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Cardiology Flashcards

1
Q

What is atherosclerosis

A

It is a combination of atheromas (fatty deposits in the artery wall)

and sclerosis (hardening of the blood vessel walls)

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2
Q

Cause of atherosclerosis

A

Chronic inflammation and activation of the immune system in the artery walls.

This causes deposition of lipids in the walls which develop into fibrous plaques.

The plaques cause the artery walls to stiffen leading to hypertension, stenosis or plaque rupture leading to thrombosis

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3
Q

Modifiable risk factors of atherosclerosis

A

Smoking, alcohol consumption, poor diet, low exercise, poor sleep, obesity, stress

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4
Q

Non-modifiable risk factors of atherosclerosis

A

age, family history, male gender

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5
Q

Medical co-morbidities that can increase risk of atherosclerosis

A

Diabetes
Hypertension
Chronic kidney disease

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6
Q

Possible end results of atherosclerosis

A

angina
myocardial infarction
strokes
peripheral vascular disease

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7
Q

What is a QRISK 3 score

A

Calculates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

Score > 10% = start a statin (atorvastatin 20mg at night)

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8
Q

Secondary prevention of cardiovascular disease is for patients that have already developed angina, MI, stroke, etc.

What are the 4As of secondary prevention

A

1 - Aspirin (plus a secondary antiplatelet such as clopidogrel for 12 months)

2 - Atorvastatin 80mg

3 - Atenolol or another beta blocker like bisoprolol titrated to a maximum dose

4 - ACE inhibitor, commonly Ramipril

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9
Q

Side effects of statins

A

Myopathy
Type 2 diabetes
Haemorrhagic strokes - rare

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10
Q

What is angina

A

Constricting chest pain which can radiate to jaw or arms

Happens when there is narrowing of the coronary arteries, so in times of high demand like exercise, there is insufficient blood supply to meet the demand

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11
Q

Stable vs unstable angina

A

Stable - symptoms are always relieved by rest or GTN glyceryl trinitrate

Unstable - symptoms come randomly at rest. This is a type of acute coronary syndrome

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12
Q

Investigation for angina

A

Gold standard - CT coronary angiography

Physical exam - heart sounds, BMI, signs of heart failure

ECG
Lipid profile
Thyroid function
HbA1C
FBC, U&Es

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13
Q

Management of angina (RAMP)

A

R - refer to cardiology

A - advise patient about diagnosis, how to manage and when to call an ambulance

M - Medical treatment

P - Procedural or surgical intervention

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14
Q

Medical management of angina

A

Immediate symptomatic relief - GTN spray (causes vasodilation) used when required.
- use when symptoms start, repeat after 5 mins if necessary, if still in pain call ambulance

Long term relief is with either
- beta blocker (bisoprolol 5mg once daily)
- calcium channel blocker (amlodipine 5mg once daily)

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15
Q

Procedural or surgical interventions for angina

A

Percutaneous Coronary Intervention (PCI) with coronary angioplasty
- put a catheter into brachial or femoral artery
- feed up to coronary arteries under xray guidance
- inject contrast to see areas of stenosis
- balloon dilation and insertion of stent

Coronary artery bypass graft (CABG)
- for patients with severe stenosis
- chest is opened along sternum (will leave scar)
- graft is taken from leg, usually great saphenous vein
- sewn onto affected coronary artery to bypass the stenosis
- slower recovery and higher complication rate than PCI

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16
Q

What is Acute Coronary Syndrome

A

It is the result of a thrombus from an atherosclerotic plaque blocking a coronary artery

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17
Q

Coronary arteries

A

Left coronary artery becomes
- CIRCUMFLEX artery
- and LAD (left anterior descending) artery

Right Coronary artery

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18
Q

Three types of Acute Coronary Syndrome

A
  • unstable angina
  • STEMI (ST elevation myocardial infarction)
  • NSTEMI
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19
Q

How to make a diagnosis when a patient presents with possible ACS symptoms

A

Perform an ECG

If there is ST elevation = STEMI

If there is no ST elevation, perform troponin test

If there is raised troponin with pathological changes (ST depression, T wave inversion, Q waves) = NSTEMI

If normal troponin and no pathological ECG changes = unstable angina or musculoskeletal chest pain

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20
Q

Symptoms of ACS

A

Central, constricting chest pain
Nausea + vomiting
Sweating and clamminess
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaws or arms

Symptoms continue at rest for 20mins. If they resolve with rest, could be angina.

