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CLASP Sudden Death > CLASP Sudden Death > Flashcards

CLASP Sudden Death Flashcards

1
Q

Define stillbirth

A

When a baby is born dead after 24 completed weeks of pregnancy

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2
Q

Define miscarriage

A

Loss of baby before 24 completed weeks of pregnancy

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3
Q

Define antepartum stillbirth and intrapartum stillbirth? What is more common?

A

Antepartum is loss of baby before labour
Intrapartum occurs during labour
Intrapartum is much less common

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4
Q

Name 8 risk factors for stillbirth?

A 
Twin pregnancy
Black or asian ethnicity
Older mum
Teen mum
Poverty
Obesity
Smoking 
Previous stillbirth
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5
Q

Name 8 categories of causes of stillbirths?

A 
Unknown
Placental causes 
Congenital abnormalities 
Intrapartum 
Maternal infections 
Medical complications 
Prolonged pregnancy 
Maternal antibodies
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6
Q

Describe intrapartum causes of stillbirth

A

Placental abruption (placenta separates from the inner wall of the uterus)
maternal and/or fetal infection
Cord prolapse (cord prolapse into vagina and this can result in hypoxia)
Idiopathic hypoxic acidosis
Uterine rupture

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7
Q

What maternal infections may cause stillbirth?

A 
CMV
Parvo
Herpes
Malaria 
Syphilis
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8
Q

What medical complications may cause stillbirth?

A

Pre-eclampsia and eclampsia (high BP in pregnancy)
Diabetes
Obstetric cholestasis (build up of bile acids)

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9
Q

Why may certain maternal antibodies cause stillbirth?

A

If mother has certain antibodies that can cross the placenta and the baby doesn’t have antibodies then can get haemolysis in the baby

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10
Q

Describe 11 pieces of advice to prevent stillbirths?

A

sleep on your side in 3rd trimester
quit smoking/ don’t smoke
stay a healthy weight
avoid alcohol and drugs
attend antenatal appointment
seek advice if have any discharge, bleeding or pain
get the flu vaccine
report itching (sign of obstetric cholestasis)
start taking folic acid before conception
take vitamin D during pregnancy
seek urgent help if reduction in baby movement

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11
Q

People have reported that they felt their baby move ____ before stillbirth

A

less

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12
Q

Describe management of a patient just diagnosed with stillbirth?

A

Need to assess maternal wellbeing e.g. exclude pre-eclampsia, chorioamnionitis, placental abruption, sepsis, DIC
if woman is rhesus D neg then need kleihauer test done to check for feto maternal haemorrhage and if found need anti-RHD gammaglobulin administered.

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13
Q

In stillbirth what conditions merit immediate steps towards delivery?

A

sepsis, pre-eclampsia, placental abruption or membrane rupture

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14
Q

What mode of delivery is recommended in most stillbirth cases?

A

Vaginal

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15
Q

Can women delay labour if stillbirth?

A

yes if they are well they can delay for a short period however need to understand there is a risk of complications if long delay and PM value may be reduced and baby appearance will deteriorate

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16
Q

If a woman decides to return home before delivery after stillbirth what should they receive?

A

A 24 hr contact no

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17
Q

Who’s choice is it to have a PM after a stillbirth?

A

Parent choice

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18
Q

What important things may a stillbirth PM reveal?

A

Conditions that may effect other family members or future pregnancies

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19
Q

What two mental health conditions are women who have had a stillbirth more at risk of?

A

Depression (4 x)

PTSD (7 x)

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20
Q

In future pregnancy after a stillbirth women are likely to have _____ delivery by _____

A

early by IOL

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21
Q

Name 12 scenarios when post mortems are legally required?

A 
Responsible clinician unable to certify death (most likely)
Procurator Fiscal request
Sudden and unexpected death
Death due to negligence
Suspected suicide or homicide 
Death due to drugs 
Death in custody
Death at work
Death due to medical or dental care 
Death of a child SUDI 
Death due to an industrial or notifiable disease
Death due to an accident
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22
Q

What is the WHO definition of sudden death?

