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Cardio Flashcards

1
Q

Give 5 complications of atherosclerosis.

A 
Angina
MI
TIA
Stroke
Peripheral vascular disease
Mesenteric ischemia
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2
Q

Describe the primary prevention of cardiovascular disease.

A

QRISK3 score - calculates risk of stroke/MI in next 10 years.
If >10%, or CKD/T1DM for more than 10 yrs, offer a statin eg atorvastatin 20mg nocte
Check lipids at 3 months and increase the dose to aim for >40% in non-HDL cholesterol.
Check LFTs within 3 months of statin and then at 12 months. statins can cause transient and mild rise in ALT/AST in first few weeks of use, often don’t need stopping though if the rise is less than 3 times the upper limit of normal.

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3
Q

Describe the secondary prevention of cardiovascular disease.

A

(after cvd)
Aspirin 75mg daily + clopidogrel 12 months
Atorvastatin 80mg
Beta blocker eg bisoprolol titrated to max tolerated dose
ACE inhibitor eg ramipril titrated to max tolerated dose

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4
Q

Give 3 side-effects of statins.

A

Myopathy - check creatinine kinase in patients with muscle pain or weakness
Type 2 diabetes
Haemorrhagic strokes (rare)

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5
Q

Give 3 modifiable and 3 non-modifiable risk factors for atherosclerosis.

A

Modifiable: smoking, alcohol, diet (high in sugar and trans fats, low in fruit and veg and omega 3), exercise, obesity, poor sleep, stress
Non modifiable; age, family history, male sex
Medical comorbidities: diabetes, htn, CKD, inflammatory conditions eg RA, atypical antipsychotics

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6
Q

What is angina? How is it classified?

A

Symptoms of chest pain due to narrowing of the coronary arteries reduces blood flow to the myocardium.
Stable = symptoms always relieved by rest or GTN
Unstable = symptoms at rest (ACS)
Also can be classified as typical or atypical.

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7
Q

What investigations would you do for ?angina?

A

gold standard = CT coronary angiogram. would show stenosis.
Baseline investigations:
ECG, FBC, U+Es, LFTs, lipid profile, TFTs, HbA1C

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8
Q

How is angina managed?

A

Think RAMP:
Refer to cardiology (urgently if unstable)
Advice about diagnosis, management and when to call 999
Medical:
-symptomatic: GTN, b-blocker, CCB
-secondary prevention of CVD: aspirin, statin, ACEI
Procedures:
- PCI with coronary angioplasty if proximal or extensive disease on CTCA
- GABG if severe stenosis.

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9
Q

When should a patient with anginal chest pain call an ambulance?

A

Try the GTN, wait 5 mins
Try GTN again, wait 5 mins
Call ambulance

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10
Q

What is a CABG and how does it work?

A

Coronary artery bypass graft.
Chest opened up along sternum, graft vein harvested from leg usually great saphenous vein, sewn on to the affected coronary artery to bypass the stenosis.
The recovery is slower and complication rate is higher than PCI

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11
Q

What is acute coronary syndrome?

A

A thrombus from an atherosclerotic plaque blocks a coronary artery, so heart is not perfused causing sx such as chest pain.
Includes unstable angina, STEMI and NSTEMI

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12
Q

What does the right coronary artery supply? Which ECG leads correspond?

A

Right atrium, right ventricle, inferior left ventricle, posterior septal area
Leads I, II and aVL

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13
Q

What are the branches of the left coronary artery and what do they supply? Which ECG leads correspond?

A 
Circumflex - 
Left atrium
Posterior left ventricle
Leads I, aVL, V5-6
Left anterior descending - 
Anterior left ventricle
anterior septum
Leads v1-4
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14
Q

What investigations would you do for acute chest pain?

A

ECG - ST elevation/new LBBB = STEMI.
serial troponin eg baseline and 6hrs after symptoms. raised = NSTEMI (but also raised in CKD, sepsis, myocarditis, aortic dissection, PE)
Both normal = unstable angina or non-cardiac cause.
ECG, FBC, U+E, LFT, lipid profile, TFTs, HbA1c, fasting glu.
CXR
Echocardiogram after the event
CTCA

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15
Q

How does acute coronary syndrome present?

A

Central constricting chest pain, N+V, sweating, clamminess, impending doom feeling, SOB, palpitations, pain radiating to jaw or arms
Sx at rest for 20 mins.
Silent MI eg in diabetic pts - no chest pain

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16
Q

What ECG changes would be seen in an MI?

