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Sharon's phase 3b/4 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Arrhythmias - look at notes on onenote, includes pictures

ECGs: https://zerotofinals.com/medicine/cardiology/arrhythmias/

A

Abnormal heart rhythms
- Cardiac arrest rhythms
- Narrow complex tachycardia
- Broad complex tachycardia
- Atrial flutter
- Prolonged QT interval
- Ventricular ectopics
- Heart block
- Bradycardias

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2
Q

Arrhythmia: Narrow Complex Tachycardia

A

Fast heart with QRS complex < 0.12s (3 small squares).

4 main differentials: sinus tachy, supraventricular tachy, AF, atrial flutter

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3
Q

Arrhythmias: sinus tachycardia

A

Normal P waves, QRS complex and T waves

Not an arrhythmia but a response to underlying cause e.g. pain/sepsis

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4
Q

Arrhythmia: supraventricular tachycardia

A
  • QRS complex followed by T wave, P waves are buried in T waves
  • Often no apperant cause
  • Tx = vagal manoeuvres and adenosine
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5
Q

Arrhythmia: atrial fibrillation

A
  • Absent P waves and irregularly irregular ventricular rhythms
  • Treat with rate and rhym control
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6
Q

Arrhythmia: Atrial flutter

A
  • Atrial rate of ~300 beats per minute, saw tooth pattern, usually two atrial contractions for every one ventricular contraction
  • Due to re-entrant pathway and rhythm in either atriumresulting in self-peretuating loop
    • Treat with rate and rhythm control e.g. anticoagulation based on CHA2DSVASc and radiofrequency ablation
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7
Q

Arrhythmias: Broad Complex Tachycardia

A

Fast heart rate with QRS complex duration > 0.12s

  • Ventricular tachycardia (tx IV amiodarone)
  • Polymorphic ventricular tachycardia, such as torsades de pointes (tx IV magnesium)
  • AF with BBB (tx as AF)
  • Supraventricular tachycardia with BBB (tx as SVT)
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8
Q

Arrhythmia: prolonged QT interval

A
  • Start of QRS complex to end of T wave
  • > 440 ms in men
  • > 460ms in women

Tx: stop causative meds, correct electrolytes, beta blocker (not sotalol), pacemaker

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9
Q

miss jasmine

Causes of prolonged QT

A
  • Long QT syndrome
  • Meds e.g. antipsychotics, citalopram, amidarone
  • Electrolyte imbalances e.g. hypokalaemia, hypomagnesaemia and hypocalaemia
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10
Q

Arrhythmia: ventricular ectopics

A

Premature ventricular beats caused by random electrical discharges outside the atria

Appears as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG

Bigeminy = every other beat is a ventricular ectopic

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11
Q

Mx of ventricular ectopics

A
  • Healthy and infrequent = reassurance
  • Specialist advice if underlying heart disease, frequent/concerning symptoms, FHx of sudden death/heart disease
  • Beta blockers
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12
Q

Arrhythmia: Heart block (look at one note for ECG + more detail)

A
  • First-degree heart block = delayed conduction through the AV node
  • Second-degree heart block = Mobitz type 1 and 2
  • Third-degree = complete heart block, no relationship between P waves and QRS complexes, significant asystole risk
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13
Q

Asystole

A

Absence of electrical activity in the heart = cardiac arrest

Mx of asystole risk
- IV atropine (1st line) - inhibits parasympathetic nervous system
- Intotropes (e.g. adrenaline)
- Temp cardiac pacing e.g. transcutaneous or transvenous
- Pacemaker

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14
Q

Chronic heart failure

A

When heart function is impaired, the LV is not as effective in pumping blood out of the heart and around the body > increased fluid in left atrium, pulmonary veins and lungs > pulmonary oedema

  • HF with preserved ejection fraction > 50% = diastolic dysfunction with impaired LV filling
  • HF with reduced ejection fraction < 50%
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15
Q

Causes of chronic heart failure

A
  • IHD
  • Valvular heart disease (e.g. aortic stenosis)
  • HTN
  • Arrhythmia (e.g. AF)
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16
Q

Clinical features of chronic HF

A
  • SOB worse on exertion
  • Cough + frothy white/pink sputum
  • Orthopnoea (how many pillows?)
  • Paroxysmal nocturnal dyspnoea (waking with sudden cough, SOB, wheeze)
  • Peripheral oedema

Signs:
- Tachycardia + tachypnoea, HTN, murmur (VHD), bilateral basal crackles (wet = pulmonary oedema), raised JVP, peripheral oedema (ankle, legs and sacrum)

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17
Q

Ix chronic heart failure

A
  • Clinical asessment
  • N-terminal pro-B-type natruretic peptide (NT-proBNP) blood test
  • ECG
  • Echo

Refer to cardiology depending NT-proBNP

  • 400 - 2000ng/L = echo within 6 weeks
  • > 2000ng/L = echo within 2 weeks
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18
Q

