NURS216A Perfusion

what is cardiovascular disease closely linked to?

diet (people underestimate caloric intake)

Basic metabolic Rate (BMR)
1. claculate
2. Who should stick to BMR?

1. 10cal/lb
2. patients who are trying to lose weight

Most common cause of high blood pressure

idiopathic

3 elements of Blood Pressure

1. Blood volume
2. Peripheral resistance.diameter of arterioles
3. Cardiac output

Elements of Blood volume

Fluid loss
- dehydration
Fluid retention
- aldosterone
- ADH

Elements of Peripheral resistance.diameter of arterioles

- sympathetic nervous system activity
- renin.angiotensin II
- increase in blood velosity

Elements of Cardiac output

stroke volume
- preload
- contractility
- afterload
Heart rate
- sympathetic nervous system
- parasympathetic nervous system
- epinephrine

Normal blood volume in adults
Normal blood volume in pediatrics

adults: 5-6L
pediatrics: 80mL/kg

blood stasis is a risk for

blood clotting

blood pressure expected findings
BP, MAP, CO

BP = 120/80 mm/Hg
MAP = 70 - 100 mm Hg
CO = cardiac output = HRxstroke volume = 70x70%

CPP = MAP - ICP

CPP - cerebral prefusion pressure (pressure required for constant flow to brain)
- minimum ; 55-60 mmHg

MAP = Mean Arterial Pressure
- 70-100 mm Hg

ICP = intracranial pressure (exerted by brain fluids; CSF, blood)
- 5-15mmHg (adults)

SBP over 180mmHg

emergency, treat immediately (risk for bleeding)

graph BP, 24 hr assessment

SBP over 135

Treat cause

3 types of hypertension

1. Essential HTN (idiopathic)
2. Secondary HTN
3. Sudden onset HTN

Essential HTN (idiopathic): Factors

-Age
-Ethnicity/Genetics (fam. hx)
-Gender
-Lifestyle: diet, sedentary (abdominal obesity), smoking, excess alcohol,...

Essential HTN (idiopathic): Tx and BW

Tx: collect data; focus on modifiable risk factors; tx BP PRN & titrate to effect; BW (blood work)

BW: glucose, electrolytes, creatinine (calculate clearance), cholesterol, lipids

Lifestyle changes recommended for people with HTN

diet
- lower sodium intake
- lower lipids and cholesterol

lifestyle
- 30-60 mins exercise
- no smoking
- less than 2 drinks a day

Physical
- abdominal obesity ( men usually store fat in this region, also women after menopause )
age and gender
men: over 102cm
women: over 88cm

How does age affect HTN? Tx for this?

Age causes decreased:
- elasticity of vessels
------=increased PVR (peripheral vascular resistance) = can't respond to blood pressure changes
-------= increase in fibrosis of intima layer tries to compensate for low elasticity of inside
- renal blood flow
- sensitivity to baroreceptors

Tx: titrate meds to effect
- monitor for orthostatic hypotension --risk of falls (over age of 60)

what is orhostatic hypotension

drop of SBP > 20 mmHg or DBP >10

cause of orthostatic hypotension

caused by venous pooling in lower extemities
- transient (compensated once baroreceptors intervene - but slow to intervene in elderly

signs and symptoms of orthostatic hypotension

faintness.dizziness (decreased CNS perfusion)

who is at risk for orthostatic hypotension

elderly
dehydrated or fluid restricted patients
antihypertensive medication patients

what is the tx for orthostatic hypotension

titrate drugs; adrenergic agonists if ER

Secondary HTN; causes and tx

causes:
- organ disease: e.g. diabetes, renal, adrenal, congenital defects
- pregnancy (gestational HTN)

tx:
BW, treat cause, tx BP

Gestational HTN (preeclampsia): explanation and tx

> 20 weeks gestation
inflammatory etiology (immune) theory
=> inflammatory cytokine release => endothelial changes => at risk for: clotting (to fix damage)
=> organ damage + placental flow compromise; + risk of DIC: clotting & thrombocytopenia


tx: sodium restriction, antihypertensive meds

what normally happend to blood volume (BV) during pregnancy?

