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4th Year Medicine 2 > Cardiology Part 2 > Flashcards

Cardiology Part 2 Flashcards

1
Q

What are the 4 cardiac arrest rhythms?

A
  1. Ventricular fibrillation
  2. Ventricular tachycardia (pulseless)
  3. PEA
  4. Asystole
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2
Q

Explain what a sinus arrhythmia is? Is it normal?

A
  • Normal sinus arrhythmia – slight variations in heart rate due to reflex changes in vagal tone during the respiratory cycle
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3
Q

Describe sinus bradycardia?

A
  • Sinus bradycardia – heart rate less than 60bpm, can be physiological, caused by drugs or ischaemia, if acute it can be treated with atropine, if chronic and causing haemodynamic compromise will need pacing
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4
Q

Describe sinus tachycardia?

A
  • Sinus tachycardia – heart rate more than 100bpm, could be due to anxiety, fever, hypotension, anaemia or drugs, should treat underlying cause and if persistent use beta blockers
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5
Q

Explain what atrial flutter is?

A
  • This is a re-entrant rhythm where electrical signal re-circulates itself stimulating atrial contraction at 300bpm, usually every second beat is passed to the ventricles so most often there is a ventricular rate of 150 bpm
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6
Q

Sawtooth appearance on ECG with P wave after p wave

A

Atrial flutter

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7
Q

Conditions associated with atrial flutter?

A
  • It is associated with hypertension, ischaemic heart disease, cardiomyopathy and hyperthyroidism
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8
Q

Management of atrial flutter?

A
  • Management is similar to AF but can also do radiofrequency ablation of the re-entrant rhythm
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9
Q

Explain what is meant by a SVT?

A
  • Technically encompasses any arrhythmia originating above the ventricles but generally atrial fibrillation and atrial flutter are considered as separate
  • SVTs usually occur due to there being some form of perpetuating electrical signal loop with no end point
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10
Q

What happens with AVRNT?

A

Atrioventricular Nodal re-entrant tachycardia (AVNRT)
* This happens when there are 2 pathways in the AV node- a slow and fast pathway

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11
Q

Explain what happens with AVRT?

A
  • This is due to accessory pathways between the atria and the ventricles
  • It is most often caused by a condition called Wolf Parkinson White Syndrome, and in this syndrome the patient has an extra pathway called “The Bundle of Kent”
  • WPW can be asymptomatic and the person may not experience tachycardia
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12
Q

Characteristic WPW ECG pattern?

A
  • Characteristic ECG patter of WPW is slurred part of the QRS called a delta wave
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13
Q

Management of a SVT (AVRT and AVNRT)

A
  • First vagal manoeuvres
  • Next adenosine (depresses SA and AV node)
  • If these not worked, try verapamil or a beta blocker
  • Last resort would be synchronised DC cardioversion
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14
Q

Explain what vagal manoeuvres are and describe some examples?

A

Vagal manoeuvres stimulate the vagus nerve increasing parasympathetic activity which can slow conduction of electrical activity in the heart potentially terminating a SVT
3 examples are:
1. Valsava manoeuvres – these increase intrathoracic pressure e.g. blowing into 10ml syringe for 10-15 seconds, other versions involves popping ears, holding breath and bearing down (appears to be several versions)
2. Carotid sinus massage – attempt to stimulate baroreceptors in the carotid sinus by massaging that area on one side of the neck at a time (avoid in patients with carotid artery stenosis, carotid bruits or previous stroke/ TIA)
3. Diving reflex involves submerging that patient’s face in cold water

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15
Q

What is torsades de pointes?

A
  • Torsades de Pointes is a form of polymorphic VT that occurs in patients with a long QT interval
  • Normal VT is monomorphic – all the waves look the same
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16
Q

Define the QT interval?

A
  • QT interval = start of QRS complex to the end of the T wave
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17
Q

When is QT interval prolonged?

A
  • QT interval is prolonged if it is more than 440 ms (11 boxes) in men or 460 ms in women (11.5 boxes)
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18
Q

Causes of long QT interval?