A

STEMI- ST elevation, new LBBB

NSTEMI - ST depression, deep T wave inversion, pathological Q waves (late sign)

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17
Q

What is the acute management of a STEMI?

A

Within 12 hrs onset:
1st line: Primary PCI if available within 2hrs of presentation
Thrombolysis if this is not possible. eg streptokinase
PCI (catheterisation and balloon stenting)

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18
Q

What is the acute management of an NSTEMI?

A 
BATMAN
Beta blockers
Aspirin 300mg stat dose
Ticagrelor 180mg stat dose 
Morphine for pain
Anticoagulant - LMWH treatment dose
(Nitrates?)
Oxygen if sats <95%
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19
Q

When would you do PCI for someone with an NSTEMI?

A

GRACE score gives 6 month risk of death or repeat MI after NSTEMI. If medium/high risk they are considered for PCI within 4 days of admission to treat underlying CAD

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20
Q

Give 5 complications of MI.

A 
DREAD
Death
Rupture of heart septum/papillary muscle
Edema/ Heart failure
Arrhythmia, aneurysm
Dressler's syndrome (pericarditis due to localised immune response, 2-3 weeks after MI)
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21
Q

Describe the secondary prevention of MI.

A

Aspirin 75mg daily
another Antiplatelet eg clopidogrel <12 months
Atorvastatin 80mg OD
ACEI eg ramipril titrated to 10mg OD
Atenolol
Aldosterone antagonist if heart failure, ie eplerenone 50mg OD
Lifestyle - smoking, alcohol, diet, cardiac rehabilitation, optimise treatment of other medical conditions.

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22
Q

What is the pathophysiology of acute left ventricular failure?

A

The LV is unable to adequately move blood through the left side of the heart and out into the body –> backlog of blood in L atrium, pulmonary veins and lungs –> leak fluid –> pulmonary oedema = interstitial fluid in lungs. This interferes with normal gas exchange causing SOB, hypoxia etc.
Can be triggered by iatrogenic stuff eg IV fluids, sepsis, MI, or arrhythmia

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23
Q

How does acute LFV present?

A

Rapid onset breathlessness worse on lying flat.
T1 resp failure (hypoxia eithout hypercapnia)
SOB, unwell, cough with frothy white/pink sputum
Signs:
Tachypnoea, tachycardia, hypoxia, 3rd heart sound, bilat basal crackles (sounds wet on auscultation

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24
Q

What investigations would you do for ?acute LVF and what would they show?

A

ECG (ischemia, arrhythmias)
ABG
CXR - cardiomegaly, venous diversion (prominent upper lobe vessels), Kerley lines (fluid in the septal lines), pleural effusions, fluid in interlobar fissures)
bloods - infection, CKD, BNP, troponin if ?MI
Echo - ejection fraction.
If clinically acuter LVF don’t let the Ix delay treatment.

