PADV CLINICAL PRESENTATIONS

• Water
• Proteins
• Lipids
• Ions
• Carbohydrates

• Lipid layer
• Structural quality
• Primarily phospholipid, cholesterol, glycolipid
• Permeable to fat soluble substances (O2, CO2)
• Impermeable to water and water soluble substances

• Functional qualities of the cell membrane
• Change the structure, change the function
• Mainly glycoproteins
• Fuctions: recognition and binding units pores or transport units, cell surface markers, cell adhesion catalysts

• usually attached to outer surface
• Functions: negative charge, attachment or adhesions, receptors, immune reactions

• Synaptic - a long arm to excrete the chemical signal, and the target cell accepts the chemical through a receptor
• Pancreatic - cell excretes signals into the extracellular space, and the receptor on the other cell accepts the signal
• Endocrine (hormonal) - chemical signal is excreted into the blood stream and then released and picked up by another cell's receptors.
• Autocrine - a cell makes its own signaling chemicals, excretes it, and then picks them up again via receptor

Cell shrinkage

Increase in size

Increase in population

transformation into another cell

Abnormal size or organization

Malignancy

Causes: Physical agents, Chemical agents, Biological agents, and nutritional imbalances.

MEchanisms of Injuries: free radical formation, hypoxia and ATP depletion, disruption of intracellular calcium

• Programmed sequence of events leads to elimination of cells without releasing harmful substances to surrounding area. Cell suicide.
• Apoptosis gone wrong - Alzheimer, huntington, parkinson

• Hormone is released from and affects the same cell. Ie insulin like
• growth factors secreted in a muscle cell has growth - promoting actions
• on the cell

• Ion - negative
• Acid - liberates hydrogen ions in solution
• Base/Alkali - accepts hydrogen ions in solution

• Arterial blood ~ 7.35-7.45
• Venous blood ~ 7.35
• Interstitial ~ 7.35
• ICF ~ 6.0-7.35

• 1. Protein buffer system
• instantaneously
• amino acids have at least one carboxyl (COOH) which releases an H+, and amino group (NH2) which accepts H+

• 2. Carbonic acid-bicarbonate buffer system
• Carbonic acid acts as a weak acid (releases H+)
• Bicarbonate acts as a weak base (holds the H+)
• CO₂ + H₂0 <---> H₂CO₃ <---> H⁺ + HCO₃^-

• 3. Phosphate buffer system
• usually intracellular
• works to buffer acid in urine
• H₂PO₄^- (dihydrogen phosphate) : weak acid that can buffer a strong base
• HPO₄²- : acts like a weak base by buffering the H+ released by a strong acid

• CO₂ blown off directly
• compensates by rate and volume
• 1-2 times more potent
• happens within minutes

• Increase in H+ in the blood stimulates peripheral chemoreceptors
• stimulates the respiratory center
• increases alveolar ventilation
• causes an increase in CO₂ elimination
• decrease in PcCO₂
• maintaining pH

• decreased ventilation
• increase PaCO₂
• Increase H₂CO₃

• Increased Ventilation
• Decrease PaCO₂
• Decrease H₂CO₃

• Excretion of H+ in urine is the only way to eliminate hyge excess
• Metabolic reactions produce 1 mEq/L of nonvolatile acid for every kg of weight
• Kidneys synthesize new bicarbonate and save filtered bicarbonate
• RF can cause death rapidly due to its role in pH balance

• pH 7.35-7.45
• PCO₂ 35-45 mmHg
• PO₂ 80-100 mmHg
• HCO₃ 22-28 mEq/L

• Acidosis : pH <7.35
• Metabolic: HC0₃- <28 mEq/L
• Respiratory: PCO₂ > 45 mmHg

• Alkalosis : pH >7.45
• Metabolic: >28 mEq/L
• Respiratory: PCO₂ <35 mmHg

• elevation of PCO₂ of blood
• from lack of CO₂ removal, ie. emphysema, pulmonary edema, brainstem injury
• Tx: ventilation therapy to increase CO₂ exhalation

