Cardiovascular

Rochee Paraon Benito, RN

Infection Control Nurse

St. Jude College of Nursing
Heart A&P
Organ that produces heart beat and
propels blood.
Location: behind ribs; padded by
lungs
Structure:
Upper chambers: atria
Lower cambers: ventricles
Valves: tricuspid, mitral,
pulmonary, aortic
Heart A&P
Blood Supply:
Coronary arteries arise from aorta by
aortic valve.
Right coronary artery: SA node (55%
of people); AV node (90%); Posterior
chambers and septum
Left coronary artery: bifurcates into
left descending artery (anterior heart)
& left circumflex artery (SA node in
45%)
Heart A&P
Charge spreads to Bundle of His in septum,
down bundle branch fibers to Purkinje
network.
Slight hesitation, then repolarization (setting
up to be ready for next SA node stimulation)
SA node = 70-100 bpm
AV node = 50-60 bpm
Purkinje fibers: 10-30 bpm

Heart A&P
Function:
Circulate blood; maintain blood pressure
Vena cava right atria tricuspid
valve right ventricle pulmonary
artery lungs where it is oxygenated
Pulmonary veins left atria mitral
valve left ventricle aortic valve
aorta body

Heart A&P
Heart Sounds:
S
1
(lub): Closure of mitral & tricuspid valves &
contraction of ventricles (Systole: Contraction)
S
2
(dub): Closure of pulmonary & aortic valves
and contraction of atria (Diastole: Relaxation)
S
3
: Filling of ventricles (follows S
3
)
S
4
: Abnormal: prior to S
1

Sinus arrhythmia: pressure of lungs on
inspiration pressure in pulm. artery late
closure of pulmonary valve splitting (l-lub-
dub)
Heart A&P
ELECTRICAL CONDUCTION:
Sinus atrial (SA) node (right upper atrium)
begins automatic heart beat.
Heart is polarized when ready to beat.
Depolarization means charge occurs (K moves
out; Na moves into cell).
Current flows across the atrium. Pauses at
the AV node.
Atrioventricular (AV) node (located in left
lower atrium) sends charge forward.
Neuro & Muscle Action
NERVE INNERVATION:
K (inside nerve cells)
Na and Calcium (in interstitial tissue)
When nerve is stimulated, channels in axian
open & Na & calcium enter (+ and - charges
produce a spark or nerve contraction.
K = Na cant enter; no contraction.
K = Na is not pulled inside; weak
contraction; fatigue; weakness.
Calcium = no contraction or rigid.
Neuro & Muscle Action
MUSCLE ACTION:
Myosin and actin (muscle proteins) in muscle
are normally kept apart by additional protein.
When stimulated by nerve, calcium enters
cells and binds with protein separating
myosin & actin allowing myosin and actin to
contact. Muscle contracts.
calcium: Fibrillation (constant contraction).
calcium: Tetany; muscles cant contract.
Heart A&P
Preload: Ability to stretch ( difficulty with
hypertrophy, ischemia; blood volume)

Afterload:Resistance of valves & blood
vessels ( viscosity; arteriosclerosis,
hypertension)

Contractility: Force of contractions
(pericardial fluid; exhaustion; ischemia)
Heart AP
Stroke volume: Amt.. of blood ejected from
ventricle with a heart beat.
Cardiac output: Amt.. of blood pumped out of
heart/minute (cardiac output = stroke
volume X heart rate)
Cardiac reserve: ability to stroke volume &
HR.
Bradycardia: Slow heart rate
Tachycardia: Rapid heart rate

Sympathetic
Parasympathetic
Heart: Increases Decreases
Blood vessels: Constrict Dilate
BP & P: Increases Brings to normal
Bronchi: Dilates Constricts
Skin: Sweats Dry
Intestine: Decreases Increases
Liver: Glycogenesis None
Pancreas: None Secretes
Salivary: Saliva None
Bladder: Relaxes Contracts
Heart A&P
Baroreceptors in carotid & aortic arch
respond to BP:
blood pressure SNS response.
Sympathetic nervous system HR; vessel
constriction (including coronary vessels)
Epinephrine (from adrenal) dilatation
BP to PNS response.
Parasympathetic nervous system: HR &
vessel dilatation.
Heart A&P
Central Chemoreceptors: medulla
PaO2 or PaCO2 ( pH)= Tachycardia
& vessel constriction.
Peripheral chemoreceptors: Carotid & aortic
arch
PaCO2 or pH = Bradycardia &
vasodilatation.
Cardiac Drugs
Block sodium influx: (class I antiarrhythmics)
Block potassium (class III antiarrhythmics)
Interfere with calcium (calcium blockers or
class IV antiarrhythmics)
Stimulate SNS: adrenergic effect: rate
(class II antiarrhythmics)
Stimulate PNS: cholinergic effect: rate.
Block SNS: antiadrenergic effect: rate.
Block PNS: anticholinergic effect: rate.