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21
Q

ECG changes in STEMI

A
  • ST segment elevation in leads that have an area of ischaemia
  • or a new left bundle branch block
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22
Q

ECG changes in NSTEMI

A
  • ST segment depression in a specific region
  • deep T wave inversion
  • pathological Q waves - suggest a deep infarct
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23
Q

Causes of raised troponins that are not due to ACS

A

Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

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24
Q

Acute STEMI treatment

A

If patient presents within 12 hours of symptoms onset, discuss urgently with local cardiac centre for either
- primary PCI (percutaneous coronary intervention) - if available within 2 hours of presentation
- thrombolysis if PCI not available

PCI is when catheter is put into brachial or femoral artery, into coronary, balloons to dilate and stent inserted

Thrombolysis - injecting fibrinolytic meds that break down fibrin and rapidly dissolve clots - streptikinase, alteplase

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25
Q

Acute NSTEMI treatment - can be remembered with BATMAN mnemonic

A

B - beta blockers, unless contraindicated

A - Aspirin 300mg stat dose

T - Ticagrelor 180mg stat dose (alternatively Clopidogrel 300mg)

M - Morphine titrated to control pain

A - Anticoagulant - LMWH at treatment dose, Enoxaparin 1mg/kg twice daily for 2-8days

N - Nitrates like GTN to relieve coronary artery spasms

Oxygen is only given if 02 saturation is dropping

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26
Q

What is the GRACE score

A

It gives a 6-month risk of death or repeat MI after having an NSTEMI
<5% - low risk
5-10% = medium risk
>10% = high risk

Medium or high risk are considered for early PCI to treat any underlying CAD

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27
Q

Complications of MI, can be remembered with DREAD

A

Death
Rupture of heart septum
Eodema
A - arrhymia or aneurysm
Dresslers syndrome

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28
Q

What is Dressler’s syndrome

A

Also called post-MI syndrome.
Occurs 2-3 weeks after MI.

Caused by a localised immune response and causes pericarditis.

Presents with pleuritic chest pain, low fever, pericardial rub on auscultation.

Diagnosis with ECG and echo.

Manages with NSAIDS like aspirin, or steroids like prednisolone in more severe cases.

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29
Q

What is Acute Left Ventricular Failure

A

When the left ventricle is unable to adequately move blood through the left side of the heart and out into the body.

This causes a backlog of blood in the left atrium, pulmonary veins and lungs.

The vessels in these areas are engorged with blood and because of the increased volume and pressure they start to leak and can’t reabsorb fluid from surrounding areas.

This causes pulmonary oedema - lung tissue and alveoli become full of interstitial fluid.

This interferes with normal gas exchange leading to SOB, reduced oxygen saturation and other symptoms

Acute LVF causes a type 1 resp failure - low oxygen without increase in CO2

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30
Q

Causes of LVF

A
  • iatrogenic - aggressive IV fluids in frail elderly patients or patients with impaired LV function
  • sepsis
  • MI
  • arrhythmias
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31
Q

Symptoms of Acute LVF

A

Presents as rapid onset of breathlessness which is exacerbated by lying flat and improved by sitting up

  • cough with frothy white or pink sputum
  • increased resp rate
  • reduced oxygen saturation
  • tachycardia
  • 3rd heart sound
  • symptoms related to underlying cause
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32
Q

Investigations to check for Acute LVF

A
  • history and clinical examination
  • ECG to check for arrhythmias
  • echo
  • ABG
  • CXR
  • FBC, BNP and troponin
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33
Q

What is BNP

A

B-type natriuretic peptide.