A

Death within 24hrs from onset of symptoms

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23
Q

What are the 4Hs and 4Ts of reversible causes of cardiac arrest?

A

Hypoxia, hypovolaemia, hyper/hypokalaemia/metabolic, hypothermia
Thrombosis, toxins, tamponade, tension pneumothorax

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24
Q

What may be some post mortem findings of hypothermia?

A 
Patches on elbows, knees and hips
Wischnewski ulcers (gastric mucosal ulcers)
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25
Q

Why may thrombosis as a cause of cardiac arrest in custody be suspicious?

A

Potentially the person was put in a situation which caused stress exacerbating an underlying medical condition

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26
Q

Name 7 complications that can occur after a MI?

A

Cardiac Rupture
VF (scarred tissue disrupts rhythm)
VSD (due to necrotic septum)
Mitral regurgitation (due to papillary muscle rupture)
Aneurysm formation
Acute pericarditis
Dresslers (pericarditis 2-5 weeks post MI)

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27
Q

What is Dresslers syndrome?

A

Thought to be an immune response that causes pericarditis and usually occurs 2-5 weeks post MI

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28
Q

Name four non suspicious causes of tamponade?

A

After MI, neoplasm, TB, aortic dissection, trauma

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29
Q

Define clinical death

A

the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery with pre-arrest central nervous system function. Clinical Death is a reversible state

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30
Q

Under normal temperature from clinical death to biologic death the period does not exceed ________

A

3-6 mins

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31
Q

Most common cause of cardiac arrest is _______

A

coronary heart disease

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32
Q

Define biologic death

A

Irreversible state of cellular destruction

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33
Q

What are 8 things that make CPR high quality?

A

1) ratio 30:2
2) Site: centre of chest lower 1/3 of sternum
3) Depth: 5-6 cm
4) Rate: 2 per second (100-120 min)
5) Chest recoil (have shoulders directly above hands with elbows locked)
6) Minimal interruptions (<5 secs)
7) Switch CPR provider every 2 min cycle to avoid fatigue
8) Continuous compressions once airway secured i.e ET Tube

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34
Q

Where do defibrillator pads go?

A

Right of sternum under clavicle and around the apex

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35
Q

What are the two shockable rhythms?

A

Pulseless VT and VF

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36
Q

When do you give amiodarone and adrenaline in cardiac arrest?

A

If shockable: give amiodarone after 3rd shock. Adrenaline should also be given after 3rd shock then after every alternate shock
If non shockable: give adrenaline straight away and every 3-5 mins / 2 cycles thereafter

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37
Q

What are the two non shockable rhythms?

A

Asytole and PEA (pulseless electrical activity)

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38
Q

Define PEA?

A

Organised cardiac electrical activity in the absence of a palpable pulse

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39
Q

Describe VF?

A

Uncoordinated electrical activity

Bizzarre, irregular, random waveforms

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40
Q

Describe VT?

A

Broad complex rhythm

Rapid rate, constant QRS morphology

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41
Q

What is torsades de pointes?

A

It is a type of VT that is polymorphic and is common in long QT syndrome

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42
Q

Describe asystole?

A

Absent ventricular activity

Rarely a completely straight line on trace though

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43
Q

Describe how electrical activity is conducted through the heart?

A

The SA node generates potential through the atria wall and to the AV node.
Propagation through the AV node is very slow which allows time for atrial contraction to finish
Impulse travels down the septum through the Bundle of His into left and right bundle branches
Bundle branches terminate in purkinje fibres which transfer the action potential to the ventricles

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44
Q

What does the P wave on an ECG signify?

A

Atrial depolarisation

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45
Q

What does the QRS complex on an ECG signify?

A

Ventricular depolarisation

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46
Q

What does the T wave on an ECG signify?

A

Ventricular repolarisation

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47
Q

What is the normal width of the QRS complex?

A

0.08 secs to 0.12 secs (2-3 small boxes)

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48
Q

What is the PR interval defined as and what is the normal length?

