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N3523 Adult and Older Adult Health Care II > Exam 2 - Study Material > Flashcards

Exam 2 - Study Material Flashcards

1
Q

Describe isotonic fluid

A

This fluid has”particles” in the solution (extracellular) that are the same as the “particles” on the inside of the cell (intracellular), there is a balance.

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2
Q

Describe hypertonic fluid

A

This fluid contains more particles in the solution (extracellular) than in the cell (intracellular), so water will travel out of the cell to try to dilute the increased concenration of “particles”.

  • This results in ↑ vascular volume of water and ↓ water in the cell
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3
Q

Describe hypotonic fluid

A

This fluid contains less “particles” in the solution (extracellular) than inside of the cell (intracellular). Therefore water will move into the cell (extracellularly → intracellularly) to dilute the realative ↑ in concentration of “particles” inside of the cell.

  • This results in ↓ vascular volume and ↑ water in the cell
  • If this happens in the brain this leads to an ↑ in ICP → brain swelling → herniation through the foramen magnum
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4
Q

What are some examples of Isotonic Solutions?

A
  • Dextrose 5%
  • 0.9% Normal saline
  • Lactated Ringers
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5
Q

What type of solution is Dextrose 5% and describe it

A
  • Isotonic Solution
  • Initially isotonic but glucose will eventually be metabolized and then the solution becomes hypotonic because the solution is just H20 now.
  • Contraindiacted in neuro problems that increase intracranial pressure such as head injury.
    *
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6
Q

What type of solution is 0.9% normal saline and describe it

A
  • Isotonic solution
  • Not used in CHF, edema, hypernatremia because it can cause overload
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7
Q

What type of solution is Lactated Ringers and describe it

A
  • Isotonic Solution
  • Electrolyte content similar to serum
  • Contains K+, don’t use in renal failure
  • Don’t use in liver disease, patient can’t metabolize lactate
  • Don’t administer if pH > 7.5
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8
Q

What type of solution is 0.45% Normal Saline and describe it

A
  • Hypotonic solution
  • Use cautiously - may cause cardiovascular collapse or increased intracranial pressure
  • Don’t use in patients with liver disease, trauma, or burns.
  • Can be used to treat hypernatremia
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9
Q

What are some Hypertonic Solutions?

A
  • D5W 0.45% Normal Saline
  • D5W 0.9% Normal Saline
  • D10W
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10
Q

What type of solution is D5W 0.45% Normal Saline and when is it used?

A
  • Hypertonic solution
  • Used in DKA when glucose falls below 250 mg/dL
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11
Q

What type of solution is D5W 0.9% Normal saline and what are some precautions for it?

A
  • Hypertonic solution
  • Don’t use in cardiac or renal patients because of danger of CHF or pulmonary edema.
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12
Q

What type of solution is D10W and what are some precautions for it?

A
  • Monitor glucose level
  • May be used if patient on TPN and has not been weaned
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13
Q

What are some important precautions that must be taken into consideration with IV medications?

A
  • IV medications act immediately
  • Know the actions, side effects, adverse reactions, & have antidote available
  • Double check calculations
  • Medications can be irritating
  • Consult incompatibility charts
  • Call hospital pharmacist if information is not in books (i.e. rate of administration)
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14
Q

What are some advantages to using IV medications?

A
  • Maintains consistent drug blood levels & fluid balance
  • Efficient for staff & convenient for patient
  • Produces rapid physiological patient response
  • Cost containment
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15
Q

What are some disadvantages to using IV medications?

A
  • Can be painful & restrictive to patient
  • Can result in complications:
    • Infiltration vs. extravasation
    • Phlebitis or thrombophlebitis
    • Bleeding & infection
    • Allergic reaction
    • Circulatory overload
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16
Q

What should you consider when choosing an IV site & Vein Selection?

A
  • Patient preferences
  • Generally, use distal veins first and work proximal
  • Avoid legs, feet, sclerotic vein, inner wrist & flexion sites
  • Have ALL equipment ready & waiting
  • Follow-up if unsuccessful with attempt (document unsuccessful attempts as well)
  • Drugs with high or low pH or with high osmolarity will irritate the vein sooner
  • Don’t start IV on same side if the patient has had a:
    • Vascular graft/fistula (dialysis)
    • Mastectomy
    • Existing phlebitis
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17
Q

What should you consider when Measuring Fluid Intake & Output?

A
  • Identify any conditions or situations that can affect I/O.
  • Must be taken atleast every 8 hours (type, amount, route)
  • Evaluate trends over 24-48 hours
    *
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18
Q

What shouldn’t you do when Measuring Fluid Intake & Output?

A
  • Don’t delegate the task of recording I & O until you are sure the person going to do it understands its importance.
  • Don’t assess output amount only, consider color, color changes, and odor
    • Ex: Pts. w/ glomerulnephritis will have cocacola color urine
  • Don’t use the same graduated container for more than 1 patient.
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19
Q

What are the different guages of needles?

A
  • The smaller the guage of the needle, the greater its diamater is.
    • Ex: A 14 guage needle has a 1.55mm diameter, whereas a 32 guage needle has a 0.1mm diameter.

Guages:

  • 16 - Typically used for adolescents & adults to infused large amounts of fluids and requires a large vein
  • 18 - Used on older children, adolescents & adults to administer blood and other viscous fluids, requires a large vein
  • 20 - Used on children, adolescents & adults for IV infusions, most commonly used
  • 22 - Used on Infants, children, adolescents & adults for slower IV infusions, easier to use on small, thin, and fragile veins.
  • 24 & 26 - Used on Neonates, infants, school age children, geriatric pts for slower IV infusions, on extremely small veins
    • Ex: Small veins of the fingers or inner arms
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20
Q

What type of complications are there with IV medications?

A

Local complications

  • Infiltration
  • phlebitis
  • thrombophlebitis

Systemic complications

  • fluid overload
  • embolus
  • infection
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21
Q

What is Infiltration?

A
  • An abnormal accumulation of fluid at the IV site and occurs when IV fluids enter the surrounding space
  • Manifestations: Raised area, coolness to the touch, edema, pallor, and pain
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22
Q

What is phlebitis?

A
  • Inflammation of the vein
  • Manifestations: red streak on the vein and warm to the touch
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23
Q

What is extravasation?

A
  • Same as infiltration except some medications can cause vasoconstriction & tissue death or necrosis (Adrenergic-blocking medication)
  • Never give Dopamine via IV
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24
Q

What is thrombophlebitis?

A
  • The swelling of a vein caused by a blood clot
  • Manifestations: Inflammation (swelling) in the part of the body affected, pain, skin redness, and warmth and tenderness over the vein.
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25
Q

What is an embolus?

A
  • A traveling intravascular mass
  • With IV’s a piece of the catheter can breaking off causing a catheter shear
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26
Q

How would you assess for IV fluid overload?

A
  • Daily Weighing –the #1 indicator of an overload
  • Listen for crackles
  • Observe for edema
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27
Q

How would you give an IM injection in the thigh?

A
  • Place one hand about the patient’s knee and the hand belowthe greater trochanter of the femur.
  • Middle 1/3 ofthe muscle is the suggested site.
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28
Q

How would you give an IM injection in the upper arm?

A
  • Palpate the lower edge of the acromion process.
  • Injection site is 1-2 inches below the process.
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29
Q

Describe the guage needle, angle, and location used for IM medications

A

Guage:

  • 22 (20-23

Angle:

  • 90°

Location:

  • Deltoid
  • ventrogluteal site
  • lateral midthigh
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30
Q

Describe the guage needle, angle, and location used for subcutaneous medications

A

Guage:

  • 25

Angle:

  • 45° or 90°

Location:

  • lateral upper arm
  • thighs
  • abdomen
  • back
  • upper hip
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31
Q

Describe the guage needle, angle, and location used for Intradermal medications

A

Guage:

  • 26-27

Angle:

  • 15°

Location:

  • medical aspects of the forearm
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32
Q

What are Intradermal injections used for?

A
  • Used for allergy testing
  • Testing for antibody formation (i.e., PPD)
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33
Q

How would you prepare the skin before giving an injection?

A
  • •To prepare skin, wash skin soiled with dirt, drainage, or feces with soap and water and dry.
  • Use friction and a circular motion while cleaning with an antiseptic swab.
  • Always swab from center of site and move outward in a 2 inch radius.
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34
Q

How would you prevent syringe contamination during an injection?

A

Avoid touching length of plunger or inner part of barrel. Keep tip of syringe covered with cap or needle.

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35
Q

How would you prevent needle contamination during an injection?

A

Avoid letting needle touch contaminated surface (e.g., outer edges of ampules or vial, outer surface of needle cap, nurse’s hands, counter top, table surface).

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36
Q

How would you prevent contamination of solution during an injection?

A

Draw medication from ampule quickly. Do not allow it to stand open.

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37
Q

What are 3 things you should consider when giving injections?

A
  1. Volume of the medication
  2. Medication’s characteristics & viscosity
  3. Location of anatomical structures underlying injections sites
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38
Q

How would you maintain IV sites?

A
  • Recommended to change IV sites every 72 to 96 hours
    • Except blood, TPN, lipid emulsions, change every 24 hours (bacterial growth)
  • Keep system sterile
  • Assist patient with self-care activities so not to disrupt system
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39
Q

What should you document when starting an IV?

