Cardiac Function Disorders

Etiology of CAD:
Spasm of the coronary arteries due to cocaine, hypercalcemia, etc. Embolisms can also
cause CAD, thromboses can form due platelets accumulating in large numbers and occlude the
artery. Atherosclerosis is the major cause and it can occur in any artery of the body, but has an
affinity for coronary arteries. (Soft deposits of fat that harden with age are the most common
kind.) Plaque is also a cause due to focal deposits of cholesterol and other lipids.
Differentiate between cholesterol, HDL, and LDL:
Cholesterol is made in our bodies, we make as much as we need, but then we also
consume it in our foods. It needs to be less than 200 (normal 140-200), and we need it to absorb
vitamins A, E, D, and K.
High Density Lipoprotein is the “good” cholesterol. It needs to be between 40-60mg/dL
or higher (men: 37-70, women: 40-88). It is important in transporting cholesterol, like a carrier or
sweeper, and delivering it to the liver to be excreted in the bile.
Low Density Lipoprotein is the “bad” cholesterol. It needs to be below160, but below
100 is optimal (< or = 130 w/out CAD, < or = 100 with CAD). It transports cholesterol into cells,
which ADDS to atherosclerotic disease.
Collateral Circulation and what encourages its development:
Collateral circulation is additional circulation through branches that develop off of main
vessels, which provide vital O2 and nutrients to the myocardium. It temporarily circumvents
obstruction. It is encouraged by angiogenesis, the ability to develop new blood vessels,
arteriogenesis, the ability to develop large vessels (arterioles and arteries), at the obstruction,
EXERCISE is best! Having chronic ischemia can also result in collateral circulation. Slow
occlusion creates a better chance for good collateral circulation. Rapid onset could result in a
severe ischemia or necrosis.
Modifiable and Non-Modifiable risk factors for CAD:
Modifiable – Serum lipids need to be within normal ranges, htn, tobacco use, obesity,
physical inactivity, diabetes, fasting blood sugar >110, increased homocysteine levels, with is an
amino acid that develops in the endothelial lining, b vitamins help reduce these levels, and
psychological states/stress. (Metabolic Syndrome R/T insulin resistance.)
Non-modifiable – age, gender (men at a higher risk till age 60 or when women hit
menopause and lose estrogen), ethnicity (Caucasian then African American, then Hispanic), and
genetics/familial history.
Health promotion for CAD:
 Manage risk factors, emphasis on prevention and early treatment (identify and manage
those at risk), decline in coronary deaths over the last 20-30 years, more education on risks,
consumers altering unhealthy and hazardous lifestyles. Exercise 5 times a week and limit alcohol
intake, achieve normal weight, health awareness at an early age. (Aerobic exercise is better than
weight lifting for cardiac health, leg exercises also easier for people with cardiac problems then
arm movements.)
For high risk people: Lipid checks every 5 years starting at age 20, no tobacco/smoking,
weight management, exercise, decrease saturated fats, cholesterol, and sodium, set realistic
values, ALWAYS respect person’s right to make own decisions.
Bile acid sequestrants and statins work to decrease serum lipids:
Normally, the body eliminates cholesterol by converting it to bile salts in the liver which
is excreted into the intestines and into our feces. Bile-Acid sequestrants bind with bile salts in the
intestines to decreases LDL and cholesterol and is excreted in the feces. TAKE WITH FOOD,
GI upset, interacts with absorption of other drugs, so do not administer simultaneously together.
Statins, HMG-CoA Reductase Inhibitor, inhibits cholesterol synthesis in the liver. Decrease LDL
and cholesterol, and slightly increase HDL. Take at night (enzyme that destroys cholesterol
works best in the evening) on an empty stomach and talk to doctor about Co Enzyme Q10
supplements, because statins block the synthesis of this. Monitor liver enzymes (ALT and AST),
muscle weakness (CK), and visual changes.
Organs at risk and considerations while on Statins:
STATINS EFFECT THE LIVER! ANY ONE ON CHOLESTEROL LOWERING
MEDS, MODIFY DIET.
