Exam 1 Flashcards
What is the most prominent tubercle in the neck?
chassaignac tubercle
Where is the chassaignac tubercle located?
the anteroir tubercle of the transverse process of the 6th cervical vertebra (correlated with the cricoid process) against which the carotid artery may be compressed by the finder (ie. carotid massage.)
Major agonists of the ANS
-Ach
-NE
-Epi
-DA
-ATP
Calcium plays a critical role in the regulation in the peripheral vessel diameter. Increase Ca2+ causes ____________ and reduced intracellular calcium leads to __________.
vasoconstriction
Vasodilation
G-protein CAMP and nitric oxide cGMp vessel effects
vasodilation
Phospholipase C vessel effects
vasoconstriction
increased cAMP and protein kinase A _______________ intracellular calcium.
increase
Protein Kinase A (PKA) affects excitation-contraction coupling by:
-inhibition of voltage gated Ca 2+ channels in the sarcolemma
-inhibition of Ca+ release from the SR
-reduced sensitivity of the myofilaments to Ca+2
-facilitation of Ca+2 reuptake into the sarcoplasmic reticulum via SERCA2 pump
What determines how well the pump is primed?
preload
What is directly related to tension developed in the ventricles?
preload
Right ventricular end diastolic volume is the product of ________
systemic venous return
Left ventricular end diastolic volume is the product of
pulmonary circulation enters the left side of the heart after it has gone through the pulmonary circulation
preload can be measured by
CVP (RVEDP) and LAP or indirectly by PCWP (LVEDP)
Frank starling principle
increased myocardial fiber length (preload) improves contractility up to a point of ultimate decompensation
What is impedance to left ventricular outflow
afterload
-can be altered with drugs that dilate or constrict vascular beds-mostly via arterial vessels
-arterial vasodilators decrease resistance to ventricular contraction but can also decrease preload
Factors influencing contractility
-appropriate amounts of potassium, sodium and calcium
-sympathetic nervous system via Beta 1 receptor stimulation (increased contractility, HR, ventricular automaticity and myocardial O2 consumption)
-increased levels of cyclic adenosine monophosphate (caMP)
-preload and afterload
Cardac output
-volume of blood the heart ejects each minute
CO=SV x HR
normal cardiac output
4-8L/min
Cardiac index (CI)
adjusts the CO value for an individual body size
CI=CO divided by BSA (2.5–4.0 L/min)
3 primary factors that determine CO (SV):
-preload
-afterload
-contractility
What is myocardial oxygen supply determined by:
oxygen content of afterial blood
coronary perfusion
What is coronary perfusion influenced by?
heart rate
slower heart rate increased diastolic time thus allowing for increased coronary perfusion
what determines coronary perfusion pressure
diastolic pressure
coronary blood flow is regulated by
coronary vascular tone
myocardial oxygen demand is influenced by
-preload
-afterload
-inotrophy
-heart rate
myocardial oxygen demand is increased by an increase in ____ and in increase in _______.
preload and inotropy
myocardial oxygen demand is decreased by a
decrease in afterload
decrease in HR
_________ is the NT responsible for most adrenergic activity of the SNS.
norepi
the action of more is terminated by reuptake into the postganglionic nerve ending
Where are alpha 1 receptors located?
in smooth muscle throughout the body
most important CV effect upon alpha 1 stimulation is
vasoconstriction
Alpha 1
increased peripheral vascular resistance
increased arterial BP
where are alpha 2 receptors located chiefly on
the presynaptic nerve terminals
stimulation of alpha 2 receptors creates a ___________
negative feedback loop that inhibits further norepinephrine release. decreases vasoconstriction.