A
  • Causes of prolonged QT include inherited long QT syndrome, medications such as antipsychotics, citalopram, flecanide, sotalol, amiodarone and macrolide antibiotics and electrolyte imbalances such as hypokalaemia, hypomagnesaemia and hypocalcaemia
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19
Q

Management of long QT?

A
  • Management of long QT involves stopping/ avoiding medications that prolong QT interval, correcting any electrolyte abnormalities, beta blockers and potentially pacemakers or implantable cardioverter defibs
  • If you have long QT syndrome generally advised to avoid strenuous exercise, swimming should be avoided, stressful situations, startling noises e.g. alarm clocks
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20
Q

Management of torsades de pointes?

A
  • Management of torsades de pointes includes correcting any underlying cause e.g. electrolyte disturbance or medications, magnesium infusion (even if serum magnesium is normal), defibrillation
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21
Q

Explain what ventricular ectopics are?

A
  • These are premature ventricular beats caused by random electrical discharges from outside the atria
  • Causes complaints of random brief palpitations and feelings of extra, missed or heavy beats
  • Common in all ages and can occur in normal healthy individuals
  • Can occur however due to a pre-existing heart conditions
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22
Q

What is bigeminy?

A
  • Bigeminy refers to when every other beat is a ventricular ectopic – ECG shows a normal beat (with a P wave, QRS and T wave) followed immediately by an ectopic beat, then a normal beat, then an ectopic and so on
  • Can also get trigeminy and quadrigeminy
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23
Q

Management of ventricular ectopics?

A
  • Reassurance an no treatment in otherwise healthy people with infrequent ectopics
  • Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g. chest pain or syncope) or a family history of heart disease/ sudden death
  • Beta blockers are sometimes used to manage symptoms
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24
Q

First degree heart block define, causes management?

A
  • This occurs when there is delayed conduction through the AV node
  • However, every atrial impulse leads to a ventricular contraction
  • Can be defined as a PR interval greater than 0.2 seconds (5 small or 1 big square)
  • Causes include ageing, damage from MI or surgery, hypothyroidism, electrolyte abnormalities, systemic disease e.g. sarcoidosis
  • Generally, doesn’t cause any symptoms and generally does not require any treatment
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25
Q

Second degree heart block, define, causes, management?

A
  • Causes of second degree heart block include coronary heart disease, cardiomyopathy, congenital heart disease, or as a result of ageing, electrolyte imbalances and some medicines
  • Mobitz type 1: progressive lengthening of PR interval until a beat is dropped
  • Mobitz type 2: PR interval is constant but every nth beat is dropped
  • In Mobitz type 1 no treatment is generally needed, body generally copes well and are often asymptomatic
  • In Mobitz type 2 this can be symptomatic and it is likely that the patient will need a pacemaker
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26
Q

Mobitz type 1?

A
  • Mobitz type 1: progressive lengthening of PR interval until a beat is dropped
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27
Q

Mobitz type 2?

A
  • Mobitz type 2: PR interval is constant but every nth beat is dropped
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28
Q

Does Mobitz type 1 or type 2 need treatment?

A

mobitz type 2 needs treatment - usually a pacemaker

mobitz type 1 does not need treatment

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29
Q

Third degree/ complete heart block, define, causes management?

A
  • Causes of complete heart block include coronary heart disease, cardiomyopathy, congenital heart disease, or as a result of ageing, electrolyte imbalances and some medicines
  • No action potentials from the SA node get through to the AV node
  • There is no observable relationship between p waves and QRS complexes
  • There is a significant risk of asystole – need a pacemaker
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30
Q

Explain what endocarditis is?

A
  • Infective Endocarditis is infection of the endocardium (generally the heart valves), it usually arises due to bacteria in the blood stream and abnormal cardiac endothelium that facilitates their adherence and growth
  • Bacteria can form vegetations on the valve after initial endothelial damage makes the valves susceptible to bacteria sticking to them
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31
Q

Explain what valves are affected in endocarditis?

A
  • Most endocarditis is left sided due to the relatively higher pressures on the left side of the heart that produces more turbulent flow across the valves predisposing them to this damage
  • Tricuspid valve endocarditis is usually due to drug use as the infective organism comes from the skin into the veins which first travel to the right side of the heart (should note that although right sided disease is most commonly due to drug users, it is still more common that drug users will have left sided disease)
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32
Q

Risk factors for endocarditis?