Fibrates: potentiate effects of Coumadin and hypoglycemic agents (monitor glucose, GI
irritability, watch for signs of bleeding, and increased liver enzymes.
Cholesterol Absorption Inhibitors: DO NOT use with liver dysfunction.
Statins: S/E stomach cramps, constipation or diarrhea, gas, nausea (stomach), rash,
LIVER DAMAGE (increased liver enzymes), myopathy, ryabdomyolysis (breakdown of skeletal
muscles), muscle aches and pain.

Alternate therapeutic agents that support that health of the cardiac system:
Niacin (Nicotinic Acid): Vit B3 lowers LDL and triglycerides (bad form of fat), by
interfering with their synthesis and increase HDL. S/E include flushing, take ASA or Motrin 30 –
60 minutes before Niacin. (diminishes after 2 wks.)
Coenzyme Q10: Naturally produced in the body, lipid soluble (need fat to absorb it, so
take around meal time) antioxidant against free radical damage, needed by every cell for energy,
and decreases with age. Supports myocardial cells and improves energy levels.
 Hawthorn: An herb that claims to be a vasodilator and cardiotonic (modest diuretic
effect), supports CV system, could potentiate drugs used for same purpose. Use with mild to
moderate HF, CAD. Berries have been used for GI complaints. Use with caution in elderly,
possible hypotension, do not take if prego or nursing, and caution when taking with other cardiac
or diuretic meds.
Policosanol: Cholesterol lowering agent, platelet aggregation blocking agent.
Omega 3 Fatty Acids: Lower amounts of lipids in bloodstream, lower BP slightly,
increase bleeding times (caution with blood thinners), increase HDL and decrease LDL.
Other strategies include garlic, read yeast rice, psyllium, phyosterols, and possibly soy.
Define Angina, pathophysiology, and participating factors:
Angina is pain in the chest, resulting from and MI (reversible cellular lack of O2 and
nutrients, increased demand for O2, or decreased amount of O2 can lead to MI), MI is expressed
symptomatically as angina.
Patho: When the demand for myocardial O2 (myocardium resting extracts 60 to 85% of
O2) is greater than the ability of the coronary arteries to supply it, MI develops; a supply or
demand problem. There is an insufficient blood flow due to narrowing of the coronary arteries
usually by atherosclerosis, spasm, or embolism. (Not enough O2 -> increased blood flow ->
obstructed area force -> needs not met -> hypoxic w/in 10secs -> complete opbstruction and
inability to reestablish blood flow results in permanent loss of myocardial cells/injury -> MI)
Circulating blood/O2 keeps heart alive, CAD -> circulation of blood/O2 into heart.
Factors: Physical exertion increases HR, decreases diastole and coronary filling time.
Coronary arteries are perfused during ventricular diastole, so you don’t get as much blood/o2 as
would like. Strong emotions stimulate SNS and increases HR, BP, and myocardial contractility.
Heavy meals takes blood from other organs and diverts it to the gut, temperature extremes that
dilate or constrict blood vessels (hot tubs, etc.), sexual activity increases SNS, Stimulants
(cocaine, amphetamines, etc.), increase HR by stimulating catecholamine and cause coronary
artery spasms. Tobacco/smoking causes increased H, nicotine stimulates catecholamine release,
which causes vasoconstriction and increases the level of carbon monoxide which displaces o2.
Circadian rhythm causes events to occur more in the mornings after waking. Hypovolemia,
pneumonia, asthma, COPD, hypoxemia, anxiety, increased BP, hyperthermia, hyperthyroidism,
dsyrythmias, heart failure, cardiac values, and coagulopathy can lead to events. Being simply
anemic can cause cardiac event with clean arteries, GI bleed, etc.