A
  • Date & time of the venipuncture
  • Number of the solution container
  • Type & amount of solution
  • Name & dosage of any additives
  • Type of venipuncture device including length and gauge
  • Flow rate
  • Any controller or pump
  • Name of person initiating the infusion
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40
Q

What is the normal range for Sodium?

A

135-145mEq/L

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41
Q

What is the normal range for Chloride?

A

98-107mEq/L

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42
Q

What is the normal range for Potassium?

A

3.5-5.0mEq/L

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43
Q

What is the normal range for Calcium?

A

8.6-10.2mEq/L

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44
Q

What is the normal range for Phosphate?

A

2.7-4.5mg/dL

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45
Q

What is the normal range for Magnesium?

A

1.5-2.5mEq/L

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46
Q

What EKG changes are seen with hypokalemia?

A

Elevated U wave

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47
Q

What EKG changes are seen with hyperkalemia?

A

Depressed ST segment

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48
Q

What is heart failure?

A

Heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet the body’s metabolic demands as a result of impaired cardiac pump function.

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49
Q

What are some causes of heart failure?

A
  • Coronary artery disease
  • Past myocardial infarction
  • Hypertension
  • Heart valve disease
  • Cardiomyopathy
  • Congenital heart defects
  • Endocarditis and/or myocarditis
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50
Q

The performance of the heart depends on what four essential components?

A
  1. Contractility (inotropic state) of the muscle
  2. Preload: amount of blood in the ventricle at the end of diastole
  3. Afterload: the pressure against which the left ventricle ejects
  4. Heart Rate
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51
Q

How does heart failure progress?

A
  • —Usually begins with left ventricular systolic dysfunction
  • —Diminished pumping power of left ventricle results in EF below 40%; remaining blood increases pressure in pulmonary vasculature; Left ventricle stiffens
  • —Right ventricular dysfunction often results from left ventricle because of high pulmonary pressures leading to high pressure in right side of heart and systemic circulation
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52
Q

What is right heart failure?

A

The inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal ventral venous pressure

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53
Q

What causes right heart failure?

A
  • LHF → back flow of blood into right side of heart → failure of right side
  • Pulmonary hypertension
  • COPD
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54
Q

What are the clinical manifestations of right heart failure?

A

Blood backs up into the venous system, resulting in:

  • Peripheral edema
  • Hepatomegaly
  • Abdominal pain
  • Ascites
  • Anorexia
  • Nausea
  • Weakness
  • Weight gain
  • Anasarca: late manifestation
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55
Q

What is left diastolic heart failure?

A

occurs when the lower left chamber (left ventricle) is not able to fill properly with blood during the diastolic (filling) phase.

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56
Q

What causes left diastolic heart failure?

A

The major caues of diastolic dysfunction include: hypertension-induced myocardial hypertrophy and myocardial ischemia with resultant ventricular remodeling. Hypertrophy and ischemia cause a impaired relaxation of the heart, which leads to:

  • Pulmonary congestion
  • Normal SV, CO, & EF%
  • ↓ LV compliance
  • Abnormal diastolic relaxation from ischemia-caused ventricular remodeling
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57
Q

What are some characteristics of left diastolic heart failure?

A
  • Prevelance: Female > Male
  • Left ventricular ejection fraction: normal
  • Left ventricular chamber size: ↓
  • Chest radiography: pulmonary congestion without cardiomegaly
  • Gallop: S4
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58
Q

What are the clinical manfiestations of left heart failure?

A

Blood backs up into the pulmonary vasculature resulting in:

  • Dyspnea, Orthopnea, PND
  • Cough
  • Crackles, wheezing
  • Impaired oxygen exchange
  • S3, S4 heart sounds, tachycardia
  • Weakness, confusion, irritability, insomnia
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59
Q

How can mitral stenosis cause left heart failure?

A
  1. Mitral stenosis → ↓ LA emptying →
  2. ↑ LA preload:
    1. Pulmonary edema → ↑PVR & ↓ O2 supply → RV failure
    2. ↓ Force of LA contraction → ↓ blood to left ventricle → ↓ LV output
  3. Which leads to → LV failure
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60
Q

What is pulmonary edema?

A

An abnormal buildup of fluid in the air sacs of the lungs, which leads to shortness of breath.

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61
Q

What causes pulmonary edema?

A
  1. Valvular dysfunction / CAD / Left ventricular dysfunction → ↑ left atrial pressure → ↑ pulmonary capillary hydrostatic pressure (pushing pressure) → Pulmonary edema
  2. Injury to capillary endothelium → ↑ capillary permeability and disruption of surfactant production by alveoli → Movement of fluid and plasma proteins from capillary to interstitial space (alveolar space) and alveoli → pulmonary edema
  3. Blockage of the lymphatic vessels → inability to remove ecess fluid from interstitial space → ↑ accumulation of fluid in intersitital space → pulmonary edema
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62
Q

What are the signs and symptoms for acute pulmonary edema?

A
  • —Severe dyspnea
  • Orthopnea
  • Pallor
  • Tachycardia
  • Expectoration of large amounts of frothy, blood-tinged sputum Frothy pink sputum)¡Fear
  • Wheezing
  • Sweating
  • Bubbling respirations
  • Cyanosis
  • Nasal flaring
  • Use of accessory breathing muscles
  • Tachypnea
  • Vasoconstriction
  • Hypoxia with ABG findings
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63
Q

What are some nursing interventions for acute pulmonary edema?

A
  • —Life threatening, medical emergency
  • —Provide supplemental oxygen
  • Begin with 100% non-rebreather mask.
  • —Cardiac monitoring and pulse oximetry
  • —IV
  • —Elevate head of bed to reduce venous return
  • —Medications: nitrates and diuretics. Morphine IV is an excellent adjunct in acute therapy.
  • ACE inhibitors may rapidly reverse hemodynamic instability and symptoms.
  • —Beta-blockers: role is unclear in acute setting.
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64
Q

How would you diagnose a patient for heart failure?

A
  • —Signs and symptoms; health history
  • —CXR: shows pulmonary congestion as white, dense areas; may show enlarged heart or liver congestion.
  • —ECG: may give clues to the cause of LVF. It my demonstrate prior MI, dysrhythmias, or left ventricular dysfunction.
  • —Echocardiogram: provides information about the chamber size and ventricular function; ejection fraction.
  • —Cardiac cath: for pts with CAD
  • —MRI or CT
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65
Q

What is BNP and what does each level indicate?

A
  • It is a protein secreted from the ventricles in response to overload.
  • This is the lab to check for heart failure
  • BNP levels below 100 pg/mL indicate no heart failure
  • BNP levels of 100-300 suggest heart failure is present
  • BNP levels above 300 indicate mild heart failure
  • BNP levels above 600 indicate moderate heart failure
  • BNP levels above 900 indicate severe heart failure.
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66
Q

What are some nursing interventions for heart failure?

A

—Reduce preload

  • High fowler’s position to reduce pulmonary congestion
  • Controlling sodium and water retention (restrict sodium intake, avoid NSAIDs)
  • Diuretics

—Reduce afterload

  • Vasodilators

—Increase ventricular contractility

  • Inotropes
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67
Q

What is the goal with heart failure patients?

A
  • —Goal is to improve cardiac performance without increasing cardiac workload; must manipulate preload, afterload, and contractility!
  • Medications are mainstay of management; make sure patients are complient with medications
  • Make sure patient is on a low Na+ diet, decrease the intake of fluids
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68
Q

How would you manage a heart failure patient’s diet?

A

—No added salt or salt substitutes because they contain potassium salts. Fluid restriction based on weight, monitor I/O, lytes, need increased Kcal and protein.

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69
Q

How would you manage activity levels with heart failure patients?

A

—Acute HF pts on bedrest to minimize O2 demands, but increase as soon as BP, HR, O2 sats stabilize.

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70
Q

What are the effects of ACE inhibitors on heart failure patients and what are some nursing implications of these drugs?

A

—Effects:

  • The decrease in afterload increases cardiac output by enhancing contractility.
  • —The neurohormonal effects include inhibition of ACE and vasodilation and a decrease in systemic blood pressure.

—Nursing implications:

  • Monitor blood pressure. May increase BUN, Creatinine, Liver enzymes, and potassium levels. May increase digoxin levels.
  • Some patients cannot tolerate due to development of a cough.
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71
Q

What are the effects of beta blockers on heart failure patients and what are the nursing implications of these medications?

A

—Effects:

  • Decrease heart rate to promote left atrium emptying and improve left ventricular volume
  • —Decrease myocardial O2 demand

—Nursing implications:

  • Patients should not stop taking medication abruptly, may cause angina or rebound tachycardia.
  • Monitor blood sugar in a diabetic patient, may cause hypoglycemia.
  • The drug should not be given to a patient with history of asthma, however, benefits may outweigh risks.
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72
Q

What are the effects of diuretics on heart failure patients and what are the nursing implications of these medications?

A

Effects:—

  • Urine output should increase, therefore reducing circulating volume. The reduction in volume decreases central venous pressure, pulmonary congestion, and peripheral edema.
  • —Used for symptom relief, does not change mortality.

—Nursing implications:

  • Monitor I/O and electrolytes, especially potassium.
  • Monitor for orthostatic hypotension.
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73
Q

What are the effects of aldosterone Antagonists on heart failure patients?

A
  • —Two agents, Spironolactone and Eplerenone, have been approved for patients with heart failure as add-on therapy.
  • —A 30% reduction in mortality and hospitalizations has been reported when spironolactone is added to standard therapy for patients with NYHA Class III or IV heart failure and a serum creatinine less than 2.5.
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74
Q

When is Digoxin used in patients with heart failure?