Congestive Heart Failure
Inability to pump enough blood to meet
bodys metabolic demands
Acute or insidious; left or right sided
LEFT SIDED:
Output of left ventricle is less than input.
Causes: hypertension; valve stenosis (
afterload); myocardial infarction
Hypertension hypertrophy & HR. Heart
grows exhausted and fails.

Congestive Heart Failure
Failure = BP stim. of SNS HR &
force of contractions & vasoconstriction
Volume of blood in lungs .
Fluid moves into interstitial lung tissue, then
into alveoli (hydrostatic pressure)
Pulmonary edema air exchange
If capillaries break, blood alveoli
RAA system constriction, NA & H20
retention.
Congestive Heart Failure
ASSESSMENT:
Dyspneic, SaO2 ; rales, anxiety,
cyanosis, urinary output; bloody
sputum with cough.
Chemoreceptors respiratory rate.
Easy fatigue; dizziness (cerebral
hypoxia)
K from NA retention
Develop Orthopnea: inability to breath
when supine; feeling of smothering.
Congestive Heart Failure
Orthopnea occurs because:
Heart ability improves with rest; fluid returns
from alveoli to capillaries & back to heart.
Overloads left ventricle LCHF
Pressure in lung capillaries and fluid shift
into alveoli worsens aeration.
Chest X-ray or MRI: left side heart size.

Congestive Heart Failure
RIGHT SIDED CONGESTIVE FAILURE
Output of right ventricle is less than input
from VC
Causes backward pressure of VC & systemic
venous circulation.
Cause: Results from LHF; COPD, CHD with
septal defect
Congestive Heart Failure
ASSESSMENT:
Back pressure in VC liver & spleen size
(hepatomegaly; splenomegaly)
pressure in abd vessels ascites
Overall systemic edema (dependent)
Jugular vein distention
pulmonary artery circulation dyspnea
(not enough blood reaches alveoli to be
oxygenated)
X-ray or MRI right side heart size
Congestive Heart Failure
When BP , kidney produces renin. Renin
acts on angiotensinogen (plasma proteins
produced by liver) angiotensin I.
Angiotensin I converted to angiotensin II by
enzyme produced by lungs.
II is potent vasoconstrictor; stim. thirst
center in hypothalamus; constricts renal
arterioles; stim. secretion of aldosterone
BP; blood volume by fluid & NA retention
( preload).
Congestive Heart Failure
NURSING DIAGNOSIS:
Activity intolerance related to congestive
heart failure.
THERAPY/INTERVENTIONS:
Rest
Diuretics to evacuate extra fluid
Drug to and strengthen heart rate.
EXPECTED OUTCOME:
Client returns to normal activities.


Digoxin
CLASSIFICATION:
Cardiac glycoside; compound derived from
foxglove plant.
BRAND NAME: Lanoxin
ACTION:
Slows impulse conduction through the AV
node (PNS stimulation) to slow and
strengthen the heart contraction (increase
calcium availability to heart muscle).
PREGNANCY RISK CATEGORY: A

Digoxin
ADMINISTRATION: P.O. OR IV (never IM)
a. A loading dose: 10-15 mcg/kg of pts
weight is given first (1/2 initially; 1/4 3-6 hrs
later; 1/4 3-6 hrs later)
b. Maintenance dose: 0.25 mg P.O daily (25%
of loading dose).
ADVERSE ACTIONS: Narrow window between
effectiveness & toxicity.Toxicity with
hypoxemia, hypokalemia, myocardial
ischemia.
Long half life (36 hrs) can lead to sustained
response.





Digoxin
GI: Nausea, vomiting.
Neuro: Headache, vision changes (halos/blue-
green color discrimination)
Cardiac: Ventricular arrhythmias; SA arrest
NURSING INPLICATIONS:
Take apical pulse b/4 administration:
Question order if 60 in adults.
Teach patients how to take their pulse b/4
administration.
Patients should report: low pulse rate;
persistent cough; SOB; weight gain; edema of
ankles, nausea/vomiting.


