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Year 4 > Medicine - Cardiology > Flashcards

Medicine - Cardiology Flashcards

1
Q

What is the definition of heart failure and describe its aetiology

A

failure of cardiac output to meet the body’s requirements

Causes = MIGHT-VAC
metabolic
infection
genetics
HTN
Toxins (alcohol/drugs)
Valvular disease
Artery disease
Aortic stenosis
Congenital
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2
Q

What is the pathophysiology of heart failure?

A

Myocardial injury
LV dysfunction
Perceived reduction in circulating volume by the body
Neurohumoral activation = RAAS, ANP, SNS
Systemic vasoconstriction and Na/H2O retention

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3
Q

What are S/Sx of L-sided HF?

A 
pink frothy sputum + cough
orthopnoea
PND
bilateral basal creps (LUNGS!)
Reduced exercise tolerance
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4
Q

What are S/Sx of R-sided HF?

A

peripheral oedema (BODY!)
ascites
epistaxis
raised JVP

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5
Q

What features of HF are seen on X-ray? and ECG

A 
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vasculature
Pleural effusion

On ECG may be normal, or show:

  • ischaemia (T wave inversion/previous MI)
  • hypertrophy (BBB)
  • AF
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6
Q

How is HF classified?

A

Systolic (HF-REF) - EF<40%, inability of ventricle to contract properly (caused by IHD, male, cardiomyopathy)

Diastolic (HF-PEV) - EF>50%, inability of ventricle to relax properly (caused y cardiac tamponade, hypertrophy, restrictive cardiomyopathy)

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7
Q

What investigations would you carry out on a patient with suspected heart failure?

A 
History and examination
FBC
U&amp;E
TFT
BNP
ECG
CXR
ECHO = confirms diagnosis
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8
Q

What is the New York classification of heart failure?

A

1 - heart disease but no undue dyspnoea
2 - comfortable at rest, dyspnoea during ordinary activities
3 - dyspnoea during less than ordinary activities which is limiting
4 - dyspnoea at rest

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9
Q

What is the acute management of heart failure?

A 
sit up
oxygen
IV access and ECG
analgesia
furosemide
GTN
?CPAP
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10
Q

What is the treatment for chronic HF?

A

ABAL!

  • ACEi (or ARB)
  • B-blocker
  • add aldosterone antagonist (spironolactone)
  • loop diuretic (furosemide)

also. ..
- valsartan
- ICD
- ivabradine
- digoxin

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11
Q

What medications should be avoided in HF?

A
  • NSAIDS/glucocorticoids (cause fluid retention)
  • verapamil (- inotrope)
  • thiazoladinediones (DM drug that causes fluid retention)
  • Class 1 anti-arrhythmics (e.g. flecianide which is a - inotrope)
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12
Q

What is the definition of infective endocarditis?

A

microbial infection of endocardium (any interior heart surface but commonly the valves)

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13
Q

What common pathogens cause native valve endocarditis?

A

strep viridans
staphylococcus
enterococcus

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14
Q

What common pathogens cause prosthetic valve endocarditis?

A

CoNS

Staph aureus

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15
Q

What common pathogens cause IVDU endocarditis?

A

staph aureus

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16
Q

What common pathogens cause prosthetic valve endocarditis early post-op?

A

staph epidermis

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17
Q

Describe the pathogenesis of IE

A

portal of entry (dental/surgery/IVDU) + causative organism (HACEK)

  • haemophilus
  • actinobacillus
  • cardiobacterium
  • eikenella
  • kingella

endocardial damage -> vegetation formation -> embolisation of vegetative particles -> lots of mini embolic events in organs

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18
Q

What are the RFx for IE development?

A 
IVDU
Immunocompromised
DM
Alcohol
Older age
Rheumatic HD
Prosthesis
poor oral hygiene
piercings
tattoos
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19
Q

What are the S/Sx of IE?

A 
often non specific: delirium, weight loss, fatigue, malaise, weakness
- fever, rigors
splenomegaly
haematuria
glomerulonephritis
janeway lesions
osler nodes
splinter haemorrhages
finger clubbing
roth spots (retinal haemorrhages)

Fever + new murmur = IE until proven otherwise

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20
Q

What valve is commonly affected and at which you would hear a murmur in IE in an IVDU

A

Tricuspid!

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21
Q

How is IE investigated?

A 
Bloods
Blood cultures x 3 (30 mins apart, different sites, prior to Abx)
Urinalysis (?haematuria)
ECHO (TTE then TOE)
ECG
CT/MRI head (infarcts?)
CT/USS abdo (splenomegaly)
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22
Q

What are Duke’s criteria and how are they used to define IE?

A

Major criteria: positive blood cultures + evidence of myocardial involvement on imaging (ECHO)
Minor criteria: VF-PEP (vascular phenomena = janeway, fever, predisposing factors, immune phenomena = osler, positive atypical blood cultures which don’t meet the major criteria)

Definite = 2 major, 1 maj + 3 min, 5 min

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23
Q

How is IE treated?

A

Bactericidal Abx, guided by sensitivities

Usually gentamicin/vancomysin, taken for 6 weeks from the 1st day that blood cultures come back negative

50% pts need surgery (open or TAVI)
Open = tissue or mechanical heart valves

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24
Q

What are the indications for surgery in IE?