A
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75
Q

What is the MOA of Digoxin?

A
  • Sodium forced out of the cell in exchange for calcium which increase force of contraction and increases CO (+ inotropic effect)
  • Slows conduction through AV node which slows HR (- chronotropic effect)
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76
Q

What are the nursing implications for digoxin?

A
  • Take HR x 1 min, hold dose if HR < 60 bpm. Teach patient and family.
  • Monitor for digoxin toxicity!
  • Narrow therapeutic index (0.8 - 2 ng/mL)
    *
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77
Q

What are some early clinical warning signs of digoxin toxicity?

A

Symptoms:—

anorexia, nausea, vomiting, malaise, lethargy, fatigue, generalized weakness, dizziness, insomnia, palpitations, irregular heart beat, confusion.

—Visual changes:

halos or rings of light around objects, seeing lights or bright spots, changes in color perception, blind spots in vision, blurred vision.

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78
Q

What is valvular disease?

A

—Occurs when heart valves that normally move blood progressively through the heart cannot fully open or fully close, perfusion of the heart and distal tissues is impaired.

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79
Q

What factors lead to the development of valvular disease?

A
  • Myocardial ischemia
  • acute rheumatic fever
  • infectious endocarditis
  • connective tissue abnormalities
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80
Q

What is the goal of nursing interventions for patients with valvular disease?

A

—Help the client maintain a normal cardiac output to prevent:

  • Manifestations of heart failure
  • Venous congestion
  • Inadequate tissue perfusion
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81
Q

What heart valvue tends to become more dysfunctional and why?

A
  • —The aortic and mitral valves become dysfunctional more often then do the pulmonary and tricuspid valves.
  • This change occurs because the left side of the heart is a system of higher pressures when compared to the lower pressures in the pulmonary circulation.
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82
Q

What is regurgitation and how does it occur?

A
  • —backflow that occurs if a valve does not close tightly. Blood leaks back into the chambers rather than flowing forward through the heart or artery.
  • Backflow is commonly due to valve prolapse, the stretching of an atrioventricular valve leaflet into the atrium during diastole.
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83
Q

What is stenosis and how does it occur?

A
  • —Stenosis occurs when the valve opening is constricted and narrowed, impeding the forward flow of blood and increases the workload of the cardiac champer proximal to the diseased valve causing hypertrophy.
  • Occurs if the flaps of a valve thicken, stiffen, or fuse together.
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84
Q

What are the different types of Valvular Disorders?

A
  • —Mitral stenosis
  • —Mitral regurgitation
  • —Mitral valve prolapse
  • —Aortic regurgitation
  • —Aortic stenosis
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85
Q

What is mitral stenosis and what causes it?

A
  • Mitral stenosis is a valve disorder that occurs when the valve becomes calcified and immobile, the vavlular orifice narrows, and this impairs the flow of blood from the left atrium to the left ventricle.
  • It is most commonly caused by acute rheumatic fever and is 2x-3x more common in women than men.
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86
Q

What changes happen in the heart as a result of mitral stenosis?

A

Because the vavlular orifice narrows, and this impairs the flow of blood from the left atrium to the left ventricle, this causes:

  • Incomplete emptying of the left ventricle
  • ↑ Artiral pressure
  • Left atrium hypertrophy
  • Pulmonary hypertension, pulmonary edema, RHF
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87
Q

What are the signs and symptoms of mitral stenosis?

A
  • Gradual in onset
  • decreased exercise tolerance
  • dyspnea
  • orthopnea
  • paroxysmal nocturnal dyspnea.
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88
Q

What would you assess for in a patient with mitral stenosis?

A
  • a low-pitched rumbling diastolic murmur heard best at the apex.
  • Manifestations of right side heart failure may be present
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89
Q

How would you manage a patient with mitral stenosis?

A
  • Anticoagulation to decrease the risk of thrombus formation
  • surgical intervention.
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90
Q

What is mitral regurgitation and what causes it?

A
  • It is a backward flow of blood from the left ventricle into the left atrium during systole.
  • Can be caused by:
    • Mitral valve prolapse (abnormally thickened mitral valve)
    • Rheumatic heart disease
    • CAD
    • connective tissue diseases
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91
Q

What changes happen in the heart as a result of mitral regurgitation?

A

The backward flow of blood from the left ventricle into the left atrium → hypertrophy of left atrium, this can lead to:

  • LV failure
  • Additionally it can lead to right-sided heart failure due to increasing pressure in the LA causing back up into the pulmonary vasculature
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92
Q

What are the signs and symptoms of mitral regurgitation?

A
  • May be asymptomatic until cardiac output falls.
  • First signs are fatigue and dyspnea then increasing to orthopnea, paroxsymal noctural dyspnea, and peripheral edema.
  • Pulmonary hypertension
  • pulmonary edema
  • RHF
  • Atypical chest pain
  • pansystolic murmur
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93
Q

What would you assess for in a patient with mitral regurgitation?

A

A blowing, high-pitched systolic murmur with radiation to the left axilla, heard best at the apex.

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94
Q

How would you manage a patient with mitral regurgitation?

A

Nitrates, digitalis, and ACE inhibitors, possibly diuretics and low sodium diet to lessen workload of the heart.

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95
Q

What is a mitral valve prolapse and what causes it?

A
  • —It occurs when one or both of the valve leaflets bulge into the left atrium during ventricular systole resulting in regurgitation into the atrium.
  • Often accompanied by mitral regurgitation
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96
Q

What are some signs and symptoms of seen in a patient with mitral valve prolapse?

A
  • Not uncommon for patient with MVP to be completely asymptomatic
  • symptoms may be vague including:
    • tachycardia
    • lightheadedness
    • syncope
    • fatigue
    • weakness
    • dyspnea
    • anxiety
    • chest pain
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97
Q

What would you assess in a patient with a mitral valve prolapse?

A

regurgitant murmur or midsystolic click

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98
Q

How would you manage a patient with a mitral valve prolapse?

A

Depends on symptoms:

  • beta-blockers for: relieving syncope, palpitations, and chest pain
  • Aspirin: to prevent TIAs
  • prophylactic antibiotics: before any invasive procedures.
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99
Q

What is aortic reguritation and what causes it?

A
  • The inability of the aortic valve leaflets to close properly during diastole resulting from abnormalities of the leaflets or the aortic root, or both; this results in blood back flowing from the aorta
  • It is most often a result of infectious disorders such as rheumatic fever, syphilis, and infective endocarditis.
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100
Q

What changes occur in the heart with aortic regurgitation?

A
  1. Blood back flows from aorta → LV during diastole.
  2. This ↑ chamber volume → dilation, which in turn
  3. ↑ workload → **hypertrophy of Left heart. **
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101
Q

What are the signs and symptoms of aortic regurgitation?

A
  • Prominent pulsations in the neck
  • Possible head-bobbing with each heart beat –> Widened pulse pressure from ↑ SV and diastolic backflow
  • palpitations
  • dyspnea on exertion
  • fatigue
  • Angina pectoris
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102
Q

What would you assess for in a patient with aortic regurgitation?

A
  • soft, high-pitched, blowing diastolic murmur radiating to the left sternal border.
  • Turbulence across the aortic valvue druing diastole → decrescendo murmur
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103
Q

How would you manage a patient with aortic regurgitation?

A
  • relief of manifestations of heart failure and prevention of infection (prophylatic antibiotics)
  • prompt surgical treatment if s/s of LV failure.
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104
Q

What is an aortic stenosis and what causes it?

A
  • It is a narrowing of the orifice between left ventricle and aorta.
  • Caused by:
    1. Congenital defects
    2. Calcification related to aging
    3. Retraction and stiffening of the valve from inflammatory damage caused by rheumatic fever
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105
Q

What changes occur in the heart as a result of an aortic stenosis?

A

—The narrowing of the orifice between left ventricle and aorta leads to an increase in pressure within the LV, this leads to:

  • ventricular hypertrophy
  • ↓ SV, ↓ Systolic BP, narrowed pulse pressure
  • Slowed HR & faint pulses
  • Decreased cardiac output and eventually heart failure.
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106
Q

What are the signs and symptoms seen in a patient with an aortic stenosis?

A
  • dyspnea on exertion
  • exercise intolerance
  • chest pain
  • syncope
  • palpitations
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107
Q

What would you assess for in a patient with an aortic stenosis?

A

Systolic murmur with diminished second heart sounds.

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108
Q

How would you manage a patient with an aortic stenosis?

A
  1. surgical intervention
  2. prophylatic antibiotics
  3. treatment of dysrhytmias.
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109
Q

What is Warfarin used for?

A

Prevention of venous thrombosis & PE

  • & in pts with prosthetic heart valves
  • ** during atrial fibrillation**
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110
Q

What is the MOA of Warfarin?

A
  • Antagonist of vitamin K (needed for factors VII, IX, X & prothrombin)
  • Anti-clotting action delayed b/c it has no effect on clotting factors already in circulation
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111
Q

What are some nursing considerations of Warfarin?

A
  • Initial response 8-12 h & several days for peak
  • INR range should be kept between 2 - 4.5
  • If using warfarin with heparin, monitor levels (blood draw) no sooner than 5 h after IV or no sooner than 24 h after SQ inj
112
Q

What should the nurse teach a patient on Warfarrin (Coumadin)?