it increases by 50%

Sudden onset HTN

sudden change of >20 mmHg

causes to asses for Sudden onset HTN; tx

Pain? (most often clinical setting)
Infection?
No voiding? (opioids cause urinary retention burst bladder)
Compensation for changes?
Hypervolemia?
Hemorrhage?
Drug induced?
e.g. stimulants: adrenergi agonists (cocaine), sympathomimetics,...

tx: treat the cause, tx BP PRN

SBP>180 =
tx

malignant HTN = medical emergency
tx: medications

Malignant HTN effects (BARKH); tx

severe uncontrolled high BP causes evidence of HT-mediated organ damage in vital organs
Brain
- stroke (ischemic or hemorrhagic)
- hypertensive encephalopathy
Arteries
- acute aortic syndromes
- preeclampsia
Retina
- grade III-IV Keith-Wagener-Barker retinopathy)
Kidney
- acute renal insufficiency
- thrombotic microangiopathy
Heart
- acute heart failure
- pulmonary edema

tx: drugs chosen according to BARKH; reduce HTN gradually so not to cause reverse effects (e.g. reflex tachycardia)

Malignant HTN = hypertensive crisis = emergency tx
Name the drug class and drugs
MOA
Side effects

Drug class = Direct Acting Vasodilators

Drugs:
- Nipride (Nitroprusside); IV/ET
- Hydralazine; PO/IV
----IV t1/2 = 2 mins

MOA:
stimulates endothelial cell-produced NITRIC OXIDE
: acetyl-choline stimulates PNS (binds to G protein receptor) -- produceing nitric oxide (enzymaticly converted from argenine) -- travels to smooth muscle cell causing muscle relaxation (dialation o blood vessels)

POTENT = not long-term tx

S/E: reflex tachycardia; hypertension, syncope, headache

HTN tx med classes (5)

1. Direct acting Vasodilaotrs (ER use mainly)
2. Diuretics
3. Renin-Angiotensin drugs
4. Calcium channel blockers (decrease CO)
5. Adrenergic agents (decrease vasocontriction and CO)

Diuretics info

= increase urine output = decrease cirulating blood volume = lower BP = lower H2O and electrolytes

- 1st line in HTN tx
- 4 types

S/E
- dehydration
- hyponatremia
- hypokalemia (thiazide, loop diuretics)
- hyperkalemia (potassium-sparing diuretics)
- nocturia (if taken too late in day)

4 types of diuretics

1. loop diuretics
2. thiazides
3. Potassium sparing
4. Osmotic

Diuretics: Loop diuretics ('high ceiling')
MOA, drug name, and S/E

Loop of Henle:
- Blocks Na+, Cl-, K+ re-absorption = increased Na, K, Cl, out = brings water out too

Drug: furosemide (Lasix)
- first line therapy for hypertension
-POTENT
-IV, PO

S/E
- hypokalemia, ototoxicity (reversible?); drug interactions (high PPB)

Diuretics: Thiazides
MOA, drug name, and S/E

Distal convoluted tubule
- decrease in re-absoption of Na, Cl, K = increased Na, K, Cl out = brings water out

Drugs:
-hydrochlorothiezide (HZTZ)
- chlorothiazide (Diuril)
- metolazone (Zaroxolyn)

S/E
- hypokalemia!

Diuretics: Potassium sparing (aka Aldosterone antagonists)
MOA, drug name, and S/E

Collecting distal tubule:
- antagonizes renal aldosterone = increases Na+ out and K+ in
--------normally aldosterone causes Na retention

Drug:
spironolactone (Aldactone)

S/E:
hyperkalemia
---long t1/2 (1-2 days)

Which foods should be avoided with potassium sparing diuretics, to avoid complications?

leafy greens, beans, nuts, dairy, banadas, starchy vegetables, borcolli

Combination meds: diuretic combo

Thiazide and K+ sparing combination:
Aldactazide

- used very frequently
- balances out K+
- PO admin
- Excellent mainenance therapy for HTN

Diuretics: Osmotic
drugs, MOA
tx

Drugs:
- mannitol (Osmitrol),
- Isosorbide

MOA:
high solute, travel unchanged
pulls water into circulation & into renal tubules (Proximal tubule & Loop of Henle)
inhibit 'Renin' release

tx:
- cereral edema
- intraocular hypertension
- low use for CV

how do you know the drugs are effective?
what would you asses?