• Arterial blood PCO2 is too low, ie Hyperventilation from HAPE, disease, stroke, anxiety, aspirin overdose
• Renal comensation involves a decrease in H+ excretion, and an increased reabsorption of bicarbonate

• Blood bicarbonate ion concentration too low, ie. ion loss via diarrhea or RF, acid accumulates
• Respiratory compensation by hyperventilation
• Tx : ventilation, correct the cause

• Blood bicarbonate levels are too high
• Non-respiratory loss of acid; ie vomiting, gastric suctioning, diuretics, dehydration, ++ alkaline drugs
• Respiratory compensation is hypoventilation
• Tx: fluid and electrolyte therapy

• Capillary beds are wrapped around the alveoli for O₂ / CO₂ exchange.
• 2 types of cells on the alveolar:
• Type 1 cells -gas exchange
• Type 2 cells - synthesizes surfactant

• Oxyhemoglobin contains 98.5% chermically combined oxygen and hemoglobin
• Only 1.5% transported dissoved in blood
• Only dissolved O₂ can diffuse into tissues

• Four polyphyrin rings, each with an oxygen binding site
• Major determinant of hemoglobin saturation in the partial pressure of oxygen in the blood
• Blood is almost fully saturated at p0₂ of 60 mm

• Hb affinity for 02
• oixygen concentration
• acidity
• carbon dioxide
• temperature
• cellular metabolism (2,3 DPB or 2,3 BPG)
• As acidity increases, O2 affinity for Hb decreases. H+ binds to Hb and alters the structure, leaving O2 behind for tissues

• decrease in temperature
• decrease in 2.3 DPG
• decrease in pCO₂
• increase in pCO
• increase in pH (alkalosis)
• high 0₂ affinity
• haemoglobin - fetal

• increase temperature
• increase in 2,3 DPG
• increase pCO₂
• decrease PCO
• decrease pH (acidosis)
• low 0₂ affinity
• adult haemoglobin

• 8% dissolved
• 80% bicarbonate ions
• 10-12 % carbamino compounds

• inadequate oxygen
• Hypoxic hypoxia - decrease oxygen in the environment
• Anemic hypoxia - impaired oxygen transport
• Histotoxic Hypoxia - cell use of oxygen impaired
• Hypoxemia - decreased oxygen in the blood

• V=Q : normal
• V>Q : dead space; normal ventilation with no perfusion
• V<Q : shunt; normal perfusion with no ventilation. usually pathologic

V=Q=0 : silent unit, no ventilation no perfusion

• PCO2 increases and PO2 decreases with no ventilation
• Decreased tissue PO2 around under-ventilated alveol constricts their arteries and diverts blood to better ventilated alveoli
• The unoxygenated blood mixes with the oxygenated blood, thus lowering the average oxygen saturation post capillaries

Solute+Solvent

One mole of solute particles

Concentration of solute in osmoles/kg (solvent - mass)

Concentration of solute in osmole/litre (solution - volume)

Grams of solute in one ml of solution

• ICF : intracellular
• 40% TBW

• ECF : Extracellular
• 1/3 intravascular
• 2/3 interstitial
• 20% TBW

Diffusion

• Primarily by hydrostatic pressure
• lesser extent by diffusion

Movement of water from an area of high water concentration to low water concentration (down its concentration).

Pressure exerted by the movement or mass of water.

Solution on opposite sides of a membrane are equal in concentration.

Inside and outside of the cell are equal pressure.

Concentration of a given solute is greater on one side of a membrane than the other.

Concentration of a given solute is less on one side of a membrane than the other.

