hemodynamics 0.1
TRANSCRIPT
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1.________
fibers
innervates
arterioles
cause them to
constrict/relax
as needed tomaintain BP
on ______
receptors
- sympathetic
- alpha
2. 1. Increasing
heart rate via?
2. Decreasing
heart rate via?
1. SNS via beta 1 receptors
2. parasympathetic and muscarinic receptors
on SA node
3. 1. Isometric
Contraction
2. Isometric
Relaxation
1. closure of AV valves (S1) all valves are
momentarily closed, no change in
ventricular volume, ventricles contract and
stroke volume is ejected, sl ight backpressure
of blood flow closes the semi-lunar valves
(S2) 2. isometric relaxation occurs with all
valves closed, no change in ventricular
volume, diastolic filling occurs, when atria
pressure exceeds ventricles AV valves open
and Rapid filling period occurs, this is where
most of filling occurs first third of diastole
(S3) during last third, atria contract (S4)
4. 1. Principles of
Blood Flow
2. What are
factors
governing the
function of the
CV System?
1.- hemodynamics=blood flow
- heart is an intermittent pump, blood flow is
PULSATILE
2. Volume, Pressure, Resistence, Flow
5. 5 types of
Lipoproteins
- LDLs and
HDLs are most
important
- as density of
lipoprotein
increases,
proportion of
triglycerides
decreases and
proportion of
cholesterol
increases
6.ACE Inhibitor
Enalaprilat is
only one that is
used?
IV
7.ACE Inhibitors
all end in PRIL
- inhibits
converting
enzyme
- commonly used
1st treatment- cause FETAL
INJURY do not
use w pregnancy
8.ACE Inhibitors
prevents
angiotensin II
- vasodilation
- decrease blood
volume
- decrease
cardiac and
vascularremodeling
- potassium
retention
(hyperkalemia)
- fetal injury
Build up of
Bradykinin
- vasodilation
- dry cough
- angioedema
(rare swelling)
Control of CardiovascularStudy online at quizlet.com/_20dqz
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9. ACEI Adverse
Effects
- bilateral renal
artery stenosis is
contraindication
- dry cough due to
bradykinin build
up
- first dosehypotension-most
prominent
- teratogenic do
not use with
pregnancy
- angioedema due
to bradykinin
Drug Interactions
- Digoxin, Lithium
Potassium
sparing-
hyperkalemia,potassium intake-
hyperkalemia
10.ACEI and HTN
- initial=reduced
formation of
angiotensin II
- prolonged
thearpy=reduction
in BP
- may cause
hyperkalemia give
with potassiumsparing diuretics
- reduce RISK OF
CV MORTALITY
- recude RISK OF
RENAL FAILURE
in diabetics
...
11.Afterload
"RESISTANCE"
- the amount of
presure the hear
must develop
during the
period of
isometric
contraction toopen the aortic
and pulmonic
valves
- arterial
pressures are
major cources of
resistance
- disease of
aortic or
pulmonic valves
leads to increase
in resistancesuch as stenosis
and diastolic
hypertension
12.Aldosterone
Antagonist
- Spironolactone
- Epleronone
- some of the
potassium
sparing drugs
Promote sodium
and waterexcretion in the
collecting tubule
and duct
13.Algorithm for
Treating HTN
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14.Alpha 1
blockers/antagonists
- not first line due to
orthostatic HTN
- all end in "zosin"
- block alpha 1
receptor on
arterioles and veins
that prevent SNSmediated
vasoconstriction
leading to
vasodilation
lowering peripheral
resistance lowering
venous return to
heart
- sexual side effects
reason for
noncompliance
- used for benignprostethic
hypertrophy BPH
15.Angiotensin II
Receptor Blockers
(ARBs)
Adverse effects
- well tolerated
- do not cause cough
- angioedema
- fetal harm
- renal failure
Drug Interactions- hypotensive effects
- do not cause
hyperkalemia but
may with potassium
sparing diuretics
...
