Shock and a bit of cardio

Question 1

Hypertrophic cardiomyopathy (HCM)

Answer 1

is a disease in which the heart muscle becomes thickened (hypertrophied).

Question 2

Arrhythmogenic Right Ventricular Cardiomyopathy?

Answer 2

fatty fibrous tissue replaces normal heart muscle. This interrupts normal electrical signals in the heart and may cause irregular and potentially life-threatening heart rhythms.

Question 3

Cardiac arrest?

Answer 3

Inability of the heart to pump blood around the body
when the heart suddenly stops beating.

Underlying cardiac disease is usually coronary: ischaemic heart disease, heart failure and arrhythmias
non-cardiac causes such as toxins, pneumothorax or severe infection.

CPR and immediate defibrillation is appropriate for ventricular fibrillation and pulseless ventricular tachycardia

Question 4

Heart failure?

Answer 4

when the heart fails to pump enough blood throughout the body.
as a result, blood backflow–> into the lungs; swelling of the feet, ankles and legs can occur; and those affected will experience tiredness and shortness of breath.
Coronary artery disease, high blood pressure, and diabetes can all cause HF.

Question 5

ischemia vs infarction?

Answer 5

Ischemia:
blood flow to a tissue has decreased, which results in hypoxia

Infarction:
infarction goes one step further and means that blood flow has been completely cut off, resulting in necrosis, or cellular death.

Question 6

Heart Attack?

Answer 6

A heart attack occurs when blood flow to the heart is blocked. Blood clots, atherosclerosis, and fat and cholesterol deposits can all cause blocked arteries that lead to a heart attack. During a heart attack, the heart continues to beat, but oxygen-rich blood can’t reach the organ. The longer someone goes without treatment, the more damage there will be to the heart.

Question 7

Reversible causes of cardiac arrest?

Answer 7

Four Hs
- Hypoxia
- Non-suspicious e.g. asthma, aspiration
- Suspicious e.g. drug related, drowning
- Hypovolaemia
- Non-suspicious e.g. upper/lower GI haemorrhage, trauma
- Suspicious e.g. trauma, stabbings
- Hypo/hyperkalaemia/metabolic
- Non-suspicious e.g. DKA, alcoholic ketoacidosis, toxins
- Suspicious e.g. toxins (poisonings)
- Hypothermia
- Non-suspicious e.g. exposure to cold, alcoholic, drugs
- Suspicious e.g. exposure to cold, water, neglect
- Signs on autopsy: Wischnewski ulcers (black spots associated with hypothermia)

Four Ts

• Thrombosis - coronary or pulmonary
  
  • Non-suspicious e.g. coronary artery thrombosis, pulmonary venous embolism
  • Suspicious e.g. controbution, deaths in custody, one punch
• Tamponade - cardiac
  
  • Non-suspicious e.g. after MI, pericarditis, aortic dissection, trauma
  • Suspicious e.g. secondary to injury blunt or sharp force trauma
• Toxins
  
  • Non-suspicious e.g. overdose, negligence
  • Suspicious e.g. third party involvement (poisoning), negligence
• Tension pneumothorax
  
  • Non-suspicious e.g. chronic lung diseases, spontaneous, trauma
  • Suspicious e.g. secondary to trauma

Question 8

Long QT Syndrome?

Answer 8

Describes an ECG where the ventricular repolarization (QT interval) is greatly prolonged.

Congenital:
Mutation in ion channel results in reduced/dysfunctional ionic current, prolonging cardiac repolarisation and therefore resulting in QT prolongation

develop syncope and palpitations as a result of polymorphic ventricular tachycardia (torsades de pointes)

Question 9

Shock?

Answer 9

a condition that generalised cellular dysfunction due to the inadequate delivery or utilisation of oxygen

Question 10

Summary of the different classes of shock?

Answer 10

Question 11

For an organ function, it needs…

Answer 11

-pluming an plumbing (e.g. heart, valves)
-oxygen
-Mitochondria
-Energy source like glucose or fat, it is the only source that doesn’t stop suddenly.

