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General Anestesia
major surgery for loss of consciousness and sensation
Analgesia: lose sensation
delirium: unconscious but restless
surgical anesthesia: deep breathing without reflexes
medullary paralysis: voluntary stops
inhibit neuronal activity throughout CNS
Administration: inhaled (slower but easier to adjust) or IV
local anesthetics
sensation loss in specific body region
chloroprocaine, lidocaine, bupivacaine, ropivocaine
Administration: topical, transdermal, peripheral nv block, neural blockage
PT implications
lack sensation and motor
Local Anesthetic Systemic Toxicity (LAST) - spreads to blood stream → CNS = sedation or cardiac = dysrhythmias or hypotension
opioids
mimic neural endorphins (dopamine) binding to receptors to block pain
strong → for severe pain
morphine, fentanyl, hydromorphone, oxymorphone
mild/moderate → moderate pain
codeine, hydrocodone, oxycodone
PT considerations
change in mental state
orthostatic hypotension
GI dysfunction
decrease RR
withdrawal → peak in 2-3 days
muscle relaxants
spasticity: exaggerated stretch reflex caused by motor neuron damage
spasm: involuntary muscle tension occurs with pain input that excites motor neuron
benzodiazepines (diazepam)
inhibitory and calming affect
polysynaptic inhibitors
cyclobenzaprine, carisoprodol, metaxalone, methocarbamol
PT consider: sedation and lethargy
Acetaminophen
analgesic (for pain) and antipyretic (for fever)
hepatotoxicity!
NSAIDs
Analgesic (pain), Anti-inflammatory, Antipyretic (fever), antithrombotic (decrease blood clot)
Aspirin has all 4
ibuprofen, naproxen, diclofenac, oxaprozin, piroxicam, indomethacin, fenoprofen, flurbiprofen, ketorolac, celecoxib
PT considerations: GI problems, bleeding, Reye’s syndrome (swelling of liver and brain due to taken with fever), KIDNEY DYSFUNCTION, problems with tissue healing
corticosteroids
cortisone, dexamethasone, hydrocortisone, prednisone, prednisolone, betamethasone, methylprednisone, methylprednisolone
PT considerations: catabolic effect (careful with manual therapy), hypertension, immunosuppression, impaired healing, Cushing’s disease (increase fat in face and abdomen)
nociceptive meds
for pain
anesthetics, opioids, muscle relaxants, acetaminophen
neuropathic
injury to axon/nvs
anticonvulsants (gabapentin)
antidepressants
Goodman Screening for Referral
client history (medical history and meds)
risk factor assessment
clinical presentation (s/s)
review of systems
general health questions
specific systems
signs and symptoms of cardiovascular disease
angina pectoris: chest pain
myocardial ischemia
dysrhythmias
dyspnea
cardiac syncope
fatigue
cough
cyanosis
edema (pitting)
claudication: leg pain due to decrease O2 delivery to muscles
abnormal vital signs
normal control of BP
moment to moment controlled by vessels → vasoconstriction
short term by baroreceptors
long term by RAAS
orthostatic hypotension
drop in BP when rising
etiology: meds, less sensitive baroreceptors, impaired nv signals
orthostasis: normal reaction = baroreceptors detect decreased BP and will increase resistance and HR in response (fail = syncope)
more often in morning
diagnosis: SBP decrease 20 and/or DBP decrease 10
treatment = contract leg muscles to get blood flowing before standing
Postural Orthostatic Tachycardic Syndrome (POTS)
excessive tachycardia upon standing (usually in females)
etiology: neuropathic, autoimmune, virus, trauma
blood pools in lower body and ANS fails to regulate change in BP
diagnosis: HR increases > 30 bpm
treatment: fluid retention, steroids, B-blockers
syncope
temporary loss of consciousness
etiology: brain deprived O2
cardiac = decreased Q = decreased BP
vasovagal: over-activated vagus nv
result in falls, but don’t remember falling → ask duration of unconsciousness
hypertension
persistent elevation of BP
essential = 90% cases unknown cause
secondary = 10% cases known cause