A

start of the P wave to the start of the QRS and is 0.12-0.2 s (3-5 small boxes)

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49
Q

What is the QT interval defined as and what is the normal length?

A

Start of QRS to end of T wave

Usually 0.44 in males and 0.46 in females (11-12 small boxes)

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50
Q

What length of time is a small box on ECG and a large box?

A

Small box =0.04 s

Large box = 0.04 x 5 = 0.2 s

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51
Q

What is the normal calibration of a ECG?

A

25mm/s

10 mm/mV

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52
Q

How do you calculate regular HR from an ECG and irregular HR?

A 
Regular = 300/no of large squares per beat
Irregular= no QRS in 30 x 10
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53
Q

What colour are the limb electrodes in a 12 lead ECG?

A

Red- right arm
Yellow- left arm
Green- left leg
Black (earthed)- right leg

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54
Q

How many electrodes are in a 12 lead ECG?

A

10

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55
Q

Lead 1 is from ____________

A

Right arm to left arm

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56
Q

Lead 2 is from ______

A

Right arm to left leg

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57
Q

Lead 3 is from ________

A

Left arm to left leg

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58
Q

Describe the placements of V1-6 electrodes?

A 
V1= 4th ICS RSE
V2= 4th ICS LSE
V3= midway between V2 + 4
V4= 5th ICS MCL 
V5= Same level as V4 but anterior axillary line
V6= Same level as V4 but mid axillary line
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59
Q

What leads provide an inferior view of the heart?

A

2, 3 and AVF

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60
Q

What leads provide a lateral view of the heart?

A

1, AVL, V5 and V6

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61
Q

What leads provide an anterior view of the heart?

A

V3, V4

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62
Q

What leads provide a septal view of the heart?

A

V1, V2

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63
Q

If there is an inferior MI which artery is likely to be blocked?

A

Right coronary artery

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64
Q

If there is a lateral MI which artery is likely to be blocked?

A

Circumflex artery

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65
Q

If there is an anterior MI which artery is likely to be blocked?

A

Right coronary artery

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66
Q

If there is a septal MI which artery is likely to be blocked?

A

LAD

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67
Q

If a STEMI is shown in leads 2, 3 and AVF which artery is likely to be blocked?

A

Right coronary artery

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68
Q

If a STEMI is shown in leads 1, AVL, V5, V6 which artery is likely to be blocked?

A

Circumflex artery

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69
Q

If a STEMI is shown in leads V3 and V4 which artery is likely to be blocked?

A

Right coronary artery

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70
Q

If a STEMI is shown in leads V1 and V2 which artery is likely to be blocked?

A

LAD artery

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71
Q

What are the five stages of the cardiac cycle?

A 
Passive filling 
Atrial contraction
Isovolumetric ventricular contraction
Ventricular ejection 
Isovolumetric ventricular relaxation
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72
Q

Describe the passive filling stage of the cardiac cycle?

A
  • Pressure in atria and ventricles close to zero
  • AV valves open so venous return flows into the ventricles
  • Aortic pressure ~ 80 mmHg, and aortic valve is closed
  • Similar events happen in the right side of the heart, but the pressures (right ventricular and pulmonary artery) are much lower
  • Ventricles become ~ 80% full by passive filling
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73
Q

Describe the atrial contraction stage of the cardiac cycle?

A
  • The P-wave in the ECG signals atrial depolarisation
  • The atria contracts between the P-wave and the QRS
  • Atrial contraction complete the EDV (~ 130 ml in resting normal adult) – the end diastolic pressure is few mmHg)
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74
Q

Describe the isovolumetric ventricular contraction stage of the cardiac cycle?

A
  • Ventricular contraction starts after the QRS (signals ventricular depolarisation) in the ECG
  • Ventricular pressure rises
  • When the ventricular pressure exceeds atrial pressure the AV valves shut
  • This produces the first heart sound (LUB)
  • The aortic valve is still shut, so no blood can enter or leave the ventricle
  • The tension rises around a closed volume “Isovolumetric Contraction”
  • The ventricular pressure rises very steeply
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75
Q

Describe the ventricular ejection stage of the cardiac cycle?

