HEMODYNAMICS 0.1

7/30/2019 HEMODYNAMICS 0.1

1/19

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


2/19

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


3/19

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


4/19

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)


5/19

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


6/19

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


7/19

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)

...


8/19

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


9/19

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


10/19

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

...


11/19

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


12/19

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


13/19

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

...


14/19

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


15/19

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


16/19

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

...


17/19

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

...


18/19

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


19/19

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

HEMODYNAMICS 0.1

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