A
  • Patient needs routine lab work to monitor coagulation times
  • Instruct patient to avoid taking aspirin or other NSAIDS unless prescribed (due to enhanced action of warfarin)
  • Inform patient to avoid significantly increasing or decreasing consumption of foods high in Vitamin K (e.g. green leafy vegetables)
  • Patient should be informed to report excessive or prolonged bleeding from skin, nose, or mouth; red, rust-colored or smoky urine; bloody or tarry stools; blood in vomit or sputum; prolonged or excessive menses; excessive bruising; severe or persistent headache; or sudden abdominal or back pain; pregnancy is suspected or breast feeding!
  • Patient should inform provider if begins ANY new prescriptions or OTC
  • Don’t take if prego
113
Q

What is the treatment for a Warfarin overdose?

A
  • Tx with vitamin K1 (phytonadione) PO, IV (avoid SQ), infuse slowly
  • If vit K1 does not work, use whole blood or fresh-frozen plasma
    • food w/ Vit K can reduce efx: mayonnaise, canola oil, soybean oil, green leafy veggies – keep intake of these constant when testing
114
Q

What are the adverse effects of Warfarin?

A
  • Hemorrhage
  • Category X (if need anticoag during pregnancy give heparin)
  • Do not use during breast feeding
115
Q

What are the drug interactions with Warfarin?

A
  • Drugs that promote bleeding
  • Drugs that ↑ anticoag effects
  • Drugs that ↓ anticoag effects
116
Q

What are ways to minimize bleeding while on Warfarrin (Coumadin) and other anti-coagulants)?

A
  • Use an electric razor rather than a straight-edge razor
  • Floss and brush teeth gently
  • Avoid putting sharp objects in mouth (e.g. toothpicks)
  • Do not walk barefoot
  • Cut nails carefully
  • Do not blow nose forcefully
  • Avoid straining to have a bowel movement
  • Instruct patient to control any bleeding by applying firm, prolonged pressure to the area if possible.
117
Q

What are septal defects?

A
  • —Abnormality in the septum between the right and left side of the heart.
    • Atrial or ventricular
  • —Congenital defects usually identified in infancy or childhood
  • —Requires close monitoring, possible surgical repair.
118
Q

What is cardiomyopathy?

A
  • —A heart muscle disorder causing impaired cardiac output and can lead to heart failure, sudden death, and/or dysrhythmias.
  • This is a result of an enlargig heart from the hypertrophy, it leads to decreased output,
119
Q

What are the different types of cardiomyopathies?

A
  • Dilated
    • Ventricular enlargement and contractile dysfunction
  • Hypertrophic
    • Disproportionate thickening of the interventricular septum
  • Restrictive
    • Excessively rigid/stiff ventricular walls
120
Q

What are some Infectious Diseases of the Heart?

A
  1. —Rheumatic Endocarditis
  2. —Infective Endocarditis
  3. —Pericarditis
121
Q

What is rheumatic endocarditis and what causes it?

A
  • —Diffuse inflammatory disease characterized by a delayed response to an infection by the group A beta-hemolytic streptococcal pharyngitis.
  • —Inflammatory process involves all layers of the heart producing permanent and severe heart damage.
122
Q

What are some complications and treatment options for rheumattic endocarditis?

A
  • —Complications include valvular disorders, cardiomegaly, and heart failure.
  • —If appropriate antibiotic therapy for group A beta-hemolytic strep started within the first 9 days, rheumatic fever can be prevented…therefore, prompt recognition key.
123
Q

What is infective endocarditis and what causes it?

A
  • —A microbial infection of the endocardium that begins from the microorganisms in the bloodstream.
  • —Vegetative growths occur that may form clots that travel to other organs and/or severely damage heart valves.
  • —Extensions of bacteria may invade the aorta or pericardium.
124
Q

What are some risk factors for infective endocarditis?

A
  • —prosthetic heart valves
  • structural cardiac defects
  • prolonged IV catheters
  • hemodialysis catheters
  • IV drug use.
125
Q

What are some clinical manifestations of infective endocarditis?

A
  • —Fever, chills alternating with sweats
  • —Malaise, weakness, anorexia, weight loss
  • —Heart murmur
  • —Clusters of petechia on body
  • —Small, painful nodes on pads of fingers or toes (Osler nodes)
  • —Irregular, red or purple, painless, flat macules on palms, fingers, hands, or soles (Janeway lesions)
  • —Cardiomegaly and heart failure may occur
  • —Central nervous system findings
126
Q

How would a patient with infective endocarditis be treated (As in the treatment plan)?

A
  • —IV Antibiotics for 2-6 weeks
  • —Antibiotic prophylaxis for future procedures
  • —Good oral hygiene
  • —No IUDs, body piercings
  • —Surgical management if medical management unsuccessful
127
Q

What is pericarditis and what causes it?

A
  • —Inflammation of the pericardium
    • Acute or chronic
  • —Many causes: infection, myocardial injury, collagen diseases, drug reaction, radiation therapy
128
Q

What are the manifestations and complications associated with pericarditis?

A
  • Manifestations: chest pain worsened by deep inspiration, lying down, and turning. Sitting up and leaning forward typically relieves/minimized pain; pericardial friction rub; fever, tachycardia, chills, malaise, anxiety, anorexia, nausea
  • —Complications: Pericardial effusion and cardiac tamponade
129
Q

How would you treat the pain associated with pericarditis?

A
  • —Analgesics and NSAIDs to help with the pain during the acute phase
  • —Corticosteroids may be prescribed if the patient does not response to NSAIDs
  • —If related to bacterial, fungal infections, antibiotic therapy.
  • —Bed rest or restricted activity
130
Q

What are the signs and symptoms of a cardiac tamponade and how would you treat it?

A

S/S:

  • Hypotension
  • Tachycardia
  • Dyspnea
  • JVD
  • Muffled heart sounds (distant)
  • Pulsus paradoxus: BP decreases by 10mmHg or more in SBP on inspiration. DBP stays the same, so pulse pressure narrows.
  • Restlessness, anxiety
  • Cyanosis of lips and nails

Treatment:

  • Pericardiocentesis
  • Fluid or air is aspirated from the pericardial sac

This is life threatening

131
Q

What are the clinical manifestations of an infection of the heart?

A
  • —Fever, chills alternating with sweats
  • —Malaise, weakness, anorexia, weight loss
  • —Heart murmur
  • —Clusters of petechia on body
  • —Small, painful nodes on pads of fingers or toes (Osler nodes)
  • —Irregular, red or purple, painless, flat macules on palms, fingers, hands, or soles (Janeway lesions)
  • —Cardiomegaly and heart failure may occur
  • —Central nervous system findings
132
Q

What is Atherosclerosis and what causes it?

A
  • A form of arteriosclerosis caused by thickening & hardening of artiral walls by accumulation of lipid-laden macrophages because of ↑ LDL & ↓ HDL (transports cholesterol to liver for processing), and is the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen.
    • This causes plaque to develop in the arteries
  • Blockages and narrowing of the coronary vessels reduce blood flow to the myocardium
133
Q

How does Atherosclerosis progress?

A
  1. Endothelium becomes damages →
  2. inflammatory cytokines released & oxygen radicals formed →
  3. Macrophages migrate & adhere to injured endothelium & release enzymes/oxidize LDL (fatty streak; lesion reversible) →
  4. Smooth muscle cell proliferation →
  5. collagen →
  6. fibrous plaque (which obstructs blood flow) →
  7. angina or intermittent claudication →
  8. Unstable plaque prone to rupture
134
Q

What are the signs and symptoms seen in a patient with coronary atherosclerosis?

A
  • Symptoms are due to myocardial ischemia, Inadequate tissue perfusion
  • Symptoms and complications are related to the location and degree of vessel obstruction
  • Angina pectoris (usually caused by significant coronary atherosclerosis)
  • Myocardial infarction
  • Heart failure
  • Sudden cardiac death
135
Q

What are some non-modifiable risk factors for coronary atherosclerosis?

A
  • Family hx of CAD
  • Increasing age
    • 45 for men
    • 55 for women
  • Gender
    • Men>women
  • Race – AA>Caucasians
136
Q

What are some modifiable risk factors for coronary atherosclerosis?

A
  • Hyperlipidemia
  • Tobacco use
  • Hypertension
  • Diabetes mellitus
  • Metabolic syndrome
  • Obesity
  • Physical inactivity –> recommended Physical activity for 30 minutes per day of moderate exercise most days
137
Q

How can you prevent coronary atherosclerosis?

A
  • Controlling Cholesterol - statins
  • Stop Smoking
  • Manage Hypertension
  • Controlling Diabetes
138
Q

What would you teach a patient with atherosclerosis in regards to their nutrition?

A

Have the patient record:

  • Total calories
  • Total fat (25%-35% of total calories)
    • –Saturated fats (< 7%)
    • –Polyunsaturated fats
    • –Monounsaturated fats
  • Carbohydrates (50-60% of total calories)
  • Dietary fiber (20-30g a day)
  • Protein (15% of total calories)
  • Cholesterol (LESS THAN 200mg / day)
139
Q

Describe the different cholesterol levels and their interpretations

A
  • Optimal lvls = < 200mg/dL
  • High lvls = 240mg/dL +
140
Q

Describe the different LDL levels and their interpretations?

A
  • Optimal lvls = < 100mg/dL
  • Borderline = 130-156mg/dL
  • High lvls = 160-189 mg/dL
141
Q

Describe the different HDL lvls and their interpretations

A
  • Optimal lvls = 60mg/dL +
  • Low HDL lvls =
142
Q

Describe triglyceride levels and their interpretations

A
  • Optimal lvls = < 150 mg/dL
  • High lvls - 200-499mg/dL
143
Q

What is angina pectoris and how does it develop?