16.Angiotensin II
Receptor Blockers
(ARBs)
Used for:
- HTN
- Heart failure -
prevent progression- Diabetic
nephropathy
- Post MI
prophylaxis
- stroke prevention
...
17.ANS and RAAS
18.ANS regulation
of BP (just the
high control
part)
- Vagus nerve via
parasympathetic
sends impulses
to muscarinicreceptors on SA
node slowing
heart rate
- Sympathetic via
Beta-1 on
ventricular cells
increases
contractility
- Sympathetic via
Beta-1 AV node
increases speed
of conduction
19.Aortic valve
controls blood
flow from left
ventricle to
aorta.
Pulmonic valve
controls blood
from right
ventricle to
pulmonary
artery
Tricuspid valve
controls blood
from right
atrium into the
right ventricle
Bicuspid valve
controls blood
from left atrium
into the left
ventricle
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20.Atheromas tend
to develop at
sites of turbulent
flow near branch
points
- causes more
constriction and
more turbulent
flow
21.Atherosclerotic
Lesion
1. fatty streak
2. fibrous
atheromatous
plaque
3. complicatedlesions
1. thin, flat, yellow discolorations that
progressively enlarge by cecoming thicker
and more elevated, present in ch ildren
and precursors to atheromata
22.Atrial Kick
- last third of
ventricular
diastole
- gives
additional
thrust to
ventricular
filling
- important
duringtachycarda or
when heart
disease impairs
ventricular
filling
- S4 when
present, occurs
here
23.AV node
- connects atria
and ventricles
- one wayconduction
- speed
determined via
ANS
- can assume
back up of
pacemaker
- 40-60 bpm
- has a pause to
allow ventricular
filling
24. Baroreceptor
Reflex
- pressure
receptors that
keep blood
pressure
regulated to the
brain
- Located inaortic arch and
carotid artery
25. Beta Blockers
for anti-HTN (
end in OLOL)
- blockage of
cardiac beta-1
receptors lowers
HR, contractility
decreasing CO
- suppress reflex
tachcardiacaused by
vasodilators
- blockade of
beta-1 receptors
in JG cells in
kidney lowers
renin release
which decreases
RAAS causing
vasoconstriction
and volume
expansion- long term use
lowers
peripheral
vascular
resistence
- some block
both beta-1 and
beta-2
(nonselective)
- some have
greater affinity
for beta-1 than
beta-2 which is
cardioselective
- some are
partial agonists
(ISA)
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26. Biggest problem with
pharmacologic treatment of HTN
- COMPLIANCE
- lifetime treatment
- many have bad side effects
- expensive
...
27. Bile Acid Sequestrants
Cholestyramine, colestipol, and
colesevam
- biologically inert, insolule in
water cannot be absorbed from GI
tract, simply pass through the
intestine excreted in feces
- work by absorbing bile acids in
the intestine and keep them from
being reabsorbed into the blood,
creating a need for cholesterol (
using up what you have thereby
lowering LDL)
- 20% in one month
1. decrease acid
reabsorption in GI
2. increasing liver
synthesis
3. inreasing need for
cholesterol from
blood
4. increasing LDL
receptors
5. causing more LDL
to be consumed
28. Bile Acid Therapeutic Use
- reduce LDL
- with good diet may reduce LDL
by 15-30%
- with statin also reduce LDL by
50%
Adverse effects
- constipation
- bloating
- indigestion
- nausea
1. INTERACTIONS
Decrease absorption
of of many drugs so
take oral medication
1 hour before or 4
hours after the bile
acid sequestrant
29. Blood flow should
be Laminar not
Turbulent
30. Calcium Channel
Blockers
-
Dihydropyridines
- promote dilation
of arterioles lil
effect on veins
- decrease BP
- Non-dihydropyridines
- promote dilation
of arterioles, lil
effect on veins
- act on heart to
slow conduction
and decrease
contractility
31. Capillaries
- single cell-thick
vessels that
connect arterialand venous
segments
- wall composed
of single layer of
endothelial cells
surrounded by a
basement
membrane
- most vascular
beds,
fenestrations
allow passage of
water and small
molecules not
large proteins
- no smooth
muscles
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32. Cardiac Conduction System
- stimulates the myocardium to contract
and pump blood
- controls rhythm of heart
Heart has 2 conduction systems
- one controls atrial activity
- one controls ventricular activity
- impulse from atrial to ventricular via
A-V node
...
