Ambulance Victoria Pathophysiology For Panel.

1st stage - From onset of Labour until full dilation of the cervix.

2nd Stage - From full dilation of the cervix until birth of the baby

3rd stage - From birth until the placenta is delivered.

1. Penetration of the lung tissue or chest wall creates a one way valve.

2. Air enters the pleural space during inspiration (low intrathoracic pressures)

4. Air trapped during expiration which increases intrathoracic pressure.

5. Intrathoracic Pressure causes lung to collapse and occlusion of SVC and IVC.

6. Reduced venous return and cardiac output result in altered conscious state and eventually PEA arrest.

1. Injury

2.Slow continuing hemorrhage

-Decrease in venous return, and cardiac output cause baroreceptors to activate Sympathetic Nervous System, and BP remains stable.

3.Vasoconstriction

-Catecholamine mediated and renin angiotensin BP remains stable

4. Tachycardia

-Optimal CO, BP remains stable.

5. Dec

1. Complete Spinal Cord Transection - Bolus 500 ml

2. Chest Injury - Consider Tension Pneumothorax

3. Penetrating Trunk Injury, AAA or uncontrolled haemorrhage - Accept Palpable pulse and transport immediately

4. GI Heamorrhage - consider less volume and accept BP of 80-100 systolic

1. Transection inhibits sympathetic innervation while parasympathetic activity remains intact.

2. Without the sympathetic stimulus, widespread vasodilation occurs resulting in hypovolaemia.

3.Parasympathetic drive causes bradycardia, and therefore patients are expected to be bradycardic and hypotensive, and additional fluid should only be administered if other injuries are consistent with hypovolaemia.

Give only a 500ml bolus.

It requires surgical intervention.

Administering fluids can accentuate bleeding by dislodging effective clots and dilute coagulation, by lowering blood viscosity.

Accept a palpable carotid pulse and transport immediately.

You must consider a Tension Pneumothorax. This needs to be either ruled out or treated by MICA.

1. Injury

2. Slow continuing haemorhagge

3. Vasoconstriction

4. Tachycardia

5. Decompensation

6. Irreversible Shock

There is a risk of neurogenic APO. Patient has large stagnant pooling blood, and no ability to increase muscle tone or increase return to the heart.

Adding fluid increases hydrostatic pressure and can tip patient into APO.

1. An injury occurs at T6 or higher

2. It disrupts the sympthatetic outflow due to disruption of the autonomic pathways.

3. Unopposed parasympathetic activity leads to Bradycardia

4. Decreased systemic resistance and pooling leads to hypotension.

Compensatory Shock - Hypotension is detected by baroreceptors anda sympathetic response is activated

- vasoconstriction and an increase in HR, to maintain perfusion.

- increase in RR and bronchodilation to blow of CO2 and reduce PH.

Decompensatory - Continued hypotension causes compensation mechanisms to fail, systolic BP falls first, and pulse pressures decrease.

- Cellular Hypoxia

- Anaerobic metabolism = acidosis

- Atriovenus shunts open, capillaries leak and blood pools

-Increased blood viscosity and decreased blood volume leads to disseminated Intravascular Coagulation,

Irreversible Shock

- Multi Organ Failure

- Death

1. Hypovolaemic (reduced circulating blood volume)

2. Cardiogenic (Ineffective Cardiac Output)

3. Hypoxic (Reduced O2 leads to anaerobic metabolism and lactic acid production = cell death

4. Neurogenic (Sympathetic Nervous System is damaged and vessels dilate)

5. Anaphylatic (Inflammatory mediators cause dialation and increase permeability of vessels + O2 exchange reduced by bronchospasm)

6. Septic (Toxins in the blood result in increased permeability, and decreased vessel resistance and pressure)

Primary Injury is the sudden profound injury to the brain which is more or less complete at the time of impact (ie. Concussion, Contusion, or Compression)