antagonism of alpha 2 receptors causes
enhanced release of NE from nerve endings
Beta 1 receptor stimulation
-increases heart rate, conduction and contractility
chronotropy, dromotropy (affects conduction speed in AV node) ,inotropy
stimulation activates adenylyl cyclase, which converts ATP to cAMP
beta 2 receptors are located on
post synaptic receptors in smooth muscle and gland cells
beta 2 receptor stimulation
relaxes smooth muscle, resulting in bronchodilation, vasodilitation and relaxation of the uterus. bladder and gut
Alpha non specific agonists
epinephrine
norepinephrine
alpha 1 agonist specific drugs
-phenylephrine
-methoxamine (Vasoxyl)
Alpha 2 selective agonist drugs
-clonidine
-dexmeditomidine
alpha non specific antagonist meds
phentolamine (regitine)
-phenoxybenzamine
alpha 1 antagonist selective meds
-prazosin (minipress)
-cardura
-hytrin
Alpha 2 antagonist selective
Yohimbine
endogenous catecholamines
-dopamine
-norepinephrine
-epinephrine
non endogenous (or synthetic sympathomimetic) catecholamines
-isoproterenol
-dobutamine
Beta 1 stimulation causes:
increase in contractility and HR which leads to increased cardiac output and MVO2 (demand)
beta 2 stimulation causes:
vasodilation in skeletal muscles and bronchial smooth muscle
-may decrease diastolic pressure
alpha 1 stimulation
increases coronary and cerebral perfusion pressures and systolic BP however stimulation of alpha 1 receptors in the skin, mucosa and hepatorenal vasculature causes vasoconstriction and decrease flow
what is the principle pharmacologic treatment for anaphylaxis and v fib
epinephrine
complications of epinephrine
-cerebral hemorrhage
-coronary ischemia
-ventricular arrhythmias
norepi receptor
direct alpha 1 stimulation resulting in vasoconstriction with increases SVR (both arterial and venous) may cause reflex bradycardia
-beta 1 stimulation increase myocardial contractility
-Beta 2 minimal to absent
Renal doses of dopamine predominate at
<2 mcg/kg/min
Beta 1 stimulation of dopamine at
2-10 mcg/kg/min resulting in increased myocardial contractility, HR and CO
Alpha 1 stimulation of dopamine at
10-20 mcg/kg/min resulting in increased PVR due to vasoconstriction
Dose of dopamine >20mcg/kg/min and higher result in
release of norepinephrine, because dopamine is an intermediate product in the enzymatic pathway leading to the production of norepinephrine, thus acts indirectly by releasing norepinephrine
high doses of dopamine can inhibit ______ and cause _________
insulin and cause hyperglycemia
What is a synthetic catecholamine with structural characteristics of dopamine and isoproteronol
dobutamine
selective Beta 1 agonist
increases cardiac contractility (inotropic effects)
-can increase myocardial oxygen demand
-increases cerebral blood flow
-decreases systemic vascular resistance (beta 2 agonist)
Dose of dobutamine
2-20mcg/kg/min
effects of isoproterenol
increased heart rate, myocardial contractility, systolic blood pressure
no alpha
-excessive tachycardia and decreased diastolic pressure and may decrease coronary flow
high incidence of cardiac dysrhythmia
examples of beta agonists
-albuterol
-terbutaline
ritodrine
beta agonist effects
-relax bronchioles and uterine smooth muscles
-used to treat bronchospasm
-in ob: used to stop uterine contraction
direct acting sympathomimetic
synthetic drugs that are used as vasopressors to reverse hypotension
-mimic effects of norepinephrine
indirect acting sympathomimetics
synthetic drugs that are used as vasopressures to reverse hypotension
-evoke release of endogenous norepinephrine
Ephedrine
-non-catecholamine
direct and indirect acting sympathomimetic