33. Cardiac Output = stroke volume x hear
rate
What are the components of stroke
volume?
1. preload -
ventricular
filling volume
2. contractility
- pumping
function of the
heart
3. afterload-
resistance to
ejection of
blood from
heart
34. Causes of Orthostatic Hypotension
- reduced blood volume (dehydration)
(reduced preload) this is the MOST
common cause of dizziness and fainting
especially in young
- drug induced
---impaired venous return: (reduced
preload) (calcium channel blocker)
---impaired baroreceptor (beta blockers,
alpha 1 blockers)
---diuretics (reduced preload)
- Aging, sluggish reflexes to includebaroreceptor
- bedrest - deconditioning
- disorders of ANS
...
35. Centrally Acting
Alpha-2 agonists
- Clonidine,
methyldopa
CHOICE FOR
chronic HTN in
pregnancy, not
for
preeclampsia- Act within
brainstem to
suppress
sympathetic
outflow to the
heart and blood
vessels
increasing
vasodilation
lowering CO and
BP
- cause drymouth, sedation,
hemolytic
anemia, liver
disorders
- rebound
hypertension if
abruptly
stopped
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36. Cholesterol Absorption Inhibitors
Ezetimibe (zetia)
MOA: acts on cells in brush border of
intestine and inhibits cholesterol
absorption, blocks absorption of
dietary cholesterol and cholesterol
secreted in bile
- lowers total cholesterol, LDL, TG
and raises HDLs- used as adjunct to diet modification
- used solo or with statin but may
make plaques worse
DRUG INTERACTIONS
- statins increase
risk of liver
damage
- fibrates also
increase
cholesterol in the
bile increasing
risk for gallstones
- bile acidsequestrants
impair the
absorption of
Ezetimibe
- cyclosporine
inhibits
metabolism of
ezetimibe and
increasing its
concentration
37. Classification of Diuretics
- Thiazide- High-ceiling loop
- potassium sparing
- osmotic diuretics
ALL DIURETICS indirectly prevent
the reabsorption of water in the
kidneys which DECREASES
PRELOAD
...
38. Classification of
LDL, Total, and
HDL
39. Clinical
Manifestations
of Vascular
Disease
40. Consequences of
HTN- long term
targets others
organs
- accelerates
atherosclerotic
vascular disease
- Heart, LV
hypertrophy,
coronary artery
disease
- Brain, stroke
or TIA- Chronic kidney
disease
- Peripheal
vascular disease
- Retinopathy
(blindness)
...
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41. Contractility
- ability of theart
to change its
force of
contraction
- strongly
influenced by
number of
calcium ionsthat are
available to
participate in
the contractile
process (actin
and myosin
interactions)
- activation of
beta-1 receptors
in the ventricles
by
norepinephrineincreases
availability of
calcium ions
...
42. Definitions
1. thrombus
2. embolus
3. stenosis
4. mural
1. clot
2. clot that breaks off from its initial
location and travels
3. narrowing or closeing off of a vessel
4. wall like clot
43. Determinants of
Blood Pressure
BP = CO x
PeripheralVascular
resistance
CO = SV x HR
What
determines
peripheral
vascular
resistance?
44. Determinants of
Blood Pressure
BP= CO x
Peripheralvascular
resistance
CO= SV x HR
...
45. Diagnosis of
HTN
- repeated BP
measurements
of average of > 2
readings taken
at > 2 visits after
an inital
screening visitover several
months
- laboratory
tests, x-rays
looking for
target organ
damage
...