Secondary Injury is the changes in the hours to days after the initial injury. A further cascade of cellular, chemical, tissue or blood vessel changes that further destruct brain tissue (ie. Hypoxia, Ischaemia, Hypercapnia)

- Caffiene

- Alcohol

- Pregnancy

- Stress

- Genetics (ie. Wolff-Parkinson White Syndrome)

- Electrolyte Imbalance

- Athlosclerotic Tissue

- Smoking

- Drugs

- Exercise

- Thyroid Disease

- Some medications/ medication changes

Sepsis

Shock

Cardiac Arrest

Carbon Monoxide Poisoning

Anaphylaxis

Major Trauma or Head Injury

Status Epilepticus

Decompression Illness

Tone

Tissue

Trauma

Thrombin

1. Muscles contained in inflexible sheaths

2. Swelling causes capillary pressures to exceed perfusion pressures within the muscle.

3. Circulation is compromised and creates muscle ischaemia.

4. After 4+ hours of ischaemia, irreversible damage has occured including rhabdomyolosis and neuropraxia

5. Gangrene and Loss of Limb

6. Generalised Rhabdomyolosis and Renal Failure.

Pain

Pallor

Pulse-lessness

Perishingly Cold

Paraesthesia

Paralysis

1. Risk factors damage endothelium

2. LDL's penetrate endothelial wall followed by...

3. Monocytes, under go differentiation and produce...

4. FOAM CELLS which turn into ...

5. Fatty streaks protrude into the lumen of the artery

6. Collegen and Elastin cover fatty streak forming fibrous cap.

7. Cap disrupted by turbulent blood flow

8. Clotting cascade begins

9. Blood flow restricted distal to occlusion causing ischaemia.

3 Zones

Coagulation, Stasis, and Hyperaemia.

Coagulation - Irreversible damage to cells. No perfusion. Tissue is necrotic.

Stasis - Cell damage can be recovered with appropriate treatment and reperfusion, but will be irreversibly damaged with no intervention. Cells are ischaemic due to clotting and vasoconstriction.

Hyperaemia - Increased blood flow due to inflammatory response.

Major loss of heat and water.

Potential infection risk.

Damage to epidermis causing pain, redness and swelling.

Damage to dermis and epidermis, causing pain, swelling redness and blistering.

Damage to all layers of tissue. Skin may feel numb. Extensive tissue destruction.

1. Severe Hyperglycaemia

2. Osmotic Diuresis and Dehydration

3. Breakdown of fat, protient and muscle. Release of pottasium

4. Loss of sodium and water. Bicarbonate prevented from forming

5. Compensation kicks in (Tachycardia, Tachypnoea)

6. PH continues to decrease as Ketones still being produced.

7. Compensation Mechanisms Fail

8. Excessive Dehydration, Osmolality, and Haemoconcentration

9. Shock,-> Coma,-> Death.

1-2 days of Upper Resp Tract infection

Tachycardia

Hypoxia (agitation, distress, cyanosis, SPO2 <92% RA)

Stridor

Rib Retraction

Barking Cough

Restlessness

Lethargy

Marked use of accessory muscles

Primarily an acute swelling of the trachea and bronchi

Generally characterised by a 'barking" seal-like cough

Usually preceeded by some form of URTI

Causes localised oedema

Trachea, Larynx and Bronchi become inflammed and cause partial airway obstruction

Decreased mobility of the vocal chords leads to associated hoarse voice.

Croup -

Viral Infection

URTI and mild fever past 1-2 days

Hoarse Voice

Barking Cough

Stridor increases with severity

Epiglottitis-

Severe bacterial infection and sudden onset of symptoms

Pt appears flushed/septic

Unable to swallow

Constant drooling

Pt sits upright with head thrust forward to keep airway open.

Locate point of compression near the umbilicus and slightly to the left.

Apply downward pressure with a closed fist through the abdominal wall.

Assess effectiveness by assessing the quality of the femoral pulse whilst pressure is applied.