-CV effects similar to those of epinephrine although ephedrine is less potent with longer DOA
-increases BP by stimulating release of norepi
-increases cardiac contractility and heartrate secondary to beta-1 receptor stimulation
-bronchodilator
Ephedrine dose
2.5-10mg bolus
diluting epi
available 50mg/ml dilute with 9ml NS to created 5mg/ml in 10 ml syringe
Phenylephrine
non-catecholamine, direct acting (mimics effects of norpi), alpha 1 agonist
-primary effect is peripheral vasoconstriction which increases systemic vascular resistance and BP
-reflex bardy
-increases cerebral blood flow
iinfusion of phenylephrine
0.25-1mcg/kg/min
phenylephrine dilution
10mg/ml availability
10mg in 250ml=40 mcg/ml
primary uses of phenoxybenzamine
chronic medical control of patients with pheochromocytoma
-raynaud’s disease by reversing vasoconstriction in the hands
moa phenoxybenzamine
-non-selective alpha antagonist
blockage at alpha 1> alpha 2
phentolamine moa
competitive alpha antagonist: smooth muscle relaxation. which leads to peripheral vasodilation, decreased BP (alpha 1) and reflex tachycardia (alpha 2)
-used to treat extravasation of alpha agonist. 5-10mg locally infiltrated to prevent tissue necrosis
dose of phentolamine
1-5 mg bolus
Prazosin MOA
-alpha 1 receptor antagonist
-dilated both arterioles and veins
-decreases SVR And preload
-virtually no tachycardia secondary to lack of alpha two antagonistic
loading dose of dexmeditomidine
0.5-2mcg/kg over 10 minutes
infusion of dexmeditomidine
0.2-0.7mcg/kg/hr
clonidine (catapress)
-central acting on alpha 2 agonist receptors located in the dorsal horn of the spinal cord
-decreases outflow of sympathetic nervous system bty reducing plasma catecholamine levels
-negative chronotropic effects
-decreased CO, SVR, BP
-sedative and analgesic effects decrease anesthesia requirements
-effective in suppressing the signs and symptoms of withdrawal from opioids
-the adverse effect is rebound HTN when abruptly d/c’d
IV dose clonidine
1-3 mcg/kg
Do beta blockers inhibit platelet aggregation?
yes
Decrease in heart rate produced by B blockers :
-prolongs diastole
-increases coronary blood flow to LV
-enhances coronary collateral perfusion to ischemic myocardium
-improves oxygen delivery to coronary microcirculation
also serves to reduce myocardial oxygen demand while increasing the supply
Propanolol (inderal) receptor action
nonselective Beta 1 and beta 2 antagonist
prototypical B-blocker
propanolol effects
decreases HR and cardiac output which deccreases myocardial oxygen requirements
-decreases myocardial contractility
-decreases spontaneous SA node firing; slows av conduction
-SVT
uses of propanolol
SVT
A-fib
A-flutter
dose of propanolol
1-3mg IV in 0.5 mg increments q 2 min
metoprolol (lopressor) receptor action
selective beta 1 antagonist
dose of metoprolol
15mg IV given 5 mg increments q 2-3 minutes
1/2 life 3-4 hours
Atenolol (tenormin) receptor action
beta one selective antagonist
dose of atenolol
mostly PO for HTN-long acting
5mg IV over 10 min
esmolol (Brevibloc) receptor
selective beta 1 antagonist
ultra short acting
dose of esmolol
10mg IVP
infusion load 250mcg/kg over 5 min f/b 25-50 mcg/kg/min
labetolol actions
-lowers bp without reflexive increase in HR
-decreases PVR, HP, HR
CO slightly depressed or unchangeed
labetolol dose
0.1-0.5mg/kg IV
1/2 life labetolol
3- 8 hours
which is a non-selective Beta blocker used in treatment of glaucoma
timolol (blocadren)
mostly used to derease IOP by decreasing formation of aqueous humor
phosphodiesterase inhibitors
inhibit PDE III (milrinone and amrinone) enzyme that breaks down caMP
