP monitoring -frequent measurements 2 per hour, use average of 14 atleast

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18
Q

management of these patients

A

[1] lifestyle and education - alter diet, lose weight, stop smoking and cut down alcohol, diabetic control
[[2] if this does not work, consider an ACEi or an ARB as a first line (Younger than 55)

unless over 55 and/or afro-Caribbean than use CCB

if this does not work consider increasing dose and combination of the 2.
Ace inhibitor+Calcium Channel blocker

if still resistant, then consider thiazide duiruetic Ace inhibitor+ thiazide-type diuretic

then consider ACEI + CCB +TD

if still no success with combination and TD then cosndier adding spironocolone or using beta blocker

Consider seeking specialist advice

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19
Q

when can beta blockers be used

A

child bearing female (or potential)

contraindication with ARB or ACEi

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20
Q

Angina— define angina?

A

angina is myocardial ischemia and presents with central chest pain/tightness/heaviness

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21
Q

what makes it better and wrose?

where may it radiate?

A

intiated by exertion
relieved with rest/GTN within about 5 minutes

mat radiate to left arm, neck, jaw or back.

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22
Q

what is unstable angina?

A

increased frequency of angina
unpredictable
rest makes no difference -still pain

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23
Q

another name for unstable angina

A

cresendo

24
Q

what is decubitius angina

A

occurs when lying flat

25
Q

risk factors

A

same as MI

Age, male, family history (counts as first degree relative has developed has developed ischaemic heart disease before the age of 50). Hyperlipidaemia, cigarette smoking, hypertension, metabolic factors (e.g. Diabetes), diet (high in fat, low in antioxidant), lack of exercise, psychosocial factors (work stress, lack of social support, depression), elevated CRP, high alcohol intake and high levels of coagulation factors.

26
Q

investigations

A

• Pathological Q waves (in particular)
• Left bundle branch block
• St-segment and T-wave abnormalities (for example ST-segment depression, T wave flattening, or T-wave inversion)
But remember a normal ECG does not confirm or exclude angina

27
Q

management

A

remove risk factors
aspirin - reduces mortality by 34%
[1] beta blocker - atenolol or CCB
nitrates-GTN spray
K channel activator -nicorandil
coronary artery bypass graft if still not working
refer if sundden onset /recurrent angina after past MI or uncontrollable

28
Q

what is contraindicated?

A

phosphodiesterase inhibitors (sildenafil, tadalafil, and vardenafil), often used in the treatment of erectile dysfunction

29
Q

differentials

A

MI, unstable angina, Prinzmetals angina (a form of angina though to be caused by vasospasm), dissecting thoracic aneurysm, pericardial pain, acute congestive heart failure, arrhythmias. GI causes (peptic ulcer disease, GORD), MSK (costochondritis, rib fracture, osteoarthritis, osteoporosis, rheumatoid arthritis), psychological causes (anxiety, panic attacks, depression), respiratory causes (PE, pneumothorax, lung tumour), referred pain from thoracic spine

30
Q

Name 3 other agents and their action

A

ivabradine - inhibit current in SA node and therefore HR
trimetazidine -inhibit FA oxidation
ranolazine - inhibit late NA curent

31
Q

what is AF

A

Chaotic irregular atrial rhythm (300-600bpm). AV node responds intermittently hence an irregular ventricular rhythm. This causes cardiac output to  by 10-20% (atria don’t prime ventricles reliably

32
Q

symptoms

A
  • May be asymptomatic
  • Chest pain
  • Palpitations
  • Dyspnoea
  • Faintness
33
Q

sign

A

Irregularly irregular pulse
Apical pulse greater than radial rate
1st heart sound of variable intensity
Signs of LVF

(Examine whole patient- AF often associated with non-cardiac disease)

34
Q

causes

A
mitral valve disease
hyperthyroidism
Heart failure
Hypertension 
IHD
PE
Mitral valve disease 
Pneumonia 
Hyperthyroidism 
Caffeine 
Alcohol 
Post-op 
Low K+ or low Mg2+ 
Rare causes; endocarditis, haemochromatosis, cardiomyopathy, constrictive pericarditis
35
Q

rf

A
age >60
diabetes
hypertension
hypercholestermia 
previous MI
heart failure
36
Q

ddx

A
  1. Atrial flutter
  2. Atrial tachycardia
  3. Wolff-Parkinson-White syndrome (extra electrical pathway between heart’s upper & lower chambers causes a rapid heartbeat
37
Q

tests

A

ECG (absent P waves, irregular QRS complexes)
Blood tests; U&E, cardiac enzymes, thyroid function tests
Echo (L atrial enlargement, mitral valve disease, poor LV function, other structural abnormalities) fibrosis diltation

38
Q

management

A

acute: first line is CCB or beta blocker, 2nd is digoxin and amoridone, then consider flecanide cardioconverison
same with chronic

anticoagulation varies - warfarin/NOAC in chronic but in acute LMWH unless emboli risk high then warfarin. If no risk factor and stable sinus rythmn thhen no antiCoagultation needed.

avoid triggers
aspirin and warfarin 
angioplasty and cathether ablation 
beta blockers
amaridone