self perpetuates
silent killer
Anti-hypertensive meds
orthostatic hypotension
B-blockers
decrease SNS → decrease HR → decrease BP
use RPE scale
end in -lol
a-blockers
decrease resistance → decrease BP
reflex tachycardia
cautious with heat therapy (since vasodilating)
end in -osin
central a-2 agonists
decrease SNS in brain → decrease BP
clonidine and methyldopa
diuretics
decrease H2O reabsorption → decrease blood volume → decrease BP
Loop diuretics end in -ide (strongest)
Thiazide Diuretics end in -thiazide
Potassium sparing diuretics (weakest)
ACE inhibitors
prevent vasoconstriction
end in -pril
Angiotensin 2 receptor blockers
cause vasodilation
end in -artan
Renin inhibitors
stop angiotensin 2 production
end in -ren
vasodilators
direct: relax vascular muscles
hydralazine, minoxidil, nitroprusside
indirect: calcium channel blockers
end in -ipine expect most common = diltiazem
heart valve disease
damage to tricuspid, pulmonic, biscuspid/mitral, aortic valve
etiology: IHD, infection, rheumatic fever
types
stenosis: narrowing of valve
regurgitation: back flow due to improper closing
prolapse: change in shape, only a problem if causing regurg
most of time asymptomatic but may cause arrhythmias or heart failure
diagnose: auscualtion (heart sounds) or echocardiogram
treat: surgery
cardiac arrhythmias
changes in circulatory dynamics
etiology: congenital, other pathology, lifestyle
risk factors: IHD/MI
due to electrical problem
abnormal automaticity: SA node not working
abnormal conduction
mild = no s/s
severe = decrease Q → cardiac failure, stroke, death
diagnose: ECG
treatment: meds, defibrillator (shock), surgical pacemaker
Anti-arrhythmic meds
all pro-arrhythmic
sodium channel blockers
disopyramide, flecainide, quinidine
B-blockers (end in -lol)
potassium channel blockers
amiodarone → toxicity of eyes, heart, thryroid, liver, blue/grey skin
calcium channel blockers
diltiazem
hyperlipidemia (high cholesterol)
leads to atherosclerosis (plaques)
etiology: lifestyle
HDL target >50 (good type)
LDL target <100 (bad type)
diagnose: blood test
treatment: lifestyle change and meds
hyperlipidemia meds
all cause GI problems
Statins
inhibit enzyme that catalyzes cholesterol synthesis (decrease production of cholesterol)
can cause muscle pain
end in -statin
Ezetimibe
inhibit cholesterol absorption
Nicotinic Acid
B vitamin that binds to receptors to decrease lipid breakdown
Fibric Acids (fenofibrate)
increase activity of lipoprotein lipase
increase free fatty acid uptake in liver
Hepatotoxicity and increase risk of gallstones
bile acid binding agents (cholestyramine)
block reabsorption of bile
PCSK-9 inhibitors (alirocumab)
block protein that normally prevents cholesterol removal
Ischemic Heart Disease (IHD)
Coronary Artery Disease
coronary arteries narrow due to arteriosclerosis
due to atherosclerosis (plaque)
risk factors: male, age, lifestyle
angina pectoris: chest pain
not enough O2 to heart due to clot (emboli)
referred pain to L chest, arm, jaw, and in females abdomen
diagnosis: lipid profile, coronary catheterization, echocardiogram
treatment: meds, lifestyle change, surgery (PTCA stenting or CABG - bypass)
Myocardial Infarction (MI) = heart attack
irreversible necrosis of heart muscle
etiology: IHD → embolism (moving clot)
risk factors: male, hypertension, hyperlipidemia, valve disease, IHD
more often in morning
diagnose: lab results, ECG, echocardiogram, angiogram
treatment: meds, surgery (PTCA or CABG)
50% deaths occur within 1 hr and usually due to dysrhythmia
IHD and MI meds
Anti-anginals
Nitrates
Nitroglycerin converted to NO in smooth muscle cells → vasodilation
make sure patient has with them before exercise
call 911 if no improvement in 15-20 min or symptoms increase
orthostatic hypotension, reflex tachycardia, edema, caution with heat therapy
B-blockers: decrease SNS → decrease HR to decrease O2 needed
calcium channel blockers
