Shock and a bit of cardio Flashcards

1
Q

Hypertrophic cardiomyopathy (HCM)

A

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

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2
Q

Arrhythmogenic Right Ventricular Cardiomyopathy?

A

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.

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3
Q

Cardiac arrest?

A

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

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4
Q

Heart failure?

A

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.

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5
Q

ischemia vs infarction?

A

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.

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6
Q

Heart Attack?

A

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.

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7
Q

Reversible causes of cardiac arrest?

A

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
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8
Q

Long QT Syndrome?

A

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)

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9
Q

Shock?

A

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

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10
Q

Summary of the different classes of shock?

A
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11
Q

For an organ function, it needs…

A

-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.

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12
Q

Function and dysfunction of cardiovascular organs like heart?

A

Function:
Blood flow (HR, BP)

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

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13
Q

Function and dysfunction of kidneys?

A

Function:
Urine production
Biochemical homeostasis

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

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14
Q

Function and dysfunction of the brain?

A

Function:
Consciousness
Specific Nerves

Dysfunction:
Decreased GCS
Nerve palsies

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15
Q

Function and dysfunction of lungs?

A

Function:
Oxygen uptake
CO2 Clearance

Dysfunction:
Hypoxia
Hypercarbia

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16
Q

Function and dysfunction of liver?

A

Function:
Glycogen store
Clotting factors
Metabolism

Dysfunction:
Hypoglycaemia
Coagulopathy
Hyperbilirubinaemia
Hepatic encephalopathy

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17
Q

Function and dysfunction of Pancreas?

A

Function
Endocrine (glucose control)
Exocrine (digestive enzymes)

Dysfunction:
Hypo/hyperglycaemia
malabsorption

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18
Q

Function and dysfunction of skin?

A

Function:
Temperature homeostasis
Barrier

Dysfunction:
Hypothermia
Breakdown
Fluid losses

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19
Q

Function and dysfunction of bone marrow?

A

Function:
Cell production- RBC, WBC,Platelets

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

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20
Q

Function and dysfunction of bowel?

A

Function:
Absorption

Dysfunction:
Stasis (Ileus)
Diarrhoea

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21
Q

Scoring methods for the shocks?

22
Q

Sudden Cardiac Death (SCD)?

A

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

23
Q

Arrhthmia?

A

A common manifestation of many genetic conditions.

24
Q

Chaleopathies? Give e.g.

A

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

25
Mechanisms of Arrhythmia?
-*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
26
Hypovolaemic Shock?
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
27
Hypovolaemic Shock - Recognition
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.
28
Hypovolaemic Shock Mx?
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 (unless hypoglycaemic) (Dextrose-Dissolve solute of electrolyte--ions become extracellular and interstional--only for hypoglycaemic, so don't give it to Hypovol)
29
Cardiogenic Shock? Clinical signs?
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
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Right side backflow- -----oedema Left side backflow- -----oedema
peripheral pulmonary
31
Cardiogenic Shock - Recognition?
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
32
Cardiogenic shock – Management ?
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 ## Footnote Be careful with the amount of the fluid as it can tip of the Stirling curve.
33
Enhancing inotrophy for the cardiogenic shock?
- 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
34
Obstructive Shock?
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
35
Obstructive Shock - Recognition?
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
36
Obstructive shock - Management?
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
37
Distributive Shock? Types?
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
38
Sepsis?
bacterial endotoxin mediated capillary dysfunction Infection (any kind) Widespread inflammatory mediators Vasodilatation Disruption of endothelium (glycocalyx) Activation of clotting factors
39
Anaphylactic?
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
40
Neurogenic?
loss of thoracic sympathetic outflow following spinal injury/trauma Septic shock Loss of Sympathetic Nervous System Tone Cord injury above T6
41
Adrenal Crisis?
Sudden mismatch of steroid requirements and availability Unclear pathophysiology Any stressful stimulus Infection Pregnancy Parturition Etc. Sheehan's syndrome Abrupt cessation of long term steroids
42
Distributive Shock - Recognition?
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
43
Distributive shock management?
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
44
Cytotoxic shock?
- uncoupling of oxygen to Hb in tissue delivery and mitochondrial oxygen uptake - Causes include carbon monoxide poisoning, cyanide poisoning
45
CPR?
- 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
46
Defibrillation?
'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. 
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
48
Asystole is never a 'flat' line but rather a wandering baseline
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.
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
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.
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