New York Heart Association Classification for heart failure

A
  • Class I: No limitation on activity
  • Class II: Comfortable at rest but symptomatic with ordinary activities
  • Class III: Comfortable at rest but symptomatic with any activity
  • Class IV: Symptomatic at rest
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19
Q

Management of chronic heart failure

A

ABAL

  • ACEi/ARB (ramipril/candesartan) - renal function, hyperkalaemia
  • Beta blocker (e.g. bisoprolol)
  • Aldosterone antagonist if above ineffective (e.g. spironolactone) - renal function, hyperkalaemia
  • Loop diuretic (e.g. furosemide) - monitor U+Es

Surgery - implantable cardioverter defibrillators

ARB = Angiotensin receptor blocker

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20
Q

Atrial Fibrillation (AF)

A

Condition where the electrical activity in the atria becomes disorganised. Choatic electrial activity in the atria overrides regular, organised electrical activity from SA node.

-Irreguarly irregular pulse
- Tachycardia
- Heart failure due to impaired filling of the ventricles during diastole
- Increased risk of stroke (x5)

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21
Q

Common causes of AF

A

SMITH

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

Alcohol and caffeine too

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22
Q

Presentation of AF

A
  • Often asymptomatic, could be dx after stroke
  • Palpitations
  • Shortness of breath
  • Dizziness or syncope (loss of consciousness)
  • Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
23
Q

Key examination finding in AF

A

Irregularly irregular pulse.

Consider ventricular ectopics as differential - VE disappear above certain HR, normal HR during exerise indicate VE

24
Q

Investigations for AF

A

ECG:
- Absent P waves
- Narrow QRS complex tachycardia
- Irregularly irregular ventricular rhythm