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25
What is BNP? What does raised BNP indicate?
B-type natriuretic peptide is a hormone released from ventricles when myocardium stretched. Therefore high BNP indicates overload (also raised in tachycardia, sepsis, PE, renal impairment, and COPD) BNP relaxes smooth muscle in blood vessels --> reduces systemic vascular resistance --> easier for heart to pump blood. Also diuretic action in kidneys, reducing circulating volume.
26
How is acute LVF managed?
Pour SOD: Stop (pour away) IV fluids, measure input and output, U+E, daily weight. Sit up Oxygen if <95%. Be cautious in pts with COPD Diuretics IV furosemide 40mg stat
27
What is chronic heart failure and how is it classified?
LV failure to pump blood around the body, due to either impaired LV contraction (systolic) or relaxation (diastolic). Reduced ejection fraction: EF <40% Preserved ejection fraction: EF >40% Can be caused by ischemic heart disease, valvular heart disease (commonly aortic stenosis), htn and arrhythmias (commonly atrial fibrillation)
28
How does chronic heart failure present?
``` SOB worse on exertion Cough, frothy white/pink sputum Orthopnoea (SOB when lying flat) Paroxysmal nocturnal dyspnoea (waking up acutely SOB at night with cough and wheeze) Peripheral oedema ```
29
Describe the pathophysiology of paroxysmal nocturnal dyspnoea.
1. More fluid on lungs 2. less active respiratory centre in brain, so does not respond to reduced O2 saturation like it does when awake 3. less adrenalin, myocardium more relaxed, lower cardiac output
30
How is chronic heart failure diagnosed?
Clinical NT-proBNP blood test echocardiogram ECG
31
How is chronic heart failure managed?
1. Refer to specialist - urgently if NT-proBNP >20,000ng/l 2. Discuss and explain the condition 3. Medical (start low go slow) - ACEI ramipril 10mg OD/ ARB if ACEI not tolerated or CI due to valvular heart disease - BB bisoprolol 10mg OD - aldosterone antagonist eg spironolactone - in HFREF not controlled with A and B - loop diuretics eg furosemide - lowest dose needed to control symptoms 4. Surgical rx in severe AS or MR 5. HF specialist nurse. 6. yearly flu+ pneumococcal vaccine, stop smoking, optimise treatment of co-morbidities, exercise as tolerated.
32
Why do you need to monitor U+Es in patients with heart failure?
ACE inhibitors, aldosterone antagonists and diuretics all cause electrolyte disturbances.
33
What is cor pulmonale? Describe the pathophysiology.
Right sided heart failure caused by respiratory disease - the increased pressure and resistance in the pulmonary arteries (pulmonary htn) results in the RV being unable to effectively pump blood out of the ventricle and into the pulmonary arteries, leading to back pressure of blood in the R atrium, vena cava and systemic venous system. Causes: COPD, PE, interstitial lung disease, CF, primary pulmonary htn.
34
How does cor pulmonale present?
``` Asymptomatic SOB (but this could be due to the causative respiratory disease) Peripheral oedema SOBOE syncope chest pain ```
35
Give 5 signs of cor pulmonale.
Hypoxia Cyanosis Raised JVP due to backlog of blood in jugular veins peripheral oedema 3rd heart sound murmurs (eg pan-systolic in TR) hepatomegaly due to backpressure in hepatic vein (pulsatile in TR)
36
What is the management and prognosis of cor pulmonale?
Treat symptoms and underlying cause long term oxygen therapy (LTOT) poor prognosis as often underlying cause is irreversible such as COPD
37
How is hypertension diagnosed and staged?
stages: 1. BP >140/90 in clinic or 135/85 at home 2. >160/100, home 150/95 3. >180/120 diagnostic process: 1. screen every 5 yrs for everyone, every year in patients with T2DM or borderline. 2. confirm BP reading with 24hr ambulatory BP/home reading to exclude white coat htn - defined at >20/10 mmHg difference between clinic and home readings. 3. Assess for end organ damage: bloods for HbA1c, renal function and lipids, urine albumin creatinine ratio and dipstick for haematuria (kidney damage), fundoscopy, ECG
38
What causes hypertension?
95% of htn is due to essential or primary htn. Secondary causes: Renal artery stenosis Obesity Pregnancy/pre-eclampsia Endocrine - esp hyperaldosteronism (Conns syndrome) - Renin aldosterone ratio blood test.
39
Give 5 complications of hypertension.
``` Ischemic heart disease CVA eg stroke, heamorrhage hypertensive retinopathy hypertensive nephropathy heart failure ```
40
Describe the management of hypertension.
1. ACEi eg ramipril starting at 1.25mg, or ARB if ACEi not tolerated, 1st line for Black pts and those over 55 (never ARB with ACEi together) 2. Add CCB eg amlodipine from 5mg 3. Add Diuretic eg indapamide 2.5mg 4. If serum K+ <4.5mmol/l try spironolactone, if >4.5mmol/l try alpha or beta blocker Treatment target <140/90 for those under 80 yrs, <150/90 for those over 80 yrs.