Nifedipine (Procardia)
CLASSIFICATION:
Calcium channel blocker
Antianginal
Antihypertensive
ACTION:
Prevent calcium from entering cardiac and
vessels cells vasodilatation & slows nerve
conduction in heart. O2 heart perfusion.


Nifedipine (Procardia)
PREGNANCY RISK CATEGORY: C
ADMINISTRATION:
PO (slow release)
ADVERSE EFFECTS:
Dizziness
NURSING IMPLICATIONS:
Dont break sustained release
capsules
Monitor BP until regulated
ECG
Measure of the electrical conduction of the
heart (measuring current flow between
negative to positive lead)
ELECTRODES (for monitoring):
- under right clavicle
+ over left lower rib
If reading a 12 lead ECG, read lead II.


ECG
PAPER:
Small blocks: 0.04 sec*
Large blocks: 0.2 seconds (5 small blocks)
5 large blocks = 1 second
6 second strip = 30 large blocks*
USUAL GRAPH:
If current is flowing + lead upward
deflection.
If current is flowing + lead downward
deflection.
ECG
P-WAVE:
Current flowing over atria.
Appearance: Smooth upward curve
Duration: 0.06-0.12 seconds(2-3 small
blocks)
Height: 2-3 blocks high
Problems:
If no wave: SA node not originating heart
beat.
If long wave: atrial hypertrophy
If irregular wave: atrial fibrillation
ECG
P-R INTERVAL:
From beginning of P-wave to beginning of
QRS wave.
Appearance: P-wave plus hesitation space
b/4 AV node.
Duration: 0.12-0.20 secs (3-5 small blocks).
Problems: Short: suggests impulse originated
outside SA node.
Long: suggests poor conduction (digitalis
toxicity or heart block)
ECG
QRS SPIKE: Ventricular contraction; High,
upward spike after P-R interval.
Appearance: Begins with downward spike
(Q); next the high R, then downward S.
Duration: 0.06-0.10 (1 1/2 -10 small blocks)
1/2 of P-R interval)
Height: 3-30 blocks.
Problems: If low: poor contraction from
pericardial fluid?
If wide: poor conduction (myocardial
infarction?)
ECG
S-T SEGMENT:
End of ventricular contraction and beginning
of repolarization (referred to as J-point)
Appearance: Space from S wave to beginning
of T-wave. Isoelectric (neither + nor -)
Problems: depressed or elevated: ischemia or
digitalis toxicity.
ECG
T-WAVE
Repolarization to prepare for next heart beat.
Duration: varies
Height: 0.5 mm (5 small blocks)
Problems:
Absent: Repolarization not occurring;
Inverted: heart damage (ischemia);
hyperkalemia

ECG
Q-T INTERVAL:
Ventricular depolarization & repolarization
(point from beginning of QRS to end of T-
wave.
Duration: Should not be greater than 1/2 the
distance between consecutive R waves.
U-WAVE
An additional small wave at end of pattern.
May indicate electrolyte interference.
ECG
1. Count the rate: (QRS spikes X 10 on a 6
second (30 block) strip
2. Assess the rhythm: (are the QRS spikes
steady?)
3. Assess the P-wave: Is there one b/4 all QRS?
Is is normal appearance and length?
4. Assess the P-R interval: Is is steady?
5. Assess the QRS spike: Are they consistent?
6. Assess the T-wave: Is there one after every
QRS?

ECG
HEART BLOCK:
Current originates in SA node but doesnt
reach the AV node.
P-R length unusually long.
1st degree: Normal rhythm; long R-R interval.
2nd degree: Regular rhythm; P-R interval
lengthens; P-waves without QRS
3rd degree: Regular rhythm but difference in
atrial & ventricle heart rates
Coronary Artery Disease
A group of disorders including
atherosclerosis, arteriosclerosis,
hypertension, and unhealthy lifestyles.
Lipids (Fats)
Made from carbon, hydrogen and O
2
the same as
carbohydrates (not water soluble).
Necessary for cell wall formation & energy (9
Kcal/gm)
Triglycerides (fats & oils)
Phospholipids (lecithin)
Sterols (cholesterol)
Digested by salivary, stomach & pancreas lipase;
cholesterol absorbed directly
Fat links to plasma proteins for transport
through blood.
Triglycerides
95% of fat in food
Main way that fat is stored in body
Most cells store little; adipose cells
can store an unlimited supply.
All have 3 carbon atoms at center;
fatty acids attached: 3=triglyceride;
2=diglyceride; 1=monoglyceride.
Short chain, intermediate & long
chain (2-24 carbon atoms); short
chain are easiest to absorb.
Lipids (fats)
SATURATED FAT (ALL CARBON SITES
ATTACHED TO HYDROGEN NO DOULBE
BONDS)

