Pathophysiology of asthma

'Intrinsic' asthma is triggered by e.g. exercise, cigarette etc.

'Extrinsic' asthma is the allergic type of asthma which involves IgE antibodies and mast cell degranulation.

The pathogenesis of asthma involves both genetic and environmental factors, and is triggered by exposure of allergens. When come into contact with antigens (allergens), dendritic cells react and present the antigens to lymphocytes. Helper T cells are then activated, releasing cytokines (IL-2, IL-4), which results in the activation of B cells to secret IgE antibodies. In extrinsic asthma, patients have a tendency to form abnormally large amounts of IgE antibodies. Migration and activation of mast cells and eosinophils are also stimulated by lymphocytes activation and cytokines generation.

The IgE antibodies attach to mast cells present in the lung interstitium. As the antigens react with the mast cell attached-antibodies, the mast cell is activated and sends signal for 1) degranulation; 2) phospholipase activation; 3) cytokine gene activation.

1) Substances released in mast cell degranulation are primary mediators of the allergic response. One of which is histamine.
2) Phospholipase activation leads to the release of leukotrienes and prostaglandin.
3) Cytokine IL-5, secreted upon cytokine gene activation, is responsible in activation of eosinophils.

Mast cell activation or, the mediators released, thus results in spasms of smooth bronchial muscles, increased mucus secretions into bronchiolar lumens, and localized oedema in the walls of the small bronchioles. The increased airway resistance creates obstruction in respiration.

The obstruction is, however, more severe during expiration. Despite the occlusion in asthmatic lungs, during inspiration, the positive pressure of the lungs in compare to the atmospheric pressure keeps the airway open. Thus the effect of obstruction is less. In expiration, the partially obstructed airway is further compressed by the greater atmospheric pressure. This gives a more reduced bronchiolar diameter and patients experience great difficulty expiring.

The activated eosinophils release mediators such as eosinophil cationic proteins that are toxic to epithelial cells. Epithelial cell loss in the chronic phase of asthma makes it more vulnerable to irritant stimuli -- resulting in bronchial hypersensitivity.

The theory behind airway remodeling is unknown. Nevertheless, various growth factors cause hypertrophy and hyperplasia of the smooth muscles in the chronic phase. Increased deposition of collagens due to fibroblasts activation creates an environment for ongoing inflammation, and eventually structural and functional alterations.


Reference: Kumar & Clark, Rang & Dale, Guyton

• Main causes of pneumonia – typical, atypical - Rushmi
• Lung function test - Ari
• Pathophysiology of asthma – dilys
• Asthma treatment - Kylie
• What is asthma
• Asthma link with other diseases – atopy – Georgia
o Eczema, hay fever
o Risk factors
• CAM treatment of asthma - Sarah
• Asthma prevention – Jackie
• Puffers - steph
o Spacers
• Asthma plan - Ambu
• Effects of smoking - Lionel
• How to help someone quit - Nathan
o Patches vs. cold turkey
• Lung function, spirometry
• Diagnosis of asthma – Jemima
• Risk factors - Hasif

CAM for Asthma - Sarah

Asthma and Selenium

Selenium deficiency may be important in chronic asthma. Observational studies have demonstrated that patients with chronic asthma may have lower levels of selenium than their control. Nevertheless, selenium supplementation has not been recommended with drug therapy for asthma

Meta-analysis


EBM Reviews - Cochrane Database of Systematic Reviews Allam, Mohamed Farouk. Lucena, Rosario A. Selenium supplementation for asthma. [Systematic Review] Cochrane Database of Systematic Reviews. 1, 2009.
Selection criteria
Randomised trials comparing patients with chronic asthma receiving selenium supplementation in conjunction with asthma medication, with patients taking asthma medication only.