A hormone released from the heart ventricles when the myocardium is stretched beyond its normal range

High BNP = heart is overloaded with blood

BNP relaxes the smooth muscle in blood vessels to reduce vascular resistance and make blood easier to pump

It also acts on kidneys a diuretic to promote excretion of water in urine, so that volume decreases and improves heart function

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34
Q

Testing for BNP is sensitive but not specific. What are other possible causes of high BNP

A
  • tachycardia
  • sepsis
  • pulmonary embolism
  • renal impairment
  • COPD
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35
Q

What is echocardiography used for

A

To assess the function of the left ventricle and any structural abnormalities in the heart

Main measure of LV function is ejection fraction - percentage of blood left in LV after ventricular contraction.

EF > 50% = normal

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36
Q

How does cardiomegaly appear on CXR

A

Cardiothoracic ratio > 0.5
Basically when the diameter or the widest part of the heart is more than half of the diameter of the widest part of the lung fields

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37
Q

Management of acute LVF, can be remembered with Pour SOD

A

POUR away - stop IV fluids
S - sit up
O - oxygen if <95% saturation
D - diuretics (IV furosemide 40mg stat)

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38
Q

What is chronic heart failure

A

It is caused by either:
- systolic heart failure - impaired LV contraction

  • diastolic heart failure - impaired LV relaxation

This impaired LV function results in chronic back-pressure of blood trying to flow into and through the left side of the heart

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39
Q

Presentation of chronic heart failure

A
  • breathlessness worsened by exertion
  • cough with frothy white sputum
  • orthopnoea - SOB when lying flat, relieved by sitting up
  • peripheral oedema
  • paroxysmal nocturnal dyspnoea - waking suddenly at night with severe SOB and cough. Feeling suffocated and have to walk around and gasp for breath
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40
Q

Diagnosis of chronic heart failure

A
  • clinical presentation
  • BNP blood test
  • echo
  • ECG
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41
Q

Causes of chronic heart failure

A
  • ischaemic heart disease
  • valvular heart disease, commonly aortic stenosis
  • hypertension
  • arrhythmias, commonly atrial fibrillation
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42
Q

Management of chronic heart failure

A
  • refer to specialist
  • medical management
  • surgical treatment of severe aortic stenosis or mitral regurgitation
  • yearly flu and pneumococcal vaccine
  • stop smoking
  • exercise
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43
Q

Medical management of chronic heart failure

A
  1. Ace inhibitor - Ramipril titrated as tolerated up to 10mg once daily

If ACE inhibitors are not tolerated then replace with ARB e.g Candesartan titrated up to 32mg once daily

  1. Beta blocker - Bisoprolol titrated as tolerated up to 10mg once daily
  2. Aldosterone antagonist such as Spironolactone if symptoms are not controlled with A and B
  3. Loop diuretics - for improvement of symptoms - Furosemide 40mg once daily

These meds can cause electrolyte disturbances so have U&Es closely monitored.

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44
Q

What is cor pulmonale

A

Right sided heart failure caused by respiratory disease.

In pulmonary hypertension there is increased pressure and resistance in the pulmonary arteries

This results in the RV being unable to effectively pump blood out of the ventricle into the pulmonary arteries

This leads to back pressure of blood in the RA, vena cava and systemic venous system.

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45
Q

Causes of cor pulmonale

A
  • COPD - most common
  • pulmonary embolism
  • cystic fibrosis
  • interstitial lung disease
  • pulmonary hypertension
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46
Q

Presentation of cor pulmonale

A

Asymptomatic in early stages.

  • SOB
  • peripheral oedema
  • breathlessness on exertion
  • syncope (dizziness and fainting)
  • chest pain
  • cyanosis
  • raised jugular venous pressure
  • third heart sound
  • pan systolic murmur
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47
Q

Management of cor pulmonale

A
  • treat underlying cause
  • long term oxygen therapy

Poor prognosis unless underlying cause is reversible

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48
Q

Primary vs secondary hypertension

A

Primary hypertension means it has developed on its own without any other cause.