A
  • When the ventricular pressure exceeds aorta/pulmonary artery pressure
  • Aortic/pulmonary valve open -this is a silent event
  • Stroke Volume (SV) is ejected by each ventricle, leaving behind the end systolic Volume (ESV)
  • SV = EDV – ESV
  • Aortic pressure rises
  • The T-wave in the ECG signals ventricular repolarisation
  • The ventricles relax and the ventricular pressure start to fall
  • When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut
  • This produces the second heart sound (DUB)
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76
Q

Describe the isovolumetric ventricular relaxation stage of the cardiac cycle?

A
  • Closure of aortic/and pulmonary valves signals the start of the isovolumetric ventricular relaxation
  • Ventricle is again a closed box, as the AV valve is shut
  • The tension falls around a closed volume “Isovolumetric Relaxation”
  • When the ventricular pressure falls below atrial pressure, AV valves open and the heart starts a new cycle
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77
Q

What heart valves are open with ventricular diastole but closed with ventricular systole?

A

AV valves (mitral and tricuspid)

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78
Q

What valves are closed with ventricular diastole but open with ventricular systole?

A

Semilunar valves (aortic and pulmonary)

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79
Q

Define stroke volume?

A

The volume of blood being pumped out of a ventricle in a single beat or contraction (60-130 ml)

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80
Q

Define cardiac output? Give an equation to calculate it?

A

Amount of blood pumped out by the ventricles per minute
= SV x HR
(4-8 L /min)

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81
Q

Define a sinus rhythm and name 4?

A

Rhythms that originate in the SA node

1) normal sinus rhythm
2) sinus bradycardia
3) sinus tachycardia
4) sinus arrhythmia

82
Q

Describe how you may identify normal sinus rhythm on an ECG?

A

60-100 bpm
atrial and ventricular rhythm is regular
P wave followed by QRS
Normal PR, QRS and QT intervals

83
Q

Describe how you may identify a sinus bradycardia?

A

Regular but slow heart rate less than 60 bpm

84
Q

What is the risk of sinus bradycardia?

A

Reduced cardiac output

85
Q

What are some potential causes of sinus bradycardia?

A

physiological, drugs, ischaemia, systemic e.g. hypothyroid, hypoglycaemia, hypothermia

86
Q

If acute sinus bradycardia how can it be treated?

A

atropine

87
Q

Describe how you may identify a sinus tachycardia?

A

Regular but fast HR more than 100 bpm

88
Q

What is the risk with a sinus tachycardia?

A

CO falls due to inadequate ventricular filling time

89
Q

What are some causes of sinus tachycardia?

A

stress, drugs, fever, systemic (e.g. hyperthyroid),

90
Q

Treatment of sinus tachycardia?

A

Aimed at treating the underlying cause

may give beta blockers

91
Q

What is a sinus arrhythmia and what causes it?

A

Slight variations in HR due to reflex changes in vagal tone during the respiratory cycle (HR still between 60-100bpm)

92
Q

What causes atrioventricular nodal re-entrant tachycardia?

A

There are both fast and slow electrical pathways in the AV node

93
Q

What are the symptoms of AVNRT and how is it treated?

A

Asymptomatic or may have episodes of palpitations

Often terminated by vagal manoeuvres e.g. valsava, right carotid massage or immersion in cold water

94
Q

What causes atrioventricular re-entrant tachycardia?

A

There are accessory pathways between the atria and ventricles which results in re-entry circuits where atria are activated after the ventricles.

95
Q

How may ECG appear with AVRT?

A

Depends on direction of pathways

In sinus rhythm may see delta waves due to pre-excitation of ventricles

96
Q

What condition can cause AVRT?

A

Wolff-Parkinson White Syndrome

97
Q

What is characteristic ECG finding of Wolff-Parkinson White syndrome?

A

Delta waves

98
Q

Define first degree heart block?

A

PR interval more than 0.2 s but every P wave is conducted through

99
Q

What is second degree heart block and what are the two types?