Authors' conclusions
There is some indication that selenium supplementation may be a useful adjunct to medication for patients with chronic asthma. This conclusion is limited because of insufficient studies and lack of improvement in the clinical parameters of lung function.
RCT’s
EBM Reviews - Cochrane Central Register of Controlled Trials Burgess CD, Bremner P, Thomson CD, Crane J, Siebers RW, Beasley R Nebulized beta 2-adrenoceptor agonists do not affect plasma selenium or glutathione peroxidase activity in patients with asthma. [Clinical Trial. Journal Article. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] International journal of clinical pharmacology and therapeutics. 32(6):290-2, 1994 Jun.
Found that selenium levels are not effected by beta 2-agonists, fenoterol and salbutamol (asthma drugs)

EBM Reviews - Cochrane Central Register of Controlled Trials Shaheen SO, Newson RB, Rayman MP, Wong AP, Tumilty MK, Phillips JM, Potts JF, Kelly FJ, White PT, Burney PG Randomised, double blind, placebo-controlled trial of selenium supplementation in adult asthma. [Journal Article. Multicenter Study. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] Thorax. 62(6):483-90, 2007 Jun.

197 participants, divided into a selenium supplement group or placebo. The primary outcome was asthma-related quality of life (QoL) score. Secondary outcomes included lung function, asthma symptom scores, peak flow and bronchodilator usage. There was an increase in selenium in the supplement group and none in the placebo. The quality of life score improved in the active treatment group, however the difference in change in score between the two groups was not significant (p=0.47), no improvements were seen in the secondary outcomes compared with placebo. CONCLUSIONS: Selenium supplementation had no clinical benefit in adults with asthma, the majority of whom were taking inhaled steroids.

EBM Reviews - Cochrane Central Register of Controlled Trials Hasselmark L, Malmgren R, Zetterstrom O, Unge G Selenium supplementation in intrinsic asthma. [Clinical Trial. Journal Article. Randomized Controlled Trial. Research Support, Non-U.S. Gov't] Allergy. 48(1):30-6, 1993 Jan.

This is the original study, with 24 patients suffering from intrinsic asthma. Two randomised groups, receiving selenium, other placebo, there was found to be a significant clinical improvement in the Se-supplemented group. However, the change could not be validated by significant changes in separate clinical tests.

Asthma and Yoga
Maybe some benefit, but not enough evidence to show conclusively. Maybe some benefit in paediatrics –

Therapeutic effects of yoga for children: a systematic review of the literature. [Review] [54 refs] Galantino ML. Galbavy R. Quinn L. Pediatric Physical Therapy. 20(1):66-80, 2008.

Pneumonia

What is it?
An inflammation of the substance of the lungs, usually due to bacteria

Classification by site
Localised – one or more lobes affected
Diffuse – affect lung lobules and bronchii and bronchioles (bronchopneumonia)

Classification by aetiology

Typical pneumonia
Due to streptococcus pneumoniae – most common

Atypical pneumonia
Due to organisms such as mycoplasma pneumoniae, legionella pneumophila, Chlamydia pneumoniae, Chlamydia psittaci, coxiella burnetti
Accounts for 1/5 of the cases of pneumonia (Kumar and Clarke).
Overlaps in clinical presentation with typical pneumonia

Viral pneumonia
Influenza and adenovirus infection are the most common causes. It can often predispose parients to bacterial pneumonia (damages epithelium - facilitates bacterial infection).

Pneumonia due to opportunistic infections
Occurs in immunocompromised patients (e.g. AIDS). It is due to Pneumocytis carinii (bacterium), actinomyces isralli (bacterium), nocardia asteroids (bacterium), cytomegalovirus, aspergillus fumigates (fungus), mycobacterium avium-intracellulare (bacterium), crytptococcus (fungus) and Karposi’s sarcoma.

Rare causes
Bordetella pertussis, typhoid bacillus, paratyphoid bacillus, brucellosis, leptospirosis, measles, chicken pox, glandular fever

Aspiration pneumonia
Occurs when gastric contents enters the lungs. Due to a trachea-oesophageal fistula, periods of impaired consciousness (e.g. sleep), reflux oesophagitis with an oesophageal stricture, or in bulbar palsy (problems with cranial nerves 7-12). The pneumonia is often due to anaerobes.