Asses: vital sings, pain, pulses (bounding =HBP?), peripheral edema (diff. than cerebral edema), BP goes down, assess eletrolytes

BW to check kidney fxn

BUN and Cr

'Angiotensin-converting enzyme' inibitors (ACE) Inhibitors
MOA, drug name, and S/E

- Inhibit ACE => vasodilate
- potent; titrate to effect!
1st line dugs in heart failure (high efficacy)

Drugs: '-prils'
- enalapril (Vasotec)
- Captopril
- Monopril
- Rampril (Altace

S/E:
- severe hypotension

'Angiotensin II receptor blockers' (ARBs)
MOA, drug name, and S/E

MOA: angiotensin II receptors antagonized
decreased afterload => decreased preload
slow onset of action (a few weeks to full effect)

Drugs:
- Losartan (Cozaar)
- Ibesartan (Avapro)

S/E:
- hypotension

****great for heart failure pts bc heart pump is tired
deploy ACE inhibitors, then transition to ARBs

Synergy combo meds ARB:

Thiazide diuretic + ARB
Brand name drugs: Hyzaar; Cosart

Calcium Channel Blockers
MOA, drug name, and S/E

MOA:
- Muscle contraction regulated by calcium (Ca 2+ enters cell = contraction initiated)
- Ca2+ influx blocked = muscle relaxation

Drugs:
1. vascular-selective: smooth muscle
---Nifedipine (Adalat)
---Amlodipine (Norvasc)
2. cardio-selective: cardiac muscle (myocardial cells)
---Verapamil (Isoptin)
---Diltiazem (Cardizem)
-------Tx of arrhythmias: Atrial Fibrillation

Overall effects of Calcium Channel Blockers on cardiac

Overall:
↓ heart rate (cardio-s.)
↓ cardiac output (cardio-s.)
optimize cardiac contractions
↓ blood pressure (smooth-s.) = lower afterload

Herbal notes: Ginseng

'Calcium channel antagonist'
- herbal (NHP)
- therapeutic dose: 20-30 mg/day

Adrenergic antagonists/'blockers'

- most body parts have PNS & SNS innervation
- only SNS: adrenal medulla, arrector pili muscles, sweat glands, some blood vessels
- alter a lot more than just BP

Adrenergic antagonists/'blockers'
MOA

MOA: antagonize the sympathetic nervous system at various adrenergic receptors => decrease catecholamine activity

Normal fxn of Alpha 1 Receptors

- Cause vasoconstriction (increased peripheral resistance)
- Pupil dilatation
- Increased closure of the internal urinary sphincter
- Secretions

Normal fxn of Alpha 2 Receptors

- Vasoconstriction of arteries
- Vasoconstriction of veins
- Decreased GI motility
- Decreased smooth muscle motility
- Contraction of male genitalia during ejaculation

Adrenergic antagonists/'blockers'
Drugs: Alpha 1 and 2 antagonists

Prazosin (alpha 1)
Phentolamine (alpha 1 and 2)

Normal fxn of Beta 1 Receptors

- Cardiac muscle- Increased myocardial activity and increased heart rate
- AV node conduction

- antagonise to calm down cardiac activity (high HR, arythmia)

Normal fxn of Beta 2 Receptors

- Smooth muscles in blood vessels, bronchi, in the periphery
- Stimulation leads to vasodilation/bronchodilation!!!
- Increased muscle and liver breakdown of glycogen and increased release of glucagon from the alpha cells in the pancreas

CONTRA: ASTHMA

Adrenergic antagonists/'blockers'
Drugs: Beta 1 and 2 antagonists

Atenolol (beta 1)

Propranolol (beta 1 and 2)

Metroprolol (beta 1 and high doses effect beta 2)
- highly used for rescue, and after myocardial infarctions

Synergy combo meds: w/ adrenergic antagonist

Diuretic (thiazide) + adrenergic antagonist
Med: Lopressor HCT

'Centrally acting alpha2 adrenergic agonists'
MOA, drugs, tx, S/E

MOA: stimulate (agonise) CNS's negative feedback mechanism at alpha 2 receptors (vasomotor center) => inhibits release of norepinephrine (NE) => decreased sympathetic tone