A 
Multidrug resistance
HF
Valve dysfunction
infection uncontrolled
repeated embolic events
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25
Q

Describe the components of the CHA2DS2VASC score

A 
Congestive HF
HTN
Age >74yrs (2)
DM
Stroke/TIA/thromboembolic event previously (2)
Vascular disease
Age 65-74
Female

Calculates risk of stroke with AF

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26
Q

Describe 2 signs of R and L sided heart failure

A

Right sided:

  • pedal oedema
  • raised JVP

Left sided:

  • pulmonary oedema (bibasal crepitations)
  • pleural effusions
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27
Q

On an ECG of someone presenting with acute chest pain, what features would you see in someone having an NSTEMI?

A

T wave inversion
ST depression
Pathological Q wave

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28
Q

On an ECG of someone presenting with acute chest pain, what are ST elevation, Q waves and a raised troponin signs of:

A

Infarction (i.e. STEMI)

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29
Q

What is Barlow syndrome?

A

Mitral valve prolapse = mid-systolic click murmur (heard loudest at apex)

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30
Q

What are the risk factors for coronary artery disease?

A

Smoking
HTN
Hyperlipidaemia
Diabetes

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31
Q

Describe the classifications from ACS

A

Acute coronary syndrome can be described as: MI or unstable angina

ST elevation and +ve cardiac markers = STEMI
No ST elevation and +ve cardiac markers = NSTEMI
No ST elevation and -ve cardiac markers = unstable angina

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32
Q

Define stable angina and its presentation

A

FIXED atheromatous stenosis in a coronary artery, angina pectoris is the symptom

Presents as central chest pain, discomfort and breathlessness precipitated by exertion/stress, and promptly relieved by rest

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33
Q

How is stable angina investigated?

A

Bloods
Resting ECG (usually normal/previous MI signs)
Stress testing and exercise ECG (may show ST depression which is indicative of ischaemia)
Cardiac biomarkers (usually normal)
Coronary arteriogram (gives info about the location and extent of artery clogging)

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34
Q

What is the treatment for stable angina?

A

Educate the patient

Medical Mg:

1) Symptomatic relief -> with GTN (they can take 2 doses of this 5 mins apart, and if 5 mins later there is still no improvement then CALL AMBULANCE)
2) Long term symptomatic relief
- > B-blocker (bisoprolol/atenolol)
- > Ca+ blocker (non-rate limiting e.g. felodipine, amlodipine, nifedipine)
- > others e.g. nicorandil, ivabradine…
3) Secondary prevention = BASE
- > B-blocker (may be on this already!)
- > Aspirin (75mg OD)
- > Statin (atorvastatin 80mg OD)
- > acE inhibitor (ramipril)

Surgical Mg:

1) PCI
2) CABG

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35
Q

2/3 of which 3 features are needed to diagnose ACS (i.e. unstable angina or MI)

A 
chest pain
cardiac enzymes (troponin)
ECG changes
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36
Q

What are the signs and symptoms of ACS?

A

Pain
anxiety
breathlessness
N&V
Collapse/syncope
Sympathetic activation -> tachycardia, sweating, pallor
vagal activating -> bradycardia and vomiting

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37
Q

How is ACS (acute chest pain) investigated?

A
  • Good history and examination
  • ECG (?ST elevation?) - if yes then STEMI, if no the NSTEMI or unstable angina
  • Biochemistry (troponin, CK, Raised WCC/CRP/ESR)
  • CXR (cardiomegaly? pulmonary oedema?)
  • ECHO (assess ventricular function and any complications e.g. valve disease)
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38
Q

Does NSTEMI suggest ischaemia or infarction?

A 
NSTEMI = suggests ischaemia
STEMI = suggests infarction
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39
Q

What is the definition of HTN and what are its causes?

A

Systemic HTN = persistent elevation of arterial BP >140/90

Optimal = <120/80

Primary causes = essential HTN accounting for 90% of cases, no attributable cause but RFx include age, gender, ethnicity, genetics, diet, obesity, alcohol…

Secondary causes = ROPE

  • Renal disease (renal artery stenosis)
  • Obesity
  • Pregnancy/pre-eclampsia
  • Endocrine
  • > hyperaldosteronism
  • > phaemchromocytoma
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40
Q

What is the presentation of hypertension?

A

Normally always asymptomatic but occasionally present with:

  • headache
  • visual changes
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41
Q

How is HTN diagnosed?

A

At least 2 high readings, taken 5 mins apart

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42
Q

How is HTN managed?

A

Lifestyle changes: exercise, weight loss, smoking cessation, diet…

Pharmacological:
Age <55 = ACEi
Age >55/afro-caribbean origin = Ca+ channel blocker

Then combine the two
Then add a thiazide-like diuretic

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43
Q 
Which tachyarrhythmia has:
A) narrow QRS and is regular
B) narrow QRS and is irregular
C) broad QRS and is regular
D) broad QRS and is irregular
A

A) SVT
B) AF
C) VT
D) VF

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44
Q

What are the adverse features associated with someone who has a tachyarrhythmia (which determine the treatment pathway in resus?)