Risk factors
· Cigarette smoking – strongest independent factor for invasive pneumococcal disease
· Strep. Pneumoniae - often follows a viral infection with influenza/parainfluenza
· Hospitalised patients – infected with Gram negative organisms
· Alcohol excess
· Bronchiectasis (abnormal and permanently dilated airways – impairs the mucocillary transport mechanism, and thus frequent bacterial infections occur)
· Bronchial obstruction, such as a carcinoma
· Immunosuppresion (AIDS, cytotoxic agents) – infection by Pneumocystis carinii, Mycobacteirum avium intracellulare and cytomegalovirus
· IV drug abuse – associated with staph.aureus infection
· Inhalation from oesophageal obstruction – associated with infection from anerobes

Clinical presentation (with strep. pneumoniae)
· Preceding history of viral infection
· High temperature – 39.5°C
· Pleuritic pain
· Dry cough
· Rusty-coloured sputum
· Breathing is rapid and shallow
· Affected side of chest moves less
· Pleural rub
· Signs of consolidation in the lungs

Diagnosis of severe community-acquired pneumonia
· Respiratory rate is greater than or equal to 30/min
· Diatolic BP is less than 60 mmHg
· Confusion
· High mortality, particularly in those over 65
· Co-morbidities

Investigations
· Chest x-ray
· In strep. pneumoniae:
o White blood cell count – is greater than 15 x 109/L (normal = 4-11 x 109/L)
o Erythrocyte sedimentation rate – greater than 100mm/h (normal = less than 20 mm/h) – measure of the settling of RBCs during 1 hour
· To detect certain types of pneumonia:
o Pneumococcal antigen – counter-immunoelectrophoresis of sputum, urine and serum (more sensitive than sputum or blood cultures)
o Mycoplasma antibodies (IgM and IgG)
o Legionella and Chlamydia antibodies – immunoflouresence tests
o Legionella antigen – in urine
· Blood gases – check for respiratory failure, and is also baseline for comparison if the patient deteriorates

Management
· Antibiotics
o Should be started once diagnosis is made
o Largely directed against strep. pneumoniae
o Mild community-acquired pneumonia – oral amoxicillin, oral erythromycin if sensitive to penicillin
o Staph. Aureus infection
§ intravenous flucloxacillin
§ if intolerant to penicillin and macrolides – fluroquinalone
o Severe cases
§ Broad-spectrum lactamase-stable beta-lactam (co-amoxiclav or cefuroxime)
§ Clarythromycin
o Antibiotics can be narrowed once test results received (however, 10% are mixed infections)
· General measures
o Fluids – avoid dehydration
o Sitting upright or where comfortable
o Cough should be encouraged (physiotherapy may be needed.)
§ If it is distressing or unproductive – codeine linctus
o Analgesia from pleuritic pain
· Hospital-acquired
o Commonly gram negative bacteria
§ Third-generation cephalosporin (cefuroxime)
§ Aminoglycosdies (gentamicin)
o Pseudomonas infection
§ IV xiprofloxacin or ceftazidime (cephalosporin)
o Aspiration pneumonia (multiple bacteria, often anaerobic)
§ Metronidazole (nitromidazole)
§ Co-amoxiclav or cefuroxime

PREVENTION OF ASTHMA

Prevention

Consideration should be given to factors which may trigger attacks of asthma. Cigarette smoke should be avoided. Exposure to animals that cause symptoms (often household pets) should be minimised or avoided, and your child may be better with non-allergenic bedding if they are affected by goosedown or feathers. In some selected cases, carpets may need to be removed to minimise dust and decrease exposure to the common house dust mite. In addition you could try avoid pollen! :)

These measures should be balanced with the need to minimise drastic changes to your child’s and your family’s living conditions. Change in environment of any significant degree may not be indicated in children with mild or minimal symptoms.

Some of these precipitating factors can and should be avoided. However, the mainstay of management of asthma is pharmacological – the appropriate use of medications to prevent and treat symptoms.

Apples prevent asthma

A new study tracked the diets of nearly 2,000 pregnant women and checked the lung health of 1,253 of their children at age five. Among a wide variety of foods eaten and recorded by the pregnant women, only apple consumption showed a consistent protective effect against childhood wheeze and asthma.