ACUTE AF
If adverse signs (e.g. shock, chest pain, ECG changes);
• ABCDE & senior help
• Direct current (DC) cardioversion (synchronized shock) +/- amiodarone
Stable & AF started <48hrs ago;
• Rhythm control- DC cardiovert or give flecainide (anti-arrhythmic drug) or amiodarone
• Start heparin
Stable & AF started >48hrs ago/ unclear time of onset;
• Rate control- bisprolol or diltiazem
• If choose rhythm control- anticoagulated >3wks first
Correct electrolyte imbalances
Treat associated illnesses
Consider anticoagulation (no anticoag if stable snus rhythm restored, no emboli risk factors & recurrence unlikely)

CHRONIC AF
Anticoagulation
Rate control;
• -blocker or rate-limiting calcium channel blocker are 1st choice (don’t give -blockers with verapamil)
• If this fails consider digoxin then amiodarone
Rhythm control;
• Elective DC cardioversion (do echo 1st- check for intracardiac thrombi)
• Elective pharmacological cardioversion- flecainide 1st choice (amiodarone if structural heart disease)
• AVN ablation with pacing or pulmonary vein ablation may be considered
Paroxysmal AF;
• Sotalol or flecainide PRN (if; Af infreq, BP >100mmHg systolic, no past LV dysfunction)
• Anticoagulate (assess need; embolic stroke risk vs risks of anticoagulation- use scores fpr each)
• Consider ablation if symptomatic or frequent episodes

39
Q

what is endocarditis?

A

inflammation of the endocardium layer of the heart tissue

usually involves valves

40
Q

what can be characteristic of it?

A

vegetations that can be seen in echocardiogram

made of fibrin, platelets and inflamationary cells on the chordiae tedniae

41
Q

causes

A

infective- 50-60% strep. viridans from mouth, s.aureus via skin coagulase negative staphylococci – prosthetic valves
can be acute or subacute
other causes
non bacterial thrombolytic endocarditis NBTE
endocarditis of SLE-libman sacks disease

42
Q

risk factors

A
ivdu 
artiifical valves 
califcation of stenosis
congential defects 
dental disease
prolonged catheters 
Gentourinary disease
dabetes
wounds
bowel cancer- s. bovis
43
Q

symptoms and signs

A
flu-like symptoms 
Fever
Roth spots
Osler nodes- digits, painful 
Murmur- associated with left IE
Janeway lesions - erythematous on palms and soles
Anaemia 
Nails- splinter haemorrhage 
Emboli

immunological conditions e.g. glumeronephritis

44
Q

differences between acute and subacute

A

subacute- less nasty, can be treated with antibiotics, lower virulence, less destructive
acute- more destructive, higher virulence, surgical treatment, more nasty

45
Q

who can vegetations be seen in and what arethey

A

small sterile aggregated along the valuve edge or on the cusp
doesn’t cause inflammation
usually during hypercoaguable state such as pregnancy, dvt
may rbeak off and lodge in brain or heart
cancer patients increase risk due to debilating state
in SLE

46
Q

what is rheumatic fever - who and how does it present

A

rheumatic feature is an inflammati0ory diseaseaffecting heart, brain joint and skin
following GROUP A STEPTOCOCCAL PHARNYNGITIS
rare
vegetations - veruccae
aschoff bodies- cardiac lesions, nodules in the heart
cause of mitral stenosis
Antibodies against M proteins of streptococci
clinical features include nose bleeds, painful joints, fever, chorea- jerky movements
carditis
sore throat
malaise

47
Q

Ix of infective endocarditis

A
bloods- culture- microorganisms, anaemia FBC 
ESR, CRP for infection 
echocardiogram for vegetations 
CXR 
ECG
48
Q

Treatment

A

abx dependent on cause
vancomycin - s.aureus

pencillin if viridans
beta lactam - naficliin and aminoglycoside

1st line gentamicin, benzypencillin and flucaxoacillin

49
Q

what is congestive heart failure

A

Chronic progressive condition affecting pumping power of heart muscles- specifically refers to stage fluid builds up around heart & causes it to pump inefficiently. Veins near heart become ‘congested’ (full of blood). Term for pts with breathlessness & abnormal Na & water retention (causing oedema)

Left sided failure (systolic or diastolic failure) & right sided failure that occur together= CCF

50
Q

what is postural hypertension

A

drop in systolic BP by 20mmHg or diastolic by 10mmHg on standing

51
Q

causes

A
hypovolemia
after long run
hypopituaritism 
addisons disease 
autonomic neuropathy 
parkinsons
pregnancy
52
Q

diagnosis

A

BP monitor in clinic
posture test
tilt test- lie for 15 mins and then stand/tilt up, monitor bp and heart rate for 45 mins - postural hypertension bp will drop instantly on standing

53
Q

management

A
compression stockings
drink more water 
stand slowly 
head of bed elevated 
avoid caffeine 
small and frequent meals
 if not managed then consider FLUDROCORTISONE AND MIIDODRINE/E[HDRINE
54
Q

What meds can cause it

A

antihypertensives
anti-psychotics
nitrates
diuretics

55
Q

symptoms

ddx

A
lightheadedness 
syncope
blurred vision 
nausea 
ddx- vertigo
asovagal syncope (collapse