46. Differences in
the 2 systems
1. Pulmonary
2. Systemic
1. low pressure system (12 mmHg), good
for gas exchange
2. high pressure system (90-100 mmHg),
good for distant transport against gravity
47. Drugs Acting on
RAAS
48. Drugs that affect
BP:- sympatholytics
-
antiadrenergics
49. ECG
Note: electrical
events PRECEDE
mechanicalevents
- P
- QRS
- T
- can have EKG
but no
contraction
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50. Endothelial
control and
smooth muscle:
What causes
vasodilation?
What causes
vasoconstriction?
- nitric oxide
- angiotensin II, prostaglandins,
endothelins
51. Fibric acid
derivatives
Adverse effects
- gallstones
- myopathy
- hepatotoxicity
- becaue of
overlapping
adverse effects,
the combo of
statin and fibric
acid derivative
should be used
with cautionDrug
Interactions
- Warfarin efficacy increased
- Statins increase risk of myopathy
52. Fibric Acid
Derivatives
(Fibrates)
Gemfibrozil +
Fenofibrate
- increase
lipoprotein lipase
decreasing
VLDLs and
increasetriglyceride
storage in
adipose storage
decreasing serum
triglycerides
- raises HDL
- no effect on
current LDL in
blood
...
53. Functional
anatomy of
Heart:1. endocardium
2. myocardium
3. visceral
pericardium
(epicardium)
4. pericardial
cavity
5. parietal
pericardium
6. fibrous
pericardium
54. HDL (scavenger of waste lipids)
- GOOD cholesterol
- carries cholesterol FROM tissues
TO liver
- high HDL prevents atherosclerosis
- HDL inhibits uptake of LDL into
cells
- exercise and moderate ETOH
increase HDL- smoking, diabetes or metabolic
syndrome decreases HDL
...
55. Heart Rate
- if HR increases CO increases
- HR increased via beta-1 and
decreased via muscarinic receptors
on SA node
- as HR increases diastolic filling
decreases
- tachycardia can be dangerous
because the heart may not have time
to fill adequately
...
56. How do diuretics decrease blood
pressure?
act on renal
tubules to promote
water excretion
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57. How does blood
get back to the
heart?
58. Hyperlipidemia
(high blood
lipids)
- insoluble in
water but soluble
in alcohol
Three biological
types1. triglycerides -
source of energy
2. phospholipids
- structural
component of
lipoprotein,
clotting
components,
myelin sheath,
cell membranes
3. cholesterol -
basis of steroid
hormones and
important cell
membrane
component
lipid transport particles
59. Hypertension
- common health problem in adults
- leading risk factor for
cardiovascular disorders (MI,
heart failure, stroke, vascular
disease)
- more common in young men than
women, blacks than whites, in
persons from lower socioeconomicgroups with increasing age, more
obese
- diabetics are more likely to have
hypertension and it is more likely
to lead to cardiovascular disease
than in nondiabetics
...
60. Hypertensive Emergencies
Symptoms of actual or impending
end organ damage
(systolic > 200 or
diastolic > 120)
Neurological
- hypertensive
encephalopathy
- CVA or cerebralinfarction
- subarachnoid
hemorrhage
- intracranial
hemorrhage
Cardiovascular
- MI
- acute left
ventricular
dysfunction
- acute pulmonary
edema- aortic dissection
Other
- acute renal
failure/insufficiency
- retinopathy
- eclampsia
(pregnant seizures)
- microangiopathic
hemolytic anemia
61. Implications of Afterload/CO curve
- In normal healthy people,
PRELOAD is important- In heart failure people,
AFTERLOAD is important
...
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62. Implications of Frank
Starling Law
- at normal volumes, as
preload increases, stretch
increases, which increases
contractility
- CO goes up becuase
increased volume and
increased contractility- increase in contractility is
INDEPENDENT of the SNS, it
is an INTRINSIC property of
heart
- at high volumes, cardiac
muscles is overstretched and
contractility decreases
...