Children of mothers who ate more than four apples per week were 37 per cent less likely to have a history of wheezing and 53 per cent less likely to have doctor-confirmed asthma, compared to mothers who ate one or no apples per week while pregnant. The specific association found with apples, and not with the total amount of fruits eaten or with citrus, fruit juice or vegetable consumption, hints at an apple-specific effect, possibly because of its unique flavonoids, which have been shown to have beneficial effects on adult lung function. To maximize apple’s benefits why not think about adding apples to your daily juice regime.

A few Things that have been tried and failed;

1)Intermittent Inhaled Corticosteroids in Infants with Episodic Wheezing

2)Although no clinical trial has tested the use of antibiotics in the first weeks of life as a strategy for the prevention of asthma, there is sufficient evidence from a number of population-based cohort studies to suggest that various antibiotic therapies administered early in life do not reduce the risk of asthma.

references;

http://www.detoxstop.com/children/apples-prevent-asthma/

http://raisingchildren.net.au/articles/asthma_treatment.html

http://content.nejm.org.ezproxy.lib.monash.edu.au/cgi/content/short/354/19/1998

http://content.nejm.org.ezproxy.lib.monash.edu.au/cgi/content/full/357/15/1545

Smoking Hx / How to Quit

Taking a Smoking History

What to ask:

• Current number of cigarettes smoked per day
• How soon after waking is first cigarette smoked
• Other tobacco use
• Number of years smoked
• Triggers
• Quitting history
• Longest quit attempt
• Most recent quit attempt
• Withdrawal symptoms

http://makesmokinghistory.org/quitworks/docs/masshealth/IntakeAssessGuide.doc

Methods of quitting smoking:

• Cold Turkey
• Must overcome both physical/pharmacological addiction as well as psychological addiction.
• Physical addiction can be overcome after 100 hours without a cigarette.
• Gradual Reduction
• Although you are weaning yourself from addiction, you are still prolonging your exposure to the cancer-causing chemicals in tobacco.
• Nicotine Replacement Therapy : NRT - Doubles chance of success
• Lower conc of nicotine. No tar, gasses
• Reduces craving and withdrawal symptoms
• Patches – continual low dose – suitable for people who smoke constantly throughout the day,
• gums, nasal spray, inhaler, lozenges and lollipops – hit of nicotine – suitable for people who smoke under stressfull situations or at certain times of the day
• Drugs:
• Bupropion – noradrenaline and dopamine RI + nicotinic antagonist. Antidepressant found later to be an aid in smoking cessation through rather unidentified means.
• Varenicline – Nicotinic receptor partial agonist (like NRT). As a partial agonist, it both reduces cravings for and decreases the pleasurable effects of cigarettes and other tobacco products, and through these mechanisms it can assist some patients in stopping smoking.

http://en.wikipedia.org/wiki/Varenicline

http://en.wikipedia.org/wiki/Bupropion

http://ezinearticles.com/?Quitting-Smoking:-How-Long-Do-The-Cravings-Last&id=360120

http://www.quitsmokingsupport.com/methods.htm

Spirometry

Sorry tried to post. Having battles.
Will just bring copies on Friday.

http://www.amicusvisualsolutions.com/obrasky/05001_02X.jpg

picture :)

Indications
Emergency
Pneumothorax
-In all patients on mechanical ventilation
-When pneumothorax is large
-In a clinically unstable patient
-For tension pneumothorax after needle decompression
-When pneumothorax is recurrent or persistent
-When pneumothorax is secondary to chest trauma
-When pneumothorax is iatrogenic, if large and clinically significant
Hemopneumothorax
Esophageal rupture with gastric leak into pleural space

Non emergency
Malignant pleural effusion
Treatment with sclerosing agents or pleurodesis
Recurrent pleural effusion
Parapneumonic effusion or empyema
Chylothorax
Postoperative care (e.g., after coronary bypass, thoracotomy, or lobectomy)

Contraindications
- when a lung is completely adherent to the chest wall throughout the hemithorax
- a risk of bleeding in patients taking anticoagulant medication or in patients with a predisposition to bleeding or abnormal clotting profiles


