ANS and CV System Flashcards
SNS: fight or flight
- Increased cardiac output
- Shunting of blood
GI tract & skin →muscle,
heart & lungs - Increased metabolism
- Increased mental alertness
- Dilate pupils
PSNS: rest and digest
- Decreased cardiac output
- Shunting of blood to
abdominal organs - Increased digestion &
absorption - Decreased metabolism
- Decreased alertness
- Focus lens/constrict pupil
Sympathetic Neurotransmitter
Sympathetic ganglion –> Nicotinic- Cholinergic Ach Receptor –> Adrenergic Norepi receptor
Parasympathetic Neurotransmitter
PNS ganglion –> Nicotinic- Cholinergic Ach Receptor –> Muscarinic Ach receptor
Ach –>
Cholinergic –> muscarinic or nicotinic
Norepinephrine –>
adrenergic receptor –> alpha or beta
cholinergic receptor –> muscarinic
primarily in the peripheral ANS at PSNS post-
ganglionic post-synaptic membrane
cholinergic receptor –> nicotinic
– CNS
– Peripheral ANS in preganglionic -postsynaptic membrane
– neuromuscular junctions
alpha one adrenergic receptor
vascular smooth muscle
alpha two adrenergic receptor
post-synaptic adrenergic membrane
beta one adrenergic receptor
heart, kidney and fat cells
beta two adrenergic receptor
certain vascular beds, bronchioles
direct agonist
drug binds to and stimulates receptor
cholinergic agonist
- bind all acetylcholine (Ach) receptors (R)
- Non-specific and wide-spread side effects
muscarinic agonist
- bind only the muscarinic subtype Ach R
- More specific to GI organs and fewer side effects
indirect cholinergic stimulant
- alter degradation of Ach
- Block acetylcholinesterase so Ach isn’t
degraded, prolonging neurotransmission - Tend to be non-specific (affecting all Ach
receptors) with a lot of side effects
Uses of muscarinic agonist
- Illius
- Atony of bladder
- glaucoma
- myasthenia gravis
- reversal of neuromuscular block or anticholinergic toxicity
Uses of muscarinic agonist - Illius
a loss of tone (atony) in GI Tract after surgery
or trauma. decreases peristalsis, distension
Uses of muscarinic agonist - Atony of bladder
decrease tone in smooth muscle and
distension of bladder. Urinary retention
uses of muscarinic agonist - glaucoma
increases in ocular pressure due to accumulation
of aqueous humor in the eye
uses of muscarinic agonist - myasthenia gravis
skeletal muscle paralysis due
(autoimmune) loss of Ach receptors
non specificity of cholinergic agonists causes:
– bronchoconstriction (acting at muscarinic R in
PSNS nerves to lung)
– excessive salivation
– bradycardia
– difficulty in visual accommodation
– flushing/sweating, especially of face due to
stimulation of special SNS neurons w/ Ach Rs
What are anti-muscarinic drugs used in treatment of?
GI disturbances, Parkinson’s Disease, bradycardia (2MI/surgery), motion
sickness, urinary frequency, asthma/breathing
difficulty, poisoning & to produce mydriasis
GI disturbances:
- hyperactivity in ANS- GI
motility/secretion - Anti-muscarinic block both secretion & motility
since both mediated by Ach at GI muscarinic Rs
what do anti- muscarinics block?
both secretion & motility
since both mediated by Ach at GI muscarinic Rs
Uses of anti-muscarinics
- irritable bowel
- peptic ulcer
- motion sickness
- bradycardia
- parkinson disease
- urinary frequency/incontinence
- reparatory distress/asthma
- produce mydrisis
- rx poisoning
uses of anti-muscarinics - irritable bowel
motility in GI tract
* Anti-muscarinic effectiveness questionable
uses of anti-muscarinics - peptic ulcer
- caused by gastric acid
- Anti-muscarinics not very effective: H2-blockers & antibiotics more efficacious
uses of anti-muscarinics - motion sickness
Scopolamine: inhibit Vestibular Sys.