Question 12

Function and dysfunction of cardiovascular organs like heart?

Answer 12

Function:
Blood flow (HR, BP)

Dysfunction:
Poor flow
Back pressure
Failure of forward pressure
Cardiac arrest

Question 13

Function and dysfunction of kidneys?

Answer 13

Function:
Urine production
Biochemical homeostasis

Dysfunction:
Decreased urine production
Biochemical derangement (especially rising urea/creatinine,high K+ and H+)

Question 14

Function and dysfunction of the brain?

Answer 14

Function:
Consciousness
Specific Nerves

Dysfunction:
Decreased GCS
Nerve palsies

Question 15

Function and dysfunction of lungs?

Answer 15

Function:
Oxygen uptake
CO2 Clearance

Dysfunction:
Hypoxia
Hypercarbia

Question 16

Function and dysfunction of liver?

Answer 16

Function:
Glycogen store
Clotting factors
Metabolism

Dysfunction:
Hypoglycaemia
Coagulopathy
Hyperbilirubinaemia
Hepatic encephalopathy

Question 17

Function and dysfunction of Pancreas?

Answer 17

Function
Endocrine (glucose control)
Exocrine (digestive enzymes)

Dysfunction:
Hypo/hyperglycaemia
malabsorption

Question 18

Function and dysfunction of skin?

Answer 18

Function:
Temperature homeostasis
Barrier

Dysfunction:
Hypothermia
Breakdown
Fluid losses

Question 19

Function and dysfunction of bone marrow?

Answer 19

Function:
Cell production- RBC, WBC,Platelets

Dysfunction:
Anaemia- low RBC
Thrombocytopenia- ^ platelets
Neutropenia/Leukopenia- ^Neutropnia/Leukopenia

Question 20

Function and dysfunction of bowel?

Answer 20

Function:
Absorption

Dysfunction:
Stasis (Ileus)
Diarrhoea

Question 21

Scoring methods for the shocks?

Answer 21

Question 22

Sudden Cardiac Death (SCD)?

Answer 22

an event that is non-traumatic, non-violent, unexpected, and resulting from sudden cardiac arrest within 6 hours of previously witness normal health

Question 23

Arrhthmia?

Answer 23

A common manifestation of many genetic conditions.

Question 24

Chaleopathies? Give e.g.

Answer 24

Arrhythmogenesis is related to ion current imbalance due to mutation of ion channel, causing development of early and late depolarisations i.e. the problem is in the ionic and electrical conduction due to protein problem.
Results in ion current imbalance and development of early and late depolarisation.

e.g.
Congenital long QT Syndrome
Short QT syndrome
Brugada Syndrome
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Progressive familial conduction disease
Familial AF
Familial WPW

Question 25

Mechanisms of Arrhythmia?

Answer 25

-Automaticity-when the SA node goes wrong
-Trigger-early/delayed depolarisation; cause electrical dispersion; ways of depo going to all the ventricles and cause VF
-Re-entry; when there is a loop of conduction before reaching the refractory period and the commonest arrhythmia is re-entry. also re-entry occurs in previously had MI or Hypertrophic Cardiomyopathy

Question 26

Hypovolaemic Shock?

Answer 26

Low volume circulation
(not necessarily blood loss)

Causes
* Loss (e.g. Bleeding, Diarrhoea, Sweating)
* Wrong place (e.g. ‘third spacing’ occurs when intravenous fluid shifts out of circulation in the blood and into the space between cells in organs and tissues; i.e fluid is in the wrong place)
* Inadequate intake–>Technically possible but very rare

Clinical features depend on the degree of hypovolaemia - classes I - IV

Question 27

Hypovolaemic Shock - Recognition

Answer 27

A
No specific Airway problems
B
Tachypnoea, may have poor reading SpO2
C
Hypotension, Tachycardia
Cool, dry peripheries, may have dry membranes, thirst,reduced skin turgor
D
Reduced GCS, agitation, maybe reduced temp
E
Bleeding, diarrhoea, burns etc.

Question 28

Hypovolaemic Shock Mx?