A

HISS

Heart failure
Ischaemia/chest pain
Syncope/reduced consciousness
Shock/low BP

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45
Q

Describe the pathophysiology of AF and its 4 main categories:

A

Underlying heart disease causes structural remodelling, myocardial stretch and fibrosis leads to disrupted cell-cell coupling and electrical remodelling

1) paroxysmal - <48hrs, can be intermittent and recurring and is normally self-terminating
2) persistent - lasts >7 days
3) long standing - >1yr
4) permanent - pt no longer in efforts to return to sinus rhythm

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46
Q

What are the S/Sx of AF

A 
SOB
chest pain
palpitations/syncope
irregularly irregular pulse
narrow QRS
no P waves
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47
Q

How is AF investigated?

A

Bloods: ECG, FBC, TFT, troponin, U&E, LFT
Blood cultures: underlying infection?
ECHO: ?any structural abnormalities? (this must be carried out anyway before cardioverson to check for clots)
CXR: ?infection

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48
Q

How is AF treated?

A

HR >120 = think about treatment, HR > 150 = definitely treat

1) treat underlying cause
2) rate control: B blocker/Ca channel blocker/digoxin
3) -> if symptoms continue despite rate control or rate control is unsuccessful, rhythm control: amiodarone or flecianide
4) anticoagulation: use CHA2DS2VASc score to determine need for it, and HAS-BLED score to determine of the risks of anticoagulation outweigh the risks of bleeding
- > with NOAC/warfarin
5) cardioversion
6) other: maze ablation/LAA surgery

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49
Q

What is the CHA2DS2VASc score?

A 
Used to determine the need for anticoagulation and the risk of stroke in AF:
congenital HF
HTN
Age >74 (2 marks)
Diabetes
Stroke/previous TIA (2 marks)
Vascular disease
Age 65-74yrs
Sex (female)
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50
Q

What is the HAS-BLED score?

A

Used to determine if the risks of bleeding from anticoagulation are outweighed by the benefits of anticoagulating:

HTN
Abnormal liver/renal function
Stroke
Bleeding history/predisposition
Labile INR (i.e. unstable, easily altered)
Elderly (>65yrs)
Drugs/alcohol
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51
Q

Describe the types of cardioversion which can be carried out and the choice:

A

Decision to cardiovert depends on the timing and onset of AF:

  • immediately cardiovert if onset <48hrs ago / pt is haemodynamically unstable
  • delayed cardioversion if onser >48hrs ago and pt is stable -> pt should then be anticoagulated for 3 WEEKS before cardioverting and get ECHO first to check

Options for cardioversion are: electrical or chemical (amiodarone)

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52
Q

What are the reasons for urgently cardioverting a patient:

A

chest pain
decompensated HF
haemodynamically unstable (low BP)

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53
Q

Describe SVT and its aetiology

A

Supraventricular tachycardia
Regular, narrow complex tachycardia
The collective name for a group of conditions where the SA/atrial tissue is the cause of the sustained arrhythmia

Disorders of impulse formation or conduction

Either due to:
Increased cardiac muscle automaticity
Re-entry circuit formation

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54
Q

What are the signs and symptoms of SVT:

A

On ECG: Regular, narrow QRS, P waves absent/present

Symptoms: palpitations, chest pain, anxiety, light headedness, SOB, syncope

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55
Q

How is SVT investigated?

A

ECG

Bloods - TFT, troponin, FBC, LFT (?alcohol), CRP, cultures

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56
Q

What is the treatment of SVT?

A

Give O2, IV access, 12 lead ECG
Look for HISS adverse features
No adverse features:
- If the rhythm is regular -> vasovagal manouvres and adenosine (slows the HR)
- If the rhythm is irregular -> probably AF

Adverse features:
- seek expert help, sedation and electrical cardioversion, amiodarone

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57
Q

What are the causes of SVT

A

Often no cause identified

Sometimes: caffeine, stress, infection, thyroid disease, medications

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58
Q

Describe VT and its causes

A

Ventricular tachycardia
Wide QRS, regular
Improper ventricular electrical activity, shows torsades de pointed (sharks teeth) on ECG

Short spells can go unnoticed, long spells can lead to VF and sudden cardiac death

Causes: aortic stenosis, CAD, cardiomyopathy, electrolyte imbalances (low K/Mg)

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59
Q

Describe the different types of VT and their causes

A
  • Monomorphic (more common)
    the shape of each heart beat on the ECG looks the same because the impulse is either being generated from increased automaticityof a single point (in either the L/R ventricle) or due to a re-entrycircuit in the ventricle
    Scarring of the heart musclefrom a previous myocardial infarction is the most common cause -> the scar cannot conduct electrical activity, so there is a potential circuitaroundthe scar that results in the tachycardia
  • Polymorphic
    Most commonly caused by abnormalities of ventricular muscle repolarization (prolonged QT interval on ECG)
    QT prolongation may be congenital or acquired
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60
Q

What are the signs and symptoms of VT?

A

short periods - asymptomatic

longer periods - headaches, chest pain, SYNCOPE

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61
Q

How is VT investigated and treated?

A

Investigation:

  • Bloods - FBC, U&E, CRP, troponin, TFTs
  • ECG
  • Blood cultures

Treatment:

  • Cardioversion (amiodarone, DC)
  • Ablation therapy
  • ICD
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62
Q

Define VF and its causes:

A 
Irregular wide QRS  complex tachycardia
80% occur within 12hrs of an MI
Due to disordered electrical activity which causes the lower heart chambers to fibrillate (quiver) and prohibit the heart from pumping blood
Can cause sudden cardiac arrest
Causes:
- sepsis
- drugs
- IHD/MI
- cardiomyopathy
- aorta problems
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63
Q

What are the signs and symptoms of VF?

