NURS 443 Lecture Notes - Lecture 8: Regular Insulin, Stroke Volume, Vascular Resistance

63 views11 pages
7 May 2018
School
Department
Course
Professor
Fluid and Electrolytes
A Hyperkalemia
a. If over 6 = severe!
b. Clinical Manifestations
i. Irritability, anxiety
ii. Abdominal cramping, diarrhea
iii. Weak lower extremity
iv. Paresthesia
v. Irregular pulse
vi. Hypoglycemia
vii. Cardiac arrest if sudden or severe-
ventricular fibrillation or cardiac standstill
viii. Flat P wave and wide QRS. Short QT interval and narrow & peaked T wave
c. Causes:
i. Renal failure, burns/ crush injury, tumor lysis, severe infection, exercise, and Metabolic
acidosis, Rapid infusion of parenteral fluids
ii. Digoxin-like drugs and beta blockers can cause higher ECF potassium concentration.
iii. Potassium-sparing diuretics & ACE Inhibitors can develop hyperkalemia
d. Nursing management
i. Monitor ECG and BP-- RISK FOR V TACH
ii. Eliminate oral and parenteral potassium intake
iii. Admit diuretics, dialysis, and ion-exchange resins like polystyrene sulfonate (Kayexalate)
1. Never give Kayex if pt has paralytic ileus
2. If given via enema, will need to stay for 30 mins and cleansing enema may be
used afterwards. Also check bowel sounds before admit
iv. Administer IV regular insulin (along with glucose) or IV sodium bicarbonate
1. Will only be temporary
v. Administer IV calcium gluconate if experiencing dangerous cardiac dysrhythmia
find more resources at oneclass.com
find more resources at oneclass.com
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 11 pages and 3 million more documents.

Already have an account? Log in
vi. If potassium elevation is mild and kidneys are fine: withhold potassium from diet and IV
sources and increase renal potassium eliminate by administering fluids and loop or
thiazide diuretics.
vii. If they have renal failure- hemodialysis is plan of care
B Hypokalemia
a. If under 2.5 then severe!
b. Clinical Manifestations:
i. Cardiac changes- weak/ thready, irregular
pulse
ii. Skeletal muscle weakness and paralysis
iii. Leg cramps
iv. Shallow respirations/ arrest
v. Paralytic ileus, N/V
vi. Hyperglycemia
vii. Decreases reflexes & paresthesia
viii. Flat T wave, presences of U wave, peaked P wave, prolonged QRS
c. Cause:
i. GI loss: diarrhea, laxative abuse, vomiting, ileostomy drainage, fistula, starvation
ii. Renal loss: diuretic mag depletion, dialysis
iii. Skin loss: diaphoresis, tissue repair
iv. increased insulin, alkalosis, low mag
v. increased epinephrine (stress), antibiotics, diuretics
vi. no K+ in parenteral fluids
d. Nursing implementation
i. RISK FOR V TACH
ii. Oral or IV potassium chloride (KCL)- not given unless urine output is at least 0.5 mL/kg
1. IV SAFETY ALERT!!!!!
a. Must check IV site every hour due to damage IV can do to veins
b. Use central line if possible
c. Do not exceed 10mEq/hr
d. Must always be diluted and never give IV push or bolus
2. PO medication
a. Must be given w/ meals can cause nausea and increases the
absorption
iii. Teach at increased risk for dig toxicity if they have hypokalemia
iv. Teach prevention for hypokalemia: S&S, if taking potassium-loosing drugs such as all
diuretics besides aldactone (increased potassium in diet) if taking potassium-sparing
(avoid salt and high potassium foods)
Potassium high foods: banana, canolope, strawberry, mangos, oranges, dates, raisins, plums,
veggies, potatoes, meat, fish, apricots, whole grain cereal, legumes
C Heart Failure
find more resources at oneclass.com
find more resources at oneclass.com
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 11 pages and 3 million more documents.

Already have an account? Log in
a. Definition: A complex process in which the heart is unable to pump enough blood to meet the
demands of the body.
i. EF should be about 55-65%
b. Patho:
i. Preload- olue of lood at ed of diastoli. Heart o’t e ale to streth or pup lood
out
ii. Afterload- resistae to heart pupig. Musle o’t e ale to fill ayore
iii. Franks Starling law- stroke volume of cardiac will increase. Causes cardiac muscle to
contract more forcefully. Cardiac workload will increase causing failure.
iv. Ventricular hypertrophy- increase contractility- increasing myocardial oxygen demand and
cellular enlargement
v. Neuroendocrine response: increased HR, BP, contractility, venous resistance, vascular
return. Renin angiotensin system will be redistributed in body causing decrease renal
perfusion, increase preload and afterload, and pulmonary congestion
c. Risk factors:
i. CAD, MI, hypertension, family history, cardiotoxic drugs, smoking, obesity, alcohol,
diabetes, African American, low ejection fraction
d. Classifications
i. Systolic vs. diastolic- ventricular fails to contract vs. Heart can’t fill & relax
1. Systolic is caused by impaired contractile function (MI), increased afterload
(hypertension), cardiomyopathy, and valvular heart disease.
a. Most common type
b. Will have symptoms of heart failure and EF <45%.
c. Left ventricle loses its ability to push blood out- weak heart
2. Diastolic is caused by left ventricle hypertrophy from hypertension, Myocardial
ischemia, valve disease (aortic/ mitral), or cardiomyopathy.
a. Will have symptoms of heart failure but normal EF
b. Thickened heart and is noncompliant. Decreased preload
3. Dilated cardiomyopathy (DCM) is in both systolic and diastolic. Pts will have
extremely low EF(<35%), high pulmonary pressure, and biventricular failure
a. May show low BP, CO, renal perfusion, and heart dysrhythmias
ii. Left ventricle vs. right ventricle- blood back up into left atrium and pulmonary veins vs
backup of blood into the right atrium and venous circulation
1. Left sided is caused by CAD and hypertension. And could lead to right sided
failure and pulmonary edema
2. Right sided is caused by Cor pulmonale, right ventricular infarction or embolism,
or left sided HF. It causes restriction of blood flow to the lungs.
iii. Low vs. high- hypertension, cardiomyopathy vs. hypermetabolic, hyperthyroid, pregnancy
iv. Acute vs. chronic- abrupt onset of myocardial injury vs. progressive deterioration of heart
muscle.
1. Acute- increase in pulmonary venous pressure causes failure of LV. Interstitial
edema may occur followed by tachypnea and SOB.
find more resources at oneclass.com
find more resources at oneclass.com
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 11 pages and 3 million more documents.

Already have an account? Log in

Get OneClass Notes+

Unlimited access to class notes and textbook notes.

YearlyBest Value
75% OFF
$8 USD/m
Monthly
$30 USD/m
You will be charged $96 USD upfront and auto renewed at the end of each cycle. You may cancel anytime under Payment Settings. For more information, see our Terms and Privacy.
Payments are encrypted using 256-bit SSL. Powered by Stripe.