Drugs: Clonidine; Methyldopa

Tx: resistant HTN

s/e: hypotension, headache

Failure to control HTN can...

damage small blood vessels, leading to
accelerated narrowing of the arteries that can result in angina,
myocardial infarction (MI), and peripheral vascular disease

One of the most serious consequences of chronic HTN is

heart must work harder to pump blood to organs and tissues = excesive cardiac overload can cause heart to fail and lungs to fill w/ fluid = heart failure

damage to the vessels that suply blood and oxygen to the brain can result in

transient ischemic attacks and cerebral ascular accidents or strokes
*renal damage and retinal damage also consequences of sustained HTN

blood pressure is regulated by

vasomotor centre in medulla oblongata: nerves travel from vasomotor centre to arteries -- smooth muscle in arteries either contricts or relaxes

regulation of blood pressure by potent vasoconstrictors

Potent vasoconstrictors, such as angiotensin II and endothelin,
and potent vasodilators, such as nitric oxide and vasodilator pros-
taglandins, that are released in the vascular endothelium exert
local effects on blood pressure

regulation of blood pressure by receptors in aorta and internal carodid artery

receptors in aorta and internal carotid artery are sensors to provide vasomotor centre w vital info on vascular system
- baroreceptors sense pressure w/in large vessels
- chemoreceptors recognize pH and O2/CO2 levels in blood
- vasomotor centre reacts to info from baroreceptors and chemoreceptors

effect of emotions on BP

emotions:
anger and stress = BP rise
depression and lethargy = BP lowers

regulation of BP by hormones

Hormones
- epinephrine and norepinephrine = immediate rise in BP
- ADH = potent vasoconstrictor; increase BP by raising blood volume
- renin-angiotensin-aldosterone system (RAAS)

diuretics are often 1st line meds for HTN because...

they have few side effects and can control minor to moderate hypertension
***often prescribed with other antihypertensive drugs

How can diuretics cause orthostatic hypotension?

Diuretics decrease circulating blood volume, which can cause dehydration and hypovolemia

How do Calcium channel blockers (CCBs) treat hypertension?

by blocking calcium ions from entering cells and cause smooth muscle in arterioles to relax = lowers peripheral resistance

How do drugs blcoking the renin-angiotensin-aldosterone system treat HTN? (2 ways)

1. by preventing the intense vasoconstriction caused by angiotensin II, and by decreasing blood volume (ACE inhibitors)
2. blocking the action of angiotensin II after it is formed (angiotensin II receptor blcokers)

renin

an enzyme secreted by kidney when BP is low or Na+ is low in kidney tubules

once in blood, renin converts inactive liver protein angiotensin to angiotensin I

when passing through the lungs, angiotensin-converting enzyme (ACE) converts angiotensin I is converted to angiotensin II = one of the most potent natural vasoconstrictors

angiotensin II causes intense vasoconstriction of arterioles caused

anguitensin II stimulates the secretion of these two hormones

aldosterone and ADH

aldosterone

hormone from the adrenal cortex
increases sodium reabsp. , helps body retain water
increases blood volume and pressure

ADH

hormone from the posterior pituitary
enhances the conservation of water by the kidneys
increases blood volume and pressure

how do ACE inhibitors treat HTN?

inhibits angiotensin-converting enwyme = block the effects of angio-
tensin II, decreasing blood pressure through two mechanisms:
lowering peripheral resistance and decreasing blood volume

How to ARBs treat HTN?

block receptors for angiotensin II in arteriolar smooth muscle and in the
adrenal gland, thus causing blood pressure to fall

Adrenergic agents

Antihypertensive autonomic agents are available to block alpha1, beta1, and/or beta2 receptors, or stimulate alpha2 receptors in the
brainstem (centrally acting).

• Blockade of alpha1 receptors in the arterioles
• Selective blockade of beta1 receptors in the heart
• Non-selective blockade of both beta1 and beta2 receptors
• Non-selective blockade of both alpha and beta receptors
• Stimulation of alpha2 receptors in the brainstem (centrally acting)
• Blockade of peripheral adrenergic neurons

direct vasodialators affect arteriolar smooth muscle and are highly effective , but

produce too many side effects to be 1st choice drugs

all direct vasodialators can produce

reflex tachycardia as a compensatory response to the sudden decrease in blood pressure