increase levels of cAMP result in vasodilation, decreased PVR and promotes ventricular filling (preload)
PDE inhibitors other action
alters intracellular Ca regulation to enhance myocardial contractility without affecting catecholamine release or activation of Beta 1 receptors
-pronounced arterial and venous vasodilation by blocking cGMP metabolism and facilitating actions of second messenger in vascular smooth muscle
-
contraindicated in tx of heart failure
Vasopressin
-peptide hormone release from posterior pituitary
-regulates water reabsorption in the kidney and exerts potent hemodtynamic effects independent of adrenoceptis
-activation of subtype triggers second messengers to increase intracellular smooth muscle cell
vasopressin uses
-intraop hypotension due to ACEIs and ARBs refractory to admin of catecholamines or sympathomimetic
-anaphylaxis
-vasoplegia: severe hypotension after prolonged CPB
-cardiac arrest from vfib, PEA asystole
nitroglycerin
-relaxes vascular smooth muscle
-venous dilatation predominates over arterial which leads to decreased myocardial o2 demand
-decreases preload
-MOA similar to sodium nitroprusside (metabolism of NO)
infusion of nitroglycerin
0.5-10mcg/kg/min
Risk of sodium nitroprusside
vascular steal snydromes:
-coronary steal: shunts blood away from compromised coronary leading to worsening ischemia and infarction
cerebral steal
avoid ni patients with cerebral ischemia and increased ICP
-rebound HTN with sudden d/c
nipride metabolism
-enters RBCs and receives an electron from iron of oxyhemoglobin (Fe2+)
-this electron transfer results in an unstable nitroprusside redical and methemoglobin (Fe3+)
-nitroprusside radicals decompose into cyanide ions
-cyanide ions bind to tissue cytochrome oxidanse which interferes with normal Oxygen utilization and prevents oxygen from being released by tissues
-risk factors include malnutrition, liver disease, CPB and hypothermia
s/s of acute cyanide toxicity
metabolic acidosis
tachyphylaxis
increased mixed venous O2
cardiac dysrhythmias
-mechanically with 100% oxygen
-administer sodium thiosulfate 150mg/kg over 15 min
-thiosulfate converts cyanide to thiocyanate which is cleared by kidneys
hydralazine effects
-decreases SVR
-decreases BP
-increases HR and CO
-relaxes arteriolar smooth muscle
hydralazine dose
5-20mg IV
onset 15-20 min
duration 2-4 hours
Calcium channel blocker tx
-HTN
-SVT
-coronary artery spasm
-angina
cerebral artery vasospasm
how do CCB work?
decreases myocardial oxygen demand by decreasing afterload, contractility, HR and conduction through AV node
-small muscle relaxation and vasodilation
what is the most potent CCB?
nifedipine (Procardia)
nifedipine uses
-coronary vasospasm
-HTN
-angina
nifedipine effects
-coronary and peripheral arterial vasodilation
-potential for hypotension and reflex tachycardia
nicardipine (Cardene)
smooth muscle relaxation produces vasodilation of peripheral and coronary arteries
-minimal cardio depressant
-does not decrease the rate of the sinus node pacemaker or slow AV conduction
nicardipine dose
1-4mcg/kg/min
what is an ultra-short-acting dihydropyridine CCB with a plasma half-life of 2 min?
clevidipine
which CCB is metabolized by plasma and tissue esterases?
clevidipine
clevidipine uses
acute HTN in cardiac surgery
pheochromocytoma
acute intracerebral hemorrhage
spinal surgery
which CCB’s primary use is to prevent cerebral artery vasospasm following subarachnoid hemorrhage which can occur 4-14 days after event?
nimodipine
Which CCB should you now use in WPW or other ventricular dysfunction conduction abnormalitiites since it inhibits the intrinsic conduction pathway?