A

Loss of responsiveness
Breathing abnormalities
PULSELESS - requires cardioversion

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64
Q

How is VF investigated and treated?

A

Investigation:

  • ECG
  • Bloods
  • Cultures

Treatment:

  • CPR
  • Defibrillation
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65
Q

Define sinus bradycardia and its causes

A

HR <60, everything else normal
Causes:
Physiological - sleep, athletes
Pathological - increased ICP, sinus node disease, sepsis, hypoxia, IHD

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66
Q

What are the signs and symptoms of sinus bradycardia?

A

Usually asymptomatic, but rarely:

  • syncope
  • hypotension
  • dyspnoea
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67
Q

How is sinus bradycardia treated?

A

Usually no treatment needed if HR >40
Sometimes:
- atropine
- pacemaker

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68
Q

What is junctional bradycardia?

A

HR <60
Regular, narrow QRS, but NO P WAVES
Due to SA node dysfunction, meaning there is no atrial activity

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69
Q

How is sinus bradycardia treated?

A

Usually no treatment needed if HR >40
Sometimes:
- atropine
- pacemaker

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70
Q

What is junctional bradycardia?

A

HR <60
Regular, narrow QRS, but NO P WAVES
Due to SA node dysfunction, meaning there is no atrial activity

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71
Q

Define bundle branch block

A
  • electrical impulses are delayed/blocked as they travel through the heart
  • always symptomatic
  • may be a sign of an underlying heart condition which requires treatment
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72
Q

What is LBBB and its causes

A
  • delayed conduction of electrical signals through the left bundle branch
    Due to:
  • CAD, cardiomyopathy, ageing
  • septum depolarises R -> L, causing W(v1) and M (v6)
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73
Q

What is RBBB and its causes

A
  • delayed conduction of electrical signals through the right bundle branch
    Due to:
  • CAD, congenital heart disease, lung conditions
    BUT can also occur in healthy individuals with no underlying heart conditions
  • septum depolarises L -> R, causing M(v1) and W(v6)
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74
Q

What are the signs and symptoms of BBB

A

Often asymptomatic
Sometimes:
- palpitations, SOB, light headed, syncope, chest pain/discomfort

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75
Q

How is BBB treated?

A

pacemaker

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76
Q

Describe 1st degree AV block

A

Rate <60

PR interval >200ms

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77
Q

Describe 2nd degree AV block - Mobitz type 1

A

Rate <60
Narrow QRS
Progressive PR prolonging with random dropping of QRS complexes

78
Q

Describe 2nd degree AV block - Mobitz type 2

A

Rate <60
Narrow QRS
Constantly prolonged PR with RATIO of P-QRS dropping
E.g. 1:3, 1:2

79
Q

Describe 3rd degree AV block (complete HB)

A

Rate <60
Regular broad QRS
No relationship between P and QRS (atria and ventricles in complete dissociation)

80
Q

How is AV block investigated?

A 
ECG
Bloods (troponin, K, Ca)
ECHO
CXR
Angiography
81
Q

What is the treatment for AV block?

A

Pharmacological = anti-cholinergics (if bradycardic)

Surgical = pacemaker

82
Q

Define postural hypotension

A

A fall in SBP of at least 20mmHg (or 30mmHg if pt has HTN) +/- a 10mmHg fall in DBP within 3 minutes of standing

Becomes clinically significant when associated with symptoms of cerebral hypoperfusion:

  • syncope
  • falls (common in elderly)
83
Q

What are the causes of postural hypotension and the pathophysiology

A 
Causes:
- ageing: impaired adaptation to BP changes and reduced autonomic buffering capacity
- drugs
- dehydration
- dementia
Aggravating factors:
- hot weather/heat
- big meals
- long periods of standing

Pathology:

  • Normally when we stand, venous return decreases -> there is a transient drop in CO -> baroreceptors are triggered -> peripheral vasoconstriction occurs to maintain BP
  • However, failing of these mechanisms leads to orthostatic (postural) hypotension
84
Q

What are the RFx for postural hypotension?

A 
ageing
prolonged bed rest
dehydration
anti-hypertensive drugs, tamsulosin
underlying medical condition affecting autonomic nerve function e.g. DM, PD
85
Q

What are the S/Sx of postural hypotension?

A

syncope/fainting -> may be associated jerking
dizzy/light-headed
visual changes
symptoms worse on standing and better/relieved by lying down

86
Q

What are the differentials for postural hypotension?

A

vasovagal episode
vertigo
non-specific fall

87
Q

What are the investigations for postural hypotension?

A 
Postural testing -> BP sitting and standing, table tilt test
ECG
Bloods (NA)
Review of all medications
CT head
88
Q

How is postural hypotension treated?

A 
Remove RFx (causative medications)
Lifestyle changes
Mineralocorticoids (increase BP)
Fluids
Correct any underlying anaemia
89
Q

Define dyslipidaemia and its components

A 
dyslipidaemia = broad term describing disturbances in fat metabolism
E.g.:
- hypercholesterolaemia
- hypertriglyceridaemia
- mixed dyslipidaemia
90
Q

What are the causes of dyslipidaemia?