41
Explain the effect of spironolactone on potassium levels. Why should U+Es be monitored carefully?
Potassium sparing diuretic, blocks aldosterone action in the kidneys. aldosterone usually causes K excretion and Na resorption, so spironolactone causes K absorption and Na excretion. Increases risk of hyperkalaemia. ACEis also cause hyperkalaemia.
42
What causes normal heart sounds (S1+S2?)
S1 caused by closing of AV valves (tricuspid +mitral) at start of systole (ventricular contraction)/ end of diastole (filling). S2 is caused by closing of pulmonary and aortic valves at end of systole.
43
What causes s3? is it always pathological?
0.1s after S2. Caused by rapid ventricular filling causing chordae tendinae to pull to their full length and twang like a guitar string. Normal in healthy people 15-40yrs, but in older people indicates HR as the ventricles and chordae are stiff/weak, so they reach their limit faster than normal.
44
What causes s4? is it always pathological?
Directly before s1, rare, always abnormal. | Indicates ventricular hypertrophy, caused by turbulent flow from an atria contracting against a non-compliant ventricle.
45
Where is the pulmonary valve area?
2nd ICS left sternal border
46
What type of murmur is heard with aortic stenosis? What would be the likely cause?
Ejection systolic high-pitched murmur at the 2nd ICS right sternal border radiating to carotids, slow-rising pulse+narrow pulse pressure Associated with exertional syncope. causes LV hypertrophy. Causes: idiopathic age-related calcification, rheumatic HD
47
Where is the tricuspic valve area?
5th ICS left sternal border
48
What type of murmur does mitral stenosis cause and what would it be caused by?
Mitral stenosis = mid-diastolic low-pitched murmur loudest at the mitral area/5th ICS mid clavicular line (apex area) (due to low velocity blood flow), Associated with loud s1 due to thickened valves requiring a large systolic force to shut, then shutting suddenly. Palpable tapping apex beat. Leads to LV hypertrophy. Caused by rheumatic heart disease and infective endocarditis.
49
What type of murmur does mitral regurgitation cause and what would be the likely cause of this?
Pan-systolic high pitched murmur at the mitral area (5th ICS mid clavicular line) due to high velocity blood flow. Can lead to congestive cardiac failure Causes: Idiopathic, ischemic heart disease, IE, rheumatic HD, CTDs eg EDS, Marfan syndrome
50
What type of murmur is heard with aortic regurgitation?
Early diastolic, soft murmur at the aortic area (2nd intercostal space, right sternal border). Associated with collapsing pulse - blood pumped out then flows back so the pulse 'disappears'. Leads to LV dilatation. Causes: age, CTDs eg EDS, Marfan syndrome
51
Give 2 differences between bioprosthetic and mechanical valves.
``` Bioprosthetic = from a pig (porcine). Lifespan of 10 yrs, biodegrade, no anticoag needed, better for older pts Mechanical = lifespan >20 yrs, lifelong anticoag with warfarin (target INR 2.5-3.5) ```
52
What are the advantages of the different types of mechanical valves?
Starr-edwards valve = ball in cage - effective but high risk of clots. Tilting disc - single disc St Jude's - bileaflet/2 tilting discs. Effective, least risk of clots.
53
Give 3 complications of heart valve replacement.
Thrombus and thromboembolism as blood stagnates IE - infection in valve Haemolysis as blood 'churned' in the valve, leading to anaemia
54
What would a metallic mitral valve sound like?
Click replaces S1
55
What would a metallic aortic valve sound like?
Click replaces S2
56
What is a TAVI and how does it compare with surgical valve replacement?
Trans catheter Aortic Valve Implantation - used for severe aortic stenosis, if pt high risk for open operation. Bioprosthetic valve implanted through the femoral artery. 1.5% risk of IE compared to 2.5% with surgical valve replacement.
57
What are the most common causative organisms in IE?
Gram +ve cocci: staphylococcus, streptococcus, enterococcus
58
What is the pathophysiology of atrial fibrillation?
Uncoordinated, rapid, irregular atrial contraction. Normally the SAN produces organised electrical activity that coordinates atrial contraction. This results in irregular conduction to the ventricles, can lead to tachycardia, HR due to poor diastole. Blood collects in the atria --> clots --> stroke ``` Causes: Sepsis Mitral valve pathology (Valvular AF = Pts with mitral stenosis/mechanical heart valve.) Ischemic HD Thyrotoxicosis Hypertension ```
59
What is seen on an ECG with AF?
Absent P waves Irregularly irregular rhythm Tachycardia