Angina pain:
Pain, pressure, an ache or unpleasant feeling that is constrictive, squeezing, heavy,
choking, or suffocating; indigestion-like or burning in the epigastric region, CAN radiate (left
arm or shoulder) or stay substernal. Myocardial nerve fibers irritated by increased lactic acid
from anaerobic metabolism. Usually lasts 3-5mins and subsides when the cause of the ischemic
event is reversed (activity-rest, emotional reaction-calmness, etc). Should not last more than
20min after rest and nitroglycerin. Some pts. are asymptomatic, still the same thing. RARELY
ever sharp and stabbing, and does not change with positions or breathing (pain of pericarditis
changes with position and resperations). Sharp, stabbing pain -> MI, Ripening -> aortic aneurism
rupture, right shoulder pain is usually gallbladder. Angina usually causes increased BP and
pulse.
Types of angina:
Chronic Stable Angina (classic): Occurs intermittently over a long period with same
pattern of onset, duration, and intensity of symptoms, never changes, usually exercise induced.
Pain at rest is unusual. Relieved typically by rest or medication. Often predictable and meds
given to provide peak effects when angina likely to occur.
Unstable Angina (progressive, crescendo, or preinfaction): Unpredictable, may be 1st
clinical manifestation of CAD, may go from stable to unstable; will describe increase in
frequency, and begins with no triggers. REQUIRES MEDICAL
ATTENTION/HOSPITALIZATION.
Prinzmetal’s Angina (variant): Often at rest, usually in response to spasm of major
coronary artery, rare, but may occur more common in people with migraines, may occur with or
without CAD. Not usually exercised induced. Pain may occur during REM sleep, or cyclical,
short bursts of pain at the same time each day. Tx is ca channel blockers and nitrates.
Nocturnal Angina: Only at night, doesn’t mean the person has to be sleeping.
Angina Decubius: Occurs while person is laying down, can be awake, and usually stops
when the stand or sit.
Nitrates and Beta-blockers:
They are antianginals.
Nitrates dilate peripheral blood vessels and dilate coronary arteries and collateral vessels.
Many forms:
Short-Acting Nitrates -> Nitroglycerin/Nitrostat; SubL or translingial spray.
(works w/in 3 min, last for 10 min)
Long-Acting Nitrates -> Isordil, Sorbitrate, and Imdur tablets that are longer
acting then SL and help prevent stable angina attacks.
Nitroglycerin ointment: Nitrol and Nitropaste, 2%
nitroglycerin topical ointment dosed by inch. Anginal prophylaxis for 6-8
hours. Good for nocturnal and unstable angina, Taper off dose if extreme
hypotension results. Take patch off an clean area if patient starts to crash.
Nitro patch: Transdermal controlled-release nitrates:
24 hour patch that delivers low continuous dose. (Suggested to remove at
bedtime and wear for 14/16 hrs a day to avoid risk of tolerance, but follow
dr orders.)
 IV Nitroglycerin: Treat hospital pts with unstable angina. Immediate onset of
action. Use a glass bottle and special PVC tubing, nitroglycerin is absorbed into plastic,
so we won’t know dose given if plastic bottle is used. Stops angina pain, reduces systolic
BP, and used in treatment of MI to dilate C.A. to maximize blood flow.
S/E for all nitrates include hypotension because everything is dilated, headache,
dizziness, flushing, orthostatic hypotension, and reflex tachycardia.
Teach pt to let dissolve below tongue if SubL, if no relief after 3 doses, call for
ambulance, NEVER drive to hospital or let someone take you! Use nitrates prophylactically
before activity known to cause angina, viable nitrates should cause a slight tingling sensation,
nitrates expire in 6 months. Stay resting or lay down when taking nitrates, headaches will stop as
body gets used to nitrates, do not combine with drugs for ED---BAD hypotension, may
antagonize effects of heparin; alcohol or drugs used for vasodilatation (ca channel blockers) can
potentiate nitrate effects.
Beta-blockers: Antianginal, antidysrhythmic, and antihypertensive (treat underlying
cause), decrease effects of SNS by blocking action of catecholamines, epinephrine and
nonepinephrine. Block b1 receptors in heart and if not beta selective, also block b2 receptors in
the lungs. Decrease afterload (resistance in the aorta to the emptying of the left ventricle to
decrease o2 demand and worload, reduce heart rate and contractility, which decreases angina
episodes, preferred drug for treatment of Chronic Stable Angina. Decreases morbidity and
mortality with CAD especially following a MI.