A

Anything that either predisposes you to more damage or predisposes you to infection essentially:
* Having a prosthetic valve
* Any form of structural heart pathology e.g. valvular heart disease, HOCM, congenital heart disease, implantable devices e.g. pacemaker
* Rheumatic heart disease
* IV drug use

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33
Q

Organisms involved in endocarditis?

A
  • Most common cause is Staph Aureus – particularly common as an acute presentations and in IV drug users (as inject from the skin into the bloodstream)
  • Strep viridans is another common cause – it is found in the mouth – endocarditis of this type would usually be related to dental disease or a dental procedure
  • Staph epidermis may be the organism involved in prosthetic heart disease
  • Enterococcus faecalis or strep gallolyticus – from the gut – can be related to disease, surgical procedure or malignancy (especially SG)
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34
Q

What criteria can be used for diagnosing endocarditis?

A

modified dukes criteria

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35
Q

Some general symptoms and signs of endocarditis?

A
  • Malaise (usually present)
  • Clubbing
  • Cardiac murmurs (usually present)
  • Cardiac failure
  • Arthralgia
  • Pyrexia (usually present)
36
Q

Describe the skin lesions you might get in endocarditis?

A
  • Osler nodes (antigen antibody complexes on hands, sore spots)
  • Splinter haemorrhages (small septic emboli seen in nails, not painful)
  • Janeway lesions (small septic emboli on palms and soles of hands and feet, not painful)
  • Petechiae
37
Q

Describe the eye lesions you might get in endocarditis?

A
  • Roth spots (antigen antibody complexes on the retina, these don’t actually cause any visual impairment)
  • Conjunctival splinter haemorrhages (rare)
38
Q

Investigations for endocarditis?

A
  • Blood cultures to determine causative organism (blood cultures should be done PRIOR to starting any antibiotic therapy if endocarditis is suspected)
  • Generally need to take 3 different sets of blood cultures from 3 different sites, 6 hours apart – obviously if the patient is very unwell then don’t wait this length of time
  • ECHO can be done to look for signs of endocarditis (trans-oseophageal echo is best and can pick up vegetations)
  • May also do ECG, CXR or MRI
39
Q

Empirical treatment for endocarditis?

A
  • In IV drug users give flucloxacillin
  • In those with native valves – amoxicillin and either gentamicin or vancomycin
  • In those with prosthetic valves – vancomycin, gentamicin, rifampicin (for biofilms)
40
Q

Specific treatments for endocarditis?

A
  • Staph A – flucloxacillin
  • Viridans – benzylpenicillin and gentamicin
  • Enterococci – amoxicillin/ vancomycin and gentamicin
  • Staph epi – vancomycin, gentamicin and rifampicin
41
Q

Explain what pericarditis is and some causes?

A
  • Inflammation of the pericardium
  • Most is either idiopathic or viral
  • Other causes includes: infections, autoimmune (e.g. SLE), post MI, post surgery, malignancy, medication induced e.g. methotrexate
42
Q

Explain what a pericardial effusion and a tamponade is?

A
  • A pericardial effusion is fluid in the pericardial space, a tamponade is when the effusion is large enough to raise intra-pericardial pressure which reduces CO and is a medical emergency
43
Q

Presentation of pericarditis?

A
  • Chest pain that is sharp, worse on inspiration (pleuritic), worse on lying down and better on leaning forward
  • Low grade fever
  • Pericardial rub may be heard on auscultation – this is a rubbing scratching sound
44
Q

Investigations for pericarditis?

A
  • Bloods will show raised inflammatory markers – WBCs, CRP and ESR
  • ECG – wide spread saddle-shaped ST-elevation and PR depression
  • ECHO can be used for diagnosis
45
Q

Management of pericarditis?

A
  • Combination of NSAIDs and colchicine is generally used as first line for patients with acute idiopathic or viral pericarditis
  • Most cases resolve within one month
  • Some patients may develop chronic pericarditis
46
Q

What is the most common cause of fainting?

A

vasovagal syncope

47
Q

Explain what is meant by vasovagal syncope?