60
How does AF present?
``` Asymptomatic Palpitations SOB Syncope/dizziness Associated conditions -stroke, sepsis, thyrotoxicosis ```
61
What can cause irregularly irregular rhythm? How are they differentiated?
Atrial fibrillation | ventricular ectopics - these disappear when HR rises, eg during exercise
62
How is AF managed?
1. Rate control: BB, CCB eg verapamil 2. Rhythm control (reverting to normal sinus rhythm) recommended if reversible cause, new onset (<48 hrs --> immediate cardioversion), AF is causing HF, symptoms remain despite rate control. Delayed cardioversion (DC) for stable pts - anticoagulate for 3 weeks to reduce risk of mobilising a clot during treatment. Cardioversion is done electrically (defibrillation under anaesthetic) or pharmacologically (flecanide or amiodarone) Long term rhythm control: BBs + Anticoagulation: 5% risk of stroke without anticoag vs 3% risk bleed. Depends on HAS-BLED and CHADSVASc score. DOAC eg apixiban (aspirin no longer used for prevention of stroke in AF)
63
What is paroxysmal AF and how is it managed?
AF episodes <48h in duration. Pts should be anticoagulared based on CHADSVASc score. Pts with infrequent episodes without underlying structural heart disease may be suitable for flecanide pill in pocket treatment.
64
When is flecanide contraindicated and why?
Atrial flutter - can cause 1:1 AV conduction resulting in significant tachycardia.
65
Give 3 differences between DOACs and warfarin.
DOACs: no monitoring required, no major interactions, shorter half life (12hrs for apixiban, 1-3 days for warfarin).
66
What does CHA2DA2VASc stand for?
``` C – Congestive heart failure H – Hypertension A2 – Age >75 (Scores 2) D – Diabetes S2 – Stroke or TIA previously (Scores 2) V – Vascular disease A – Age 65-74 S – Sex (female) ```
67
What does HAS-BLED stand for?
``` H – Hypertension A – Abnormal renal and liver function S – Stroke B – Bleeding L – Labile INRs (whilst on warfarin) E – Elderly D – Drugs or alcohol ```
68
What are the cardiac arrest rhythms and which are shockable?
Shockable: ventricular tachycardia, ventricular fibrillation | Non-shockable: pulseless electrical activity, asystole.
69
How is tachycardia in an unstable patient managed?
Up to 3 synchronised shocks | Amiodarone infusion
70
How is tachycardia in a stable patient managed?
Depends on ECG: Narrow complex could be Atrial fibrillation --> rate control with BB/CCB Atrial flutter --> BB SVT --> vagal manouvres, adenosine Broad complex indicates ventricular pathology - amiodarone if potential VT If known SVT with BBB treat as normal SVT If irregular may be AF variation - seek expert help
71
What is atrial flutter?
Re-entrant rhythm in atrium causing atrial contraction at 300bpm. Signal may make its way into the ventricles every 2nd lap due to the long refractory period to the AVN, causing 150bpm ventricular contraction (2:1). Sawtooth appearance on ECG with P wave after P wave. Associated with htn, ischemic HD, cardiomyopathy, and thyrotoxicosis.
72
How is atrial flutter managed?
Rate/rhythm control with BB or cardioversion Treat underlying condition (eg htn, thyrotoxicosis) Radiofrequency ablation of re-entrant pathway Anticoagulation based on CHA2DS2VASc
73
What is SVT?
Electrical signal re-entering the atria from the ventricles, travels back through the AVN and causes another ventricular beat. Results in narrow complex tachycardia. Can be paroxysmal. Types: AVNRT: re-entry through AVN ANRT (accessory pathway eg WPW) Atrial tachycardia: electrical signal originates in the atria but not in the SAN, causing atrial rate >100bpm.
74
Describe the acute management of stable patients with SVT.
Continuous ECG monitoring 1. Valsalva manouevre eg blowing into a syringe 2. Carotid sinus massage 3. Adenosine 4. Verapamil 5. DC cardioversion Note: antiarrhythmics CIs in WPW with AF/flutter.
75
What is Wolff-Parkinson White syndrome?
Normally the AVN is the only AV pathway, but in WPW there is an extra AV pathway called the Bundle of Kent.
76
What is seen on an ECG in WPW?
Short PR interval, wide QRS complex, delta wave (slurred upstroke on QRS complex).
77
How is WPW treated?
Radiofrequency ablation (RFA) of the accessory pathway.
78
How does adenosine work?
Slows conduction through the AVN thereby interrupting the AVN/accessory pathway during SVT and resetting it to sinus rhythm. Needs to be given as a rapid bolus in a large proximal cannula eg a grey cannula in the antecubital fossa. Avoid in asthma/COPD/ HF/HB/severe hypotension.
79
When should you avoid anti-arrhythmic medications in WPW?
If there is also atrial fibrillation/flutter, because this chaotic electrical activity could pass through the accessory pathway into the ventricles causing polymorphic VT.