A

Intermittent block get Mobitz type 1 and mobitz type 2

100
Q

What happens in mobitz type 1?

A

Progressive lengthening of the PR interval until a beat is dropped

101
Q

What happens in mobitz type 2?

A

PR interval is constant but every nth beat is dropped

102
Q

What is being described?

PR interval is constant but every nth beat is dropped

A

mobitz type 2

103
Q

What is being described

progressive lengthening of the PR interval until a beat is dropped

A

mobitz type 1

104
Q

Define third degree heart block?

A

No action potentials from the SA node get through the AV node
P waves are completely unrelated to QRS complexes

105
Q

What is atrial flutter?

A

An arrhythmia similar to AF but the heart rate is regular

106
Q

What do AF and atrial flutter both risk? What must be given to reduce risk?

A

Clot formation in the atria which could result in a stroke or a PE
Blood thinners

107
Q

Sawtooth pattern on ECG?

A

Atrial flutter

108
Q

Describe the ECG of atrial flutter?

A

Regular HR
Normal P waves are absent but flutter (f) waves are present
sawtooth pattern

109
Q

What may treatment of atrial flutter involve?

A

Rhythm control with procainamide or rate control with dilimiazem, verapamil or a beta blocker

110
Q

What are some causes of atrial fibrillation?

A

Rheumatic heart disease, alcohol intoxication, hyperthyroidism, hypertension, sometimes no cause can be identified

111
Q

What happens in atrial fibrillation?

A

There is continuous rapid activation of the atria by re-entry wavelets. The atria respond electrically at this rate but there is no coordinated mechanical action. Only a proportion of impulses are conducted to the ventricles.

112
Q

Symptoms of atrial fibrillation?

A

Rapid palpitations, dyspnoea or chest pain

113
Q

What are the three types of AF?

A

Paroxysmal
Persistent
Permanent

114
Q

Define paroxysmal AF?

A

Lasts less than 48 hrs often recurrent

115
Q

Define persistent AF?

A

Episodes last more than 48hrs but can still be cardioverted to normal sinus rhythm

116
Q

Define permanent AF?

A

Inability of pharmacologic or non pharmacologic methods to restore NSR

117
Q

What does AF look like on ECG?

A

Irregularly irregular HR, no p waves but there are f waves

118
Q

Irregularly irregular HR arrhythmia?

A

AF

119
Q

Treatment of AF?

A

ventricular rate control with digoxin, beta blockers, verapamil/dilitiazem
rhythm control by converting electrically or with drugs
always need to do anticoagulation

120
Q

What happens in ventricular ectopics?

A

ectopic beats arise from an irritable site in the ventricles

121
Q

What symptoms can VT result in?

A

pre-syncope, syncope, hypotension and cardiac arrest

122
Q

Wide QRS tachycardia with a history or CAD/HF =

A

VT until proven otherwise

123
Q

What is the most common shockable rhythm?

A

ventricular fibrillation

124
Q

Treatment of VF?

A

it causes cardiac arrest so need CPR and defibrillates

125
Q

What happens in VF?

A

rapid and irregular ventricular activation with no mechanical effect

126
Q

What happens in asystole?

A

ventricular standstill

127
Q

Most common cause of sudden cardiac death in young people?

A

HOCM

128
Q

Define penetrance

A

the likelihood of having a disease if you have a mutation. If something has 100% penetrance you will get the disease if you have the mutation. Mendelian disorders are high penetrance.

129
Q

Describe why next generation sequencing is used if you want to sequence several genes as opposed to sequencing them separately

A

Next generation sequencing allows sequence of whole genome. It is cheaper and more efficient to sequence the whole genome if several genes you want to sequence. Sequence lots but only analyse the bits you want to.

130
Q

Describe reference sequences

A

Sequences are compared to “reference sequences” which re the commonest sequence for an American caucasian male

131
Q

Define the central dogma

A

The two step process of transcription and translation

132
Q

What 3 things may any genetic change be?