S/E bradycardia, hypotension, wheezing, GI complaints, weight gain, depression, sexual
dysfunction. Be careful with diabetics, because hypoglycemia could be masked and with
asthmatics, because if not beta-selective bronchoconstriction/bronchospasm could result.
DO NOT discontinue abruptly, could risk rebound hypertension and return of ischemic
heart disease symptoms
Nursing considerations for administering diuretics:
Monitor E’s, esp. K/Mg before and after dosing. May need to hold drug until E’s are
replaced, safer to hold diuretic until replaced. Monitor urinary output, weight, edema and lung
sounds. Monitor for hypotension/orthostatic. Monitor for signs of K and Mg depletion -> muscle
weakness, leg cramps, and cardiac dysrhythmias.
Teach pt/family to take diuretics in the morning, rise slowly from a lying position, avoid
licorice -> increase K loss, and NOTIFY PHYSICIAN OF WEIGHT GAIN OF 3LBS IN 2
DAYS OR 5LBS IN ONE WEEK.
Loop, Thiazide, and Osmotic are potassium-wasting.
Nursing Assessment for pt with chest pain:
PQRST(A)
Participating factors –> what were you doing when the pain began? Quality of pain ->
feels like, what makes better or worse, Radiation of pain -> where is it located?, Severity of pain
-> scale of 0-10, Timing -> when did it begin? Change? Had it before? Associated symptoms ->
SOB, N/V, doom, etc. associated symptoms rarely ever occur with angina, but are a sign of an
even worse cardiac event. Vital signs ->BP, P, R, Pulse Ox, Temp, Targeted PMH, 12 lead EKG
and probable continuous cardiac monitoring.
HF and its pathology:
HF is an abnormal cardiovascular condition (NOT a disease, other things cause it),
involving impaired cardiac pumping. The heart is unable to pump an adequate amount of blood
to meet metabolic needs of the body’s tissues. It can have a sudden onset, or a slow insidious
one.
Impaired ventricular emptying is a defect in systolic function, it is the most common
cause of HR. Impaired contractility is a defect in the ability of the cardiac muscle cells to pump
blood forward, which causes an increase in accumulation in the pulmonary vascular bed.
Etiology includes valvular disease, loss of myocardial cells due to an MI, HTN, and
cardiomyopathies.
Impaired ventricular filling is a defect in diastolic function. Impaired ability of the
ventricle to relax and fill due to a stiff, noncompliant ventricle. Results in decreased stroke
volume and cardiac output and venous enlargement of pulmonary and systemic vascular systems.
Usually the result of hypertrophy from chronic HTN, aortic stenosis, or cardiomyopathies.
(NEED small, tight, pressurized chamber surrounded by lots of muscle.)
Endolthelin increase vasoconstriction (bad).
Nitric Oxide released by the vascular endothelium is a vasodilator.
Right and left HF:
Left-sided failure is usually the initial type, and the most common type. Results from a
back up of blood into the atrium then into pulmonary veins (left side receives blood from the
lungs, which isn’t how it should be), resulting in pulmonary congestion (CFH!!) and edema.
Usually leads to right-sided failure. Common causes include disease of coronary arteries, htn,
cardiomyopathy, and rheumatic heart disease.
**Tachycardia, crackles (lungs) with dry hacking cough to pink frothy sputum
with pulmonary edema, S3, S4 heart sounds, changes in mental status,
restlessness or confusion, decreased PO2 and increased PCO2, displaced PMI,
anxious, cranky, depressed, orthopnea, paroxsysmal nocturnal dyspnea (PND).
Right-sided heart failure doesn’t involve the lungs. Results from back flow to right atrium
and systemic venous circulation. Congested systemic venous circulation results in jugular venous
distention, peripheral edema, hepatomegaly (liver is spongy and can hold a lot of fluid;
hepatojugular reflex test), splenomegaly, and vascular congestion of the GI tract. Can occur by
itself, but some causes include left-sided failure (primary cause), right ventricular MI, or Cor
pulmonale (RV dilation and hypertrophy caused by lung disease).