80
What is Torsades de pointes?
A type of polymorphic VT in which the QRS complex appears to twist around the baseline. Occurs in patients with long QT because random spontaneous depolarisation in some areas of myocytes called afterdepolarisation) lead to ventricular contraction prior to proper repolarisation occurring --> Torsade de pointes -> usually self resolves but can become VT --> cardiac arrest. Correct the cause (eg electrolyte disturbance, see long QT causes), Mg infusion (even if serum mg normal), defib if in VT.
81
What does the QT interval represent and what does it mean if is it prolonged?
(Prolonged) repolarisation of muscle cells after contraction. Can result in random depolarisations --> torsade de pointes.
82
Give 3 causes of long QT syndrome.
``` Causes of long QT: inherited long QT syndrome medications: antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics Electrolyte disturbance (hypokalaemia, hypomagnesaemia, hypocalceamia). ```
83
What are ventricular ectopics and how do they present?
Premature ventricular beats caused by random electrical discharges not in the atria. ECG: random abnormal broad QRS complexes. Palpitations. Usually normal but more common in patients with heart conditions.
84
What is bigeminy?
Ventricular ectopics occurring after every sinus beat.
85
What is the management of ventricular ectopics?
Bloods - anaemia, electrolyte disturbance, thyroid Reassure if healthy If other cardiac symptoms/conditions seek expert advice.
86
What is first degree heart block?
Delayed AV conduction (through AVN), leading to long PR (>0.2s) but where every atrial impulse still leads to a QRS complex.
87
What is second degree heart block?
Some atrial impulses do not make it through AVN to ventricles --> P waves don't always lead to QRS complexes. Classified as Mobitz 1 or 2 depending on ECG findings.
88
What is Mobitz type 1 block?
A type of 2nd degree heart block. Atrial input becomes weaker and weaker until it fails to stimulate ventricular contraction, then it gets stronger and the cycle repeats. PR interval gets longer until there is a non-conducted P wave, then becomes normal and repeats.
89
What is Mobitz type 2 block? What is the associated risk?
A type of 2nd degree hear block in which intermittent failure of AV conduction results in missing QRS complexes, with normal PR interval. There may be a set ratio of P waves to QRS complexes eg 3:1. Risk of asystole.
90
What causes 2:1 heart block?
Just means 2 P waves for each QRS complex. Every 2nd P wave is not strong enough to stimulate a QRS complex. A type of 2nd degree heart block but can be caused by mobitz type 1 or 2.
91
What is complete heart block? What is the associated risk?
Aka 3rd degree heart block, no relationship between P waves and QRS complexes. Significant risk of asystole.
92
How would you manage heart block?
Depends how stable they are and the risk of asystole. If unstable or risk of asystole (Mobitz 2, 3rd degree, or previous asystole) --> atropine 500cmg IV. then if no improvement, repeat the atropine same dose until 3mg reached, try other inotropes eg noradrenalin, then defibrillator/cardiac pacing.
93
How does atropine work? What are its side-effects?
Antimuscarinic, inhibits PNS --> urinary retention, dry eyes, constipation, pupil dilatation.
94
How do pacemakers work?
Deliver electrical impulses to heart to restore normal electrical activity and improve heart function. Pulse generator (box) + pacing leads (in either one, two or three heart chambers). Modern pacemakers have a computer that monitors the natural electrical activity and only intervenes if necessary. Batteries last 5 years.
95
What do you need to consider in patients with pacemakers?
MRI scans - check MRI compatible TENS Diathermy Cremation form - has the pacemaker been removed yet
96
Give 3 indications for pacemakers.
Symptomatic bradycardia Mobitz 2 AV block 3rd degree heart block Severe heart failure (biventricular pacemaker) Hypertrophic obstructive cardiomyopathy (ICDs)
97
When are single-chamber pacemakers used?
R atrium --> for issue with SAN only. ECG shows line before P wave R ventricle--> for issue with AV conduction only. ECG shows line before QRS complex. (Eg AV block)
98
In which chambers do the leads sit in a dual chamber pacemaker, and how would you identify one on an ECG?
Leads in RA and RV to synchronise contractions of atria and ventricles. ECG: vertical line in all leads before P wave and before QRS complexes.
99
When are biventricular pacemakers used?
Leads in RA, RV and LV. For patients with severe heart failure to optimise heart function. Also called CRT (Cardiac resynchronisation therapy) pacemakers.

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