A

genetics + lifestyle
Primary = genetic mutation -> altered LDL production and clearance
Secondary = sedentary life style, diet
medical conditions -> DM, obesity, renal failure, hypothyroid, alcoholism
drugs -> diuretics, oestrogens, antipsychotics, steroids

91
Q

What are S/Sx of hyperlipidaemia

A 
xanthelasmas
tendinous xanthomas
obesity
CVD: angina, stroke, MI
T2DM
hypothyroidism
92
Q

What are the differentials of dyslipidaemia

A

liver disease
nephrotic syndrome
chronic renal insufficiency
hypothyroidism

93
Q

How is dyslipidaemia treated?

A

Diet/lifestyle - smoking cessation, weight loss, increased physical activity
Pharmacological - statins

94
Q

Which of the heart valves is bicuspid in shape (and all the rest are tricuspid)

A

Mitral valve = bicuspid

95
Q

Which type of murmurs radiate, and which can be accentuated?

A

Systolic murmurs = radiate

Diastolic murmurs = can be accentuated

96
Q

What issues can occur to heart valves:

A

calcification, infection, thickening, prolapse, annulus changes

97
Q

What investigations should be carried out if a murmur is heard?

A 
ECG (?hypertrophy)
CXR (?cardiomegaly)
Colour doppler (?regurgitation)
Exercise testing
Coronary angiography
98
Q

What is the general treatment for a faulty heart valve?

A

if symptomatic -> diuretics, ACEi/ARB

Surgery:
older = tissue valve (no anti-coagulation needed)
younger = mechanical valve

99
Q

Describe rheumatic valve disease

A

caused by acute rheumatic fever due to a group A strep (normally would present as pharyngeal infection)
Features: fever, joint pain and rash
Cross reactivity of antibodies against the infection lead to damage to connective tissues including heart valves

100
Q

What type of murmur is pulmonary regurgitation?

A

diastolic (continuous, decrescendo)

101
Q

What type of murmur is pulmonary stenosis?

A

late (ejection?) systolic

102
Q

Describe aortic stenosis

  1. sound
  2. causes
  3. other S/Sx
A
  1. ejection systolic murmur (crescendo-decrescendo)
  2. Idiopathic age related calcification, or RF
  3. Slow rising pulse, narrow pulse pressure, radiates to carotids, SAD (syncope, angina and dyspnoea)
103
Q

What is Corrigan’s sign?

A

visibly exaggerated carotid pulses (suggests a hyperdynamic circulation and seen in advanced aortic REGURGITATION)

104
Q

What type of murmurs does marfans predispose to?

A

usually aortic (normally regurg)

105
Q

Describe aortic regurgitation:

  1. sound
  2. causes
  3. S/Sx
A
  1. diastolic blowing
  2. idiopathic age related, CTD
  3. collapsing pulse, wide PP, corrigan’s sign, Austin flint murmur, L-sided HF (PND, orthopnoea, exertional dyspnoea)
106
Q

Describe tricuspid stenosis and its S/Sx

A 
a late diastolic murmur
presents with:
- raised JVP
- AF
- fatigue
- ascites
- oedema
107
Q

Describe tricuspid regurgitation and its S/Sx

A 
pan systolic
presents with:
- raised JVP
- ?jaundice (due to raised hepatic venous pressure)
- RV heave
- ascites
- fatigue
- oedema
108
Q

Describe mitral stenosis

  1. sound
  2. cause
  3. other signs
A
  1. diastolic rumbling, may have an opening snap (if the valve is calcified)
  2. caused by congenital (mitral valve disease) or RF
  3. tapping apex beat palpable, malar flush (due to backpressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation)
109
Q

Describe mitral regurgitation

  1. sound
  2. causes
  3. other S/Sx
A
  1. pansystolic blowing (radiates to axilla)
  2. Caused by old age, post MI, CTD, RF, IE
  3. Congestive heart failure (R-sided signs)
110
Q

Define ‘cardiomyopathies’ and the three classifications of types

A

= heterogeneous group of diseases affecting the heart MUSCLE associated with mechanical or electrical dysfunction
= can be primary or part of a systemic disorder

1) genetic cardiomyopathies
2) acquired cardiomyopathies
3) genetic + acquired cardiomyopathies

111
Q

Describe a genetic cardiomyopathy

A

Hypertrophic cardiomyopathy = formation of a hypertrophied LV in the absence of a pre-disposing condition

112
Q

Describe 2 acquired cardiomyopathies

A

1) inflammatory myocarditis

2) tako-tsubo (broken heart syndrome) = stress-provoked

113
Q

Describe 2 genetic + acquired cardiomyopathies

A

1) dilated cardiomyopathy (LV and RV dilatation)

2) restrictive cardiomyopathy (restrictive heart filling physiology in the presence of normal/reduced diastolic volumes)

114
Q

Name S/Sx of cardiomyopathies

A 
arrhythmias
chest pain
ECG changes
HF symptoms
INDIVIDUALS ARE AT RISK OF THROMBOEMBOLISM
115
Q

What is congenital heart disease?

A

Any structural abnormality of the heart present from birth

116
Q

what is dextrocardia?

A

Apex of the heart point to the LHS instead of the RHS

117
Q

Describe three differences between the foetal and adult circulatory systems:

A

1) foramen ovale = allows blood to flow from RA -> LA to avoid going to the lungs which in the foetus are not yet functioning (blood does not yet need baby oxygenation)
2) ductus arteriosus (PA -> aorta) = later becomes ligamentum arteriosum, as a back up to (1) so that any blood which does reach the RV is still diverted away from the lungs
3) Ductus venosus = shunts blood from the umbilical vein -> aorta, allowing blood to bypass the liver

118
Q

What is ‘shunting’ of blood?