A

refers to fainting due to the vagus nerve receiving a strong stimulus such as an emotional event, painful sensation or change in temperature
* When the vagus nerve receives a strong stimulus it can activate the parasympathetic nervous system, which can then cause blood vessels delivering blood to the brain to relax and cerebral hypoperfusion
* The patient then loses consciousness and faints

48
Q

What is meant by haemochromatosis?

A
  • This refers to iron overload
  • It can be primary or secondary
49
Q

Describe primary haemochromatosis?

A
  • Long term excess iron absorption with parenchymal rather than macrophage iron loading
  • The commonest form is due to mutations in HFE gene which causes a decreased synthesis of hepcidin resulting in increased iron absorption
50
Q

Describe secondary haemochromatosis?

A
  • Sources of secondary iron overload include repeated red cell transfusions and excessive iron absorption related to over-active erythropoiesis
  • This can occur in thalassaemia, sideroblastic anaemia, red cell aplasia and myelodysplasia
51
Q

Describe presentation of haemochromatosis?

A
  • Iron deposition in the liver causes fibrosis and cirrhosis
  • Deposition in the heart can cause cardiomyopathies and arrhythmias and in the skin there can be bronzing, the pancreas can be damaged leading to malabsorption (damage of exocrine portion) and diabetes (damage of endocrine portion)
  • Classic presentation is the “bronzed diabetic” although it’s usually picked up much earlier than this now
  • Although primary haemochromatosis is present from birth people tend not to present until later on in life, men at about 40 and women at about 60 (as they’ve been able to lose iron through menstruation previously)
52
Q

Investigations for haemochromatosis?

A
  • Transferrin % saturation is high
  • Total iron binding capacity is reduced (because you are running out of stuff for iron to bind to)
  • Increased ferritin levels (ferritin helps store iron)
  • Genetic testing for hereditary haemochromatosis
  • Used to need liver biopsy with prussian blue staining but genetic tests are more accurate now so this is generally not necessary
53
Q

Management of haemochromatosis?

A
  • Primary: repeated venesection (basically remove the iron rich blood every week or two)
  • Secondary: you cannot do venesection because they are already anaemic, need to give iron chelating drugs e.g. desferrioxamine
54
Q

Explain what myocarditis is?

A
  • Inflammation of the heart muscle
  • Inflammation causes swelling which makes it harder for heart to contract
  • Once inflammation resolved heart typically returns to normal
  • Occasionally can cause fibrosis and long term problems
55
Q

Causes of myocarditis?

A
  • Viral infections are a common cause: coxsackie B virus, HIV
  • Bacterial infections: diptheria, clostridia, lyme disease
  • Protozoa: chagas disease (trypanosoma cruzi), toxoplasma (in immunocompromised)
  • Autoimmune cause: SLE, sarcoidosis, polymyositis
  • Drug induced e.g. clozapine, acetazolamide, amitriptyline, colchicine etc. (these all cause a hypersensitivity reaction)
  • Toxic myocarditis – this occurs with ethanol, cytotoxic antibiotics, amfetamines, cocaine
56
Q

Presentation of myocarditis?

A
  • This can be very variable
  • Fatigue
  • Chest pain – which may be positional ie. Gets worse or better in particular positions
  • Arrythmias
  • Palpitations
  • Dyspnoea
  • Heart sounds – soft S1 or S4 gallop rhythm
  • Signs of heart failure
57
Q

Investigations for myocarditis?

A
  • ECG changes: ST segment elevation or depression, t wave inversions, arrhythmias, transient AV node block
  • Blood tests: FBC, U and E, creatinine kinase, ESR or CRP, LFT
  • CXR
  • ECHO
  • Looking for underlying cause e.g. viral serology
  • May want to do biopsy but this has risks associated
58
Q

Management of myocarditis?

A
  • Treatment of underlying condition
  • Treatment of myocarditis itself is mainly supportive
59
Q

What is angina?

A
  • It is a clinical diagnosis
  • Chest pain caused by myocardial ischaemia
  • The chest pain occurs on exertion when blood flow cannot meet demand
60
Q

Presentation of angina?

A
  • Chest pain – heavy, tight and gripping, it may be difficult for patients to describe
  • Has a characteristic pattern of being brought on by exertion but fading at rest
61
Q

Examination of angina?