H H H
| | |
H--CCCH
| | |
H H H


MONOUNSATURATED FAT (1 DOUBLE BOND)

H H H
| | |
C=CCH
| | |
H H H

POLYUNSATURATED FAT (2 OR MORE DOUBLE BONDS)

H H H H
| | | |
C=C=C=C
| | | |
H H H H

Triglycerides
Low density lipids (LDL):
Transport fat to body cells
Bad fat
Derived from animal sources
High density lipids (HDL):
Transport fat back to liver
Good fat
Omega-3 Fats
Unsaturated
The first double bond is at the 3rd
position.
Found in fatty fish: mackerel, salmon,
tuna, sardines & trout.
Plants: canola oil, soybean, hazelnuts,
green leafy vegetables.
triglycerides, BP, anti-inflammatory;
maybe cancer.
Lipids (fats)
How to tell saturated from unsaturated
fats:
Unsaturated: From plants; liquid at room
temperature, spoil easily: Mono= olive &
canola
Saturated: From animals; hard at room
temperature, high melting point: coconut,
palm oil, butter, meat.
Hydrogenated & TransFats
Hydrogenated: Hydrogen is added to
unsaturated fats. Changes them to saturated.
Makes the best French fries, flaky pie crusts)
Loses cardiovascular protection effect.
Transfat: Hydrogen bonds are rearranged;
becomes partially hydrogenated oil (stick
margarine, microwave popcorn)
Acts like saturated fat
Phospholipids
A phosphate compound (SO4) attaches to last
carbon.
Water soluble
Necessary in body for prostaglandins, lung
surfactant
Sterols (Cholesterol)
Necessary for bile, sex hormones
(testosterone & estrogen); adrenocortical
hormones myelin sheaths, & vitamin D.
Found in all animal products.
Not essential to eat any as liver produces
it by enzyme HMG-CoA.
Bile digests fat, then is reabsorbed and
returned to liver.
Fiber removes bile so helps cholesterol.


Cholesterol
Blood Levels:
Cholesterol: 200 mg/dL
LDL = 130 mg/dL
HDL= 29-77 mg/dL (should be 50)
If LDL to HDL is 3:1; if risk for CVD


Hypertension
Largest untreated disease in U.S.
Silent killer
Essential or Primary:
Genetic (paternal); excessive sodium
intake; sensitivity to sodium; renin-
angiotensinI - angiotensinII release;
abnormal sympathetic NS response; stress;
obesity; insulin resistance.
Secondary:
Kidney, adrenal gland, coarctation/aorta)

Hypertension
Thickening of arterial walls occurs
afterload.
Sodium retention promotes volume
to preload and cardiac output
Cardiac Output = Cardiac volume X
heart rate. (80 ml is usual stroke
volume)
Na leads to potassium.
Renin angiotensin I to angiotensin
II BP.


Blood Pressure
Category: Systolic: Diastolic:
Optimal: 120 80
Normal: 130 85
High normal: 130-139 85-89
Stage I HTN 140-150 90-99
Sage II HTN 160-179 100-109
Stage III HTN 180 110


Hypertension
Systolic BP reflects cardiac output
(pressure in arteries)
Diastolic BP reflects peripheral resistance
(pressure while heart is filling)
Hypertension
Lifestyle Changes:
Weight: q 2 lbs = 1 mm decrease
Salt intake: reduce to 6 gm/table salt
(Usual is 15 gm/day).
Saturated fats & cholesterol
Nicotine (nicotine BP by
vasoconstriction)
Alcohol (not over 1-2 oz daily)
Stress (stress to SNS response)