Secondary hypertension has secondary causes, remembered by ROPE
- Renal disease
- Obesity
- Pregnancy - pre-eclampsia
- Endocrine - hyperaldosteronism

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49
Q

Complications of hypertension

A
  • ischaemic heart disease
  • stroke
  • hypertensive retinopathy or nephropathy
  • heart failure
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50
Q

Values for stage 1 and 2 hypertension

A

Stage 1
- clinic >140/90
- home > 135/85

Stage 2
- clinic >160/100
- home >150/95

51
Q

Medical management of hypertension

A
  1. ACE inhibitors - Ramipril 1.25mg up to 10mg once daily
  2. Beta blocker - Bisoprolol 5mg up to 20mg once daily
  3. Calcium-channel blocker - Amlodipine 5mg up to 10mg once daily
  4. Diuretic
    - If serum potassium >4.5mmol/l then give a thiazide like diuretic such as Indapamide 2.5mg once daily
  • If serum potassium is or <4.5mmol/l then potassium sparing diuretic like Spironolactone
  1. ARB - Candesartan 8mg up to 32mg once daily (used in patients that cannot tolerate ACE inhibitors)
52
Q

S1 - first heart sound

A

caused by the closing of the atrioventricular valves (tricuspid and mitral)

at the start of systolic contraction of the ventricles

53
Q

S2 - second heart sound

A

caused by closing of the semilunar valves (pulmonary and aortic)

once systolic contraction is complete

54
Q

S3 - third heart sound

A

heard 0.1s after S2

rapid ventricular filling causes the chordae tendinae to pull to their full length and twang like a guitar string

normal in younger patients, in older patients can indicate heart failure

55
Q

S4 - fourth heart sound

A

heard directly before S1

always abnormal and rare

indicates a stiff or hypertrophic ventricle

56
Q

Where would you place the stethoscope to listen to murmurs

A

Pulmonary valve - 2nd intercostal space, left sternal border

Aortic valve - 2nd intercostal space, right sternal border

Tricuspid valve - 5th intercostal space, left sternal border

Mitral valve - 5th intercostal space, mid clavicular line

Erb’s point - 3rd intercostal space, left sternal border. Best area to listen to S1 and S2

57
Q

How to assess a murmur (SCRIPT)

A

S - Site - where is the murmur loudest

C - Character - soft/ blowing/ crescendo (getting louder) / decrescendo / crescendo-decrescendo

R - Radiation - can it be heard over carotids (indicates aortic stenosis) or left axilla (mitral regurgitation)

I - Intensity - what grade is the murmur

P - Pitch - high pitch or low and grumbling. Pitch indicates velocity

T - Timing - systolic or diastolic

58
Q

Grades of murmurs

A
  1. difficult to hear
  2. quiet
  3. easy to hear
  4. easy to hear with a palpable thrill
  5. can hear with stethoscope barely touching chest
  6. can hear with stethoscope off chest
59
Q

Myocardial hypertrophy vs dilation

A

When pushing against a stenotic valve, the myocardium has to try harder resulting in HYPERTROPHY
- mitral stenosis causes LA hypertrophy
- aortic stenosis causes LV hypertrophy

When a leaky valve allows blood back into the chamber, it stretches the muscle and causes dilation
- mitral regurgitation causes LA dilation
- aortic regurgitation causes LV dilation

60
Q

What is mitral stenosis

A

Narrowing of the mitral valve
making it difficult for LA to push blood through to the ventricle

61
Q

What is mitral stenosis caused by

A

Rheumatic heart disease
Infective endocarditis

62
Q

Murmur caused by mitral stenosis

A

mid-diastolic

low pitched rumbling due to low velocity

loud S1 due to thick valves

can palpate a tapping apex beat

63
Q

What is mitral regurgitation

A

when an incompetent mitral valve allows blood to leak back through
during systolic contraction of the LV

it results in congestive cardiac failure because the leaking valve causes a backlog of blood waiting to be pumped through the left side of the heart

64
Q

Causes of mitral regurgitation

A

idiopathic weakening of valve with age

ischaemic heart disease

infective endocarditis

rheumatic heart disease

connective tissue disorders - Marfan’s or Ehler’s Danlos

65
Q

Murmur caused by mitral regurgitation

A

pan-systolic
high pitched, whistling murmur
radiates to left axilla
S3 can be heart