A
  • There are generally no abnormal findings on examination
  • Occasionally a fourth heart sound may be heard
  • Should check for signs of anaemia, thyroid disease and hyperlipidaemia
  • It is also important to exclude aortic stenosis as this is a possible cause of angina
  • Blood pressure should be taken to identify coexistent hypertension
62
Q

Investigations for angina?

A
  • Laboratory tests: FBCs, Thyroid function, fasting glucose, HbA1c, fasting lipid profile, eGFR
  • 12 lead ECG
  • ECHO
  • Ambulatory ECG
  • CXR
63
Q

Management of angina?

A
  • First step is always to give education about condition and lifestyle advice, prognosis is good
  • Patients should be given short acting nitrates e.g. GTN spray for treating episodes of angina
  • Patients should be advised to repeat the dose of GTN after five minutes if the pain has not gone and to call an emergency ambulance if the pain has not gone five minutes after taking a second dose
  • Side effects of GTN to note are flushing, headache and light-headedness
  • Should also be on a beta blocker, 2nd choice would be verapamil or dilitiazem, or can give beta blocker with amlodipine, then may add a long acting nitrate
  • Drugs for secondary prevention should also be used aspirin, statins, ACEi and other anti-hypertensives
  • Revascularisation may be considered in some patients this could involve PCI (dilating arteries by putting in a balloon and stent) or CABG (anastomose other veins or arteries to make sure the stenosed area is still getting blood)
64
Q

Side effects of GTN?

A

flushing, headache and lightheadedness

65
Q

What are the 3 acute coronary syndromes? Define the differences?

A
  • Unstable Angina: anginal symptoms at rest or occurring at less physical exertion, cardiac enzymes remain normal and there is no necrosis
  • NSTEMI: anginal symptoms at rest but resulting in myocardial necrosis with elevated cardiac enzymes but no ST elevation on ECG, this is caused by extreme narrowing of the luminal area but not complete occlusion of the vessel
  • STEMI: anginal symptoms at rest but resulting in myocardial necrosis with elevated cardiac enzymes and ST elevation on ECG, this is caused by spontaneous plaque rupture resulting in complete occlusion of the artery
66
Q

Explain the difference between unstable angina and NSTEMI?

A
  • Both involve anginal symptoms at rest
  • NSTEMI involves myocardial necrosis indicated by elevated cardiac enzymes, unstable angina does not
  • It is likely a sort of spectrum of disease as opposed to clear cut divisions between the two
67
Q

Management of NSTEMI and unstable angina?

A
  • NSTEMI and unstable angina are managed similarly
  • Should get an initial 300mg dose of aspirin
  • Use established GRACE scoring system to predict 6 month mortality and risk of cardiovascular event
  • If low risk (predicted 6 month mortality < 3%) – consider conservative management without angiography, offer tiagrelor with aspirin, ischaemia testing before discharge, can reconsider angiography (with follow on PCI if indicated) if ischaemia develops or shown on testing
  • If intermediate or higher risk (predicted 6 month mortality > 3%) offer angiography (immediately if unstable or within 72 hours if stable) with follow on PCI if indicated
  • Those who have had NSTEMI should have an ECHO and left ventricular function assessed and should consider this in unstable angina
  • Cardiac rehabilitation and secondary prevention should be done like in STEMI
68
Q

Describe the scoring system that is used for management of unstable angina and NSTEMI?

A

GRACE scoring system
* Use established GRACE scoring system to predict 6 month mortality and risk of cardiovascular event
* If low risk (predicted 6 month mortality < 3%) – consider conservative management without angiography,
* If intermediate or higher risk (predicted 6 month mortality > 3%) offer angiography (immediately if unstable or within 72 hours if stable) with follow on PCI if indicated

69
Q

Management of NSTEMI?

A

B- base decision re angiography and PCI on GRACE Score
A- Aspirin 300mg stat dose
T- ticagrelor 180mg stat dose (clopidogrel if high bleeding risk or plasugrel if having angiography)
M- morphine titrated to control pain
A- Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N- Nitrate (GTN)

70
Q

Why is aspirin helpful in a MI?

