100b Flashcards
upper air way
- Pharynx
- Nasopharynx – nose to uvula
- Oropharynx – Nasopharynx to epiglottis - Larynx – epiglottis to glottis
- Thyroid cartilage
- Glottic opening
- Arytenoid cartilage – false vocal cords
- Pyriform fossae
- Cricoid ring
- Vallecula – base of tongue meeting epiglottis, hyoid epiglottic ligament
lower air way
Functions to exchange O2 and CO2
Trachea – glottis to bronchi bifurcation, 16-20 cartilaginous incomplete rings, carina
Bronchi
Bronchioles – smallest airway without alveoli
Alveoli
Lungs – L 2 lobes, R 3 Lobes
pharynx
nasopharynx
oropharynx
(epiglottis sits between oro and hypo)
hypopharynx
larynx
vocal cords
thyroid cartilage
cricoid cartilage
esophagus
attaches to the stomach, runs postieor to the larynx
minute volume
tidal volume x ventolations per min
tidal volume
amount of air inhaled in one breath
dead space
the air that fills the upper and lower airways but doesnt actually get used by the body simply fills the cavities
approx 150ml
perfusion
delivery of oxygenated blood to tissues
shock
lack of end organ perfusion leading to anaerobic metabolism
effects of anaerobic metabolism
cause build up of waste products acids eg. latic acid and pyruvic acid. and cell death
anaerobic metabolism
- which can be defined as ATP production without oxygen
- much less effective
- occurs in 3 stages glycolysis , the Krebs cycle , and electron transport
fick principle
- adequate supply of O2
- on loading of O2 to RBCs
- delivery of oxygenated RBCs to tissue
- off loading of O2 from RBC to tissue
cellular respiration
chemical reactions breaking down food to use as energy
increased H+ in the body
causes decreased PH causing metabolic acidosis
brain damage
heart damage
organ damage
4-6 min
starts 30-60 seconds
minutes to hours depending on the organ
norepinephrine
released causing peripheral vasoconstriction
increased chrontropic, inotropic effects increasing organ perfusion
stroke volume
amount of blood pumped by the heart in one contraction
approx 70ml
perload
- passive stretching on the walls of the heart
- more blood in, increased stretching, increased contraction, increased output
blood pressure
force that blood exerts on artery walls
cardiac out put
stroke volume x heart rate (BPM)
blood buffer system
- almost instant
- protects form changes in H+
- chemical sponge absorbing H+ when there is excess and releasing H+ when levels are low
ratio of Bicarb to H+
20:1
respiratory buffer
-aids in correcting acid base imbalance by controlling CO2 levels
-CO2 in the body increase, resp rate increases to blow off CO2
-increased resp = decreased CO2 and H2CO3 = increased PH
decreased resp = increased CO2 and H2CO3 = decreased PH
decreased CO2
increased blood PH
increased CO2
decreased blood PH
renal buffer
- slowest to act but most effective
- kidneys excrete H+ and form HCO3
CO2 + H2O = H2CO3 = H + HCO3
uses buffer systems to shift back and forth to maintain PH (homeostasis)
4 types of imblances
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
respiratory acidosis
- decreased resp rate causing the body to retain CO2
- increased CO2 in blood causing decreased PH and a surplus of H2CO3
- easily correctable by increasing resp rate and blowing off CO2
respiratory alkalosis
- increased resp rate causing excess CO2 to be exhaled
- decreased CO2 leads to increased PH and decreased H2CO3
metabolic acidosis
- renal impairment
- decreased HCO3 increased H2CO3
- increased PH
metabolic alkalosis
- ingestion of alkaline products (baking soda, tums)
- prolonged vomiting (decreasing acid in body)
- increased HCO3 and decreased H2CO3
- decreased PH
3 stages of shock
compensated - < 15% blood loss
decompensated - 15%-25% blood loss
irreversible - > 25% blood loss
compensated shock (stage 1)
- body recognizes a problem and attempts to correct it by initiating a sympathetic response
- norepi and epi released, increased HR, peripheral vasoconstriction, increased BP
- shunting blood from limbs
- decreased urine out put
- increased resp rate (combat metabolic acidosis)
decompensated shock (stage 2)
body cant compensate forever, condition worsens and compensatory mechanisms begin to fail
- BP decreased with increased HR and RR
- epi is still being released in an attempt to oxygenate vital organs
- peripheral cells are now hypoxic and anaerobic metabolism is the only option, this produces greater amounts of acid and increases the acidity (decreased PH) in the body.