A
  • A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow.
  • Physical exertion or emotional stress increases myocardial oxygen demand and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand.
144
Q

What are some collaborative problems with angina pectoris?

A
  • Acute pulmonary edema
  • Heart failure
  • Cardiogenic shock
  • Dysrhythmias and cardiac arrest
  • Myocardial infarction
145
Q

What are the differnt types of angina?

A
  • Stable Angina
  • Unstable Angina
  • Refractory angina
  • Variant (Prinzmetal’s) - happens more likely at night
  • Silent ischemia (EKG changes with a stress test), patient reports no pain
146
Q

What is stable angina and what causes it?

A
  • Stable angina (a.k.a. Angina pectrois) is substernal, transient chest pain that is usually relieved by rest and/or nitrates
  • It is caused by gradual luminal narrowing and hardening of the arterials so that the affected vessels cannot dilate in response to increased myocardial demand associated w/ PHYS exertion or emotional stress.
147
Q

What is unstable angina?

A

Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention!

148
Q

What is prinzmetal angina?

A
  • Transient, unpredictable chest pain from coronary vasospasm that occurs at rest
149
Q

What is silent ischemia?

A
  • Ischemia that has no symptoms (no chest pain)
  • Occurs more often in women
  • It can also occur in some people during mental stress
150
Q

What are the EKG changes seen in unstable angina?

A

the patient has clinical manifestations of coronary ischemia, but ECG and cardiac biomarkers show no evidence of MI

151
Q

Describe the pain associated with angina pectoris

A
  • Pain described as tightness, choking, or a heavy sensation.
  • Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left).
  • Anxiety frequently accompanies the pain.
  • The pain of typical angina subsides with rest or NTG.
  • Diabetes – may not feel pain (diabetic neuropathy)
  • Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention!
152
Q

What are some classic signs of angina pectoris?

A
  • dyspnea/shortness of breath
  • dizziness
  • nausea and vomiting.
153
Q

What is metabolic syndrome?

A
154
Q

How would you manage angina pectoris?

A
  • Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply
  • Medications - dialate the arteries – Nitroglycerin
  • Start patient on oxygen
  • Reduce and control risk factors
  • Reperfusion therapy may also be done
155
Q

What are some medications used for angina pectoris?

A
  • Nitroglycerin
  • Beta-adrenergic blocking agents
  • Calcium channel blocking agents
  • Antiplatelet and anticoagulant medications
  • Aspirin
  • Clopidogrel and ticlopidine
  • Heparin
  • Glycoprotein IIB/IIIa agents
156
Q

What are the effects of nitrates?

A
  • Cause vasodilation, reduce blood return to heart from veins, decrease preload & workload on heart, decrease O demand;
  • Dilate peripheral arteries to decrease afterload & decrease in O demand
  • Dilate coronary arteries to increase collateral flow to ischemic heart
157
Q

What are the effects of beta blockers in relation to coronary artery disease?

A
  • Decrease myocardial O2 demand by decreasing force of contraction, slowing heart rate, & slowing impulse conduction
  • Slowed HR increases filling time & increases CA perfusion
  • Decrease BP to decrease afterload & O2 demand
158
Q

What does the acrynom MONA-B mean and why is this used?

A

The goal is to increase O2 supply & decrease O2 demand

  • Morphine 1-5 mg IVP
  • Oxygen 2L
  • Nitro 0.4mg SL 5 min x 3
  • ASA 160mg – 325mg
  • Beta Blockers 5mg IV q5-15 min x 3
159
Q

What would you assess for in a patient with angina pectoris?

A

You would assess for:

  • Symptoms and activities, especially those that precede and precipitate attacks
    • Ask about the pain, location, quality, etc, activities the patient was doing when the pain started
  • Risk factors, lifestyle, and health promotion activities
  • Patient and family knowledge
  • Adherence to the plan of care ( compliance is a big thing)
160
Q

What are some nursing diagnoses for a patient with angina pectoris?

A
  • Ineffective cardiac tissue perfusion
  • Death anxiety
  • Deficient knowledge
  • Noncompliance, ineffective management of therapeutic regimen
161
Q

What would you teach a patient with angina pectoris?

A
  1. Lifestyle changes and reduction of risk factors
  2. Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of ischemia
  3. Teaching regarding disease process
  4. Medications
  5. Stress reduction
  6. When to seek emergency care
162
Q

What is actue coronary syndrome?

A

An umbrella term covering ST elevation MI’s and Non-ST elevation MI’s

NSTEMI: = unstable angina

STEMI: = MI heart attack, worst one to have, immediate concern, head to cath lab

163
Q

What is a myocardial infarction?

A

An area of the myocardium is permanently destroyed. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.

164
Q

What causes a myocardial infarction?

A
  • Prolonged ischemia → cellular death & irreversible damage to heart muscle caused by:
    • Plaque progression, rupture, & clot formation (most common etiology)
    • Coronary artery vasospasm
    • Coronary artery embolism
165
Q

What are the signs and symptoms of a myocardio infarction and what are some lab values associated with it?

A
  • Pallor
  • diaphoresis,
  • sense of unease,
  • palpitations,
  • nausea/vomiting (blood flow, reflex stimulation of vomiting center by pain fibers),
  • dyspnea
  • fatigue
  • chest pain
  • 12 lead ECG ( rule out an acute MI)

Laboratory tests—biomarkers

  • CK-MB - peaks at 24 hours
  • Myoglobin - peaks at 12 hours
  • Troponin T or I - levels are elevated for 3 weeks
  • Patient history
166
Q

What are some treatment options for an acute myocardial infarction?

A
  • Obtain diagnostic tests including ECG within 10 minutes of admission to the ED
  • Start Oxygen
  • Aspirin, nitroglycerin, morphine, beta-blockers
  • Angiotensin-converting enzyme inhibitor within 24 hours
  • Evaluate for percutaneous coronary intervention or thrombolytic therapy
  • As indicated; IV heparin or LMWH, clopidogrel or ticlopidine, glycoprotein IIb/IIIa inhibitor
  • Bed rest - to prevent fatigue, DOE
167
Q

What are some nursing interventions for a patient with an AMI?

A
  • Frequent VS
  • Telemetry
  • I & O; daily weights
  • Careful assessment of restlessness, dyspnea, or chest pain - indicates that tissue damage is worsening
  • Assessment for S/S of CHF
  • Assessment of skin color
168
Q

How would you care for patient 72 hours after post AMI?

A
  • Rest is a priority – injured heart must have time to start repairing itself
  • Bedside commode for bowel movement – preferred over bedpan if can. Stool softeners may be ordered
  • Assist with isometric exercises
    • Provide muscle exercise without causing exhaustion
  • Sequental compression devices to prevent DVT
  • Place all necessary items within patient’s reach. Call light available. Prevents stretching or straining
  • Perform physical care – provides rest & comfort
  • After assistance with ADLs – provide ample time for rest. Place in semi-Fowler’s position – position assists with breathing and relieves pain
169
Q

How would you assess a patient with ACS?

A
  • Assess all symptoms carefully and compare to previous and baseline data to detect any changes or complications.
  • Monitor ECG.
170
Q

What are some nursing diagnoses for a patient with ACS?

A
  • Ineffective cardiac tissue perfusion
  • Risk for fluid imbalance
  • Risk for ineffective peripheral tissue perfusion
  • Death anxiety
  • Deficient knowledge
171
Q

What are the goals of care for a patient with ACS?

A

Goals include the relief of pain or ischemic signs and symptoms, prevention of further myocardial damage, absence of respiratory dysfunction, maintenance of or attainment of adequate tissues perfusion, reduced anxiety, adherence to the self-care program, and absence or early recognition of complications

172
Q

What changes would you see in an EKG with a myocardial infarction?

A

ST segment elevation is a classic sign of an AMI: Resolves with restoration of blood flow or completion of MI

173
Q

What are some coronary artery disease diagnostic tests?

A
  • Other blood tests
    • Chemistry & CBC to determine concurrent diseases
    • ESR rises 1st week after infarct
  • Stress test shows significance of blockage related to patient functioning
  • Cardiac cath–for patients with recurring symptoms to monitor heart structure & function
174
Q

What are some treatments for CAD?

A

Intraaortic balloon pump:

  • pts with s/s of hemodynamic instability
  • balloon inserted into descending thoracic artery & inflated during diastole
  • changes early diastolic pressure & coronary artery perfusion
  • deflates at end diastole, decrease afterload, increases CO

Coronary angioplasty & intracoronary stents:

  • sheath inserted into femoral artery & cath is guided through arteries to aorta & radiopaque dye is inserted into coronary arteries
  • lesion identified to see if PTCA possible
  • cath with balloon inserted & positioned central to blockage then inflated to reconfigure blockage
    • WATCH OUT FOR INFECTION
    • MONITOR THE SITE for any changes
  • Stent may be inserted to prevent restenosis
175
Q

What kind of a diet is a CAD patient on?

A
  • NPO while evaluated for acute chest pain to prevent blood from being redirected to GI tract
  • Prevents vomiting from vagal effects
  • If not NPO then diet is low fat low cholesterol
  • Saturated fats should be less than 10% Kcals since large amounts saturated fats raises cholesterol; polyunsaturated fats help lower cholesterol
176
Q

What kind of activity will a CAD patient participate in?