63. LDL (primary or secondary)
- family defects in LDL
receptor called familial
hypercholesterolemia
- inadequate or defectivehepatic uptake of LDL
allowing more to circulate in
the blood and cause build up
- receptor disease
1. Diagnosis and Screening
1. all adults 20 years of
age and older should have
a fasting lipoprotein
profile done every 5 years
- total cholesterol, LDL,HDL, TG
64. Lifestyle risk factors for
Hypertension
- diet high in sodium and
saturated fats
- obesity
- physical inactivity
- excessive alcoholconsumption
- oral contraceptives in
predisposed women
...
65. Lipid lowering Drugs
1. affect cholesterol
production by liver
2. remove cholesterol from
blood
3. increase LDL receptors
4. decrease cholesterol
absorption
5. decrease intravascularconversion of VLDL and IDL
to LDL
...
66. Long-term
Regulation of BP
- primarily
controlled by
kidneys
- nueral
mechanisms act
rapidly, but can't
maintain theireffectiveness
over time
- kidneys control
in long term is
through
regulation of
sodium and H2O
balance via:
--- RAAS
--- Vasopressin
...
67. Loop Diuretics -
Furosemide(Lasix)
- prevent the re-
absorption of
sodium from
ascending loop
of HENLE
- second-line
diuretic for HTN
- used for
pulmonary
edema
w/congestiveheart failure
- promotes
diuresis in renal
impairment
Adverse Effects
-
HYPOKALEMIA,
Orthostatic
hypotension,
Ototoxicity
Drug
Interactions
- Digoxin,
nitrates, lithium,
NSAIDS
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68. LV hypertrophy
is major risk
for?
ischemic heart disease, dysrhythmias,
heart failure, sudden death
69. Managment of
Atherosclerosis
- reduction in
LDL is
PRIMARY target
especially in
cardioheart
disease
- atheromatous
changes can
regress
- dietary changes
- lifestyle
changes
- meds
...
70. Mechanisms of
BP Regulation
- arterial
pressure must
remain relatively
constant as
blood flow shifts
from one area of
body to another
- method by
which arterial
pressure is
regulated
depends on
whether short-
term or long-
term adaptation
is needed
- ANS=short term
- RAAS=longer term
- kidneys= control blood volume as well
as the RAAS (renin-angiotensin-
aldosterone system)
71. More Calcium
Channel
Blockers used
for hypertensive
crisis
1. Fenoldepam
2. Nicardipine
3. Clevidipine
All cause
________ and
________
1. long half life
2. long half life
3. shor half life, easy to titrate
reflex tachycardia and hypotension so
give beta blocker
72. Neurotransmitters
Review
73. Nicotinic Acid
(Niacin)
- decreases
production of
VLDLs by
inhibiting lipolysis
in adipose tissue
reducing LDL
Effect on plasma
lipoproteins
- reduce
triglycerides (20-50%) LDLs (5-
25%)
- raises HDL (15-
33%)
- DRUG OF
CHOICE to lower
triglycerides in
pancreatitis
patients
- triple therapy
(w/statin+bile
acid) decrease
LDL 70%
- also a vitamin B
but doses are small
than as a lipid-
lowering drug
ADVERSE
EFFECTS
- intense flushing (use ASA)
- GI upset
- Hepatotoxic
- hyperglycemia
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74. Nifedipine and Amlodipine
- dihydropyridines
- calcium channel blocker
- dilation of peripheal vessels
decreasing BP
- dilation of coronary
arteries increasing perfusion
- DO NOT BLOCK CARDIAC
calcium at therapeutic dosesINDIRECT EFFECTS
- lowering BP stimulating
baroreceptor reflext to
increase firing of SNS to
beta receptors for
compensation in the heart
- can lack direct
cardiosuppressant actions
and increase HR and
contractility, you canprevent this by also g iving
beta blocker
- net effect is sum of direct
effect vasodilation and
indirect effect of (reflex
cardac stimulation)
75. Nifedipine and amlodipine
USES
- angina pectoris
- HTN
---Essential HTN
---Nifedipine only usesustained release for HTN
---Amlodipine has longer half
life and no sustained release
ADVERSE EFFECTS
- flushin, dizziness,
headache, edema
- gingival hyperplasia
- constipation
- does not make conduction
abnormalites worse- does cause reflex
tachycardia (give beta
blocker)
76. Nifedipine blocks calcium
channels in arterioles, this
results in?