Hypertension
Potassium Na (citrus fruit & bananas)
Exercise (30-45 min/3-4 X week)
Arteriosclerosis
Stiffening and thickening of arterial walls.
Affects small arterioles.
BP because compliance falls.
Atherosclerosis
Large vessels and points of turbulence
(bifurcation & rapid flow)
Begins with fatty streak in artery.
Fat is irritating to artery wall; produces
inflammation when in contact by O2.
(oxidized)
Macrophages invade. Platelets enter and
produce clotting.
Calcium walls off macrophages to produce
stiff plaques.
Angina
Pain from myocardial ischemic pain
An imbalance between O2 demand and
coronary blood supply.
O2 demand increases with exercise, sex.
O2 supply limited by stress, smoking
ASSESSMENT:
Pain over left chest that radiates to left
arm (nagging to sharp)
Angina
Two Types:
Stable:
I: Prolonged exercise
II: Walking over 2 blocks.
III: Walking under 2 blocks
IV: Minimal exertion or rest

Easily relieved with rest and
nitroglycerin
Angina
Unstable:
Pain occurs at rest, after meals
Depression of ST segment
Atherosclerosis
RISKS:
Dyslipidemia; sedentary life style; high fat diet.
COMPLICATIONS:
Renal Disease:
Sclerotic changes glomerulo destruction.
Microalbuminurea; Creatine clearance will be .



Atherosclerosis
Retinal Disease:
Papilledema (cotton-wool spots), tortuous
arteries; retinal infarction
Cardiac Disorders:
Poor coronary artery perfusion from
narrowed lumen

Atherosclerosis
Cerebral Disorders:
Temporary ischemic Attacks (TIAs):
2-15 minutes of weakness, paralysis,
confusion, difficulty speaking, writing,
calculating (a senior moment).
50% of people having a TIA will have a CVA
(stroke) in 5 yrs.
Atherosclerosis
Cerebral Vascular Accident (stroke)
Males/females; elderly
Embolus breaks loose from vessel plaques
Blocks artery so cuts off circulation to tissue
beyond that; ruptures and cuts off
circulation as well as bleeds into tissue.
Leads to paralysis; loss of speech, motor
function, etc.
NURSING DIAGNOSIS:
Ineffective tissue perfusion related to
involved blood vessels


Atherosclerosis
THERAPY/INTERVENTIONS:
Change lifestyle:
LDL
weight
exercise
fiber in diet
saturated fat (all fat = 30% of total
calories; saturated fat = 10% - step 1;
7% = step 2 diet)
Atherosclerosis
Pharmacology: Reduce dyslipidemia:
Inhibit enzyme that promotes liver
production of cholesterol (HMG-
CoA) (statins)
Bile acid sequestrants excretion
of cholesterol
Reduce hypertension:
SNS response.
blood volume
RAA system response


Atherosclerosis
Diuretics (thiazides & loop) and beta blockers
(#1)
ACE inhibitors (#2)
Calcium channel blockers (#3)
EXPECTED OUTCOME:
Client follows modified lifestyle; triglycerides
& cholesterol at normal levels.

Hypertension of Pregnancy
10% of pregnancies.
3 classic symptoms: hypertension
(140/90); albuminuria; weight gain &
edema
Probably results from foreign protein;
causes vasospasm.
Severe Preeclampsia (160/110) &
eclampsia (if seizures occur)
Malignant Hypertension

Rapid HTN development leads to kidney
failure, retinal damage and congestive
heart failure.
Need to caution this is not a malignancy.
Coronary Artery Disease
RISK:
White male
Women develop it ten years later than men;
35-55=m/w
55= even
Over 55= w/m
Heart does not receive enough oxygen
(perfused during relaxation or diastole)
Associated with hypertension &
atherosclerosis.
Peripheral Vascular Disease
RISK:
Diabetes mellitus; elderly
ASSESSMENT:
Cold, numbness of extremities.
Hairless and dry skin
Cramps in legs with exercise
(intermittent claudication)
TIAs
Dizziness on movement
Erectile dysfunction
Diuretics
Afferent artery Efferent artery
| |
------- | |---------
| | - Na+ is reabsorbed
| | - Potassium sparing diuretics
proximal | | - K+ is reabsorbed
descending -- | | - Na+ is reabsorbed
tubule | | - Thiazide diuretics
| | - Distal ascending tubule
-----------
Loop of Henle ( H2O is reabsorbed)
Osmotic (loop) diuretics
Chlorothiazide HCl (Diuril)
CLASSIFICATION:
Thiazide diuretic
ACTION:
Inhibits reabsorption of sodium in distal
renal tubule; excretion of sodium &
H2O.
PREGNANCY RISK CATEGORY: C
ADMINISTRATION:
PO, IV
Chlorothiazide HCl (Diuril)
ADVERSE EFFECTS:
Dizziness; dry mouth, orthostatic hypotension,
erectile dysfunction, muscle cramps
NURSING IMPLICATIONS:
Take drug early in the day so sleep is not
disrupted by voiding.
Increased urination will occur.
Stand up slowly to prevent dizziness.
Supplement diet with potassium (citrus fruit &
bananas)