A
  • Bedrest when initially experience chest pain to decrease O demand until AMI dx made
  • After pt stable activity gradually increased
  • Pts assessed for activity tolerance based on orthostatic changes in BP, dysrthymias, s/s; can indicate possible ischemia
  • Post infarct pts have stress test to determine safe exercise level
  • Cardiac rehab for activity progression
177
Q

What is the rehabilitation plan for a patient post-MI?

A
  • In hospital, gradual increase in the patient’s activity level as prescribed
  • Exercise tolerance test and exercise progression
  • Graded exercise program with monitoring of tolerance based on BP and HR – cardiac rehab
  • Emotional support & counseling
  • Stress management
  • Sexual counseling
  • Lifestyle changes if needed (e.g. stop smoking)
  • Risk factor management
  • Dietary changes
  • Medication adherence
178
Q

What is a coronary artery bypass graft?

A

Internal mammary artery or saphenous vein grafted to coronary artery beyond the point of blockage to reestablish blood flow

179
Q

What are some characeristics of a coronary artery bypass graft?

A
  • Internal mammary artery or saphenous vein grafted to coronary artery beyond the point of blockage to reestablish blood flow
  • Consider anatomy of occlusion & surgical risk/benefit
  • Not curative since grafts can occlude but it can improve quality of life
  • Cardiopulmonary bypass machine during procedure
180
Q

How would you assess a CAD patient preop for a coronary artery bypass graft?

A
  • Goals include accurate H & P, preop teaching for pt & family regarding surgery, preparing pt & family physically & psychosocially
  • Dx testing to evaluate severity of disease
  • Assess risk factors which could hinder recovery & teach lifestyle changes
  • Obtain baseline data: apical & radial HR, bilat BP, peripheral pulses, neuro, nutrition
  • Withhold ASA 1 to 3 days before surgery
  • NPO at midnight
181
Q

How would you assess a CAD patient postop for a coronary artery bypass graft?

A

Postop care: promoting patent airway & effective gas exchange

  • intubation & MV until pt stable
  • assess resp, breath sounds, cough, sputum, ABGs, pulse ox, CXR to check lung reexpansion, pulm care q1-2h
  • pain meds to promote T, C, DB
  • splint incision, change position
  • Preventing infection
  • Monitoring neurological status
  • Monitoring fluid balance: I/O (should have urine output 30 cc/hour), limit fluids to reduce chance of overload, daily weights, possible diuretics (watch K levels), H & H, PT, serum glucose (may be elevated from stress of surgery), plasma expanders
  • STOP METFORMIN
182
Q

What are some nursing interventions for a CAD patient postop?

A
  • promote comfort, rest, sleep
  • support nutrition
  • promote activity
  • promote psychosocial adaptation
  • monitor anticoagulation
  • pt/family discharge teaching
183
Q

What are some complications with CAD patients involving coronary artery bypass graft?

A
  • pulmonary most common; atelectasis, pleural effusion, pneumonia
  • cardiac instability & dysrhythmias
  • neuro changes
  • fluid imbalance & fever
  • immobility
  • sleep disturbance
184
Q

How do Calcium Channel Blockers work?

A
  • Drugs that prevent calcium ions from entering cells
  • Also known as calcium antagonists and slow channel blockers
185
Q

What are calcium channel blockers used to treat?

A

Used to treat:

  1. Hypertension
  2. angina pectoris
  3. cardiac dysrhythmias
186
Q

What are Beta-blockers used for?

A

To treat Pts w/ :

  • Angina
  • HTN
  • Cardiac dysrhythmias
  • MI
  • Heart failure
  • Hyperthyroidism
  • Migraine
  • Stage fright
  • Pheochromocytoma
  • Glaucoma

All of these are due almost entirely to blocking β1 receptors

187
Q

What are the 3 generations of Beta-blockers?

A
  • 1st gen: nonselective – block β1 & β2 (ex. propranolol)
  • 2nd gen: selective – block β1 (ex. metoprolol)
  • 3rd gen:
    • nonselective - β1&2, α1 (carvedilol & labetalol)
    • selective (β1) - nebivolol

All end in “LOL”

188
Q

What do 1st gen Beta-blockers do?

A
  • They block β1 & β2, resulting in:
    • Reduced HR (β1)
    • Decreases the force of ventricular contraction (β1)
    • Slows impulse conduction through AV node (β1)
    • Suppresses secretion of renin (β1)
    • Bronchoconstriction - β2 blockade in the lung
    • Casoconstriction - β2 arteriole blockade in heart, lung, skeletal muscle
    • Reduces glycogenolysis (β2 blockade in skeletal muscle & liver)
189
Q

Abrupt d/c of a Beta-blocker can cause what?

A

Rebound cardiac excitation

190
Q

What are some nursing interventions with Beta-Blockers?

A
  • Teach pts to carry enough medication on away trips!
  • Teach pts s & sx of HF:
    • SOB, night coughs, edema of extremities
    • Nurse should assess for ↑ resp, ↑ BP, ↑ HR & auscultate lungs for crackles
191
Q

What are some examples of “statin” drugs?

A
  • Atorvastatin
  • Lovastatin
  • Rosuvastatin
  • Simvastatin
  • Pravastin
  • Fluvastatin
192
Q

What are “statin” durgs used for?

A
  • decrease LDL levels , triglycerides
  • Increase HDL levels

Nonlipid CV Benefits:

  • ↑ plaque stability
  • ↓ inflammation @ site
  • Slow CAD calcification
193
Q

What are some adverse effects of “statins”?

A
  • HA
  • Rashes
  • GI disturbances
  • Myopathy/rhabdomylolysis (RARE)
  • Hepatoxicity (RARE)

These are PREG X drugs

194
Q

What is the MOA of nitroglycerin?

A

Dilates the veins and leads to:

  • ↓cardiac preload
  • ↓blood return = ↓ventricular filling
  • ↓cardiac work = ↓CO/perfusion
195
Q

What is nitroglycerin used for?

A
  • Primary HTN
  • Hypertensive crisis
  • Heart failure
196
Q

What is the MOA for heparin?

A

Inhibit the activity of clotting factors

197
Q

What is heparin used for?

A

1st line tx in DVTs

198
Q

What are some nursing considerations for heparin?

A
  • Monitor for bleeding
  • Watch out for heparin induced thrombocytopenia, it will decrease platelet count
  • Hypersensitivity (small test dose 1st)
199
Q

What are aneurysms and what causes them?

A
  • It is an abnormal widening or ballooning of a portion of an artery due to weakness, dilation, or outpouching in the wall of the blood vessel and are at least 1.5 times their normal size
  • Caused by atherosclerosis, trauma, syphilis, infection, connective tissue disorders, cigarette smoking, HTN

50% all aneurysms larger than 6cm in diameter will rupture within 1 year

200
Q

What causes aneurysms?

A
  • chest trauma from MVA, and atherosclerosis
  • strongly linked to HTN & instability
201
Q

What are some characteristics of aneurysms?

A
  • Abdominal aorta most common site
  • Growth unpredictable but larger the aneurysm the greater the risk of rupture
  • Commonly asymptomatic; but can be felt as palpable mass, bruit heard
  • May have thoracic, abdominal, or back pain; anterior chest wall, back, flank, pain; s/s shock if leakage, dyspnea, cough, & wheezing
  • If ruptures: severe pain, s/s shock, decreased RBC, increased WBC, death
202
Q

How are aneurysms diagnosed?

A

Trans esophageal echocardiogram or X-ray, CT

Maintain BP is high priority

203
Q

What would you teach a patient with an aneurysms?

A

info regarding surgery, care of wound, s/s infection, diet, activity, pain meds, avoid constipation /straining

204
Q

What is Chronic Arterial Occlusive Disease?

A
  • It is a progressive narrowing, degeneration, & obstruction of arteries of extremities; usually lower involved
  • Arteriosclerosis obliterans most common: atherosclerosis (plaque) combines with ateriosclerosis (calcification) to produce widespread slowly progressive narrowing of arteries
205
Q

What causes chronic arterial occlusive disease?

A
  • Plaque formation causes thickening of intima & media causing partial or complete obstruction
  • Calcification of arteriosclerosis weakens arterial wall & increases chance of thrombus & aneurysm
  • Occurs segmentally; s/s appear with >50% occlusion
206
Q

What are some risk factors for chronic arterial occlusive disease?

A
  • Age
  • Smoking
  • Hypertension
  • Atherosclerosis
  • Obesity
  • Diabetes
  • Stress
  • Family hx PVD
  • Sedentary lifestyle
  • Hyperlipidemia
207
Q

What are the signs of Chronic Occlusive Disease? (ADD PIC)

A
  • Intermittent claudication– aching pain or cramp distal to blockage occurring with exercise & relieved by rest
  • Rest pain– severe disease usually at night; has numbness, coldness, tingling
  • Hair loss on affected extremity
  • Thick, brittle, slow growing nails
  • Shiny, thin, tight, fragile skin is dry & scaly
  • Cool to touch
  • Diminished or absent pulses
  • Pale appearance with elevated extremity
  • Reddish color with extremity dependent
  • Decreased motor function
  • Ulcer formation with advanced disease
208
Q

What are some diagnostic tests for Chronic Occlusive Disease?

A
  • ultrasound
  • segmental limb pressure & pulse volume record
  • exercise testing
  • arteriogram
  • Ankle-brachial index (ABI)– measures degree of stenosis
209
Q

What are some medications used to treat chornic occlusive disease?