A

Mixing of oxygenated and deoxygenated blood in any direction

  • cyanotic = deoxygenated blood mixes with oxygenated blood
  • acyanotic = O2 blood spreads into deoxygenated blood
119
Q

What is ccTGA?

A

congenitally corrected transposition of the great arteries

- double discordance, acyanotic, no shunting

120
Q

What is ASD?

A

Atrioseptal defect (acyanotic, blood shunted from LA -> RA)
E.g. a patent foramen ovale
can lead to eisenmenger syndrome

121
Q

What is Eisenmenger syndrome?

A

ASD and an acyanotic shunt, but which overtime becomes cyanotic as RV hypertrophy occurs and RV pressure > LV pressure, blood moves from RA -> LA

122
Q

What is coarctation of the aorta?

A

a congenitally narrowed area of the aorta which can be surgically repaired, HTN above and hypoTN below the area of narrowing

123
Q

What is transposition of the great arteries?

A

VA discordance = aorta and pulmonary artery are switched over
Cyanotic
2 completely separate independent circuits
Incompatible with life after birth so must be corrected with atrial/arterial switch

124
Q

What is tetralogy of fallot?

A

4 characteristic congenital lesions:

  • VSD
  • misplaced aorta (aorta sits over the VSD allowing the RV to pump some deoxygenated blood into it)
  • pulmonary valve stenosis
  • RV hypertrophy
125
Q

What is tricuspid atresia?

A

malformation of the tricuspid valve means blood cannot flow from RA -> RV
cyanotic
blood moves from one side of the heart to the other through:
- VSD
- ASD
- patent ductus arteriosus
Treated with a fontan operation

126
Q

What is a fontan operation?

A

Detach IVC/SVC and graft onto pulmonary artery
Detach the pulmonary artery from the heart so that only the aorta leaves the heart
This means you are left with one common ventricle to support the body (blood returns in IVC/SVC and goes straight to the lungs)

127
Q

What is acute pericarditis and its classical triad of presentation?

A

Inflammation of the pericardium, which can be idiopathic or secondary to viral/bacterial infection, autoimmune causes or drugs

Presents:

1) chest pain (relieved by sitting up and worse when lying flat)
2) pericardial friction rub (heard when leaning forwards)
3) ECG changes:
- PR depression
- Saddle shaped ST elevation

May also have:

  • raised troponin
  • FEVER
  • CXR may show pericardial effusion
128
Q

What is a pericardial effusion and its causes?

A 
Accumulation of fluid in the pericardial sac (10-50ml)
Causes:
- pericarditis
- myocardial rupture
- malignancy
- aortic dissection
129
Q

What are the S/Sx of pericardial effusion

A 
dyspnoea
chest pain
muffled HS
enlarged heart on CXR
ECG -> low voltage QRS complexes with alternating QRS morphology
130
Q

In pericardial effusions, local structures can becomes compressed. How does compression of:
A) phrenic nerve
B) diaphragm
C) Left lower lung lobe

present?

A

A) hiccups
B) nausea
C) bronchial breathing at the left base (Ewart’s sign)

131
Q

Describe constrictive pericarditis, its causes and presentation

A

When the heart is encaged in a rigid pericardium
Cause often unknown but can be due to TB/after pericarditis
S/Sx: Right sided HF, raised JVP, Kussmaul’s sign, ascites, oedema, splenomegaly, quiet HS

132
Q

What is a cardiac tamponade and what can cause it?

A 
A pericardial effusion which increases intra-peritoneal pressure leading to reduced ventricular filling and reduced CO
Causes:
- malignancy
- kidney failure
- chest trauma
- pericarditis
133
Q

How does cardiac tamponade present?

A

Beck’s triad: low BP, raised JVP and muffled HS

Fast HR and pulse
Kussmauls sign
Pulsus parodoxus (= a large reduction in stroke volume and SBP during inspiration)
- intrathoracic pressure swings are exaggerated and this is due to the fluid around the heart
- SBP falls >10mmHg during inspiration

134
Q

What are the normal layers of the aorta?

A
  • lumen
  • tunica intima
  • tunica media
  • adventitia
135
Q

Define aortic dissection and its causes

A
  • separation of the tunica media in the aortic wall
  • causes blood to flow into a new channel made between the inner/outer layers of the tunica media
  • as the dissection extends, it can occlude branches of the aorta leading to -> hemi/paraplegia, limb ischaemia, anuria (renal arteries blocked)

causes

  • CTD (marfan’s/ED)
  • iatrogenic
  • idiopathic
136
Q

What are type A and B aortic dissections?

A

Type A) involves the ascending aorta +/- descending aorta/aortic arch

Type B) no involvement of the ascending aorta, mainly the descending and abdominal aorta that are involved

137
Q

What are the signs/symptoms of aortic dissection?