66
Q

What is aortic stenosis

A

Narrowing of the aortic valve, restricting blood flow from LV to aorta

Patients may complain of exertional syncope - light headedness or fainting during exercise

67
Q

Murmur in aortic stenosis

A

ejection-systolic murmur

high pitched

crescendo-decrescendo character due to blood flow being very slow at start and end, and fast in middle of systole

radiates to carotids

68
Q

Causes of aortic stenosis

A

idiopathic age related calcifications

rheumatic heart disease

69
Q

What is TAVI

A

Transcatheter Aortic Valve Implantation

treatment for severe aortic stenosis
for patients at high risk for open valve replacement

Catheter inserted into femoral artery, then fed to aortic valve under x ray guidance.
Balloon to inflate the stenosed aortic valve, and then bioprosthetic valve implanted

70
Q

What is aortic regurgitation

A

The aortic valve doesn’t close properly so during ventricular diastole, blood flows back from the aorta into the LV

71
Q

Murmur in aortic regurgitation

A

early diastolic, soft murmur

associated with Corrigan’s pulse - rapidly appearing and disappearing pulse at the carotid as blood is pumped out by ventricles and then immediately flows back in

72
Q

Causes of aortic regurgitation

A

idiopathic age related
connective tissue disorders

73
Q

Bioprosthetic vs mechanical valves

A

Bioprosthetic have a limited life span of around 10 years. Come from a pig.

Mechanical valves have a life span >20 years but require lifelong anticoagulation with warfarin. Cause a click.

74
Q

What is atrial fibrillation

A

normally the sinoatrial node produces electrical activity that coordinates the contraction of the atria.

in atrial fib, the contraction of the atria is uncoordinated, rapid and irregular.

this is because of disorganised electrical activity that overrides the normal SAN activity.

the function of the atria is to pump blood into the ventricles. When the contractions of the atria are uncoordinated, the ventricles have to fill up by suction and gravity.

this leads to irregular conduction of electrical impulses to the ventricles, resulting in
- irregularly irregular ventricular contractions
- tachycardia
- heart failure due to poor ventricular filling during diastole
- risk of stroke

the higher the heart rate, the less time there is for the ventricles to fill with blood, so the cardiac output is lower

75
Q

Symptoms of atrial fibrillation

A

patients are usually asymptomatic and atrial fib is picked up incidentally.

otherwise:
- palpitations
- SOB
- syncope (dizziness, fainting)

76
Q

How does atrial fibrillation present on an ECG

A
  • absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricular rhythm
77
Q

What are the 2 diagnoses for an irregularly irregular pulse

A
  • atrial fibrillation
  • ventricular ectopics

they are differentiated with an ECG.

ventricular ectopics disappear over a certain heart rate - so pt will have regular heart rate during exercise

78
Q

Common causes of atrial fibrillation (SMITH)

A

Sepsis
Mitral valve stenosis/regurgitation
Ischaemic heart disease
Thyrotoxicosis
Hypertension

79
Q

What are the 2 principles to treating atrial fibrillation

A
  1. rate or rhythm control
  2. anticoagulation to prevent stroke
80
Q

Rate control is first line treatment for atrial fibrillation unless

A
  • there is a reversible cause for the AF
  • new onset (within last 48hrs)
  • AF is causing heart failure
81
Q

What are the options for rate control when treating atrial fibrillation

A
  1. First line - beta blocker
    Atenolol 50-100mg once daily
  2. Calcium-channel blocker
    Diltiazem - not preferable in heart failure
  3. Digoxin - only in people with a sedentary lifestyle. Need to be monitored as there is risk of toxicity
82
Q

What is the aim of rhythm control when treating atrial fib

A

The aim is to return the patient to normal sinus rhythm.