A
  • Pentoxifylline (Trental) and cilostazol (Pleta) are the only medications specifically indicated for the treatment of claudication.
  • Antiplatelet agents such as aspirin or clopidogrel (Plavix) help prevent the formation of thromboemboli, which can lead to myocardial infarction and stroke.
210
Q

What are some treatments for chronic occlusive disease?

A
  • Treatments:
    • pt assisted to improve management of other chronic conditions; smoking cessation
    • may use angioplasty & stents when condition is incapacitating
  • Surgical Management: Bypass grafts & endarterectomy, amputation
  • Activity
  • Referrals
211
Q

What would you assess in a patient with Chronic Occlusive Disease?

A

Subjective:

  • presence, severity, location of intermittent claudication & rest pain
  • Hx HTN, diabetes, CAD (include tx adherence)
  • smoking hx & attempts to quit
  • diet patterns; exercise patterns
  • ADLs & social impact of disease
  • numbness or tingling

Objective:

  • Peripheral pulses palpated or doppler
  • Appearance of skin, nails, hair on extremity
  • Skin breakdown
  • Postural color changes
  • Presence of muscle wasting
  • Ankle-Brachial index
  • Weight
212
Q

What are some nursing diagnoses for patients with Chronic Occlusive Disease?

A
  • Ineffective peripheral tissue perfusion related to impaired arterial circulation.
  • Pain related to decreased oxygen supply to tissues.
  • Risk for impaired skin integrity related to compromised tissue perfusion.
  • Fear and anxiety related to actual or potential lifestyle changes.
213
Q

What are some nursing interventions to provide proper positioning for a patient with Chronic Occlusive Disease

A
  • Place the client’s legs in a dependent position in relation to the heart to improve peripheral blood flow
  • Avoid raising the client’s feet above heart level unless specifically prescribed by the health care providers
  • Keep the client in a neutral, flat, supine position if in doubt about the nature of his peripheral vascular problems.
214
Q

What are some nursing interventions to **promote vasodilation **for a patient with Chronic Occlusive Disease

A
  • Teach the client to avoid constricting clothes, such as garters, knee-high stockings and belts.
  • If overreplacement of glucocortiocoid is indicated, inform the client about the purpose of therapy and possible adverse effects such as cushingoid appearance, weight gain, acne, hirsutism, peptic ulcer, diabetes mellitus, osteoporosis, infection, muscular weakness, mood swings, cataracts and hypertension.
  • Provide insulating warmth with gloves, socks and other outerwear as appropriate.
  • Keep room temperatures comfortably warm.
  • Instruct the client to warm himself with warm drinks or baths.
  • Never apply a direct heat source to the extremities. Limited blood flow combined occur with normal circulation.
  • Teach the client about the vasoconstrictive effects of nicotine and caffeine, emotional stress, and chilling, discuss ways to avoid or minimize these risk factors.
215
Q

How would you promote activity and mobility for a patient with Chronic Occlusive Disease?

A

For a client with decreased arterial function but without activity-limiting tissue damage, encourage a program of balanced exercise and rest to promote development of collateral circulation.

216
Q

What are some complications for patients with Chronic Occlusive Disease?

A
  • lInjury
  • lInfection
  • lGangrene
  • lThrombus
  • lArterial ulcers
  • lAmputation
217
Q

What is Acute Arterial Occlusive Disease?

A
  • A sudden process in which an artey is blocked
  • Can occur in healthy & diseased arteries resulting from thrombosis, embolism in healthy artery or trauma
  • Typically occurs at site of vessel bifurcation or narrowing
218
Q

What are some risk factors for Acute Arterial Occlusive Disease?

A

Risk factors are conditions causing thrombus formation, which are:

  • Rheumatic heart disease
  • artificial heart valves
  • MI
  • atrial fib
  • postop vascular surgery
  • trauma with lacerated or compressed arteries
219
Q

What are the signs for Acute Arterial Occlusive Disease?

A
  • Severe constant pain not relieved by rest
  • Pallor or mottled appearance
  • Pulselessness or diminished over affected area
  • Paresthesia – numbness, tingling, burning
  • Poikilothermia – cool or cold to touch
  • Paralysis – mobility is limited; indicates ischemic death of nerves
220
Q

What are some diagnostic tests for Acute Occlusive Disease?

A
  • physical exam, Doppler ultrasound, ABI, MRI
221
Q

What are medications used to treat Acute Occlusive Disease?

A

Medications: to dissolve clot & prevent further clot formation

  • heparin– prevent further clots
  • urokinase– dissolves clot over 24-48 hours
  • spasmolytic agents – relieve arterial spasms
  • calcium channel blockers– spasms
  • coumadin– prevent future episodes
222
Q

What are some nursing interventions preop for patient’s with Acute Occlusive Disease Surgery?

A
  • physical, emotional, & psychosocial prep of pt & family
  • teach procedures, meds, postop care; provide as much info as possible for better decisions
  • frequent VS & neurovascular checks
223
Q

What are some nursing interventions postop for patient’s with Acute Occlusive Disease Surgery?

A
  • Support circulation & perfusion: monitor graft patency; check peripheral pulses, VS, neuro- vascular status, limb temp, ABGs, pulse ox, cardiac enzymes, cardiac monitor. Test pt output (drains & tubes) for blood. Measure abd girth & limb circumference
  • Prevent respiratory complications: atelectasis, resp. infection; TCDB, pain meds, ambulation
  • Support fluid balance: kidneys at risk from low CO (hypotension, hypovolemia, trauma); can lead to acute postop renal failure. I/O, daily weight, BUN, creatinine, lytes, UA
  • Promote wound healing: Infections common especially with diabetic & malnourished pt; perform & teach proper wound care; graft infection has high fever, ileus, high WBC
  • Patient/family teaching: have brief hospitalization so care for self at home
    • standard dc teaching: diet, activity, wound care, resuming normal activities
    • risk factor reduction
    • avoid constipation & straining
    • use pain meds for rest & activity
224
Q

What are some complications postop for patients with Acute Occlusive Disease?

A
  • Infection at graft site
  • Reoccclusion & restenosis
  • Multi-system injury
  • Ischemia leading to necrosis & gangrene
  • MI, dysrhythmias, stroke
225
Q

What are some characteristics of DVT?

A
  • More common in women & elderly
  • 50% DVT pts will develop PE as result & @ 50,000 will die from PE/year
  • Thrombi develop in areas of slow or turbulent blood flow
  • Spasm & change in pressure dislodge thrombi & move them toward heart
226
Q

What are some risk factors for DVT’s?

A
  • Age: elderly (have lots of risk factors)
  • Female
  • Pos. hx thrombosis
  • Immobility/ stasis
  • Increased viscosity
  • Intimal damage
  • Associated conditions
  • Trauma
  • Use of oral contraceptives (estrogen)
  • Chronic lung & heart disease
227
Q

What is a DVT?

A

a blood clot that forms in a vein deep inside a part of the body. It mainly affects the large veins in the lower leg and thigh.

228
Q

What are the s/s of DVT?

A

Presentation: s/s vary according to size & location of thrombus

  • 50% pts asymptomatic
  • local pain or tenderness
  • edema or swelling
  • local warmth, redness; mild fever
    *
229
Q

What are some diagnostic tests for DVT’s?

A

venogram is criterion standard but is not always accurate; also use ultrasound & venous agglutination test

230
Q

What are some medications used to treat DVT?

A
  • §low dose heparin (sc) q12h
  • coumadin
  • other thrombolytic therapy to dissolve existing thrombi
231
Q

What are some treatments for DVT?

A

Treatments: mostly preventative; to increase venous return & prevent venous stasis

  • antiembolism stockings
  • graduated compression stockings– different degrees of compression to different parts of leg
  • external pneumatic compression sleeves– uses air pump by inflating & deflating sleeves at regular intervals to stimulate venous return
  • Surgery: not major role in acute DVT, but used when other treatments ineffective
    • thrombectomy when circulation compromised
    • placement of transvenous filtration device in vena cava to trap thrombi before they reach heart & lungs; Greenfield filter, bird’s nest filter
232
Q

What kind of diet and activity will a patient with DVT be on, and what referrals would be made?

A
  • Diet: only major restriction for Coumadin pts– consistent Vitamin K intake
  • Activity: ambulate as tolerated after therapeutic heparin level achieved; if edema or pain present, bed rest with leg elevated
  • Referrals: home health agency, APNs for monitoring anticoagulation
233
Q

What would you assess (subjective and objective) for in a patient with DVT?

A

Subjective Assessment:

  • pain or tenderness in calf or thigh muscle with rest or exercise
  • tenderness with palpation
  • previous hx DVT
  • risk factors
  • sudden onset chest pain, dyspnea, tachypnea
  • pain starting in leg but moving to chest

Objective Assessment:

  • unilateral or bilateral extremity edema
  • increase circumference in affected area
  • warmth/redness
  • abrupt pain with dorsiflexion
  • engorgement of collateral veins
  • positive dx results
234
Q

What are some nursing interventions for a patient with DVT?

A

Support tissue perfusion:

  • neurovascular assessment, distal pulses, pain, paresthesia, swelling, calf/thigh circumferences
  • initial bedrest with pain
  • avoid prolonged standing & sitting
  • avoid crossing the legs at knee or ankle
  • use compression devices if possible
  • **DO NOT MASSAGE LEGS!!!! **
  • Watch labs, use bleeding precautions

Promote Comfort:

  • pts have physical & psychosocial discomfort
  • use mild analgesics
  • elevate effected leg, warm soaks,
  • NSAIDs
  • encourage expression of fear & anxiety since risk of PE (potentially fatal) is very real
235
Q

What would you educate a patient with a DVT on?