Transport: respiratory gases, nutrients, resgulatory substances, waste products

Thermoregulation: temperature

• RBC 45%
• Electrolytes, enzymes, fats, proteins, carbohydrates

• WBC and Platelets 1%
• Monocyte, neutrophyil, basophil, eosinophil, lymphocyte, platelets

Plasma 54%

RBC = Hematocrit = percentage of blood occupied by red blood cells

• responsible for removal of interstitial fluid from tissues
• absorbs and transports fatty acids from circulation
• transports WBC to and from lymph to bones

• Areas drained by:
• right lymphatic - head and right chest/arm
• thoracic ducts - left chest/arm and lower body

Loss of total body water

Isotonic - H₂0, Na+ lost in equal proportions; bleeding, diarrhea

Hyponatremic - increased loss of sodium; sweating, diuretics

Hypernatremic - decreased loss of sodium; increased salt intake


Thirst is stimulated by dry mucous membranes, dehydration of osmoreceptors, angiotensin II, and sympathetic nervous system (baroreceptor stimulation).

Stimulated by high osmotic pressure in the blood (high concentration of solutes, but low water).

• Osmoreceptors ->
• Synthesizesd + ADH ->
• Into bloodstream ->
• Kidneys retain H₂0 ->
• decrease urine; arterioles constrict ->
• increase in BP ->
• Decreased blood osmotic inhibits hypothalamic osmoreceptors ->
• inhibition of osmoreceptors reduce or stops ADH secretions

R-A : Stimulated by a decrease in glomerular filtration rate (GFR)

• A : stimulated by angiotensin II or increase in serum K+
• :Stimulates increase in Na+ reabsorption and water reabsorption in the distal convoluted tubule

• -Dehydration, Na+ deficiency
• -Decrease in blood volume
• -Decrease in blood pressure
• -Increased renin (from juxtaglomerular cells of the kidneys)
• -Angiotensin is released from the liver
• -Increased Angiotensin I goes to the lungs
• -Angiotensin Converting Enzyme (ACE) from the lungs converts Angiotensin I to Angiotensin II
• -Vasoconstriction of arterioles
• -Increased Aldosterone (via adrenal cortex)
• -Kidneys increase Na+ and H₂O reabsorption
• increased blood volume
• -blood pressure increases until it returns to normal

• 1- Higher (cortical) brain: information, conscious control
• 2- Lower brain: vegetative body process
• 3- Spinal cord: reflexes

• Brainstem: midbrain, pons, medulla oblongata
• Cerebellum:
• Diencephalon: thalamus, hypothalamus
• Cerebrum: sensory, motor, associative areas; basal ganglia, limbic system

• Dura Mater
• Arachnoid Mater
• Pia Mater

• transitions between spinal cord and brain
• vegetative functions

• involuntary motor reflexes to sudden auditory and visual stimulus
• motor nuclei for cranial nerves II, IV
• reticular activating system (RAS): consciousness

• involuntary control of pace and depth of respiration
• sensory and motor nuclei of cranial nerves (V-VIII)

• physically connects brain and spinal cord
• relay station for ascending and descending tracts
• cardiovascular centre (heart rate, vasomotor centre)
• respiratory rhythmicity

• Relay point for ascending sensory information that will reach conscious awareness
• Filters sensory information
• Relay information from cerebellum and basal ganglia to primary motor area of cortex

• ANS Control
• produces hormones (ADH, oxytocin)
• Emotional and behavioural patterns
• Eating and drinking regulation
• Maintains body temperature
• Circadian rhythms

• Inferior and posterior aspects of cranial cavity
• 1/10 brain mass, half the neurons
• rapid adjustments in muscle tone and position to maintain balance and equilibrium
• fine tunes voluntary and involuntary movements

• gray matter layer on cerebral surface
• outer layer of the brain
• responsible for consciousness
• impulse distribution to cerebrum
• cerebrum contours

• 1. Sensory: primary - auditory, visual, etc. secondary - adjacent
• 2. Motor: mostly anterior, Broca's speech, motor, etc
• 3. Associative: motor and sensory areas connected by tracts