A
  • Acute coronary syndromes result from a thrombus blocking a coronary artery, when a thrombus forms in a fast flowing artery such as the coronary artery it is mainly made of platelets which is why aspirin is used
71
Q

What do pathological q waves (abnormally wide or abnormally deep) suggest?

A

suggests a deep MI involving full thickness of the heart, typically 6 or more hours after symptom onset

72
Q

Presentation of STEMI?

A
  • Severe crushing chest pain radiating to jaw and arms, especially the left, symptoms are similar to angina but not relieved by GTN (MI pain usually need opiates!)
  • May have sweating, nausea and/or pallor
73
Q

Investigations for STEMI?

A

ECG changes:
- ST elevation
- T wave inversion
- Leads correspond to what area is damaged

Enzymes:
- There is often not time to wait for enzymes
- CK only peaks after 24 hours
- Troponin is better at detecting small amounts of cardiac necrosis and will be in bloodstream 2-3 hours after initial onset of chest pain
- However, it should be noted that CK and troponins are not specific markers and can be elevated in other conditions, everything needs to be interpreted in context

74
Q

ECG changes for STEMI which artery which area?

A

Right coronary artery – inferior aspect of the heart – II, III and aVF
Left coronary artery – anterolateral aspect of the heart – I, aVL, V3-V6
Left circumflex – lateral aspect of the heart – I, aVL, V5-V6
Left anterior descending – anterior aspect of the heart – V1-V4

75
Q

Right coronary artery STEMI?

A

inferior aspect of the heart – II, III and aVF

76
Q

Left coronary artery STEMI?

A

anterolateral aspect of the heart – I, aVL, V3-V6

77
Q

Left circumflex STEMI?

A

lateral aspect of the heart – I, aVL, V5-V6

78
Q

Left anterior descending STEMI?

A

anterior aspect of the heart – V1-V4

79
Q

Management of STEMI?

A

Early Treatment (MONAT) – MORPHINE, OXYGEN, NITRATES, TICAGRELOR
1. Morphine plus an anti-emetic
2. Oxygen if the patient is hypoxic
3. GTN if BP > 90
4. Aspirin 300 mg
5. Ticagrelor 180mg

If a patient is more than 2 hours from hospital they are given thrombolysis therapy, if they are less than 2 hours they are prepped for PCI and taken to hospital

80
Q

Rehabilitation and secondary prevention of MI?

A
  • Appointments with rehabilitation nurses looking at physical activity and diet etc.

Drugs for secondary prevention include:
- ACE inhibitor (continue indefinitely)
- dual antiplatelet therapy (aspirin plus another for up to 12 months)
- Beta blocker (continue indefinitely)
- Statin lifelong (usually atorvastatin 80mg)

81
Q

List some complications post MI?

A

heart failure
myocardial rupture and aneurysmal dilatation
ventricular septal defect
mitral regurgitation
cardiac arrhythmias
conduction disturbance
Post MI pericarditis (in days) or Dresslers syndrome (weeks)

82
Q

Explain what Dresslers syndrome is?

A
  • Dresslers syndrome is an autoimmune response to cardiac damage occurring 2-10 weeks post infarct, autoimmune reaction to myocardial damage is the main aetiology and antimyocardial antibodies can be found
  • causes a pericarditis
83
Q

Causes of cardiac tamponade?

A

Acute (less blood heart doesn’t have time to adapt so it causes tamponade): penetrating or blunt trauma, post MI, heart surgery, aortic dissection

chronic (much more blood as heart has time to adapt): after pericarditis, cancers, due to inflammation in CTD

84
Q

What is Becks triad?

A

signs of cardiac tamponade:

raised JVP
hypotension
muffled heart sounds

85
Q

Explain what pulsus paradoxus is?

A

this is a sign of cardiac tamponade - drop in BP on inspiration - pulse may disappear on inspiration when examining

86
Q

What does a posterior MI often occur with?

A

can occur on its own but often occurs with inferior or inferolateral MI

87
Q

Appearance of posterior MI on ECG?

A

wont see ST elevation of normal ECG (as this is viewing the anterior part of the heart)
ST depression in leads V1-V3
if cooccurring with inferior or inferolateral may see ST elevation in these leads

4th Year Medicine 2 (14 decks)

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