uses of anti-muscarinics - bradycardia
Atropine: blocks vagal tone after MI or with
anesthesia during surgery
uses of anti-muscarinics - parkinson disease
blocks Ach inhibition in BG
uses of anti-muscarinics - urinary frequency/incontinence
decreases bladder tone/spasm
uses of anti-muscarinics - respiratory distress/asthma
block vagal bronchial constriction
uses of anti-muscarinics - produce mydriasis
dilate the papillary muscle to allow
for ophthalmologic examination
uses of anti-muscarinics - treat poisoning
insecticides, mushrooms, chemical
weapons and other common poisons
side effects of anticholinergics
- similar for all drugs in this class
– dry mouth
– blurred vision
– urinary retention
– constipation
– tachycardia
– CNS symptoms: confusion, nervousness,
drowsiness (especially anticholinergics)
urinary retention
– Muscarinic agonists may be given to patients w/ SCI in first few weeks to prevent urinary retention
– decrease the risk of UTI
Neurogenic bladder (incontinence or frequency)
– Anti-cholinergic agents may be given to patients w/ SCI after reflexes return to decrease activity in the bladder and prevent incontinence
Rx of autonomic dysreflexia
-remove noxious stimulus
- block SNS: Non-specific adrenergic antagonists (Acebutolol), Beta adrenergic blockers (Propranolol), Alpha adrenergic blockers (Phentolamine)
- Alpha 2 receptor agonist –> Clonadine (Catapress)
definition of HTN
bp > 140/90
primary or essential HTN:
– cannot be attributed to another disease process
– no straight forward underlying pathology or cause is u/k
– 95% of all patients with HTN
secondary HTN
– HTN that is due to another disease process
– example: HTN due to chronic renal disease
– only 5% of cases of HTN
pathophysiology of HTN on slide 25
causes of HTN
– Complex interaction of genetic & environment
– Genetic factors are variable depending on individual
– Environmental factors: smoking, sedentary life style, obesity, alcohol, personality trait
major categories of drugs for HTN
– diuretics
– sympatholytic drugs
– vasodilators
– angiotensin converting enzyme (ACE)
inhibitors
– calcium channel blockers
Diuretics
- work in kidney
- decrease plasma volume
Sympatholytics
- works on SNS and in hypothalamus
- decreases SNS influence on heart and vasculature
Vasodilators
- peripheral vasculature
- lower vascular resistance by direct vasodilation
ace inhibitors
- work in peripheral vasculature, heart, kidney
- inhibit ACE enzyme, blocking Ang II formation
Ca-channel blockers
- works in Ca channels in smooth and cardiac muscle
- decrease smooth muscle tone, vasodilation, decrease force and rate of cardiac contraction
Thiazide Diuretics
Chlorothiazide (Diuril)
Hydrochlorothiazide (Esidrix)
pathophysiology of angina pectoris
- Occurs when myocardial O2 demand is
insufficient to meet the demands of body.
– Often brought on by exercise/exertion
symptoms of angina pectoris
- resulting from myocardial ischemia
– chest pain (may also be in jaw, shoulder or back)
– diaphoresis (sweating)
– chest pressure (intense tightness or constriction)
– anxiety/ denial
– SOB or dyspnea
see slide 34
drugs used to treat angina
All drugs used to Rx angina either decrease the hearts work load or increase O2 delivery to the heart:
– 1) Drugs that decrease the afterload (force against
which heart pumps)
– 2) Drugs that decrease the preload (thereby
decrease work of the heart)
– 3) Drugs that decrease cardiac contractility
– 4) Drugs that vasodilate coronary arteries
how do nitrates work?
primarily by decreasing the
workload on the heart, not by coronary
vasodilatation as previously thought
Best delivery of nitrates
- Not absorbed well in GI tract so sublingual, buccal or patch works best
- Sublingual is fastest (2 min) for acute angina attack
can tolerance to nitrates develop?
yes - remove for at least a few hours
side effects of nitrates
- associated with vasodilation
– headache (secondary to hypotension)
– orthostatic hypotension
– nausea
how do beta blockers work?
- Directly decrease the work of the heart by
decreasing contractility - Prophylactically to prevent angina attack
how do calcium channel blockers work?
primarily by blocking Ca2+ entry into
smooth muscle, causing vasodilatation and
decreasing the afterload and preload
what is the primary effect of calcium channel blockers
- vasodilation of the coronary arteries: increases myocardial blood flow
- Also limit Ca2+ entry to myocardium, but this
affect is important for Rx arrhythmias
stable angina
- myocardial oxygen demand exceeds supply during cardiovascular stress in predictable manner
- treat with beta blockers and/or nitrate
variant angina
- myocardial oxygen demand exceeds supply, secondary vasospasm, may occur at rest
- treat with calcium channel blockers
unstable angina
- myocardial oxygen demand exceeds supply at any time
- treat with combination of calcium channel blocker ply beta blockers and/or nitrate
use of nitrates during PT
– If a patient is taking nitrates (by patch or
sublingual) then the med should be taken with the patient to PT!