• Nuclei deep in hemispheres
• Receive input from cortex and output back to motor parts of cortex
• Regulates initiation and termination of movement, some cognitive functions
• Associated with several psychiatric disorders

• Ring of structures on inner border of cerebrum
• Emotional part of the brain
• Hippocamups has a role in memory

• Olfactory - smell
• Optic - vision
• Occumomotor - eye movement, pupils
• Trochlear - eye movement
• Trigeminal - chewing
• Abducens - lateral eye movement
• Facial - facial expressions
• Vestibulocechlear - hearing, equilibrium
• Glossopharyngeal - swallowing, throat
• Vagus - autonomic function, heart
• Spinal Accessory - shoulder movement, head rotation
• Hypoglossal - tongue movement

• Dendrites - extensions to receive incoming impulses
• Cell body - controls metabolism of cell
• Axon - contains fibre that carries outgoing impulses to end organ fibres (skeletal and smooth muscle; central nervous system)

Activation of sodium channel to open by means of a voltage stimulus across the membrane. The activation is transferred between nerve cells

activation of cell membrane by chemical irritant/mediator (neurotransmitter)

ACh released into synapse, timed by acetylcholinesterase. Choline is taken back via presynaptic membrane for resynthesis.

Presynaptic receptors provide a negative feedback loop, monitoring the total amount of ACh.

• PNS: activates muscles, ANS major transmitter
• ACh binds to ACh receptors, which opens the Na+ channels in the cell membrane.

CNS: ACh with associated neurons forms a system, called the cholinergic system; anti-excitatory actions.

• 2 major types or ACh receptors:
• Nicotinic receptors, Muscarinic receptors.

Dopamine, norepinephrine, epinephrine, serotonin, histamine.

Involved in limbic system, hypothalamus, basal ganglia.

• NE is released at SNS post ganglionic nerve endings.
• DA, NE, and seotonin regulating thought processes and moods. Antipsychotic and mood-altering drugs change their activities.

• Excitatory: Glutamate, Asparate (NMDA)
• Glutamate - widely spread through the brain, considered the primary excitatory neurotransmitter. Involved in memory, and considered neurotoxin when found in excess amounts within the synapse.

• NMDA - will not open unless the binding is paired with a cotransmitter and concurrent depolarization of the membrane. Ligand-gated calcium ion channel, blocked by Mg ion when postsynaptic membrane is polarizerd. Responsible for long-term changes in the synapse, and may be related to long term memroy.
• Drugs that interfere with NMDA receptors block memory; activating drugs produce hallucination and nightmares.

• Inhibitory: Glycine, y-Aminobutyric acid (GABA)
• GABA - formed by decarboxylation (CO₂ removal) of glutamate, changing it from an excitatory to an inhibitory substance. GABA_A is a classic ligand-gated CL- channel that produces an IPSP (inhibitory postsynaptic potential) when activated and GABA_B is a metabotropic receptor that also produces IPSP and is linked to cytoplasmic signaling cascades within the cell.

Barbituates and benzodiazepines exert their depressive effects by increasing GABA activity.

Vasopressin, oxytocin, growth hormone; corticotropin, and thyrotropin releasing hormones; glucagon, angiotensin II, endorphins.

Functions as primary neurotransmitter in the synapse, more often released with other polypeptides. Released in very small quantities.

Neuropeptides have long-lasting effects on post synaptic cell, mediating changes in receptor number orr structure and altering the response of intracellular signalling pathways.

Ex - transmission and perception of pain: substance P, endorphins, and enkphalins

• Adenosine triphosphate (ATP), adenosine.
• Neurotransmitters in various brain regions.

• Adenosine:
• -Continuously released by most neurons and modulates neurotransmission by blocking neurotransmitter release.
• -May prevent seizure activity, but the main ATP role is elucidated.