Answer 28

Call for help
High flow O2
IV access and IV fluids
Stop the losses like
* Haemorrhage control
* Treat the diarrhoea
* Wrap the burns
Give fluid=Colloid protein like solution–stays in the blood and produce high osmosis; water into the cell
Give like-for-like
DO NOT GIVE DEXTROSE (unlesshypoglycaemic)
(Dextrose-Dissolve solute of electrolyte–ions become extracellular and interstional–only for hypoglycaemic, so don’t give it to Hypovol)

Question 29

Cardiogenic Shock? Clinical signs?

Answer 29

Pump failure
Cannot create adequate cardiac output to meet body’s needs
CO=HRxSV
SV=EDV-ESV

Causes:
* Massive MI
* Myocarditis
* Endocarditis
* arrhythmias
* Certain overdoses

• Clinical signs:
  
  • Poor forward flow - hypotension/shock, fatigue, syncope
  • Backpressure - pulmonary oedema, elevated JVP, hepatic congestion

Question 30

Right side backflow- —–oedema
Left side backflow- —–oedema

Answer 30

peripheral
pulmonary

Question 31

Cardiogenic Shock - Recognition?

Answer 31

A
Nil specific
B
Tachypnoea, pulmonary oedema (widespread crackles)
C
Tachy(or brady)cardia, hypotension
Cool, sweaty peripheries,slow CRT
New murmurs (which is damaged to the heart muscles)
May have relevant ECG changes–Signs of MI (ST elevation, LBBB), Tachyarrhythmias, bradyarrhythmias, complete heart block
Chest pain
D
Low GCS, Agitation, syncope
E-Nil

Question 32

Cardiogenic shock – Management?

Answer 32

Call for help
High flow O2
IV access, cautious with fluids

Treat underlying cause
* PCI (thromboysis in rural centres)
* Cardioversion
* Antiarrhythmics
Supportive measures
* Inotropes
* Vasopressors
* Mechanical devices Balloon pumps, Ventricular Assist Devices

Be careful with the amount of the fluid as it can tip of the Stirling curve.

Question 33

Enhancing inotrophy for the cardiogenic shock?

Answer 33

• Positive inotrophy is an increase in force of cardiac contraction for any given preload
• This is physiologically achieved by the sympathetic nervous system
• Can be replicated pharmacologically by beta and dopaminergic stimulation
  
  • Dobutamine, adrenaline
  • Dopamine, dopexamine
  • Others e.g. milrinone. levosimendin

Question 34

Obstructive Shock?

Answer 34

Obstruction to flow (mesle eine k pato bezari roo shelang), physical obstruction to filling of the heart → reduced preload and cardiac output

There are 3 parts of the lumen; endoluminal, intraluminal and extraluminal. The endo and extraluminal are the most common ones.

Massive pulmonary embolism-intraluminal
Cardiac Tamponade-extraluminal
Tension Pneumothorax-extraluminal effect on SV and IVC

Constrictive pericarditis
Aortic stenosis
Abdominal Compartment syndrome

Question 35

Obstructive Shock - Recognition?

Answer 35

A
Normally nil specific
B
Tachypnoea, reduced SpO2
Reduced air entry unilaterally, hyperresonance
C
Tachycardia, hypotension
Chest pain, recent surgery
Dilated neck veins
Cool peripheries, sweaty
D
Agitation, reduced GCS, Normothermia
E
Recent thoracotomy, chest wall trauma, evidence of DVT

Question 36

Obstructive shock - Management?

Answer 36

Call for Help
High Flow O2
IV access, Cautious fluids

Relieve the obstruction
Thrombolysis
Thrombectomy
Pericardiocentesis

• PE - anticoagulation +/- thrombolysis
• Cardiac tamponade - pericardial drainage
• Tension pneumothorax - decompression and chest drainage

Question 37

Distributive Shock?
Types?

Answer 37

significant reduction in SVR beyond the compensatory limits of increased cardiac output; Farz kon mikhay az ye loole kheyli bozorg foot koni k badiam akhar darnemiad

Types:
Septic
Anaphylactic
Neurogenic (NOT spinal)
Adrenal Crisis

Question 38

Sepsis?