dilation of peripheral
vessels
77. Orthostatic Hypotension
- abnormal drop in BP on
assumption of the standing
position
- defined as a drop in systolic
pressure of > 20 mm Hg or
drop in diastolic pressure >
10 mm Hg when going from
lying to standing
- in absence of normal
circulatory reflexes and or if
blood volume is decreased,
blood pools in lower part of
the body when the standing
position is assumed
(decreased venous return),
CO decreases and blood flowto the brain is inadequate
causing dizziness or syncope
78. Osmotic
Diuretics -
Mannitol
- given
parenterally
- used for
prophylaxis of
renal failure,
reduceintracranial
pressure,
increased intra-
ocular pressure
- increases
osmotic
pressure of
blood drawing
edema into
vascular system
- filtered into
glomerulus,holding excess
water in renal
tubules
Adverse effects
- Edema,
dehydration,
orthostatic
hypotension
No Drug
interaction, not
metabolized
(inert)
79. Perfusion of
Organs
- regulated
minute to
minute basis
- neural
mechanisms
regulate CO and
systemic
vascular
resistance (BP)
to support local
mechanisms
- local control
includes
preferential
vasoconstriction
or vasodilation
mediated by the
SNS or by
intrinsic
mechanisms
within the organ
...
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80. Pericardial Effusion ? virtual space filled
with lubrication but
can be filled with
fluid or blood
81. Potassium-Sparing
(Spironolactone)
Used for:
- HTN, Edema, commonly used
with combo therapy (thiazide or
loop)
-effects are delayed
Adverse effects
- HYPERkalemia, avoid
potassium intake
- synergistic with ACE inhibitors
and ARBs
- has steroid structure causing
gynecomastia, impotence,
mentrual irregularities,
hursutism, deep voice
Drug interactions- potassium supplements or salt
substitutes
- ACE inhibitors or ARBs
exacerbate kyperkalemia
...
82. Potassium-Sparing (Triamterene)
- used with thiazide
Adverse effect
- HYPERKALEMIA, avoid
potassium intake
Drug interactions
- ACE inhibitors, ARBs, NSAIDS
blunt effect precipitate renalfailure, take after meals in AM
...
83. Potassium-
Sparing
Diuretics
- prevent re-
absorption of
sodium from the
collecting tubule
and duct
84. Pre-Clinical
Phase
85. Preload"VOLUME"
- represents the
volume of blood
the heart must
pump with each
beat
- largely
dtermined by
venous return
and stretch of
muscle fibers
- venous return -
64% blood
volume in veins
and mediated by
alpha 1
receptors SNS
86. Pulmonary and
Systemic
Circulation
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87. Purkinje Fibers
- supply the
ventricles
- large fibers, rapid
conduction, efficient
ejection of blood
from heart
- back up to the back
up pacemaker- 15-40
88. RAAS
89. Recommended
drugs for initial
therapy with high-
risk comorbid
conditions
90. Renin Inhibitor
- prevents all
activation of the
renin-angiotensin
aldosterone system
- only one drug
(Aliskiren) use as
monotherapy or
combination with
hydrochlorothiazide
...
91. Risk Factors of
Atherosclerosis
- Age (men>45,
women>55,
premature
menopause)
- family history
(MI before 55 of
father or 65 inmother)
- SMOKING
- HTN
- hyperlipidemia
(low HDL or
high LDL)
- Diabetes
Blood tests
- CRP is marker of inflammation if they
have no other factors and can be better
than LDL
- Homocysteine inhibits coagulation
- Serum Lipoprotein part of LDL promotes
foam cells
- Infections agents like chlamydia
pneumoniae
92. Risk factors of
Hypertension
- family hx
- age relatedchanges
- insulin
resistance,
metabolic
syndrome,
diabetes
- race (blacks are
highest risk)
...