Nitric oxide, Carbon monoxide

• -Diffuse through cell membrane, doesn't need synaptic receptors
• -Binds and stimulate guanylyl cyclase, an enzyme that produces cGMP (cyclic guanosine monophosphate) a second messenger in the cell. Or alter the activity or ion pumps, metabolic enzymes and DNA transcription factors.
• -NO can be synthesized in postsynaptic neuron and diffuse locally to affect presynaptic neurons

Anything that enhances a transmitters effects

Anything that reduces the action of a transmitter

• Components in both CNS and PNS
• 2 neuron system: preganglionic neurons (myelinated); postganglionic (unmyelinated). No two sympathetic responses are ever the same.

Sympathetic: arise out of the spinal cord, T1 - L2. Thoracolumbar division, some preganglionic fibres go straight to adrenal medulla.

Parasympathetic: arise from cranial nerves III, VII, IX, X and sacrum.

Spinal Cord - Preganglionic Neuron (myelinated) ACh - Postganglionic Neuron (unmyelinated) - effectors.

Spinal - Somatic Motor Neuron (myelinated) - ACh - effectors

• Alpha 1 - primarily vasoconstriction in a larger blood vessel
• Alpha 2 - vasodilation in some smalle (skeletal) blood
• vessels
• Beta 1 - vascular smooth muscle
• Beta 2 - extravascular smooth muscle
• Beta 3 - appear to play a role in lipolysis

Muscarinic and Nicotinic

• ACh to Adrenal medulla - Epi - Various Organs
• ACh to Ganglion - NE - Various Organs
• ACh to Ganglion - ACh - Sweat Glands

ACh to Ganglion - ACh - Various Organs

• Alpha 1 - Smooth muscle fibers (excitation -> contraction = constriction and pupil dilation)
• Alpha 2 - Pancreatic Islets secrete insulin (B cells) (decrease insulin secretion)
• Beta 1 - Cardiac muscle cells (excitation = increase rate/force)
• Beta 2 - Smooth muscles in A/W walls (inhibition -> relaxation, dilates A/W, vasodilation, etc.)

• closely packed iceratinized epithelial cells
• mucous membranes
• gastric juices
• perspiration and lysozymes
• hair
• tears and salvia
• urine, defecation, vomiting, vaginal secretions

• Antimicrobial proteins
• Phagocytes and natural killers
• Inflammation
• Fever

• Rubor (redness)
• Tumor (swelling) colour (heat)
• Dolor (pain)
• Functio laesa (decrease function)

• local damage to tissues cause local response
• release of chemical mediators
• vasodilation and increased vessel permeability
• clotting factors leak into area, also to trap microbes

• Histamine:
• -Performed in mast cell, released with antigen exposure
• -Important to asthma; smooth muscle contraction, vascular permeability, edema, irritant receptors
• -Antihistamines not effective in asthma

• Leukotrienes:
• -Synthesized in and released from mast cells and basophils
• -Direct bronchoconstrictor effector on smooth muscle
• -Increased vascular permeability

• Prostaglandins:
• -Released from damaged cells and mast cells
• -Direct bronchoconstrictor effect on smoth muscle
• -Increased vascular permeability
• -Both leukotrienes and prostaglandins come from same chemical precursor

• 1 to 24 hours, sustained increased vessel permeability
• Monocytes infiltrate area within an hour via emigration
• Granulocytes take longer (basophils, neutrophils, and eosinophils)

• Types of white blood cells
• Neutrophils and macrophages
• Neutrophils and monocytes migrate to the injury site
• Monocytes become wandering or fixed macrophages

• Chemotaxis
• Adherance
• Injection
• Digestion
• Killing

• Emigration - cell leaves the blood stream
• Chemotaxis - cell starts to wrap around the injury
• Phagocytosis - cell completely wraps around injury

• group of diseases with all the same characgtristics
• leading cause of M+M
• chronic bronchitis, emphysema, asthma, cystic fibrosis