This can be through:
- pharmacological cardioversion
- electrical cardioversion
- long term medical rhythm control

83
Q

According to NICE, what are the first line options for pharmacological cardioversion

A

Flecanide

or Amiodarone in patients with structural heart disease

84
Q

What is electrical cardioversion

A

The heart is rapidly shocked back into sinus rhythm

the patient is first sedated or given a general anaesthetic

and then using a cardiac defibrillator machine, controlled shocks are delivered

85
Q

What are the medicines used for long term rhythm control

A
  1. Beta blockers - first line
  2. Dronedarone - used to maintain normal rhythm in patients that have had successful cardioversion
  3. Amiodarone - in patients with heart failure of LV dysfunction
86
Q

Immediate vs delayed cardioversion

A

Immediate - if the AF has been present for <48hrs, or if patient is haemodynamically unstable

Delayed - if AF has been present for >48hrs and patient is stable.

In delayed cardioversion, the patient should be anticoagulated for at least 3 weeks before cardioversion - otherwise the patient may develop a clot in the atria and cardioversion would mobilise that clot and cause a stroke

87
Q

What is paroxysmal atrial fibrillation

A

When AF comes and goes in episodes, but doesn’t last for more than 48hrs.

Patient takes Flecanide when they feel the symptoms of AF starting

88
Q

Why are patients with atrial fibrillation at higher risk of stroke

A

The uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in the atrial appendage

Eventually this stagnated blood can lead to a clot (thrombus).

This clot mobilises and travels with the blood, from the atria to the ventricle, then to the aorta and up into the carotid arteries to the brain

it can lodge in the cerebral artery and cause an ischaemic stroke

therefore patients should be on anticoag

89
Q

How does warfarin work

A

it is a vitamin K antagonist

warfarin blocks vitamin K which is essential for the functioning of clotting factors.

it also prolongs the prothrombin time (time taken for blood to clot)

90
Q

What is INR

A

International Normalised Ratio
- this compared the prothrombin time of the patient to that of a normal healthy adult

It is used to assess how anticoagulated a patient is.

INR 1 = normal
INR 2 = twice that of a normal adult

Target INR for atrial fib is 2-3

91
Q

What are the advantages of DOACs over Warfarin?

A

Direct Oral AntiCoagulants
- Apixiban and Dabigatran - taken twice daily
- Rivaroxaban - once daily

They have a lower bleeding risk
and relatively short half life
no major interaction problems
no monitoring required

They are much more expensive though, around £27 a month, whereas warfarin costs £1

92
Q

What is the CHA2DS2-VASc score

A

This is a tool for assessing whether a patient with atrial fibrillation is at risk of stroke and should be started on anticoagulation.

Higher score = higher risk of stroke

0 = no anticoag
1 = consider it
>1 = start it

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

93
Q

What is the HAS-BLED score?

A

A tool for calculating a patients risk of major bleeding whilst on anticoagulation.

Can be used before starting anticoagulation
or to monitor whilst on anticoag

H - hypertension
A - Abnormal renal or liver function
S - Stroke
B - bleeding
L - Labile INRs (whilst on warfarin)
E - Elderly
D - Drugs or alcohol

94
Q

What are the four possible rhythms that you could see in a pulseless unresponsive patient?

Which of these are shockable and which are non-shockable?

A

Shockable rhythms:
- ventricular tachycardia
- ventricular fibrillation

Non-shockable rhythms:
- asystole (no significant electrical activity)
- all electrical activity except V fib or tach

95
Q

Treatment of tachycardia in an unstable patient

A
  • up to 2 synchronised shocks
  • amiodarone infusion
96
Q

What are the 3 narrow complex tachycardias? And what are their treatments?

A

Narrow complex means QRS < 0.12s

  1. Atrial fibrillation - rate control with a beta blocker or diltiazem
  2. Atrial flutter - rate control with beta blocker
  3. Supraventricular tachycardia - treat with vagal manoeuvres and adenosine
97
Q

What are the broad complex tachycardias? And what are their treatments?

A
  1. Ventricular tachycardia - amiodarone infusion
  2. SVT with bundle branch block - vagal manoeuvres and adenosine
98
Q

What is atrial flutter?

A

Normally, the electrical signal passes through the atria once, stimulates a contraction and then disappears through the AV node into the ventricles.

In atrial flutter, there is a re-entrant rhythm in either atrium. So the electrical signal recirculates due to an extra electrical pathway in the atria.

So it goes round and round without interruption.

It goes into the ventricles every second lap due to the long refractory period of the AV node.