 **JVD, edema, weight gain, tachycardia, ascites, hepatomegaly, anxious, cranky,
depressed.
Complications of HF:
Dysrhythmias, LV thrombus, hepatomegaly, renal failure, and pleural effusion/hypoxia.
BNP:
B-type natriuretic peptide/Brain Natriuretic Factor (BNF)/Peptide or Brain Type-B is a
cardiac neurohormone secreted from the ventricular myocytes in response to volume expansion
and pressure overload. BNP levels are proportional to the severity of HF, prognostic and
therapeutic monitoring values. Goal is to maintain BNP concentration of less than 100pg/mL; >
or = 400 is a diagnostic for HF. BNP levels are understandably elevated in ventricular
hypertrophy, severe hypertension, with increasing age, and declining renal function. 4 natriuretic
peptides (including ANF) have a natriuretic (natural diuretic) and vasodilatory effect and
suppress the rennin-angiotension system so increased diuresis and decreased BP.
3 benefits of morphine sulfate for a patient with HF:
*opioid analgesic * vasodilates so decreased venous return (decreased preload)
*decrease anxiety
(2 5mg IV push over 5 minutes, dilute with at least 5ml of sterile water or NSS)
CAUTION: respiratory depressed/narcan reverses effects
Digoxin (CARDIAC GLYCOSIDE):
Actions of: Positive Inotrope (increases the force of strength of cardiac contraction –
PRIMARY FUNCTION with the HF group!) Negative chronotropic action – slows HR.
Negative dromotropic action – slows conduction speed of the impulse at the AV node (or
increases refractory period). SOOOO, decreases dysrhytmias and can reestablish a normal
rhythm.
Normal Serum Level: 08 – 2ng/ml
S/S of digitalis toxicity: anorexia, nausea, vomiting, diarrhea, yellow-green halos,
headache, blurred vision, drowsiness, fatigue, confusion, arrhythmias (bradycardia first, then
tachycardia too) ; caused by hypokalemia (WATCH with diuretics), hypercalcemia,
hypomagnesium, impaired liver and kidney function and slowed body metabolism can lead to
digitalis accumulation and toxicity.
Antidote is DIGIBAND; it binds with Digoxin so it can be excreted by the kidneys.
Nursing responsibilities: Assess apical pulse, if rate <60 hold med, recheck apical rate,
and notify doc. Teach pt. to call dr if on digoxin and apical pulse is less than 60 because <50 may
be acceptable, DEPENDS on dr. Monitor K labs, too much k inhibits action of digitalis, and too
little enhances the actions of digitalis (toxicity). Monitor digoxin level once pt is digitalized.
Teach pt/family how and when to monitor apical pulse, s/s of dig toxicity and not to take 2 doses
close together if one missed.
Teaching needs of patient with HF:
Educate patient about physiological changes that have occurred, help pt adapt to
physiological and psychological changes, PREVENTIVE CARE, focus on slowing disease, rest,
drug therapy, compliance!, teach them foods with high sodium contents, use alternate flavorings
– lemon juices, spice (not salt related), avoid extreme temps, and know the s/s of worsening HF
and seek medical attention.
GOALS: decreased peripheral edema, decreased SOB, increased exercise tolerance,
compliance with med prescribed, and no complications related to HF.
Nutritional Therapy for a pt. with HF:
Nutritional therapy is CRITICAL to the success or failure of the overall treatment. Try to
adapt diet teaching to culture/social/personal preferences. Teach pt/family to read food labels for
sodium content, worse the HF, more restricted sodium. Avoid adding salt to anything. Start with
no more than 2.5g Na/day for mild too 500mg for severe. (Average diet is 7-15 grams Na/day!)
DASH diet (restrict foods like milk, cheese, bread, cereals, canned soups, some veggies, and
most processed foods), optimize weight, weight at same time each day (am), eat small, frequent
meals.
****Notify physician of weight gain of 2lbs in 3 days or 5lbs in 5 days!!***