– Monitor patients response to exercise
– Use caution with heat or whirlpool
arrhythmia
any significant or abnormal deviation in the hearts conduction pattern
consequences of arrhythmia
syncope, TIA/CVA, MI, heart failure, death
R heart failure
accumulation in periphery: limbs,
abdomen, liver or other systemic organ
L heart failure
accumulation in lungs
what does “congestive” refer to
“backward” failure with fluid accumulation
cycle of CHF slide 46
effects of Digitalis
- Increases the pumping ability of the heart
- Very narrow “therapeutic window”: the
dose must be carefully titrated to patient
side effects of Digitalis
– drug toxicity: 20-25 % of the patients taking it
– GI distress, N&V
– CNS disturbances: drowsiness, fatigue,
confusion, visual disturbances
– Rhythm disturbances: premature atrial and
ventricular contractions, paroxysmal atrial
tachycardia, AV-blocks
Target of ACE inhibitors in CHF
– cardiac lesion (HTN)
– neurohumoral compensation
– limit the increased cardiac workload
– cell adaptations (cardiac hypertrophy)
Treatment of coagulation disorders
Body requires a delicate balance between
coagulation an anti-coagulation for vascular
function
inadequate clotting
hemophilia, hemorrhage
excessive clotting
embolism & thrombosis
Classes of anticoagulants:
Heparins
Low molecular weight heparins
oral anticoagulants
- All Inhibit synthesis and function of clotting factors; used primarily to prevent and treat
venous thromboembolism
Heparin sodium and LMWH
Used for preventing and treating MI AND:
– DVT prophylaxis (prior to THA, TKA surgery,
during periods of immobilization, etc…)
– Treatment of thromboembolism
– Treatment of pulmonary embolism
Antiplatelet Drugs (GP-2b3a Inhibitors):
Clopidogrel (Plavix) & Ticlopidine (Ticlid)
– New anti-platelet drugs
– Member of the ticlopidin family
– Reduces the risk of re-infarction by 30-35% after MI
– Clopidogrel has fewer adverse effects than other ticlopidins
– Reduces expression of glycoprotein IIb/IIIa (GP-2b-3a), the fibrinogen receptor on platelet surface
– Inhibits ADP-dependent platelet aggregation
Heparin
primary anticoagulant used clinically, given
parentally for prevention of clots in venous system
Warfarin (Coumadin)
long term anticoagulation. inhibits production of Vit-K from Vit-K epoxide, preventing completion of clotting cascade
* given orally, but lag time (2-days) before works
Aspirin
– Anti-platelet action: impairs hepatic synthesis of Factors VII, IX & X
– Rx w/ aspirin shown torisk for MI, or recurrence
What do thrombolytic drugs do
– Convert plasminogen (profibrinolysin) to plasmin (fibrinolysin)
– Plasmin is the active form of this endogenous enzyme
and dissolves the clot
– Actually break-up clots that already exist
uses of thrombolytic drugs
MI, stroke, PE, peripheral arterial occlusion
- must be administered within 3-6 hrs
hemophilia
– Hereditary disease in which a clotting factor is
not produced or produced inadequately
– Hemophilia A: F-VIII (most common)
– Hemophilia A: F-IX (second most common)
– Rx: replacing appropriate F, but it is still obtained from human blood and very expensive (25,000/y)
– risk of HIV, hepatitis-B or C, other viruses
Vitamin K deficiencies
treat with vitamin supplement
excessive bleeding after surgery
secondary to over-activation of fibrinolytic system
causes of hyperlipidemia
familial, diet and life style
how are lipids transferred
- as lipo-proteins in blood (HDL, VLDL, LDL and IDL)
– HDL- removes lipids from vessel wall
– VLDL, IDL and LDL- deposit lipids on vessel wall
Pharmacological strategies to decrease lipids
– prevent endogenous formation
* HMG-CoA reductase inhibitors or STATINS
– rid body of cholesterol
Special Concern for PT
- Many pt’s seen in PT are on thrombolytic Rx
secondary to bed rest increases risk of
embolism/ thrombosis (DVT)
– hip, knee or other joint surgery
– post-MI, post-CABG, any re-vascularization
– valve surgery
– especially patients Rx w/ streptokinase or t-PA - Rehab procedures dealing with open wounds
(WP, unwrapping dressings) should be done
with caution secondary to risk of hemorrhage