verapamil
hypotensive episodes occur more frequently after anesthetic induction in patients receiving ARBs than other antiHTN and can be refractory to tx with ephedrine or phenylephrine
Class IA Na channel blockers
Quinidine
procainamide
disopyramide
class 1 B Na Channel blockers
Lidocaine
Mexiletine
Tocainide
Class IC Na Channel blockers
Flecainide
propafenone
moricizine
Class III K channel blockers (prolong repolarization)
amiodarone
bretylium
Sotolol (also Class II)
Arterial BP
radial SBP> aortic
more distal site steeper anacrotic limb/higher SBP
pulsus alternans
-alternating beats of larger and smaller pulse pressure
-signs of severe LV dysfunction
pulsus paradoxus
spontaneous respiration
decrease in SBP>10mmHg=P. Paradoxus
-inspiration normally decreases SBP secondary to pulmonary venous capacitance increase in venous return
common in tamponade or pericardial constriction
causes of overdamping
kinks
air/clots
long tubing
hypotension/hypovolemia
underdampening causes
hyperdynamic
HTN
CVP contraindications
TV vegetation
anticoagulated patients
ipsilateral carotid endarterectomy
Limintations of CVP
unhealthy hearts
-pulmonary HTN
-right or light heart failure
-tricuspid regurg
-positive pressure ventilation with PEEP >10cm H20
CVP risks
-arrythmias
-infection
-clot formation
air embolism
-RA/RV perforamtion
-pneumo
a wave
atrial contraction
C wave
tending into RA during isovolumetric contraction
V wave
atrial filling (during ventricular systole)
x descent
atrial relaxation
y decent
atrial emptying (passive)
contraindications of PA cath
WPW
LBBB
giant V waves
secondary to severe MR
indirect measure of LA pressure (preload)
PCWP
Perfect world PCWP=LVEDP=LVEDV
distance from RIJ to RA, RV and PA
RA 20
RV 30
PA 45
distance from SC to RA, RV and PA
RA 15
RV 25
PA 40
distance from LIJ to RA, RV, PA
RA 25
RV 35
PA 50
distance from fem to RA, RV, PA
RA 30
RV 40
PA 55
dromotropic agent
affects the conduction speed (the magnitude of delay) in the AV node of the heart and influences the rate of electrical impulse propagation in the heart
Does diltiazem have a negative dromotropic effect?
yes, its prolongation of AV node conduction is useful in treating a-fub and flutter and SVT.
-may have negative inotropic effects on cardiac muscle not the AV node.
Diltiazem would have negative chronotropic effect at the SA node
dose of Atropine effect at 0.5-1.0mg
-increased HR
-dry mouth
-lack of sweating
-thirst
-mild pupillary dilation
atropine dose 2-5mg effect
-tachycardia
-palpitations
-mydriasis
-cycloplegia
-restlessness
-confusion
atropine dose >5mg
profound tachycardia
-mydriasis
-cycloplegia
-hot flushed skin
-fever
-hallucinations
-coma
-death
dihydropyridine class of Ca channel blockers
-nifedipine
-nimodipine
-nicardipine
-clevidipine
benzothiazepine Ca channel blockers
diltiazem
phenylalkylamines
verapamil
Which Ca channel blockers have better control of HR?
verapamil and diltiazem are good for tachycardia, a-fib, or a-flutter
Which Ca channel blcokers have better control of vascular tone?
nifedipine and nicardipine are vasodilators best used in the tx of HTN form elevated SVR
-nicardipine is useful as a coronary antispasmodic
PDE5 inhibitors
SVT
Sildenafil
Vardenafil
Tadalafil
-increased levels of cGMP and target lungs and penis (think viagra)
-enhances nitric oxide mediated by its inhibition of cGMP breakdown
-induce smooth muscle relaxation an increase blood flow
-promote pulmonary vasodilation and decrease pulmonary artery pressure
PDE 4 inhibitos
IRA
Ibudilast
Roflumilast
Apremilast
-increase levels of cAMP targeting airways, skin and immune system
-aiways smooth muscle relaxation with hyperreactive airways
PDE3 inhibitors
Milrinone
Cilostazole
increased levels of cAMP and cGMP
-increased intropy and relaxation of vascular and airway smooth muscle
-inodilations
-promote vasodilation in peripheral vessels and tx intermittent claudication
nonspecific phosphodiesterase inhibitors
theophylLINE
methyxanthine
-increased levels of cAMP in the airways
tx asthma and COPD
V1
CV (increased CVR)
V2
kidneys, antidiuretic
V3
pituitary gland and modulate autocoids
What are the intrinsic (intraocular) muscles of the eye?
