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CLASP Sudden Death > Sudden Death > Flashcards

Sudden Death Flashcards

1
Q

What are the potential complications of grief following a sudden death

A

High risk of PTSD

Prolonged/complex grief

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2
Q

What is the definition of a sudden death

A

Death within 24hrs of the onset of symptoms

May have had the underlying illness for some time

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3
Q

Under what conditions does the procurator fiscal require an autopsy

A 
Sudden and unexpected death
Responsible clinician unable to certify death
Death due to negligence
Suspected suicide
Suspected homicide
Death due to drugs
Death in custody
Death at work
Death due to medical or dental care
Death of a child
Death due to an industrial or notifiable disease
Death due to an accident
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4
Q

Do you need familial consent for a hospital autopsy

A

Yes
Requires consent from the family or NOK
May be requested by clinician or family if unsure why patient died

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5
Q

What is a channelopathy

A

Heart conditions where there are arrhythmias related to the ion current imbalance and development of early/late depolarizations

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6
Q

Give examples of channelopathies

A

Congenital long QT syndrome
Brugada syndrome
CPVT
Short QT syndrome

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7
Q

What is a cardiomyopathy

A

Heart is dilated or thickened, and rhythm doesn’t work properly
Patients will be completely healthy until have a cardiac event

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8
Q

Which drugs can prolong the QT

A

Clarithromycin/ erythromycin

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9
Q

What is congenital long QT syndrome

A

Genetic heart condition which prolongs the QT segement of the heart rhythm
Can have Polymorphic VT (torsades de pointes) triggered by adrenergic stimulation
Autosomal dominant version is called romano-ward
Autosomal recessive is jervell and lange-nielsen syndrome

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10
Q

How do you diagnose congenital long QT syndrome

A

ECG - Repeated (3, 3 weeks apart) and stress testing

Corrected QT interval >480ms in repeated 12 lead ECGs

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11
Q

What are the ECG features of congenital long QT syndrome

A

Large T wave with long QT
Extra notch in middle of T wave with long QT
Delayed T wave

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12
Q

How do you manage congenital long QT syndrome

A

In some B-blockers can be effective
Most need an ICD
Avoid QT prolonging drugs
Avoid electrolyte abnormalities (hypokalaemia etc)
Avoid strenuous exertion (sprinting etc) in LQTS1
LQTS2; avoid loud noises

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13
Q

How does congenital long QT present

A

Syncope - 5%
Sudden cardiac death
Most are asymptomatic

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14
Q

Describe short QT syndrome

A

Genetic heart condition - very malignant
Causes a short QT
Don’t usually live very long - risk of SCD
Usually young children

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15
Q

What can trigger VF in those with Brugada syndrome

A

Usually rest or sleep
Fever
Excess alcohol or large meals
Can be provoked using certain drugs when testing -flecainide

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16
Q

What type of inheritance does Brugada syndrome show

A

Autosomal dominant

8x more common in men

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17
Q

How does Brugada syndrome present on an ECG

A

ST elevation and RBBB in V1-3

Can be triggered by flecainide

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18
Q

How does Brugada syndrome present

A 
Blackouts 
Fits
Palpitations 
May be intermittent and related to times of illness/fever 
Risk of SCD
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19
Q

How do you manage Brugada syndrome

A

Avoid certain drugs
Early paracetamol for fever (preventing fever)
ICD in some cases
Avoid drinking lots of alcohol

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20
Q

Describe Catecholaminergic Polymorphic Ventricular Tachycardia

A

CPVT is an arrhythmia disorder caused by an abnormal response to adrenaline
Triggered by emotional stress/physical activity

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21
Q

How do you manage Catecholaminergic Polymorphic Ventricular Tachycardia

A

High dose B-blocker
ICD
ICU admission
Avoid high intensity sport

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22
Q

How does Wolff-Parkinson White syndrome present on an ECG

A

Short PR interval

Delta wave

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23
Q

What causes Wolff-Parkinson White syndrome

A

Extra bit of conducting tissue (accessory pathway)

Can bypass AV node to cause VF as a result of AF

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24
Q

How do you diagnose Wolff-Parkinson White syndrome

A

Exercise ECG

If doing exercise with High HR do they sustain the rhythm problems

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25
Q

How do you manage Wolff-Parkinson White syndrome

A

Ablation of the accessory pathway

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26
Q

What causes hypertrophic cardiomyopathy

A

Genetic disorder
Mutation in sarcomeric genes
The heart wall muscle thickens which leads to rhythm and outflow tract problems