A

a disease causing mutation, a known polymorphism, a variant of unknown significance

133
Q

Define variant

A

any change in DNA sequence (may be pathogenic or benign)

134
Q

Define mutation

A

A pathogenic variant

135
Q

Define polymorphism

A

A variant prevalent in population, often implies benign but can have a low penetrance effect on common disease

136
Q

Define highly conserved gene

A

Gene that is found in lots of species so is likely to be important for function

137
Q

Name 4 things that may hint that a variant is pathogenic?

A
  • causes a frame shift
  • results in a premature stop
  • is in a highly conserved area
  • splice site causes intron to stay in
138
Q

Long QT syndrome can be acquired or ______

A

congenital

139
Q

What are two major syndromes that cause congenital long QT?

A 
Jervell Lange Nielson (autosomal recessive and associated with deafness)
Romano ward (autosomal dominant NOT associated with deafness)
140
Q

What may provoke congenital long QT?

A

Exercise, particularly swimming

141
Q

Describe symptoms and presentation of long QT?

A

Patients with long QT develop syncope and palpitations as a result of polymorphic ventricular tachycardia (torsades de pointes). They usually terminate spontaneously but may degenerate to VF resulting in sudden death.

142
Q

In long QT syndrome what does ECG show when not in VT?

A

Prolonged QT interval

143
Q

How is congenital long QT syndrome usually treated?

A

Beta blockade, pacemaker therapy, occasionally left cardiac sympathetic denervation

144
Q

What is hypertrophic obstructive cardiomyopathy?

A

A group of inherited conditions that produce hypertrophy of the myocardium in the absence of an alternative cause

145
Q

Most cases of HOCM are autosomal _________

A

dominant

146
Q

What happens to the heart function in HOCM?

A

There is diastolic dysfunction as the heart cannot relax, eventually there is outflow obstruction due to the bulging inter ventricular septum

147
Q

Presentation of HOCM?

A

May be asymptomatic but can cause chest pain, dyspnoea, syncope, pre-syncope, cardiac arrhythmias or sudden death
May have an ejection systolic murmur and a jerky carotid pulse

148
Q

What is arrhythmogenic right ventricular dysplasia?

A

A genetic condition that cause fatty or fibro-fatty replacement of myocytes in the right ventricle which leads to dilatation

149
Q

Presentation of arrhythmogenic right ventricular dysplasia?

A

Most patients are asymptomatic. Symptomatic ventricular arrhythmia, syncope or sudden death can occur though. Occasionally patients can present with symptoms and signs of right heart failure.

150
Q

Signs and symptoms of a PE?

A
  • Sudden onset SOB is most common symptom
  • Pleuritic chest pain and haemoptysis are only present when infarction of lung tissue has occurred
  • On exam may have a localized pleural rub and coarse crackles over the area involved
  • They may have a fever
  • signs of DVT
151
Q

What is the investigation of choice for those with high clinical probability of PE, or non-high clinical probability and a positive D-dimer test?

A

CTPA

CT pulmonary angiography

152
Q

Describe management of a PE?

A
  • High flow oxygen should be given to everyone unless they have chronic lung disease
  • Usually given thrombolysis therapy (drugs that dissolve clots) then anticoagulation (drugs that help prevent clots)
  • Apixaban and Rivaroxaban are first line oral anticoagulants
153
Q

List 8 risk factors for PE and DVT?

A

1) Surgery Trauma
2) Pregnancy
3) Contraceptive pill and hormone therapies
4) Varicose veins
5) Obesity
6) Malignancy
7) Smoking
8) Genetic Conditions

154
Q

Describe symptoms of a MI?

A

severe crushing chest pain radiating to jaw and arms especially the left, similar to angina but not relieved by GTN, sweating, nausea, pallor, sense of impending doom.

155
Q

What may ECG look like in MI?

A

ST elevation, T wave inversion

May go into VF

156
Q

What is the early treatment for a MI?

A 
MONA T
Morphine and anti emetic 
Oxygen if hypoxic 
GTN if BP > 90
Aspirin 
Ticagrelor

If patient is more than 2hrs from hospital they are given thrombolytic therapy e.g. streptokinase. If less that 2hrs patient prepped for PCI and taken to hospital.