-cililary muscle
-sphincter pupillae (circular) muscle
-dilator pupillae (radial) muscle
all are smooth muscle
contraction of which muscle of the iris causes mydriasis?
contraction of the dilator pupillae (radial) muscle
-sympatheti drive causes release of NE that acts on alpha-1 adrenoreceptors in the radial muscle
contraction of which muscle of the iris causes miosis?
contraction of the sphincter pupillae (circular) muscle
parasympathetic fibers course through CN3 and travel to M3 cholinergic receptors on the sphincter (or constrictor) muscle or the iris
if tyrosine supply is low, cells can generate tyrosine from ___________.
phenyclalanine
tyrosine is converted to L-dopa by_______
tyrosine hydroxylase (rate limiting step)
tyrosin hydroxylase activity is subjected to feedback inhibition by dopamine and NE
L-dopa is converted to dopamine by___________
L-amino acid decarboxylase
dopamine is converted to norepi by _________
dopamine beta-hydroxylasenor
norepinephrine is converted to epi by _______________
enzyme phenylethanolamine N-methyltransferase in the cytoplasm of adrenergic cells
nicotonic receptors are___________
ion channelsm
muscarinic receptors are _____________
g-protein
layers of the pericardium
- fibrous portion: tough, loose-fitting, inelastic sac around the heart
- serous portion:
a. pariestal layer: lining inside of the fibrous pericardium
b. visceral layer (epicardium) adheres to outside of the heart
Pericardial space: lies between the parietal and visceral layers
Epicardium
outler layer of the heart wall; serous pericardium
myocardium
-thick, contractile, middle layer of specially constructed and arranged cardiac muscle cells
-if the myocardium is damaged this can cause a myocardial infarction
endocardium
-the lining of the interior of the myocardial wall and covers the trabeculae carnage (this helps add force to inward contraction of the heart wall
structural features
nucleus: single (sometimes double); near the center of the cell
striations: present
t tubules: larger diameter; form diads with the SR, regulate Ca ++ entry into sarcoplasm
Sarcoplasmic reticulum: less extensive than in skeletal muscle
cell junctions: intercalated disks (gap junctions and desmosomes)
contraction style: syncytium (mass) of fibers compress the heart chambers in slow, separate contractions (does not exhibit tetanus or fatigue); exhibits autorhythmicity
transverse (“t”) tubules
deep invaginations. penetrate the myoplasm and facilitate rapid, synchronous transmission of cellular depolarization
What is the contractile unit of the cardiac myocyte?
-contains myofilaments in parallel-cross striated bundles of thin (actin, tropomyosin, troponin complex) and thick (myosin and proteins) fiber
-connected in a series, have long and short axes and simultaneously shorten and thicken during contraction
-A-band contains thick and thin filaments
-I-band contains thin filaments only
-Z-line
3 interdigitating spiral muscle layers
-deep sinospiral
-superficial sinospiral
-superficial bulbospiral
Which layer of the ventricle reduces the LV diameter, and constricts the lumen?
mid-myocardium : circumferential layer
Which ventricular muscle layers are perpendicular, oblique, and helical routes from the base to the apex
subendocardial and subepicardial layers
-shorten the longitudinal axis of the LV
-pulls the apex of the heart toward the base
-systolic “twisting” or “wringing” motion of the fibers
Which ventricle accomodates volume overload more easily?
right ventricle
low pressure right ventricle in mmHg
2-10 mmHg
o2 saturation of RV?
60-70%
atrioventricular valve
tricuspid
mitral
semilunar valves
pulmonary valve
aortic valve
What is the aortic valve located
right 2nd intercostal space
pulmonic location
left 2nd intercostal space
Erb’s point location
left 3rd intercostal space
Mitral location
left 5th intercostal medial to midclavicular line
palpable point of maximal impulse (PMI)
-point in the chest where impulse of LV is the strongest
-also apical impulse
-5th Intercostal space intercostal space
-midclavicular
PMI lateral or below 6th ICS can mean what?
ventricular enlargement