93. SA node
- pacemaker
- impulses
originate here- located in
posterior wall
RA
- 60-100 bpm
- rate
determined by
ANS (beta-1
increase,
muscarinic
decrease)
94. Sensory
components ofthe
Baroreceptor
Reflex
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95. Sodium
nitroprusside
(nitropress)
- powerful arterial
vasodilator use in
hypertensive crisis
(short half life)
- no reflex
tachycardia- can overshoot
hypotension but can
be slowed
- titrate to blood
pressure, BP check
frequently
Adverse Effects
- cyanide poisoning with liver issues,
avoid prolonged rapid infusions
- thiocyanate toxicity likely when
drug given over days, CNS effects,
avoid infusions > 3 days, monitor
plasa thicyanate
96. Stages of
Hypertension
1. prehypertension
2. hypertension
stage I3. stage II
4. stage III
1. 120-139/80-89
2. 140-159/90-99
3. 160-179/100-109
4. >180/>110
97. Statin Side Effects
- myopathy
- rhabdomyolysis
(break down of
muscle, kidney
failure)
- hepatotoxicity,
monitor every 6-12
months, avoid use
for patients withviral, alcohol
hepatitits
1. Drug Interactions
1. Fibrates and ezetimibe also lower
cholesterol causing myopathy
2. inhibitors of cytochrome P450 like
ketoconazole, erythromycin, HIV
protease inhibitors inhibit the
metabolism of statins and raise blood
levels increasing the risks and
toxicity
98. Statins Beneficial
Actions:
- increase LDL
receptors (most
important)
- reduce cholesterol
synthesis in liver
- decrease LDL
levels- increase HDLs
- decrease TG
- results within 2
weeks, max 4-6
weeks
...
99. Statins Cardiovascular actions:
- reduce inflammation at plaque sites
- improve endothelial cell function
- enhance blood vessel dilation
- reduce risk of thrombus
Increase bone formation
- enhance osteoblast activity reducing
osteoporosis and fractures
...
100. Statins: Therapeutic Uses
(antiinflammatory)
- hypercholesterolemia
- prevention of cardiovascular events
Diabetes
ADA- prefer pts >40 years with total
cholesterol >135 regardless of LDL
ACP- all patients with type 2 diabetes with
coronary artery disease regardless of
cholesterol level
...
101. Terms to Know
- CO, amount of blood the heart pumps per
minute
--- 3.5 to 8.0 L/minute
- SV, amount of blood the heart pumps
each beat
--- 70 mL/beat
...
102. The heart, brain, liver, and kidney
require?
Skin, skeletal muscle require?
- large
continuous
flow
- varying
flow
103. Therapeutic use of ACEI
- HTN- Heart Failure
- protect effects in diabetic nephropathy
- post MI prophylaxis
- prevent MI, stroke and suddent death
...
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104. Thiazides:
hydrochlorthiazide
& chlorthalidone
- used for Essential
HTN, often first
drug used and can
be used as part of
multiple therapy
- used for edemaAdverse effects
- HYPOKALEMIA
(low potassium),
orthostatic
hypotension
(dehydration)
Drug Interactions
- Digoxin (toxicity),
Lithium
(contraindicated),
NSAIDS (reduce
effects)105. Time table of
Atherosclerosis
- takes time usually
4th decade
- progression can
be slowed by
controlling lipids
and exercise
- MI are occuring
later in life now
- can also be
accelerated(obesity)
106. Tissue factors and
local control:
What increases
blood flow?
What decreases
blood flow?