- metabolic acidosis increases and vital organs began to get affected
irreversible shock (stage 3)
- body can no longer compensate even with medical interventions
- BP, HR, RR and perfusion decline and begin to fail
- blood shunted from liver, kidneys and lungs in an attempt to oxygenate heart and brain
- organs start to die
- decreased LOC, feeling of impending doom
hypovolemic shock
- caused by fluid loss
- can be blood, or fluid volume
- internal or external loss
cardiogenic shock
-caused by heart failure, most common the left ventricle. If L ventricle is 40% damaged the heart is unable to properly pump blood
neurogenic shock
- disconnect between nervous system and body
- unable to control blood vessels, they relax and dilate creating to large a space for the volume of blood to full
- no compensated phase
septic shock
- caused by infection
- toxins released cause vasodilation
anaphylactic shock
- caused by exposure to allergen triggering a histamine release
- bronchoconstriction
- vasodilation
stage 1 vasoconstriction
15%
stage 2 capillary and venule opening
15%-25%
stage 3 disseminated coagulation
25%-35%
stage 4 multiple organ failure
greater than 35%
beta 1
increased chronotropic, inotopic and dromotropic
beta 2
bronchodilation
smooth muscle dilation
norepinephrine
- primary alpha 1 and 2
- vasoconstriction
- increased PVR and afterload
AVP arginine vasopressin
also known as ADH
released from pituitatry glad
increased water absorption and decreased urine out put
renin-angiotensin
- renin released from kidneys
- renin and angiotensin combine and produce angiotensin I
- angiotensin I converted to agiotensin II by enzymes
- potent vasoconstrition
- sodium reabsorption
- inotropic and chrontropic
aldosterone
defends fluid volume
sodium reabsorption
water retention
decreased urine output
Drug Sources
Five major sources of drugs
- Plants
- Animals/humans
- Minerals
- Microorganisms
- Chemical substances
Drug Names
- Chemical
- chemical make up or structure - Generic or Non-proprietary
- Not capitalized
- abbreviated chemical name - Trade, Brand or proprietary name
- copyright name designed by selling drug company - Official
- usually the same as generic name followed by USP or NF
Drug Control in Canada
- Department of health Canada – bureau of drug surveillance
- Canada food and drugs act & regulation
- Narcotics Control act & regulations
General Properties of Drugs
1-Action – what the drug does and how it goes about this
2-Indications - what the drug is used for
3-Contraindications – conditions for which the drug should not be given
4-Therapeutic effects – desirable drug actions
5-Major Side Effects – undesirable or harmful drug actions
6-Precautions – conditions or potential problems of which you should be aware
7-Preparations – how the drug comes packaged
8-Dosage – how much is given to achieve desired effects
Potential Reactions to Drug Therapy
- Antagonists
- Contraindication
- Cumulative action
- Depressant
- Allergy
- Dependence
- Interaction
- Idiosyncrasy
- Potentiation
- Stimulant
- Summation
- Synergism
- Therapeutic action
- Tolerance
- Untoward effect
Antagonist
agents designed to inhibit or counteract effects of other drugs or undesired effects caused by normal or hyperactive physiological mechanisms
contraindication
medical or physiological factors that make it harmful to admin a drug
cumulative action
tendency for repeated doses to accumulate in blood and organs causing increased and sometimes toxic effects
depressant
substance which decreases a function or activity
allergy
systemic reaction to a drug resulting from a previous sensitizing exposure and development of immunological mechanism. Can be initiated by drug itself or a metabolite of
dependance
state of which withdrawal of a drug causes intense physical or emotional disturbance
interacton
beneficial or detrimental modification of the effects of one drug by the prior or concurrent admin of another drug
idosyscrasy
abnormal or peculiar response to a drug
potentiation
enhancement of effects caused by concurrent admin of two drugs in which one drug increases effects of the other
stimulant
drug that enhances or increases body function or activity
Summation
combined effect of two drugs such that the total effects equals sum of individual effects (1+1=2)
Synergism
the combined action of two drugs such that the total effect exceeds the sum of the individual effects (1+1=3)
Therapeutic action
desired intended actions of drug
Tolerance
decreased physiological response to repeated admin of a drug
Untoward effect
side effect proving harmful