157
Q

What is an abdominal aortic aneurysm?

A

Abnormal fixed dilation of the abdominal aorta

158
Q

What may cause aortic aneurysm formation?

A

May be secondary to athersclerosis, infection (syphilis, E coli. salmonella), trauma or may be genetic (marfans or ehlers danlos)

159
Q

Describe presentation of ruptured AAA?

A

sudden onset epigastric pain that may radiate to the back, hypotension, pulsatile expansive mass in the abdomen, sudden collapse and death

160
Q

Most aneurysm are ________ unless ruptured

A

asymptomatic

161
Q

What is an aortic dissection?

A

A tear in the intima with blood tracking down the wall of the aorta

162
Q

What patients have a pre-disposition to aortic dissection?

A

Those with auto-immune rheumatic heart disorders, those with Marfans or Ehlers Danlos

163
Q

Describe presentation of aortic dissection? How is diagnosis confirmed?

A

Sudden onset of severe and central chest pain that often radiates to the back and down the arms mimicking MI

confirmed with trans oesophageal echo or MRI

164
Q

What drugs can cause long QT?

A

Clarithromycin, erythromycin (macrolides)

165
Q

Define shock?

A

Condition of inadequate perfusion to sustain normal organ function

166
Q

What are the five types of shock?

A 
Hypovolaemic shock 
Cardiogenic shock
Obstructive shock 
Distributive shock
Cytotoxic shock
167
Q

Explain what happens in hypovolaemic shock?

A

Loss of intravascular volume results in decreased cardiac output which results in a decrease in blood pressure and inadequate tissue perfusion

168
Q

List some causes of hypovolaemic shock

A

Trauma is the leading cause but other causes include fluid lost from gut in D and V, renal fluid losses, skin loss in hot climates and intravascular fluid in the interstitium.

169
Q

Describe the features of hypovolaemic shock?

A

Features depend on volume loss. As blood loss increases so does RR, HR. Pulse pressure and urine output decrease and so does mental status.

Younger and fitter patients will compensate well until they suddenly don’t.

CHILDREN WHO HAVE A LOW BP NEED TREATED URGENTLY THIS IS A VERY LATE SIGN IN CHILDREN

170
Q

Explain what is meant by cardiogenic shock?

A

Inability of the heart as a pump to meet circulatory demand.

171
Q

List some causes of cardiogenic shock?

A

Most commonly a complication of acute MI but can also be caused by acute valve dysfunction, myocarditis, cardiomyopathy or myocardial contusion

172
Q

Presentation of cardiogenic shock?

A

Hypotension, fatigue, syncope, also symptoms of back pressure > pulmonary oedema, elevated JVP, hepatic congestion

173
Q

Treatment of cardiogenic shock?

A

Positive inotropic drugs e.g. dobutamine, adrenaline, when refractory may use intra-aortic balloon pump

174
Q

Explain what is meant by obstructive shock?

A

Involves a physical obstruction to either the heart or great vessels, usually affects cardiac filing as opposed to ejection

175
Q

List some causes of obstructive shock?

List a treatment for each one?

A

Main three are PE (anticoagulation +/- thrombolysis), cardiac tamponade (pericardial drainage) and tension pneumothorax (decompression and chest drainage)

176
Q

Explain what is meant by distributive shock?

A

Massive vasodilation, initially there is a high cardiac output but this is insufficient to maintain forward perfusion

177
Q

Explain the three main subtypes of distributive shock?

A

SEPTIC > bacterial endotoxin mediated capillary dysfunction
ANAPHYLACTIC > mast cell release of histaminergic vasodilators
NEUROGENIC > loss of thoracic sympathetic outflow

178
Q

Apart from the three main subtypes give an another occasion when distributive shock can occur?

A

Adrenal dysfunction

179
Q

3 important things to do in septic shock?