Furosemide (Lasix)
CLASSIFICATION:
Loop diuretic
ACTION:
Inhibit reabsorption of sodium & H2O from
proximal tubules excretion of sodium &
H2O.
PREGNANCY RISK CATEGORY: C
ADMINISTRATION:
PO, IV

Furosemide (Lasix)
ADVERSE ACTIONS:
Same
NURSING IMPLICATIONS:
Same

Ethacrynic Acid (Edecrin) a second common
loop diuretic
Spironolactone (Aldactone)
CLASSIFICATION:
Potassium sparing diuretic
ACTION:
blocks the effect of aldosterone in distal
tubule sodium & H2O (spares K+)
PREGNANCY RISK CATEGORY: D
ADMINISTRATION: PO
ADVERSE EFFECTS: Same
NURSING IMPLICATIONS:
No need for K+ supplement
Propranol (Inderol)
CLASSIFICATION:
B-adrengenic blocker
Antihypertensive
Antianginal
Antiarrhythmic
ACTION:
SNS response vasodilatation;
HR; afterload; BP to renin
release
PREGNANCY RISK CATEGORY: C

Propranol (Inderol)
ADMINISTRATION:
PO, IV
ADVERSE EFFECTS:
Dizziness, bradycardia, heart block;
bronchospasm, pulmonary edema
NURSING IMPLICATIONS
: Should be tapered gradually
Captopril (ACE Inhibitor)
CLASSIFICATION:
Antihypertensive
angiotensin converting enzyme
inhibitor (ACE inhibitor)
ACTION:
Blocks conversion of angiotensin I to
angiotensin II so blocks
vasoconstriction & aldosterone
secretion BP & sodium excretion
& H2O excretion


Captopril (ACE Inhibitor)
PREGNANCY RISK CATEGORY: C
ADMINISTRATION: PO
ADVERSE EFFECTS:
Tachycardia, MI, GI irritation
NURSING IMPLICATIONS:
Take in-between meals for best absorption
Must be tapered before being stopped
Change position slowly to prevent dizziness

Losartan (Cozaar)
CLASSIFICATION:
Angiotensin II Receptor Blocker
Antihypertenive
ACTION:
Blocks binding of angiotensin II to tissues
PREGNANCY RISK CATEGORY: D (fetal
death)
ADMINISTRATION: PO
ADVERSE EFFECTS: Dizziness

Losartan (Cozaar)
NURSING IMPLICATIONS:
Assess for pregnancy or breast feeding
Can take without regard for meals
Should be tapering before stopping

Atorvastatin (Lipitor)
CLASSIFICATION:
Antilipidemic
HMG-CoA Inhibitor
ACTION:
Inhibits action of the enzyme that
begins cholesterol synthesis so
serum cholesterol & LDL; HDL.
ADMINISTRATION:
Oral (adjunct to diet and lifestyle
changes)

Atorvastatin (Lipitor)
PREGNANCY RISK CATEGORY: X
ADVERSE EFFECTS:
Liver dysfunction.
Myopathy.
NURSING IMPLICATIONS:
Must accompany lifestyle changes.
Liver function tests are necessary (q
6mo to 1 yr).
Caution it is pregnancy risk X.
Nitroglycerin
CLASSIFICATION:
Antianginal agent
ACTION:
Vasodilation BP & afterload.
ADMINISTRATION:
Oral form is rapidly transformed by liver so is
ineffective. Given sublingual (action in 1-3
minutes; peak 30-60 minutes) or by
transdermal patch (30-60 minutes; peak 8-12
hours).
Nitroglycerin
ADVERSE EFFECTS:
Hypotension
NURSING IMPLICATIONS:
Teach how to use sublingual (dont
chew) or apply patch.
Dont apply patches over hair.
Change patch to bath, swim, etc.
Rise from lying or sitting position
slowly.
Restricted Fat Diets
General Rules:
Cholesterol 300 mg/day.
Limit egg yolks to 3-4/week.
Use fatty fish, omega-3 plant sources
Trim fat from meat
Avoid frying food; use herbs for taste
Use unsaturated fats (canola or olive)
Use new omega-3 spreads (Benecol)
Use fat free milk; no-fat cheese