A 
Sudden tearing chest pain
May radiate to back
Underlying CTD
BP different on RHS vs LHS
Syncope
138
Q

Describe the murmur grades

A

1 - barely audible/difficult to hear
2 - quiet
3 - easy to hear
4 - easy to hear + palpable thrill
5 - easy to hear with stethoscope barely touching chest
6 - audible with stethoscope hovering above chest

139
Q

Describe the pathophysiology of atherosclerosis

A
  1. Endothelial damage
  2. Chronic inflammation
  3. Immune cells attracted -> become foam cells as they ingest LDL -> fatty plaque forms
  4. Plaque ulcerates and attracts more platelets
140
Q

List modifiable and non-modifiable RFx for atherosclerosis (and CVD)

A

Modifiable:
- Lifestyle, diet, alcohol, smoking, stress, sleep, obesity

Non-modifiable:
- Age, gender (male), genetics, ethnicity, FHx

141
Q

Name some side effects of statins

A

Myopathy (raised CK)

T2DM

142
Q

List primary prevention for someone from CVD

A

Lifestyle factors (diet, alcohol, smoking, sleep, managing stress)

Do a QRISK3 score (calculates their risk of having a stroke/MI in the next 10 years) - a score of >10% means start a statin!

143
Q

Which diseases can result from atherosclerosis

A 
MI
HTN
Angina
PVD
Stroke
Mesenteric ischaemic
144
Q

Define ‘stable’ angina vs unstable angina

A

Stable = symptoms are predictable and come on with rest, and are relieved by GTN

Unstable = symptoms not related to activity or rest

145
Q

What investigations would you do for a patient presenting with angina?

A

Bloods (FBC to check anaemia (which can precipitate), U&E, TFT, lipids, HbA1C)
ECG
Exercise ECG
Cardiac biomarkers (troponin)
CT with coronary angiogram (GOLD STANDARD)

146
Q

How is stable angina managed?

A

RAMP

  • refer to cardiology
  • advise about diagnosis and when to phone ambulance
  • medical therapies
  • procedural (surgical) therapies
147
Q

Describe the 3 categories of medical treatment for angina

A
  1. Immediate symptomatic relief - GTN
  2. Long term symptomatic relief - B-blocker, Ca blocker, or nicorandil/ivabradine
  3. Secondary prevention of CVD = BASE
    - b-blocker
    - aspirin
    - statin
    - acE inhibitor
148
Q

What are the revascularisation options for stable angina?

A

PCI - balloon opens the lumen of stenosed vessel, and normally a stent is added too

CABG - open heart surgery, uses tissue from:

  • Great saphenous vein
  • Internal mammary arteries
  • Radial arteries
149
Q

As troponin is non-specific, list other pathologies in which it can be raised in

A
  • sepsis
  • aortic dissection
  • PE
  • chronic renal failure
150
Q

Describe the management of STEMI

A

If presenting <12 hrs - PCI

If >12hrs = consider for thrombolysis

Also give MONA

  • morphine
  • oxygen
  • nitrates
  • aspirin
151
Q

Describe the management of an NSTEMI

A

BATMAN

  • beta-blocker (unless contraindicated e.g. asthma)
  • aspirin
  • ticagrelor
  • morphine
  • anticoagulant (LMW heparin e.g. enoxaparin)
  • nitrates (GTN)

Give O2 if sats <95%

152
Q

What is the GRACE score?

A

Used post-NSTEMI, gives the patient a score to tell them their 6 month risk of a repeat MI or death (after their NSTEMI)
- if score >10% then they are high risk and should be considered for PCI to treat their underlying CAD

153
Q

What are the complications of an MI?

A

DREAD

  • death
  • rupture of septum/papillary muscles
  • oEdema
  • Arrhythmias/aneurysms
  • dressler’s syndrome
154
Q

What is dressler’s syndrome and how is it diagnosed/treated

A

Pericarditis developing 2/3 weeks post MI
Immune response
Presents with pleuritic chest pain, fever, pericardial rub/effusion/tamponade

Diagnosed by

  • ECG (ST elevation, T wave inversion)
  • ECHO (pericardial effusion)
  • inflammatory markers (raised ESR/CRP)

Treat:

  • NSAIDs
  • steroids
  • may need pericardiocentesis
155
Q

Describe secondary prevention for ACS

A 
BASE
- beta blocker
- aspirin
- statin
- acE inhibitor
PLUS
- another antiplatelet (ticagrelor)
- aldosterone antagonist (if pt has clinical HF e.g. epleronone)
156
Q

What is a type 1 MI?

A

Traditional MI due to an acute coronary event

157
Q

What is a type 2 MI?

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

158
Q

What is a type 3 MI?

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

159
Q

What is a type 4 MI?

A

MI associated with PCI / coronary stunting / CABG

160
Q

What is LVF

A

Left ventricular failure

  • LV unable to pump blood adequately
  • causes back log of blood
  • leads to pulmonary oedema (accumulation of interstitial fluid in lung tissues and alveoli)
161
Q

How is LVF caused?

A

Cardiogenic causes e.g. arrhythmias, MI

Non-cardiogenic causes e.g. XS fluids, AKI/CKD (Fluid overload), PE, ARDS

162
Q

What type of respiratory failure are patients with LVF in?

A

T1 RF

163
Q

WHat are the S/Sx of LVF?

A

SOB

Pink frothy sputum and cough

164
Q

What is the function of BNP?

A

B-natriuretic peptide (hormone released from ventricles when the cardiac muscle is stretched beyond normal range)

Function: relax smooth muscle in blood vessels to cause dilation and reduce peripheral vascular resistance
Also BNP acts on kidneys as ADH

BNP will be raised in heart failure

165
Q

List reasons other than heart failure as to why BNP may be raised

A
  • tachycardia
  • sepsis
  • PE
  • COPD
166
Q

What is the treatment of acute heart failure?