So atrial contraction is at 300bpm, and ventricular contraction at 150bpm.

There is a sawtooth appearance on the ECG, with P wave after P wave.

99
Q

Conditions associated with atrial flutter

A

hypertension
ischaemic heart disease
cardiomyopathy
thyrotoxicosis

100
Q

Treatment of atrial flutter

A
  • similar to A Fib, with rate/rhythm control with beta blockers or cardioversion
  • treat underlying cause
  • radiofrequency ablation of the re-entrant rhythm
  • anticoagulation based on CHA2DS2VASc score
101
Q

What is supraventricular tachycardia

A

Caused by the electrical signal re-entering the atria from the ventricles (normally only goes from atria to ventricles).

Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction.

This happens again and again in a loop and results in fast narrow complex tachycardia (QRS <0.12s)

On ECG looks like QRS followed immediately by a T wave and this is repeated.

102
Q

What is paroxysmal supraventricular tachycardia?

A

Where SVT reoccurs in the same patient over time

103
Q

What are the 3 main types of supraventricular tachycardia based on the source of the electrical signal

A
  1. Atrioventricular nodal re-entrant tachycardia = the re-entry is through the AV node
  2. Atrioventricular re-entrant tachycardia = where the re-entry point is an accessory pathway, like in Wolff-Parksinson White
  3. Atrial tachycardia = electrical signal originates in the atria somewhere other than the SAN. So its not a re-entry, but rather the signal is abnormally generated in the atria
104
Q

Acute management of stable patients with SVT

A
  1. continuous ECG monitoring
  2. Valsalva manoeuvre - ask the patient to blow hard against resistance - e.g. pinch nose and blow into a syringe
  3. Adenosine as a rapid bolus
    or Verapamil as an alternative
  4. if above treatment fails, then direct current cardioversion
105
Q

How does Adenosine work?

A

It interrupts the AV node/accessory pathway during SVT and ‘resets’ it back to sinus rhythm

by slowing down cardiac conduction through the AV node

it is given as a rapid bolus so that it reached the heart with enough impact to interrupt the pathway

it causes a brief period of asystole or bradycardia - can be scary for patient because they might feel like they are dying or impending doom

106
Q

How is adenosine administered?

A

fast IV bolus into a large proximal cannula
e.g. grey cannula in antecubital fossa

initially 6mg, then 12mg and then a further 12mg if no improvement

DO NOT give to patients with asthma, COPD, heart failure, heart block or hypotension

107
Q

Management of patients with long term paroxysmal SVT

A

Medication - beta blockers, calcium channel blockers or amiodarone

Radiofrequency ablation

108
Q

What is Wolff-Parkinson-White Syndrome

A

caused by an extra electrical pathway connecting the atria and ventricles
(normally only one, the AV node)

this extra pathway is called the Bundle of Kent

presents on ECG with a short PR interval, wide QRS complex and a delta wave (upstroke on the QRS complex)

definitive treatment is radiofrequency ablation of the accessory pathway

109
Q

What is radiofrequency ablation?

A

patient is given local or general anaesthetic

catheter inserted into femoral vein and fed through the venous system under x-ray guidance to the heart

once in the heart, it is placed against different areas to test for electrical signals

when any abnormal electrical pathways are identified, radiofrequency ablation (heat) is applied to burn the abnormal area

this leaves a scar tissue that does not conduct any electrical activity

110
Q

What is Torsades de Pointes

A

a type of polymorphic (multiple shapes) ventricular tachycardia

it looks like a normal v tach on ECG, but the QRS complex progressively gets smaller, then bigger, then smaller, and so on

it occurs in patients with a prolonged QT interval

this means prolonged repolarisation of the muscle cells in the heart after a contraction

so normally depolarisation leads to heart contracting

and repolarisation is the period of recovery before the myocytes are ready to depolarise again

but if there is prolonged repolarisation, there can be random spontaneous depolarisations that occur in some areas of the heart

these spread through the ventricles and cause ventricular contraction without a proper repolarisation occurring

so when the ventricles continue to stimulate contractions without a proper repolarisation, this is torsades de pointes

