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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
How do you manage Wolff-Parkinson White syndrome
Ablation of the accessory pathway
26
What causes hypertrophic cardiomyopathy
Genetic disorder Mutation in sarcomeric genes The heart wall muscle thickens which leads to rhythm and outflow tract problems
27
How do you manage hypertrophic cardiomyopathy
Avoid competitive sports B-blockers, CCB etc ICD for those who have had cardiac arrest
28
How can hypertrophic cardiomyopathy present
``` Palpitations Chest pain Dizziness and syncope Breathlessness Sudden cardiac death ```
29
Which sex is more likely to have dilated cardiomyopathy
Men
30
Describe the pathophysiology of dilated cardiomyopathy
Heart muscle slowly dilates and scars Becomes ineffective heart tissue Leads to arrhythmias
31
Describe the pathophysiology of Arrhythmogenic Right Ventricular Cardiomyopathy
Fibro-fatty replacement of cardiomyocytes | This can affect the electrical activity of the heart and causes arrhythmias.
32
How do you manage Arrhythmogenic Right Ventricular Cardiomyopathy
Usually ICD to protect from rhythm problems | Avoid competitive sports
33
What are the risks of using an ICD
- Infection - Endocarditis - Leads break - Lead dislodgement
34
What is SUDI
Sudden unexpected death in infancy All infant deaths which happen suddenly for no apparent reason (unexpected) May be called cot death
35
Can SUDI be used as an official cause of death
Yes | If death is still unexplained after PM
36
What is SIDS
Sudden infant death Diagnosis of exclusion - used if no pathology or risk factors present Subset of SUDI May be called cot death syndrome
37
What maternal factors can increase risk of SUDI/SIDS
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
What environmental factors can increase risk of SUDI/SIDS
``` Poor housing or overcrowding Sleeping on a pillow or other soft surface Co-sleeping Sleeping on tummy or side Overheating Head covering ```
39
What infant factors can increase risk of SUDI/SIDS
``` Acute illness (e.g. URTI Being preterm Congenital abnormality Small for gestational age Being male Multiple births ```
40
What is the safe sleep advice
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
If a baby dies of suspected SUDI/SIDS do they need a post mortem
YES | Most common cause is infection but need to rule out NAI etc
42
What is the definition of a stillbirth
When a baby dies after 24 weeks of pregnancy and before or during birth
43
What is the definition of a miscarriage
The loss of a baby before 24 weeks of pregnancy
44
What are some of the risk factors for stillbirth
``` Intrauterine Growth restriction Congenital abnormalities Maternal infection Extremes of age Medical complications in pregnancy Multiple pregnancy Obesity Placental issues - abruption, haemorrhage etc ```
45
How can mum reduce risk of stillbirth
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
What is penetrance
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
How do you write down a mutation
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
How might familial hypercholesterolaemia present
``` Young MI may be the presenting problem Tendon xanthoma Corneal arcus – rare in a young person Family history of young MI High cholesterol ```
49
How can you manage familial hypercholesterolaemia
Recommendation is to treat everyone over the age of 10 with statins
50
What is the difference between clinical death and biological death
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
What are the shockable rhythms
VF | Pulseless VT
52
What are the non-shockable rhythms
Asystole | Pulseless electrical activity
53
How do you treat a non-shockable rhythm
CPR | Adrenaline 1 mg IV then every 3-5 min
54
Which drugs are given during resuscitation
Give adrenaline every 3-5 min | Give amiodarone after 3 shocks
55
How do you treat hyperkalaemia
calcium chloride - protects the heart | insulin/dextrose
56
What are the 5 main classes of shock
``` Hypovolaemic Cardiogenic Obstructive Distributive Cytotoxic ```
57
What causes hypovolaemic shock
Loss of circulating volume which leads to reduced preload and CO Can be due to bleeding or dehydration
58
What causes cardiogenic shock
- 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
What causes obstructive shock
Physical obstruction to filling of the heart which leads to reduced preload and cardiac output Can be due to tamponade, PE
60
What causes distributive shock
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
What causes cytotoxic shock
Uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake Can be due to CO poisoning, CN- poisoning
62
How can the heart increase CO
It can increase HR Increase stroke volume (although young children cannot do this) Increase both
63
Which patients require a lower fluid dose
Those with heart failure | At risk of being overloaded
64
What is the aim of fluid resuscitation
To increase the end diastolic volume | Try to compensate for the lower SV
65
List the body's compensatory mechanisms for hypovolaemia
Baroreceptor response Sympathetic mediated neurohormonal response - release of vasoconstrictors etc Capillary absorption of interstitial fluid Hypothalamo-pituitary-adrenal response
66
What are the clinical signs of cardiogenic shock
Poor forward flow – Hypotension/shock, fatigue, syncope | Backpressure – Pulmonary oedema, elevated JVP, hepatic congestion
67
What is positive inotropy
An increase in force of cardiac contraction for any given preload
68
How can you increase cardiac contractility
Physiological achieved by sympathetic nervous system Replicated pharmacological by β and dopaminergic stimulation - dobutamine, adrenaline, dopamine etc
69
How does an intra-aortic balloon pump work
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
Which part of the cardiac cycle is most affected by obstructive shock
Mainly affects cardiac filling rather than ejection
71
How do you manage obstructive shock
Treatment involves removing the underlying cause - PE – anticoagulation +/- thrombolysis - Cardiac tamponade – pericardial drainage - Tension pneumothorax – decompression and a chest drain
72
What are the 3 subtypes of distributive shock
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
What is the early sign of hypoperfusion in septic shock
Rising lactate levels
74
How do you treat septic shock
Early use of vasopressors Appropriate antibiotics Sepsis 6
75
How do you treat anaphylactic shock
Give adrenaline as it acts as a vasoconstrictor and a mast cell stabiliser
76
How do you confirm a diagnosis of anaphylactic shock
Serum mast cell tryptase levels
77
How do you treat neurogenic shock
Dopamine alongside vasopressors are the mainstays
78
Why do patients with neurogenic shock have inappropriate bradycardia
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
What are the reversible causes of cardiac arrest
4H’s – hypovolemia, hypothermia, hypoxia, hypokalaemia | 4T’s – tamponade, tension pneumothorax, thrombosis, toxins
80
What is the most common cause of pulseless electrical activity
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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