Procedure
Preperation
-Patient in supine position
-Maximally abduct the ipsilateral arm or place behind head.
-The area for incision is 4th to 5th intercostal space in the anterior axillary line at the horizontal level of the nipple.
-Triangle of safety: Ant border of lat dorsi, lat border of pectoralis major muscle, the apex just below the axilla and a line above the horizontal level of the nipple.
-Ensure sterile field is created.
-Use LA for deeper subcut tissue & intercostal muscles and periosteal surface & parietal pleura. (lidocaine)

Incision
-Incise 1.5-2cm parallel to rib
-Cut through subcut layers & intercostal muscles
-Path should transverse diagonally up toward the next superior intercostal space. Push thru the paretal pleura, you may also digitally penetrate the pleura to avoid puncturing lung tissue, using your index finger to explore and palpate within the pleural layer & ensure the lung falls away from the pleura. If it does not, this may show e presence of an adhension.

Tube Insertion
-Once the distal tip of the tube has passed through the incision, unclamp the Kelly
clamps or forceps & advance the tube.
-Aim the tube apically for evacuation of a pneumothorax and basally for evacuation of any fluid.

Securing the Tube
-Sutures should be used on both sides of the incision to close the ends.
-Use the loose ends of the sutures to wrap around the tube and tie them off
-Tape the tube to the side of the patient & wrap gauze dressing & multiple pressure dressings around the tube.
[Purse-string sutures are not recommended owing to poor cosmetic results and increased risk of skin necrosis; the seal they provide does not prevent air leaks.]
-Connect the distal end of the chest tube to a sterile pleural drainage system,unclamp
the distal end; Do not reclamp the chest tube, once released, may lead to the redevelopment of a pneumothorax and may create a tension pneumothorax.

Chest Radiograph Confirmation
-AP chest radiograph to confirm placement,If the proximal drainage hole is outside the pleural space,drainage may be ineffective and an air leak may result. In this circumstance, remove & a new chest tube inserted.

Complications
-bleeding and hemothorax due to intercostal artery perforation
-perforation of visceral organs (lung, heart, diaphragm, or intraabdominal organs)
-perforation of major vascular structures such as the aorta or subclavian vessels
-intercostal neuralgia due to trauma of neurovascular bundles,
-subcutaneous emphysema
-reexpansion pulmonary edema
-infection
-pneumonia
-empyema.

I shall not talk about chest-tube removals.. haha I will bore you guys to death:)

Source: NEJM

liability / responsibility and duty/standard of care

Plaintiff must establish, on the balance of probabilities, that:
• The defendant (doctor/health care provider) owed a duty of care
o What is a duty of care
 In tort law, a duty of care is a legal obligation imposed on an individual requiring that they adhere to a reasonable standard of care while performing any acts that could foreseeably harm others
o What makes the doctor owe a duty of care (VIC)
 Where a doctor agrees to treat a patient or commences to treat a patient.
 Occurs both where a patient expressively or implicatively agrees to be treated and to patients who are unable to agree to treatment (unconscious, mental illness – not of sound mind)
o Did Josh owe a duty of care?
• The defendant failed to meet the standard of reasonable care
o Was there a breach of duty of care and why
 The standard of reasonable skill and care required is that of the ordinary skilled person exercising and professing to have that special skill.
 That standard is peer-assessed
 For junior doctors: An inexperienced junior doctor will be judged according to the standard of a reasonably competent medical practitioner in a particular are of medical expertise. Junior doctors are rarely assigned to complex procedures – however if a junior doctor is found in a situation which is beyond his competence, the fault lies not so much in not having the skills, which he does not possess, but in undertaking the task at all.
 In such situations – obligation to consult more experienced physicians – judged by their standard of care.
 “If a doctor lacks a minimum competence to carry out a particular procedure but it is proper for him to be present then whatever he does must be done under the supervision of the experienced doctor. The negligence if any will now be that of the experienced doctor for failure to supervise.”
o Did Josh fail to meet the duty of care?
• The breach caused the plaintiff’s injuries (causation-covered in rushmis section)
o Did Josh’s actions cause injury
• The injury/loss was reasonably foreseeable
o What makes a loss foreseeable
 Insignificant risks include, but are not limited to, risks that are far-fetched or fanciful
 Inherent risks are defined as risks that cannot be avoided by the exercise of reasonable care. Liability for injuries occasioned as a result of the materialisation of an inherent risk is specifically excluded.
 Severity of injury/loss vs likelihood of injury/loss
o Was the injury a foreseeable risk?