• hereditary disorder of the exocrine glands and the epithelial lining of the respiratory, GI and reproduction tracts
• results in abnormal and viscous secretions by exocrine glands
• high electrolyte concentration in sweat
• Patho: abnormal, viscous secretions; GI tract: malabsorption, malnutrition; Respiratory: mucous secreted from bronchial glands, obstructs small A/W (bronchi, bronchioles) physical damage to epithelial surfaces
• Clinical: failure to thrive, chronic infection, alveolar damage, chronic A/Q obstruction (V/Q mismatch) pulmonary hypertension (cor pulmonale)

• chronic diffuse infiltrative diseases of the lungs
• 150 diseases sharing clinical features
• decreased lung volumes with normal expiratory flows
• usually a reduction in fuddusing capacity
• usually chronic
• Ie. Pulmonary fibrosis

• inflammation and scarring of alveolar tissue
• idiopathic or secondary
• Interstitial diseases (known etiology - silicosis, asbestosis, coal miners pneumoconiosis, farmers lungs, drug or radiation induced)
• Patho: functionally smaller lungs, decreased lung complication/lung volume, V/Q mismatch, pulmonary hypertension, impaired diffusion

• occlusion of pulmonary arter or one of its branches by matter carried in blood (fat, air, embolus, amniotic fluid)
• often misdiagnosed
• contributing factors: abnormal vessel walls, stagnation, increased coagulability
• Patho: most ventilation locations, hemorrhage with congestive atelectasis +/- pleural effusion. pathologic increas in dead space ventilation
• Clinical: dyspnea, pleuritic chest pain, hemoptsis, pleural effusion, pleural friction rub

• acute respiratory failure
• shock lung or non-cardiogenic pulmonary edema
• lung injury characterized by breakdown of normal barrier between pulmonary capillaries and interstitial space/alveoli
• Etiology includes aspiration, gas inhalation, pneumo sepsis, shock, trauma, drugs, neurogenic
• Pathogenesis: underlying causes result in a variety of cells and mediator involvement: pulmonary capillary endothelial cells (interstitial edema); alveolar epithelial cells (alveolar edema/collapse), shunting, V/Q mismatch, decreased pulmonary compliance
• Clinical: dyspnea, wet crackles, >50% mortality, pulmonary edema, no response to normal therapy.

• acute inflammation of gas exchange units of lungs
• variety of microorganisms (viral, bacteria, aspiration)
• hospital or community acquired
• immune status of the host
• Patho: reaches distal area, intense inflammatory reaction occurs, worse case (consolidation, necrotizing pneumonia, destroys lung tissue, scar formation, decreased lung function)
• Clinical: generalized malaise, fever, cough, dyspnea, areas of consolidation, crackles

Pleurisy (pleuritis) - inflammation of the pleura, characteristic pain pattern

Pleural Effusion - fluid build up in the pleural space

Pleural Pain - abrupt onset, usually unilateral and localized, made worse by inspiration and movement, tidal volume reduced

Atelectasis - alveolar collapse, resulting in incomplete lung expansion. Caused by increased alveolar recoil due to surfactant loss, lung compression, airway obstruction

• -Disease of the neuromuscular end plate
• autoimmune disorder where antibodies to cholinergic receptors are produced
• -Slow onset, muscle weakness and fatigue, from ocular to facial to throat
• Dx: usually by history, cholinesterase inhibitor to confirm diagnosis
• Tx: maintained with cholinesterase inhibitors therapy neostigmine, pyridostigmine, ambenonium. Immunosupressives, intubation, ventilation
• Myasthenia crisis: stressor origin, exacerbates disease process, respiratory involvement