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27
Q

How do you manage hypertrophic cardiomyopathy

A

Avoid competitive sports
B-blockers, CCB etc
ICD for those who have had cardiac arrest

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28
Q

How can hypertrophic cardiomyopathy present

A 
Palpitations
Chest pain 
Dizziness and syncope 
Breathlessness 
Sudden cardiac death
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29
Q

Which sex is more likely to have dilated cardiomyopathy

A

Men

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30
Q

Describe the pathophysiology of dilated cardiomyopathy

A

Heart muscle slowly dilates and scars
Becomes ineffective heart tissue
Leads to arrhythmias

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31
Q

Describe the pathophysiology of Arrhythmogenic Right Ventricular Cardiomyopathy

A

Fibro-fatty replacement of cardiomyocytes

This can affect the electrical activity of the heart and causes arrhythmias.

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32
Q

How do you manage Arrhythmogenic Right Ventricular Cardiomyopathy

A

Usually ICD to protect from rhythm problems

Avoid competitive sports

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33
Q

What are the risks of using an ICD

A
  • Infection
  • Endocarditis
  • Leads break
  • Lead dislodgement
34
Q

What is SUDI

A

Sudden unexpected death in infancy
All infant deaths which happen suddenly for no apparent reason (unexpected)
May be called cot death

35
Q

Can SUDI be used as an official cause of death

A

Yes

If death is still unexplained after PM

36
Q

What is SIDS

A

Sudden infant death
Diagnosis of exclusion - used if no pathology or risk factors present
Subset of SUDI
May be called cot death syndrome

37
Q

What maternal factors can increase risk of SUDI/SIDS

A

There is an association with social deprivation
Symptomatic depression in mother or primary carer
Alcohol use by mother >2 unit
Substance misuse by the parent
Smoking by mum in pregnancy or postnatally
Domestic violence

38
Q

What environmental factors can increase risk of SUDI/SIDS

A 
Poor housing or overcrowding 
Sleeping on a pillow or other soft surface 
Co-sleeping 
Sleeping on tummy or side 
Overheating
Head covering
39
Q

What infant factors can increase risk of SUDI/SIDS

A 
Acute illness (e.g. URTI
Being preterm 
Congenital abnormality 
Small for gestational age 
Being male 
Multiple births
40
Q

What is the safe sleep advice

A

Information about how to put a baby down to sleep to reduce risk of SIDS
Keep them away from smoke
Put baby in a cot, crib or moses to sleep
Never fall asleep with them on a sofa/chair
Never fall asleep with baby after drinking or taking drugs
Put baby to sleep on their back with their feet at the bottom of the cot
Ensure their face/head is uncovered and the do not overheat
Don’t let them sleep in your bed

41
Q

If a baby dies of suspected SUDI/SIDS do they need a post mortem

A

YES

Most common cause is infection but need to rule out NAI etc

42
Q

What is the definition of a stillbirth

A

When a baby dies after 24 weeks of pregnancy and before or during birth

43
Q

What is the definition of a miscarriage

A

The loss of a baby before 24 weeks of pregnancy

44
Q

What are some of the risk factors for stillbirth

A 
Intrauterine Growth restriction
Congenital abnormalities 
Maternal infection 
Extremes of age 
Medical complications in pregnancy 
Multiple pregnancy 
Obesity 
Placental issues - abruption, haemorrhage etc
45
Q

How can mum reduce risk of stillbirth

A

Going to sleep on your side in the third trimester
Quitting smoking
Staying a healthy weight during your pregnancy
Avoid alcohol and drugs
Attend all antenatal appointments
Get flu vaccine

46
Q

What is penetrance

A

The likelihood of having a disease if you have a gene mutation
100% penetrance means you will always get the disease if you have the mutation

47
Q

How do you write down a mutation

A

Gene name
First AA name listed was the original one
The number is the position on the gene
The second AA name is the one that is there now
Stop codon can be denoted by an Asterix

48
Q

How might familial hypercholesterolaemia present

A 
Young MI may be the presenting problem 
Tendon xanthoma 
Corneal arcus – rare in a young person
Family history of young MI 
High cholesterol
49
Q

How can you manage familial hypercholesterolaemia

A

Recommendation is to treat everyone over the age of 10 with statins

50
Q

What is the difference between clinical death and biological death

A

Clinical = the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery (reversible)

Biological = an irreversible state of cellular destruction.
Occurs after around 6 mins