Prevention

Wonderful task...

Well, not really researchable, so my response was to sit in the library in silence for 45 mins and brainstorm. Here goes:

For the individual, Josh in this case, there is little chance of him actually repeating the error. Presumably, after the event he would both research the relevent anatomy and procedural details, and would also probably ask for specific instruction and demonstration from a senior doctor.

In terms of the Hospital, or the overall system, they could help prevent such errors in the future by:
-Reinforcing emergency protocol and hierarchy affairs (eg what can be expected of new doctors)
-Hospital training on emergency management and procedures
-systems design of the ED - locations and proximity of staff, triage grading system
-Procedural instructions made available with the instrument (chest tube)
-Upgrading/renewing reporting and reviewing systems
-Clinical schooling upon induction to the hospital, to assure an appropriate level of knowledge.

sources: none really, though there's an interesting text called "To Err is Human"

Anatomy

A very broad topic, so I thought it would be best to concentrate on what is most relevant to this case:

The Original Penetrative Wound
The patient was stabbed with a kitchen knife, causing a penetrative wound 15x1.5cm deep, entering in the right chest, in the mid-clavicular line at the level of the right nipple.
As it was entering, the knife would have passed through many layers and structures before entering the thoracic cage, including:
 Skin (dermis)
 Mammary tissue + associated glands
 Subcutaneous tissue
 Pectoral fascia
 Pectoralis major
 Pectoralis minor
The knife is likely to then have passed through an intercostal space, likely the fourth or fifth, damaging the following structures
 The external, inner and innermost intercostal muscles
 The neurovascular bundle, consisting of a vein, an artery and a nerve which runs between the inner and innermost intercostal muscles.
From here, the knife would have pierced the parietal, then the visceral pleural membranes before puncturing the lung.

The Drainage Tube
A correctly placed drainage tube is inserted in an intercostal space (usually the 2nd-6th) “just above the rib below” in order to avoid the neurovascular bundle at the top of the space. Its purpose is to drain fluid or air from the pleural cavity, and hence the chest tube is inserted into this space. The layers the chest tube is passed through before reaching the pleural cavity are:
 Skin (dermis)
 Subcutaneous tissue
 Fascia
 Muscles of the upper limb eg. Pectoralis major and minor/Serratus anterior (which ones depend on the where the tube is being inserted)
 The external, inner and innermost intercostal muscles
 The parietal pleural membrane

In our case however, the drainage tube was placed at an intercostal space too low, so that instead of being inserted into the pleural cavity, it was put into the liver, at the level of about the 8th intercostal space. The layers the chest tube passed through in this case are likely to be:
 Skin (dermis)
 Subcutaneous tissue
 Fascia
 Latissimus dorsi
 The external, inner and innermost intercostal muscles
 The diaphragm
 The liver

References: Moore's, Last's, Netter's
By Steph

Oops... forgot references!

http://www.acem.org.au/home.aspx?docId=1
http://en.wikipedia.org/wiki/Triage
http://www.answerbag.com/q_view/4880

Hierarchy in the Hospital

In the hospital -

PGY1
PGY2
INTERN
RESIDENT
REGISTRAR 1
REGISTRAR 2
REGISTRAR 3
(Years as a Registrar are dependent on the Training Program undertaken)
CONSULTANT

In the Emergency Department
1. All patients are assessed on arrival, usually by a nurse
2. Urgency of each patients' condition is assessed
3. All patients are assigned a 'triage' category
Then
- Category 1 Patients are treated immediately
- Category 2-5 Patients are transferred to a waiting area

Triage

In Australia the Australasian Triage Scale (ATS) is used in Hospital emergency department in an attempt to have reproducibility in Emergency Departments across Australia.