Answer 38

bacterial endotoxin mediated capillary dysfunction
Infection (any kind)
Widespread inflammatory mediators
Vasodilatation
Disruption of endothelium (glycocalyx)
Activation of clotting factors

Question 39

Anaphylactic?

Answer 39

mast cell release of histamnergic vasodilators
- Uncontrolled activation and degranulation of mast cells
- Release of histamine with resulting uncontrolled vasodilation

OR

Due to a trigger
Antigen-bound IgE
Degranulation of mast cells
Histamine release
Widespread vasodilatation

Question 40

Neurogenic?

Answer 40

loss of thoracic sympathetic outflow following spinal injury/trauma
Septic shock
Loss of Sympathetic Nervous System
Tone
Cord injury above T6

Question 41

Adrenal Crisis?

Answer 41

Sudden mismatch of steroid requirements and availability
Unclearpathophysiology

Any stressful stimulus
Infection
Pregnancy
Parturition
Etc.
Sheehan’s syndrome
Abrupt cessation of long term steroids

Question 42

Distributive Shock - Recognition?

Answer 42

A
Airway swelling (stridor, see-saw breathing, etc)
B
Tachypnoea, Hypoxia, wheeze
C
Hot or cold peripheries, slow CRT, tachycardia, hypotension
D
Agitation, reduced GCS
E
Rash, swelling, causative agent, recent trauma, suddenly stopped steroids, signs of infection

Question 43

Distributive shock management?

Answer 43

Call for help
IV access
IV fluids
General
IV fluids
Consideration of underlying cause
Vasopressors (ICU/HDU only)

Specific to subtypes?
* Septic
Source control
Antibiotic
* Anaphylactic
Remove antigen (1st mx)
Adrenaline (1st Mx)-both acts as a vasoconstrictor and a mast cell stabiliser
Steroids
antihistamines
* Neurogenic
Vasopressors
Antimuscarinics
Dopamine alongside vasopressors
* Adrenal Crisis
Hydrocortisone

Question 44

Cytotoxic shock?

Answer 44

• uncoupling of oxygen to Hb in tissue delivery and mitochondrial oxygen uptake
• Causes include carbon monoxide poisoning, cyanide poisoning

Question 45

CPR?

Answer 45

• CPR involves cyclical changes in intrathoracic pressure serving to create a gradient for forward blood flow and organ perfusion as well as filling of the cardiac chambers by artificially augmenting venous return
• Explains importance of allowing recoil between compressions

CO = HR x SV
BP = CO x SVR
In CPR
HR = Rate of compressions
SV = Quality of depth and recoil
SVR = ‘squeeze’ from adrenaline

Question 46

Defibrillation?

Answer 46

‘Shockable’ Rhythms
Ventricular Fibrillation
Pulseless Ventricular Tachycardia

‘Non-Shockable’ Rhythms
Pulseless Electrical Activity
Asystole

Defibrillation works by interrupting aberrant conduction. Pulseless VT and VF have aberrant conduction and thus can be defibrillated, PEA and Asystole do not: In PEA conduction is normal but there is a mechanical reason that there is no cardiac output, and in Asystole there is no conduction at all (or no ventricular conduction) therefor neither of these arrest rhythms can be defibrillated.

Question 47

Answer 47

Ventricular Tachycardia. It is impossible to tell from an ECG if this is pulseless as you must feel for a pulse. Note the regular, uniform broad complexes. This is characteristic of VT

Question 48

Answer 48

Asystole is never a ‘flat’ line but rather a wandering baseline

Question 49

Answer 49

This is Atrial Fibrillation with a fast ventricular response. It may or may not be PEA. Again, it must be coupled with pulselessness to be PEA.

Question 50

Answer 50

Ventricular Fibrillation. Note the course pattern with no coordination. This is as the electrical impulse is travelling around and around the ventricles with no coordination

Question 51

Answer 51

This is Asystole. There are p-waves but no ventricular complexes. Although the atria have electrical activity it is not being transmitted to the ventricals and therefor systole cannot occur.