A

Measure lactate which will show hypo perfusion before hypotension occurs
Early broad spectrum antibiotics after venipuncture for blood puncture done
Early use of vasopressors improves perfusion and minimises excessive fluid volumes

180
Q

What happens in anaphylactic shock?

A

There is uncontrolled activation and degranulation of mast cells which release histamine resulting in uncontrolled vasodilation

181
Q

What can be taken during reaction to confirm diagnosis of anaphylaxis at a later date?

A

Serum try-tase (this will be raised during anaphylaxis)

182
Q

Treatment of anaphylactic shock?

A

Adrenaline

183
Q

Explain what neurogenic shock is?

A

Hypotension following loss of descending sympathetic tone most commonly following a spinal cord injury or central trauma. There is usually inappropriate bradycardia due to unopposed vagal tone.

184
Q

Why is there usually inappropriate bradycardia in neurogenic shock?

A

With loss of sympathetic system there is unopposed vagal tone

185
Q

Treatment of neurogenic shock?

A

Treat underlying cause, give vasopressors, dopamine or other chronotropes

186
Q

Explain what cytotoxic shock is?

A

Uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake
For example in CO poisonings, CN poisoning

187
Q

Define SUDI?

A

Sudden Unexpected Death of an Infant. This is used to describe all infant deaths which happen suddenly for which there is no apparent reason. If the death is still unexplained following PM the term SUDI may be given as classification on death certificate.

188
Q

Define SIDS?

A

Sudden Infant Death Syndrome. This term is used when there is no pathology or risk factors present. The term is therefore a diagnosis of exclusion and is regarded as a subset of all SUDIs investigated.

189
Q

Define Cot Death?

A

Popular description for SUDI/ SIDS

190
Q

What accounts for the largest number of infant deaths in those age 2-6 months?

A

SUDI

191
Q

Describe the triple risk model for SUDI?

A

Describes the intersection of 3 risks > vulnerable infant, a critical development period in homeostatic control and an exogenous stressor.

192
Q

List six factors that may make a child vulnerable to SUDI?

A
  • acute illness e.g. URTI, otitis media with symptoms present but not enough to cause death
  • preterm
  • congenital anomaly (but not bad enough to cause the death on its own)
  • multiple birth
  • small for gestational age
  • male infant
193
Q

Name some exogenous factors that may make a child more vulnerable to SUDI?

A
  • Symptomatic depression in mother or primary caregiver at the time of death
  • alcohol use by mother > 2 units in the last 24 hrs
  • substance misuse by parent
  • smoking by mother in pregnancy or post natally
  • poor housing or overcrowding
  • domestic violence
  • co sleeping
  • sleeping on pillow duvet or other soft surface
  • sleeping prone or on side
194
Q

6 steps for parents to reduce baby’s risk of SUDI?

A

1) keep baby away from smoke, before and after birth
2) put baby in a cot, crib or moses basket to sleep, never fall asleep with them on a sofa or chair
3) never fall asleep with baby after drinking or taking drugs/ medication
4) put baby to sleep on their back with their feet to the foot of the cot
5) keep baby’s head and face uncovered and make sure they don’t get too hot
6) breastfeed your baby

195
Q

Define sudden cardiac death

A

Sudden cardiac death is defined as an event that is non-traumatic, non-violent, unexpected, and resulting from sudden cardiac death within 6 hours of previously witnessed normal health

196
Q

What is Brugada syndrome?

A

inherited syndrome that accounts for patients with ventricular fibrillation with no causative structural cardiac disease identified

197
Q

ECG of someone with Brugada syndrome?

A

ECG findings intermittent
May have VT or VF
Atrial fibrillation is common
right bundle branch block with coved ST elevation in leads V1-3.

198
Q

What causes Brugada syndrome?

A

Inherited loss of sodium channel function

199
Q

What can be used to confirm diagnosis of Brugada syndrome?

A

Provocative testing with class 1 anti-arrhythmics e.g. flecainide or ajmaline

200
Q

Typical presentation of Brugada syndrome

A

Acutely unwell, very pale and grey and then unresponsive. Spontaneously recovers.

CLASP Sudden Death (1 decks)

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