25
Paroxysmal AF
Episodes of AF that occur spontaneously and resolve back to sinus rhythm - 24-hr ambulatory RCG (Holter monitor) - Cardiac event recorder for 1 - 2 weeks
26
Management of AF
- Rate or rhythm control - Anticoagulation to prevent strokes - Rate control is first-line* ## Footnote * Unless reversible cause of AF, new onset (within 48hrs), HF caused by AF, rate control ineffective
27
AF: options for rate control
1st line: beta blockers e.g. bisoprolol 1st line anticoagulation: DOAC (e.g. apixaban), warfarin as alternative | Remember most patients treated with bisprolol and DOAC for anticoag.
28
AF: options for rhythm control
Cadioversion - Immediate (<48hrs, life-threatening haem instability): electrical or pharmacological with flecainide/amiodarone (structual heart disease) - Delayed (>48 hrs, stable): electrical - anticoagulation 3 weeks before. Long-term = 1st line beta-blockers
29
AF: when is ablation considered?
When rate and rhythm control not effective - Left atrial ablation - identifying areas of abnormal signals and destroying them - Atrioventricular node ablation and a permanent pacemaker
30
CHA2DS2-VASC
Stroke risk score for patient with AF, and whether to start anticoagulation. C – Congestive heart failure H – Hypertension A2 – Age above 75 (scores 2) D – Diabetes S2 – Stroke or TIA previously (scores 2) V – Vascular disease A – Age 65 – 74 S – Sex (female) - 0 – no anticoagulation - 1 – consider anticoagulation in men (women automatically score 1) - 2 or more – offer anticoagulation Aspirin alone is not used for stroke prevention in AF.
31
AF: Orbit score
Assesses risk of major bleeding in patients with AF taking anticoagulation: O – Older age (age 75 or above) R – Renal impairment (GFR less than 60) B – Bleeding previously (history of gastrointestinal or intracranial bleeding) I – Iron (low haemoglobin or haematocrit) T – Taking antiplatelet medication ## Footnote Most pts with AF = risk of stroke with no anticoag. > bleeding risk on anticoag.
32
Management of Paroxysmal Atrial Fibrillation
- "Pill-in-pocket" - take flecainide+ when symptoms start - Anticoagulation based on CHA2DSVASc ## Footnote * Risk of atrial flutter, 1:1 AV conduction to ventricles = high ventricular rate
33
Thoracic Aortic Aneurysms
Dilatation of the thoracic aorta, most commonly ascending aorta (normally < 4.5cm) True aneursym = all three layers (intima, media and adventitia) intact, but dilated False aneurysms: intima and media rupture and blood enters adventitia = dilation
34
Risk factors for thoracic aortic aneurysm
- Men affected when younger and more often than women - Increased age - Smoking - HTN - FHx - Existing CVD - Marfan symdrome
35
Presentation and diagnosis of thoracic aortic aneurysms
Usually asymptomatic, incidental finding on CXR, echo or CT DIagnosis: echo, CT or MRI angiogram
36
Management of thoracic aortic aneurysm
Prevent progression by tx of modifiable RFs: stop smoking, healthy diet + exercise, optimise HTN, diabetes + hyperlipidaemia Depends on size: - Surveillance with regular imaging - Thoracic endovascular aortic repair (TEVAR) - Open surgery (midline sternotomy) Complications: aortic dissection, rupture, aortic regurgitation | TEVAR - stent via catheter via femoral artery to affected area of aorta ## Footnote Open surgery - remove affected section and replace with sythetic graft
37
Rupture of thoracic aortic aneuysms
Bigger = increase risk of rupture Bleeding into the mediastinum, oesophagus (haematemesis), lungs (haemoptysis), pericardial cavity (cardiac tamponade) - Severe chest/back pain - Haemodynamic instability - Collapse - Death (often patients do not reach hospital) Tx = emergency open surgery
38
Abdominal aortic aneursym (AAA)
39
Management and prevention of AAA
- One USS screening for males aged 65 - Manage risk factors e.g. smoking and optimise HTN, diabets and hyperlipidaemia - For large AAAs, surgery = endovascular repair (EVAR) or open surgery
40
Aortic dissection
Break or tear in the intima of the aorta, allowing blood to pool in between the intima and media = false lumen
41
Risk factors for aortic dissection
Same as PAD - Increasing age - Smoking - HTN (weight lifting, coacine, primary) - Poor diet - Male - Sedentary lifestyle Conditions/surgery: bicuspid aortic valve, coarctation of aorta, aortic valve replacement, Marfan's
42
Presentation of aortic dissection
- Often missed, typically old man with PMHx of HTN with sudden "tearing" or "ripping" chest pain if ascending aorta or back if descending aorta - Pain migrates, some pts don't have chest pain - DIfference in BP of arms (>20mmHg) - Radial pulse deficit - Collapse - Hypotension as dissection progresses - Focal neuro deficits (e.g. limb weakness)
43
DIagnosis of aortic dissection
ECG and CXR to rule ddx CT angiogram = 1st line to confirm dx
44
Management of aortic dissection
- Surgrical emergency with experienced seniors, vascular surgeons, anaesthetists, ICU team, high mortality - Analgesia e.g. morphine - Control BP and HR = beta blockers - Surgical intervention: type A = open surgery, Type B = TEVAR (see thoracic aortic aneurysm for details)
45
46
Complications of aortic dissection
- Myocardial infarction - Stroke - Paraplegia (motor or sensory impairment in the legs) - Cardiac tamponade - Aortic valve regurgitation - Death
47
Aortic stenosis
- Narrowing of aortic valve - Most common valve pathology + replacement - Ejection-systolic, high-pitched murmur, crescendo-decrescendo - Causes LVH (pump harder to overcome narrowing) - Causes: idiopathic age-related calcification (MC), bicuspid aortic valve
48
Aortic regurgitation
- Incompentent aortic valve, allowing blood to flow back from aorta into LV - Causes: age-related, biscuspid, Marfans or Ehlers-Danlos - Early diastolic, soft murmur or Austin-Flint murmur, "rumbling" at apex - Collapsing/Water hammer pulse (forcefully appearing then disappearing radial pulse)
49
Arterial ulcers
Due to insufficient blood supply to skin due to PAD Features (to distinguish it from venous ulcer): - DIstal, affecting the toes or dorsum of the foot - Associated with PAD, with absent pulses, pallor and intermittent claudication - Smaller than venous ulcers - Deeper than venous ulcers - Well defined borders - “punched-out” appearance - Pale colour due to poor blood supply - Less likely to bleed - Painful -Pain worse at night (when lying horizontally) - Pain worse on elevating and improved by lowering the leg (gravity helps the circulation)
50
Venous ulcer
- Gaiter area (between the top of the foot and bottom of the calf muscle) - Are associated with chronic venous changes, such as hyperpigmentation, venous eczema and lipodermatosclerosis - After minor injury to the leg - Larger than arterial ulcers - More superficial than arterial ulcers - Irregular, gently sloping border - More likely to bleed - Less painful than arterial ulcers - Pain relieved by elevation and worse on lowering the leg
51
Investigations for arterial/venous ulcers
- Ankle-brachial pressure index (ABPI) - Bloods (FBC (infection/anaemia), CRP, HbA1c, Albumin (malnutrition)) - Charcoal swab (infection) - Skin biopsy, 2WW to dermatology if skin skin cancer suspected
52
Management of arterial ulcers
- Same as PAD, urgent vascular sugery referral to consider surgical revascularisation - If tx effective, ulcer should heal quickly
53
Management of venous ulcers
NICE CKS Might need referral for: - Vascular surgery if mixed/arterial ulcers suspected - Tissue viability / specialist leg ulcer clinics in complex or non-healing ulcers - Dermatology if skin cancer suspected - Pain clinics if the pain is difficult to manage - Diabetic ulcer services (for patients with diabetic ulcers) - Wound care by experienced nurses: clean, debridment, dress - Compression therapy - Abx for infection - Analgesia (not NSAIDs)

Sharon's phase 3b/4 (15 decks)

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