A

Pour SOD

  • stop fluids
  • sit up
  • oxygen
  • diuretics (furosemide)
167
Q

What is cor pulmonale?

A

right ventricular dysfunction secondary to chronic respiratory disease (usually pulmonary HTN)

168
Q

List causes of cor pulmonale

A
  1. Obstructive lung disease e.g. COPD, bronchiectasis
  2. Restrictive lung disease e.g. pulmonary fibrosis, NMD
  3. Vascular disease e.g. primary pulmonary HTN, PE
  4. Central issue e.g. obesity, sleep apnoea
169
Q

How does cor pulmonale present?

A 
SOB
Syncope
R-sided signs:
- Peripheral oedema
- Raised JVP
- Hepatomegaly
170
Q

Describe S3 and when (relative to S1/2) it would be heard

A

subtle
heart straight after S2
Caused by rapid ventricular filling and the chordae then snap tensely
- can be heard in young people (normal)
- can be heard in old people with stiffened chordae tendinae

171
Q

Describe S4 and when (relative to S1/2) it would be heard

A

ALWAYS PATHOLOGICAL
indicates a stiff ventricle
caused by turbulent blood flow from a forceful atria and then blood floods into the ventricle

172
Q

Describe which side of the stethoscope is used for what

A

Bell - deep sounds

Diaphragm = high pitched sounds

173
Q

How do you assess a murmur?

A

S–Site: where is the murmur loudest?
C–Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter)
R–Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?
I–Intensity: what grade is the murmur?
P–Pitch: is it high pitched or low and grumbling? Pitch indicates velocity.
T–Timing: is it systolic or diastolic?

174
Q

What is an Austin Flint murmur?

A
  • Early diastolic rumbling murmur heart loudest at the apex
  • The bloodjets from the aortic regurgitation strike the anterior leaflets of the mitral valve, causing them to vibrate, which often results in premature closure of the mitral leaflets. This can be mistaken for mitral stenosis.
175
Q

What could a midline sternotomy scar be from?

A
  • mitral valve replacement
  • aortic valve replacement
  • CABG
176
Q

Describe the two types of heart valve replacements and their pros/cons

A

Bioprosthetic

  • come from pig ‘porcine’
  • limited lifespan of 10yrs

Mechanical

  • good lifespan >20yrs
  • need to be on lifelong anticoagulation
  • INR targets 2.5-3.5
177
Q

Name the 2 most common types of heart valves used:

A
  • Tilting disc valve (single tilting disc)

- St Jude valve (2 tilting metal discs, less risk of thrombus formation)

178
Q

What complications can arise from prosthetic valves?

A
  • thrombus formation
  • haemolysis and anaemia (blood cells get churned up in the valve)
    infective endocarditis
179
Q

What is a TAVI used for and how is it carried out?

A

Treatment of severe AS (usually in patients who are at high risk from open surgery)

Wire fed through femoral artery under x-ray guidance and into aortic valve, then balloon inflates to stretch the stenosed valve, then a bioprosthetic valve may be left in the valve

180
Q

List 5 causes of AF

A

AF affects Mrs SMITH

  • sepsis
  • Mitral valve disease
  • infarction (post MI)
  • thyroid disease
  • HTN
181
Q

How to pacemakers work and what are their components?

A
  • deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function
  • made up of a pulse generator (the box) and then pacing leads (carry the impulses to the relevant part of the heart)
182
Q

What are the indications for a pacemaker?

A
  • Symptomatic bradycardias
  • Mobitz Type 2 AV block
  • Third degree heart block
  • Severe heart failure (biventricular pacemakers)
  • Hypertrophic obstructive cardiomyopathy -> (ICDs)
183
Q

What are the 4 main types of pacemaker?

A
  • Single chamber
  • Dual chamber
  • Triple chamber
  • ICD
184
Q

Describe how a single chamber pacemaker works

A
  • have leads in a single chamber, either in the right atrium or the right ventricle
  • if the issue is with the SA node, then the lead is placed in the RA
  • if the issue is in the AV node, lead is placed in the RV
185
Q

Describe how a dual chamber pacemaker works

A
  • leads placed in both RA and RV

- the pacemaker can then allow synchronised contractions of both the atria and ventricles

186
Q

Describe how triple chamber (biventricular) pacemakers work

A
  • leads in right atrium, right ventricle and left ventricle

- used for pts with HF

187
Q

How do ICD’s work?

A
  • continually monitor the heart and apply defibrillator shock to cardiovert the patient back in to sinus rhythm if they identify a shockable arrhythmia e.g. VF/VT
188
Q

What ECG changes would you see with a single-chamber pace maker?

A

Line before EITHER the P OR QRS

189
Q

What ECG changes would you see with a dual-chamber pace maker?

A

Line before both P and QRS complexes

190
Q

Describe HOCM (hypertrophic obstructive cardiomyopathy)

A

Cause of sudden cardiac death in young males -> AD inheritance
Muscle disorder caused by defects in genes encoding for contractile proteins
Relatively common (1/500)
Characterised by the development of a hypertrophied, non-dilated LV in the absence of another predisposing condition (like HTN or aortic stenosis)
Ejection systolic murmur -> increases with valsalva manoeuvre

Year 4 (28 decks)

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