111
Q

What are possible causes of prolonged QT

A
  • long QT syndrome which is an inherited condition
  • medications - antipsychotics, amiodarone, flecainide, macrolide antibiotics
  • electrolyte disturbances - hypokalaemia, hypomagnesemia, hypocalcemia
112
Q

Management of torsades de pointes

A
  • correct the cause - electrolyte disturbances or meds
  • magnesium infusion (even if serum mg is normal)
  • defibrillation if VT occurs
113
Q

What are ventricular ectopics

A

premature ventricular beats that are caused by random electrical discharges from outside the atria

patients often complain of random, brief palpitations

common in all ages and in healthy patients, but more common in patients with pre-existing heart conditions

diagnosed on ECG - appear as random, abnormal, broad QRS complexes on an otherwise normal ECG

114
Q

What is first degree heart block

A

when there is delayed atrioventricular conduction through the AV node (from the atria to the ventricles)

but every atrial impulse will lead to a ventricular contraction

so every P wave is followed by a QRS complex, but PR interval will be > 0.2s

patients are usually asymptomatic

patient usually stable, so can just observe

115
Q

What is second degree heart block

A

When some of the atrial impulses do not make it through the AV node to the ventricles

so sometimes P waves are not followed by a QRS complex

there are 2 patterns of second degree heart block - Mobitz type 1 and 2

116
Q

What is Mobitz type 1

A

a type of second degree heart block

where the atrial impulses become gradually weaker until they do not pass through the AV node

when it is too weak it fails to stimulate a ventricular contraction

after this, the atrial impulse becomes strong again and the cycle repeats

on ECG it appears as progressive prolongation of the PR interval until eventually the QRS complex is dropped. Then it returns to normal and the cycle repeats

usually due to a functional suppression of AV conduction (e.g. due to drugs like beta blockers or digoxin, reversible ischaemia, or after cardiac surgery)

117
Q

What is Mobitz type 2

A

a type of second degree heart block

where there is intermittent failure or interruption of AV conduction

on ECG it appears as intermittent non-conducted P waves without progressive prolongation of the PR interval, followed by a missing QRS complex

there is usually a set ration of P waves to QRS complexes, so 3:1 or 2:1

Mobitz 2 is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis)

Patients typically have a pre-existing LBBB or bifascicular block

118
Q

What is third degree heart block

A

Complete heart block

There is no electrical communication between the atria and ventricles due to complete failure of conduction

On ECG, no observational relationship between P wave and QRS complexes

Patient needs pacemaker

119
Q

Treatment of second and third degree heart block (if patient is not stable)

A
  1. Atropine 500mcg IV

If there is no improvement,
- repeat Atropine 500mcg, up to 6 doses for a total of 3mg

  • other inotropes, such as noradrenaline
  • transcutaneous cardiac pacing

Permanent pacemaker when available

120
Q

What is atropine

A

It is an antimuscarinic medication

works by inhibiting parasympathetic nervous system

side effects = pupil dilation, urinary retention, dry eyes and constipation

121
Q

How do pacemakers work

A

they deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function

consist of a pulse generator - little pacemaker box which is implanted under the skin, most commonly in the left anterior chest wall or axilla

and pacing leads that carry electrical impulses to the relevant parts of the heart

batteries last up to 5 years

might be a contraindication for MRI scans, but most modern ones are compatible

must be removed prior to cremation

122
Q

Single chamber vs dual chamber vs biventricular pacemakers

A

Single chamber pacemakers - have leads in a single chamber, either the

right atrium - if AV conduction is normal and problem is with SA node

or right ventricle - if AV conduction is abnormal

Dual chamber pacemakers - leads in both right atrium and right ventricles

Biventricular pacemakers - leads in right atrium, right ventricle and left ventricle.
Usually in patients with heart failure, used to synchronise the contractions in these chambers to optimise heart function

123
Q

What ECG changes do pacemakers cause

A

Pacemakers can be seen as a sharp vertical line on all leads on the ECG tact

A line before each P wave = lead in atria
A line before each QRS complex = lead in ventricles

Line before only one = single chamber
Line before both = dual chamber

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