• Acute inflammatory polyneuritis of unknown cause affecting primarily peripheral motor and sensory neurons
• viral or traumatic
• involves segmental loss of myelin sheath (delayed hypersensitivity reaction again myelin sheath)
• Sensory abnormalities progressing to paralysis
• Usually self limiting and effects reverse with time
• Tx: symptomatic, usually needs ventilatory support, monitoring respiratory reserve volumes

• Bacterial infection transmitted by airborn dust (myobacterium tb)
• Stage 1 - bacterium inhaled into lungs, inflammatory response, may be contained at this point
• Stage 2 - bacteria multiply rapidly, from tubercles, may spread to other organs
• Stage 3 - two to three weeks, infection contained but granulomas form, tissue destruction, can lay dormant for years
• Stage 4 - tubercle erodes, releases bacteria to reinfect
• Clinical: productive cough, fever, weight loss, hemoptysis, chest pain, fatigue, night sweats

• Disease process resulting in reduced air flow and ventilation
• V/Q mismatch and pathologic shunt (oxygenated and deoxygenated blood mixed)

Characterized by hyper-responsiveness of the airways - bronchospasm/constriction, increased mucous secretion, injury to mucosal lining, inflammation of the airway.

• Catagories: Catagories are often misleading and inaccurate.
• Allergic/Extrinsic (result of antigen-antibody reaction on mast cells of the respiratory tract. Childhood).
• Idiopathic/Intrinsic (implies its a result of imbalance of autonomic nervous system, generally no antibodies formed).

Early phase: occurs within minutes, bronchospasm, mucosal edema, generally inhibited or reversed by bronchodilators (B2 agonists)

Late phase: 4-8 hours later, can last longer, might be associated with an early phase, invasion of inflammatory cells into damaged tissue (basophils, eosinophils, neutrophils), produced epithelial injury and edema.

Common provocative stimuli: exposure to allergen, inhaled irritants, respiratory tract infection, exercise, cold air, humid air.

• Patho:
• -epithelial damage,
• -hypertrophy and hyperplasia of smooth muscle layer
• -thickening of epithelial basement membrane
• -enlargement of mucous secreting apparatus -edema/infiltrates or eosinophils in bronchial wall
• inflammation
• -narrowing of the airways (smooth muscle contractions, mucosal/submucosal edema)
• -increased airway resistance (espec. expiration)
• -non-uniform distribution of disease process (A/W resistance variable, ventilation variable, V/Q mismatch)

Clinical: usually childhood asthma, wheezing/dyspnea with symptom free intervals, cough, dyspnea, wheezing chest tightness.

• Allergen
• Mast cells (release histamine, leukotrienes, prostaglandins)
• Infiltration of Inflammatory cells (cytokines, interleukins, other inflammatory mediators)
• Airway Inflammation including
• -edema
• -impaired mucociliary function
• -epithelial injury
• -airflow limitation
• -bronchospasm
• -increased A/W responsiveness

Doesn't respond to conventional therapy. Severe hypoxemia, lacticacidosis, respiratory failure

• -Hypersecretions of mucous and a chronic productive cough for at least 3 months of the year for at least two years
• -Increased incidence in smoking and air pollution exposure

• Patho:
• -Influx of inflammatory cells into airway wall
• -Increased size and number of mucous secreting cells
• -Decreased ciliary function
• -Altered mucous composition (tick and tenacious)

• Consequences
• -A/W inflammation leads to a thickened wall (decreased lumen size, increased A/W resistance), mucous alterations, chronic productive cause, bronchospasm, progression (affects large bronchi till all a/w are involved. narrows and closes, V/Q mismatch)

• -Blue bloater: extreme presentation of disease.
• -Fat, obese, build up of fluids due to heart disease
• -Blue - chronic hypoxemia, polycythemia
• -Elderly blue bloater are rare due to presence of cor pulmonale

• -Disease resulting in the destruction of alveolar walls distal to the terminal bronchioles
• -Obstruction from changes in lung tissue and not inflammation
• -Major mechanism of impaired airflow in the loss of elastic recoil.