51
Q

What are the shockable rhythms

A

VF

Pulseless VT

52
Q

What are the non-shockable rhythms

A

Asystole

Pulseless electrical activity

53
Q

How do you treat a non-shockable rhythm

A

CPR

Adrenaline 1 mg IV then every 3-5 min

54
Q

Which drugs are given during resuscitation

A

Give adrenaline every 3-5 min

Give amiodarone after 3 shocks

55
Q

How do you treat hyperkalaemia

A

calcium chloride - protects the heart

insulin/dextrose

56
Q

What are the 5 main classes of shock

A 
Hypovolaemic
Cardiogenic
Obstructive 
Distributive
Cytotoxic
57
Q

What causes hypovolaemic shock

A

Loss of circulating volume which leads to reduced preload and CO
Can be due to bleeding or dehydration

58
Q

What causes cardiogenic shock

A
  • Failure of the heart as a pump (myocardial dysfunction)
    Leads to reduction in systolic function and CO
    Can be due to acute MI, acute valve lesion
59
Q

What causes obstructive shock

A

Physical obstruction to filling of the heart which leads to reduced preload and cardiac output
Can be due to tamponade, PE

60
Q

What causes distributive shock

A

Significant reduction in SVR beyond the compensatory limits of increased cardiac output - circulation becomes larger
Can be caused by sepsis, anaphylaxis or neurogenic factors

61
Q

What causes cytotoxic shock

A

Uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake
Can be due to CO poisoning, CN- poisoning

62
Q

How can the heart increase CO

A

It can increase HR
Increase stroke volume (although young children cannot do this)
Increase both

63
Q

Which patients require a lower fluid dose

A

Those with heart failure

At risk of being overloaded

64
Q

What is the aim of fluid resuscitation

A

To increase the end diastolic volume

Try to compensate for the lower SV

65
Q

List the body’s compensatory mechanisms for hypovolaemia

A

Baroreceptor response
Sympathetic mediated neurohormonal response - release of vasoconstrictors etc
Capillary absorption of interstitial fluid
Hypothalamo-pituitary-adrenal response

66
Q

What are the clinical signs of cardiogenic shock

A

Poor forward flow – Hypotension/shock, fatigue, syncope

Backpressure – Pulmonary oedema, elevated JVP, hepatic congestion

67
Q

What is positive inotropy

A

An increase in force of cardiac contraction for any given preload

68
Q

How can you increase cardiac contractility

A

Physiological achieved by sympathetic nervous system

Replicated pharmacological by β and dopaminergic stimulation - dobutamine, adrenaline, dopamine etc

69
Q

How does an intra-aortic balloon pump work

A

It inflates during ventricular diastole to increase diastolic pressure which helps perfuse the coronary arteries
Deflates during systole = reduced afterload to reduce O2 demand and myocardial stress

70
Q

Which part of the cardiac cycle is most affected by obstructive shock

A

Mainly affects cardiac filling rather than ejection

71
Q

How do you manage obstructive shock

A

Treatment involves removing the underlying cause

  • PE – anticoagulation +/- thrombolysis
  • Cardiac tamponade – pericardial drainage
  • Tension pneumothorax – decompression and a chest drain
72
Q

What are the 3 subtypes of distributive shock

A

Septic – bacterial endotoxin causes capillary dysfunction
Anaphylactic – inappropriate release of vasodilators (histamine) from mast cells in response to allergen
Neurogenic – loss of thoracic sympathetic outflow after a spinal injury leading to massive vasodilatation

73
Q

What is the early sign of hypoperfusion in septic shock

A

Rising lactate levels

74
Q

How do you treat septic shock

A

Early use of vasopressors
Appropriate antibiotics
Sepsis 6

75
Q

How do you treat anaphylactic shock

A

Give adrenaline as it acts as a vasoconstrictor and a mast cell stabiliser

76
Q

How do you confirm a diagnosis of anaphylactic shock

A

Serum mast cell tryptase levels

77
Q

How do you treat neurogenic shock

A

Dopamine alongside vasopressors are the mainstays

78
Q

Why do patients with neurogenic shock have inappropriate bradycardia

A

There is stimulation of the vagus nerve (which cause brady) that is no longer opposed by the sympathetic system (as it has been lost)

79
Q

What are the reversible causes of cardiac arrest

A

4H’s – hypovolemia, hypothermia, hypoxia, hypokalaemia

4T’s – tamponade, tension pneumothorax, thrombosis, toxins

80
Q

What is the most common cause of pulseless electrical activity

A

Most commonly caused by hypovolemia

The heart is still pumping normally but there is no real output (therefore pulseless)

CLASP Sudden Death (1 decks)

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