- histamine
- serotonin
107. Total of 5 liters of
blood in a person
- 4% heart
- 16% arterioles
- 4% capillary- 64% veins blood is
stored here
108. Treatment for
Orthostatic
Hypotension
- alleviating the
cause: rehydrate,
change meds
- help cope with
disorder, prevent
falls, injury---gradual
ambulation
---avoid venodilation
(alcohol, exercising
in warm weather)
---maintain
hydration
...
109. Treatment of HTN
- LIFESTYLE
modification is
FIRST LINE
treatment, weightloss, exercise, diet,
less sodium,
moderate alcohol
- pharmacologic
treatment
- GOAL is to achieve
and maintain
systolic BP below 140
mm Hg and diastolic
BP below 90 mm Hg
110. Two types of
Hypertension:1. Primary
2. Secondary
1. a lso called Essential
Hypertension, chronic elevation ofBP without evidence of other
diseases, 90-95% of cases
2. Elevation of BP occurs from some
other disorder such as kidney
disease, chronic renal failure,
disorders of adrenocorticoid
hormones, comorbidity
111. Vascular damage of
HTN
- coronary arteries
lead to MI
- peripheal bloodvessels causing
peripheal vascular
disease
- kidney causing
renal failure
- cerebral blood
vessels leading to
stroke
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112. Vascular
Smooth Muscle
and SNS
1.
norepinephrine
2. beta-2 via
epinephrine
3. calcium
4. calciumblocker
1. activated alpha receptors cause calcium
channels in vascular smooth muscle to
open which produces vasoconstriction
2. beta 2 promote vasodilation by
decreasing calcium
3. calcium causes contraction
4. calcium blockers prevent
vasoconstriction
113. Vasopressin
(Antidiuretic
Hormone ADH)
114. Veins, Venules
- collect blood
from capillaries,
carry back to
heart
- enlarge and
store large
quantities of
blood
-
contract/expand
to accomodate
varying amounts
- innervated by
SNS (alpha
receptors)
- Venous
constriction can
increase the
preload to the
heart by
conducting
stored bloodinto the vena
cava
115. Verapamil
- calcium
channel blocker
in arterioles,
heart
- dilation of
peripheral
vessels,
decrease BP- dilation of
coronary
arteries,
increase
coronary
perfusion
- blockade at SA
node, decrease
HR
- blockade at AV
node, decrease
conduction- blockade in
myocardium,
decrease
contractility
- used for
angina pectoris,
HTN,
dysrhythmias
Side Effects
- constipation, decrease in contractility
has affect on GI also
- dizziness, facial flushing, headache,
edema of ankles, feet, why? if you dilate
veins will cause pooling of blood in feet
and means it is not getting to head
-Bradycardia due to slowing of SA node
and conduction defects due to AV node
116. Volume and
Pressure
DistributionArterioles
which are
innervated by
the sympathetic
system and
alpha receptors
and
constriction
determines the
pressure of the
rest of the
system
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117. What are 3
layers of blood
vessels
Intima - elastic layer
Media - smooth muscle
Externa - fibrous and connective tissue
for support
118. What are the
major resistance
vessels for thecirculatory
system and
determine
systemic
vascular
resistance?
Arterioles
119. Which Beta
Blocker would
athletes prefer to
use?
Beta blockers are
not used for?
- Pindolol
- stage fright
120. Which drug are
insoluble in
water, cannot be
absorbed from
GI and passed
through the
intestine?
Bile acid sequestrants
121. Which drugs has
been shown to
reverse
athrosclerotic
changes?
statins
122. Which is an
important
determinant of
cardiac output
in NORMAL
person?
person with
heart failure?
- preload
- afterload
123. Why are increased blood lipids bad?
- can cause atherosclerosis
- increase risk of clot formation
- occluded arteries can cause MI,
stroke, and peripheral vascular
disease
- lead to arteriosclerosis (hardening of
artery)
- increase risk of aneurysms1. Atheros
2. Sclerosis
3. Atheromas
1. glue/paste
2. hardening
3. formation of
fibrofatty
lesions