• Patho:
• -breakdown of elastin in alveolar walls
• -leads to destruction of alveolar walls
• -decrease elastic recoil (hyperinflation, decreased diffusion)
• -Enlargement of air spaces (bullae) and air spaces adjacent to pleura (blebs - incrased air trapping)
• -V/Q mismatch

• Clinicals:
• -Dyspnea and SOB OE (chronic hypoxia with minimal reserve)
• -Barrel chested (air trapping, flat costal angle)
• -Chronical accessory muscle use leads to hypertrophy
• -Muscle wasting and weight loss
• -Clubbing
• -Pursed lipped breathing

• Pink Puffer
• -extreme presentation
• -pink - not initially hypoxic (oxygen levels maintained by increased respiratory rate)
• -puffing - pursed lipped breathing (attempt to build and maintain reserve volume)

• small number of patients
• chronic increased levels of CO₂ alters the stimulation of chemoreceptors
• switch from an increase of CO₂ to decrease of O₂ levels as prime stimulus
• potential that oxygen therapy could reduce ventilatory drive
• no hypoxic patient should have oxygen withheld

• decrease PO₂
• increase pulmonary vasoconstriction
• increase right ventricular workload
• right ventricular failure

• inferior/suprerior vena cava
• right atrium
• tricuspid valve
• right ventricle
• pulmonary valve
• pulmonary trunk
• left pulmonary arteries
• lungs
• left pulmonary veins
• left atrium
• mitral valve
• left ventricle
• aorta
• body

• Left Anterior Descending (lt ventricle and septum)
• Circumflex (lt atrium, posterior and lateral left ventricle)
• Mainly anterior and left ventricle

• Supplies right and posterior and inferior left ventricle
• SA, AV node

• Specialized excitatory and conductive muscle
• Same general structure as musclecells but with fever contractile fibres

Ability of cells or groups of cells to generate their own impulses

Impulses tend to fire rhythmically from focus'

Cells ability to transmit impulses to adjacent

Fibrous connective tissue rings support the AV valves

• Electrical potential difference accross the membrane at rest
• Dependant upon sodium/potassium pump, voltage dependant channels, protein molecules
• Cardiac cells ~-85mV

Change in cell membrane electrical potential difference that will result in a dramatic change in cell membrane permeability

Change in cell membrane electrical potential difference that will stimulate a response

• Phase 0 - rapid depolarization (Na+ in via fast channels)
• Phase 1 - early rapid repolarization (Na+ close, K+ out)
• Phase 2 - plateau phase ( Ca+ moves into cell, K+ out)
• Phase 3 - Terminal rapid repolarization (Ca+ stops, K+ out)
• Phase 4 - resting membrane potential difference (Na+/K+ returns to original levels)

• Time when cells cannot respond to another impulse
• Onset of QRS to peak of T wave
• Phase 0 to halfway through phase 3

• Time during which cells could be depolarized if the impulse were strong enough
• Peak of T wave to end of T wave
• Halfway through phase 3 to early phase 4

• Enhanced Automaticity
• Re-entry
• Escape Beats
• Conduction Disturbances

• generally re-entry phenomenon
• rate problem
• -inadequate time for ventricles to fill
• -inadequate time for the coronary perfusion
• -increased myocardial workload
• Includes: SVT/PSVT, A-Fib, A-Flutter, V-Tach,

• Generally caused by re-entry phenomenon close to the normal conduction pathways in the atria
• pre-excitation syndrome

• Multiple re-entry phenomenon through out the atria
• lots of cuases
• rate problem for the first 24 hours, then evolves into embolus formation, and an embolic stroke

• Re-entry outside the normal conduction pathways in the atria (strong enough to take over)
• Variety of causes, usually paroxysmal onset

• Re-entry outside the normal conduction pathways in the ventricles
• Rarely occurs in patients that do not have some level of heart disease
• May actually result in AV dissociation