When arriving in the emergency department a patient presents to the Triage Nurse who then places them into one of five different categories:

See handout


All patients should be sorted using this model, including pediatrics.

References:
http://www.medeserv.com.au/acem/open/documents/triage.htm
http://www.medeserv.com.au/acem/open/documents/triageguide.htm

Triage

Shock

When SHOCK occurs, generally there is an inadequate delivery of nutrients to critical tissues and organs, and also an inadequate removal of cellular waste products from the tissues. The cause of this inadequacy can be of cardio- / hypovolemic- / neurogenic- / anaphylactic-/ septic origin, however ultimately, lead to the deterioration of different body parts.

In the case of cell hypoxia, the non-progressive phase of shock then kicks in, in which our body’s negative feedback mechanisms attempt to return normal cardiac output and arterial pressure i.e. to recover from shock, by, namely, baroreceptors, renin-angiotensin system etc. However, when failing to recover from shock, shock proceeds to the progressive phase. The cause of shock and its resulting effects on, say, low systemic filling pressure, or reduced venous return etc., become a vicious circle that eventually leads to an irreversible deterioration of circulation and, to death.

Cadiogenic shock
i.e. body suffers from lack of nutrition and deteriorates due to inadequate cardiac pumping, in which, 1) often occurs after acute heart attacks or prolonged periods of slow progressive cardiac deterioration; 2) caused by a decreased venous return
- problem can be compounded by a low arterial pressure e.g. in circulatory shock, which reduces the coronary blood supply even more
- the condition thus becomes a vicious circle i.e. shock causes more shock
∴elevate arterial pressure!!! By infusion of whole blood / plasma, or blood-pressure raising drug

Hypovolemic shock
i.e. diminished blood volume caused by, most commonly, haemorrhage, which then decreases the filling pressure of the circulation and, as a consequence, decreases venous return; as the result, cardiac output falls, and shock comes after.

Neurogenic shock
When there is massive dilation of veins, mean systemic filling pressure decreases; thus, filling the circulatory system adequately had become incapable even with a normal amount of blood. Venous pooling of blood reduces cardiac output, therefore limits the gaseous and nutrition exchange around the body.

Anaphylactic shock
In anaphylaxis, basophils and mast cells release histamine, which causes dilation of veins and arterioles, as well as an increased permeability in capillaries. The effect of these is a great reduction in venous return, and shock.

Septic shock
A septic shock occurs when a blood-borne bacterial infection widely spread around the body, causing extensive damage. Signs of circulatory collapse often include marked vasodilation in patients with septic shock, while high fever from the infection is a possible cause. As the infection becomes more severe, the circulatory system deteriorates at the same time, and shock becomes more progressive.

Reference: Guyton

Shock

Shock – acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia.

Hypovolaemic – loss of circulatory volume (eg. haemorrhage, burns)

Cardiogenic – failure of the heart to act as an effective pump (eg. ischaemic heart disease)

Obstructive – mechanical impediments to forward flow

Obstruction to outflow (eg. pulmonary embolus)

Restricted cardiac filling (eg. cardiac tamponade, tension pneumothorax)

Distributive – abnormalities of the peripheral circulation (eg. sepsis, anaphylaxis)

Stages of shock

1. Non-progressive phase

Baroreceptor reflex, adrenaline and noradrenaline release (increased TPR, HR, CO).

Renin-angiotensin activation, release of vasopressin from pituitary (increased blood volume).

Net effect is to increase blood pressure back to normal.

2. Progressive phase

Generalised tissue hypoxia leads to cells switching to anaerobic respiration and eventually lactic acidosis occurs. The lactic acid causes vasodilation and blood starts to pool in microcirculation and more blood fluids will leak into surrounding tissue.

3. Irreversible phase

Generalised tissue injury leads to irreversible organ failure. Death eventuates.

References: Kumar and Clark Clinical Medicine, Robbins Basic Pathology