Types of Drug Reactions
Type I – Anaphylaxis, IgE antibody and antigen complexes stimulating release of histamines
Type II – Cytotoxic, IgG antibody and antigen stimulating hemolysis and platelet destruction
Type III – Serum Sickness, IgG antibody and antigen complexes producing inflammatory reaction
Type IV – Contact dermatitis reaction – topical application stimulates T lymphocyte production causing dermatitis
biotransomation
- process by which the drug is chemically converted to a metabolite
- liver is the primary site and aim is to “detoxify” the drug
agonists
drug that binds to a receptor and causes a response
antagonists
drug that binds to a receptor to inhibit a response or block something else from binding to that site
Sympathetic (adrenergic)
Parasympathetic (cholinergic)
Sympathetic exits from thoracic and lumbar regions of spinal cord
Parasympathetic exits from cranial and sacral portion of spinal cord
Sympathetic ganglia are found near spinal column
Parasympathetic ganglia are found near the effector organ
Types of Nerve Fibers
Visceral Afferent – Sensory – convey impulses from organs to CNS
Visceral Efferent – Motor – convey impulses from CNS to organs
Somatic Afferent – Sensory – Convey impulses from head, body wall and extremities to CNS
Somatic Efferent – Motor -Convey impulses from CNS to striated muscle
preganglionic neuron
located in CNS passes between CNS and ganglia
fibers are autonomic
postganglionic neuron
located in the periphery, passes between ganglia and effector organ
fibers are sympathetic
synapse
junction between 2 neurons
acetylcholine (ACH)
neurotransmitter
fibers that release ACH are cholinergic
nicotinic
excitatory response
muscarinic
can excite or inhibit
sympathetic
alpha and beta recptors
parapympathetic
nicotinic and muscarinic receptors
cholinergic is parasympathomimetic (mimic parasysmpathic)
cholinergic blocking is parasympatholytic
adrenergic is sympathomimetic
adrenergic blocking is sympatholytic
Respiration
exchange of oxygen and carbon dioxide between an organism and the environment
External Respiration
transfer of oxygen and carbon dioxide between inspired air and capillaries
Internal Respiration
Transfer of oxygen and carbon dioxide between peripheral blood capillaries and tissue cells
Pressure gradient (required for gas flow into lungs) produced by differences in
Atmospheric pressure
Intrapulmonic pressure
Intrapleural (intrathoracic pressure)
Inspiration and Expiration Based on
Muscles of respiration
Compliance
Work of breathing
Pulmonary surfactant – lipoproteins reduce surface tension allowing alveoli to stay open
Airway resistance
Structural Changes in lungs or thorax
gass pressures
PaO2 - partial pressure of arterial O2, normal 80-100mmHg
PO2 - partial pressure of venous O2
PaCO2 - partial pressure arterial CO2, normal 35-45mmHg
PCO2 - partial pressure of venous CO2
Oxy-Hemoglobin Dissociation Curve
Offloading of O2 based on need, in exercising tissues percentage of saturation of hemoglobin can decrease to 25%, results in release of 75% of transported O2
Partial pressure can maintain for a while but will then drop off quick
`BOHR Effect
High CO2 equals drop in pH and decrease of O2 affinity for Hgb
Low CO2 equal rise in pH and increase in O2 affinity for Hgb
6 P’s of RSI
- Preparation
- Preoxygenation
- Pretreatment
- Paralysis with induction
- Placement of tube
- Postintubation management
Phernic nerve
responsible for moving the diaphragm
right upper quadrant
liver gallbladder pylorus duodenum pancreas head R adrenal glad top of R kidney colon- ascending and transverse
left upper quadrant
left lobe of liver spleen stomach body of pancreas left adrenal glad portion of left kidney transverse and descending colon
right lower
lower pole of kidney appendix ascending colon bladder ovary uterus
left lower
lower pole of kidney sigmoid colon descending colon bladder ovary uterus
cranial nerves
1-Olfactory 7-Facial 2-Optic 8-Acoustic 3-Oculomotor 9-Glossopharyngeal 4-Trachlear 10-Vagus 5-Trigeminal 11-Spinal accessory 6-Abducens 12-Hypoglossal
cranial nerve 1
olfactory- sensor nerve
cranial nerve 2
optic- sensory nerve
cranial nerve 3
oculomotor- motor nerve
cranial nerve 4
trachlear- motor nerve
cranial nerve 5
trigeminal- both
cranial nerve 6
abducens- motor
cranial nerve 7
facial- both
cranial nerve 8
acoustic- sensory
cranial nerve 9
glossopharyngeal- both
cranial nerve 10
vagus- both
cranial nerve 11
spinal- motor
cranial nerve 12
hypoglossal- motor
percussion sounds
loudest to quietest tympany hyperresonance resonance dullnes flatness