IHD and MI meds
Anticoagulants
heparin: increase clot time
monitor with aPTT
low aPTT = increase risk of clotting
high aPTT = increase risk of bleeding
Warfarin: increase clot time
monitor with Prothrombin Time (PT) or INR
Direct Thrombin Inhibitors
fondaparinux or rivaroxaban
PT consideration: increased risk of bleeding, patient must reach level aPTT or PT/INR before starting
IHD and MI meds
Anti-platlets
stop platelets from sticking together
salicylates → aspirin
PT consideration: increase risk of bleeding
IHD and MI meds
fibrinolytics
dissolve clot
tenecteplase
increase risk of bleeding and usually on bed rest for a little while
Heart Failure
condition where heart is unable. to pump sufficient quantity of blood to meet needs of tissues
risk factors: hypertension, aging, IHD, etc
Classifications
New York Heart Association functional classifications: based on function → for PT
AHA/American College of Cardiology stages: more on anatomy
Left side = congested heart failure
increase SNS, RAAS system, and ADH to compensate
difficulty breathing because backs up into lungs
cyanosis
Right side
backs up to body (edema, jugular vein distension, weight gain (ascites)
jaundice
Affecting ejection fraction?
diastolic: dysfunction of relaxation
systolic: dysfunction of contraction
diagnosis: echocardiogram, ECG, stress test, cardiac catheterization
treatment: lifestyle change!, meds, surgery, heart transplant
Heart failure meds
inotropic: affects contractility
chronotropic: affects HR
dromotropic: increase rate of conduction through AV node
Heart failure meds
Cardiac Glyosides (digoxin)
positive inotropic
neg chronotropic and dromotropic
digoxin toxicity: narrow therapeutic window → yellow visual halos
risk dysrhythmias
phosphodiesterase inhibitor (milrinone)
positive inotropic
risk dysrhythmias and OH
vasopressors and positive inotropes
for ICU patients
to decrease work of heart
ACE inhibitors
Angiotensin Receptor blockers
diuretics
vasodilators
B-blockers
Peripheral vascular disease
more often in LEs
changes in skin = first sign
vasculitis: vessel inflammation
arterial occlusive disease
result of arteriosclerosis, trauma, or vasculitis
claudication: pain due to lack of blood flow
s/s: thin skin, elevate = pain worse, rubor of dependency (redness), wound = round
thrombophlebitis
swelling of vein
DVT: 3rd most common cardiac disease
venous stasis + hypercoagulation + vessel injury
s/s: dull ache/pain in area, edema, red and warm
diagnose: Doppler ultrasound , Well’s Clinical Prediction Rule (2+ = high risk)
varicose veins
due to elevated venous pressure
risk factors: female
chronic venous insufficiency
inadequate venous return → pooling
pain improves with elevation
s/s: edema, red/blown skin, wounds=irregular
compression socks
vasomotor disorders - Raynaud’s
usually women 20-50
disease: unknown cause, hypersensitive to cold → vasospasm
phenomenon: due to underlying disease
white → blue → red
calcium channel blockers and avoid triggers
aneurysms
etiology: trauma, infection, inflammation
risk factors: AGE and smoking!
arterial aneurysms
Aortic, Thoracic, Abdominal
asymptomatic
tachycardic if ruptured
intracranial
Epidural hematoma: sudden onset, bleeding on brain
subdural hematoma: slower, take longer to find, minor trauma
subarachnoid hemorrhage: sudden excruciating headache
diagnose: palpation, imaging
treatment: watch and wait (control BP)
prognosis: rupture = death
Cerebral Vasular Accident (CVA) - stroke
etiology: arteries in brain damaged
risk factors: F more in young and over lifetime
Transient ischemic attack (mini stroke)
reversible damage
Ischemic stroke (85%)
occlusion (blood clot) usually from heart
Hemorrhagic stroke (15%)
most deadly → bleeding in brain
s/s: representative of area of brain affected
Face Arm(leg) Speech Time
diagnose: presentation or CT/MRI
treatment: PT
3rd leading cause of death and 1st cause of disability in adults