A

Patient & Family Education:

  • Coumadin - action, dosage, side effects of meds; take at same time qd; no ASA monitor s/s bleeding
  • keep follow-up appointments
  • life style modifications to decrease risk factors
  • diet, limit alcohol intake, Medic Alert tag
236
Q

What are some complications with DVT?

A
  • DVT recurrence
  • Pulmonary Embolism
237
Q

What are some common symptoms in patients with a PE?

A
  • Dyspnea
  • Chest pain
  • Apprehension
  • Cough
  • Hemoptysis
  • Sweating / diaphoresis
  • Syncope
  • Palpitations
  • Wheezing
  • Leg pain
  • Leg Swelling
238
Q

What are some characteristics of stasis ulcers?

A
  • Usually have a brownish discoloration around the medial malleolus of the ankle
  • Skin is dry, cracked and itchy
  • Subcutaneous tissue is fibrotic and atrophied
  • Complications: dermatitis and cellulitis
239
Q

How would you prevent stasis ulcers?

A
  • Elevate legs
  • Compression of superficial veins with elastic compression stockings
  • Walking encouraged
  • Avoid crossing legs when sitting
  • Avoid clothes that constrict
  • Keep skin clean and free of injury
240
Q

What are dysrhythmias?

A
  • Disorders of formation or conduction (or both) of electrical impulses within heart
  • Can cause disturbances of:
    • Rate (too fast, too slow)
    • Rhythm (regularity)
    • Both
  • Potentially can alter blood flow, cause hemodynamic changes and instability
  • Diagnosed by analysis of ECG
241
Q

What occurs during each part of the PQRST complex?

A
  • P wave - Atrial depolarization (atrial contraction)
  • QRS - Ventricular depolarization (ventricles are contrating)
  • T wave - Ventricular repolarization (ventricles relaxing)
242
Q

What occurs during the PR interval on an EKG?

A

Atrial depolarization + delay in AV junction (AV node/Bundle of His)

(delay allows time for the atria to contract before the ventricles contract)

243
Q

Describe the impulse conduction in the heart

A

Sinoatrial node –> AV node –> Bundle of His –> Bundle Branches –> Purkinje fibers

244
Q

What are the differnt nodes of the heart?

A
  • SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.
  • AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.
  • Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.
245
Q

What are the characteristics of a P-wave? (ADD PIC)

A
  • Represents depolarization of the atria
  • Present or Absent
  • Shape: gently rounded, does not exceed 2 to 3 mm in amplitude and is
246
Q

What are some characteristics of the PR interval? (ADD PIC)

A
  • Measures the amount of time it takes for the impulse to travel from the SA node to the ventricles
  • Measured from beginning of the P wave to the beginning of the QRS complex
  • Normal range: 0.12-0.20 sec
247
Q

What are some characteristics of the QRS complex? (ADD PIC)

A
  • Represents depolarization of the ventricles
  • Often the most significant portion of the EKG
  • Shape: 0.06-0.12 sec
248
Q

What are some characteristics of the ST segment? (ADD PIC)

A
  • Represents the plateau (phase 2) of the action potential
  • Normally isoelectic because all cells are at zero potential and no current flows
  • Shape: baseline, elevation or depression by 1 mm above or below is abnormal
  • If above isoelectric line =
249
Q

What are some characteristics of the T wave? (ADD PIC)

A
  • Represents the ventricles being rapidly repolarized
  • Shape: rounded, slightly asymmetric, same direction as QRS, height should not exceed 5 mm
250
Q

What are some characteristics of the QT interval? (ADD PIC)

A
  • Measures entire duration of ventricular depolarization and repolarization
  • Varies with age, gender and heart rate
  • Should be less than half the preceding R-R interval
251
Q

What are some characteristics of the U wave? (ADD PIC)

A
  • Represents a part of the latter phase of ventricular repolarization
  • Usually not seen
  • Shape: < 2 mm in height
252
Q

What is the Six step approach to analyze ECG?

A
  1. What is the Rate (Too fast ,too slow)
  2. Is the rhythm Regular ( How does it look)
  3. Are the P waves present & in which direction (upright?)
  4. Are the QRS complexes present ( wide or narrow)
  5. P and QRS related
  6. PR interval ( prolonged or short. Conduction problems)
253
Q

What are the differnt types of arrhythmias?

A
  • Sinus Rhythms
  • Premature beats
  • Ventricular Arrhythmias
  • AV Junctional Blocks
254
Q

How do you measure heartrate from an EKG stip?

A

Count the PQRS complexes in a 6 sec strip and multiply by 10

255
Q

What are sinus Rhythms?

A
  • Sinus Rhythms are those that originate from the SA node.
  • P wave before every QRS
  • P wave in same direction as QRS
  • Normal Sinus Rhythm
  • Sinus Bradycardia
  • Sinus Tachycardia
256
Q

What causes sinus bradycardia?

A

SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

257
Q

What causes sinus tachycardia?

A
  • SA node is depolarizing faster than normal, impulse is conducted normally.
  • Remember: sinus tachycardia is a response to physical or psychological stress, IT IS NOT a primary arrhythmia.
  • 100bpm+
258
Q

What causes premature atrial contractions and what are some characteristics of it?

A

Caused by:

Excitation of an atrial cell forms an impulse that is then conducted normally through the AV node and ventricles.

Characteristics:

  • Deviation from NSR
  • These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.
  • When an impulse originates anywhere in the atria (SA node, atrial cells, AV node, Bundle of His) and then is conducted normally through the ventricles, the QRS will be narrow .
259
Q

What are Premature Ventricular Contractions?

A

One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles (wide QRS complex).

THEY ARE A RED FLAG, NO Cardiac Output!!

260
Q

What are some characteristics of PVC’s?

A
  • Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes.
  • When there are more than 1 premature beats and look alike, they are called “uniform”. When they look different, they are called “multiform”.
  • They don’t have a pulse, and don’t increase cardiac output
  • You don’t count them in your rate
  • They can be inverted or can appear widened.
261
Q

What are the different types of Supraventricular arrhythmias?

A
  • Atrial Fibrillation
  • Atrial Flutter
  • Paroxysmal Supraventricular Tachycardia
262
Q

What causes atrial fibrillation?

A

Recent theories suggest that it is due to multiple re-entrant wavelets conducted between the R & L atria. Either way, impulses are formed in a totally unpredictable fashion. The AV node allows some of the impulses to pass through at variable intervals (so rhythm is irregularly irregular).

263
Q

What are some characteristics of atrial fibrillation?

A
  • No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node).
  • Atrial activity is chaotic (resulting in an irregularly irregular rate).
  • Decrease in CO
264
Q

What causes atrial flutter?

A

Reentrant pathway in the right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in the AV node as the node repolarizes).

265
Q

What are some characteristics of atrial flutter?

A
  • No P waves. Instead flutter waves (note “sawtooth” pattern) are formed at a rate of 250 - 350 bpm.
  • Only some impulses conduct through the AV node (usually every other impulse).
  • In atrial flutter, the heart’s atria beat very fast but at a regular rate. Atrial flutter is caused by irregular circuitry within the atria.
  • The fast rate results in weak contractions of the atria. The rapid signals entering the AV
266
Q

What are the differences between atrial flutter and atrial fibrillation?

A
  • Regularity - Atrial fib has no organization whereas flutter has a pattern
  • Shape - Atrial flutter doesn’t have P waves
267
Q

What causes Paroxysmal Supraventricular Tachycardia (PSVT)?

A
  • Etiology: There are several types of PSVT but all originate above the ventricles (therefore the QRS is narrow).
  • Most common: abnormal conduction in the AV node (reentrant circuit looping in the AV node).
  • Can be caused by PAC
268
Q

What are some characteristics of Paroxysmal Supraventricular Tachycardia?

A
  • The heart rate suddenly speeds up, often triggered by a PAC (not seen here) and the P waves are lost.
  • Super high BPM
  • It is an emergency, intervene
269
Q

What are the different types of ventricular arrhythmias?

A
  • Ventricular Tachycardia
  • Ventricular Fibrillation
270
Q

What is ventricular tachycardia?

A
  • It is a rapid heart rate that originates with abnormal electrical signals in the ventricles.
  • The rapid heart rate doesn’t allow the ventricles to fill and contract efficiently to pump enough blood to the body.
  • Ventricular tachycardia is often a life-threatening medical emergency.
271
Q

What causes ventricular tachycardia?

A
  • There is a re-entrant pathway looping in a ventricle (most common cause).
  • Ventricular tachycardia can sometimes generate enough cardiac output to produce a pulse; at other times no pulse can be felt.
272
Q

What are some characteristics of ventricular tachycardia?

A
  • Impulse is originating in the ventricles (no P waves, wide QRS).
  • Lethal
273
Q

What occurs during ventricular fibrillation?

A
  • It is a rapid, chaotic electrical impulses cause your ventricles to quiver uselessly instead of pumping blood.
  • Without an effective heartbeat, your blood pressure plummets, instantly cutting off blood supply to your vital organs — including your brain.
  • Most people lose consciousness within seconds and require immediate medical assistance, including cardiopulmonary resuscitation (CPR).
274
Q

What causes Ventricular Fibrillation?

A
  • A problem in the electrical impulses traveling through your heart after a first heart attack, or problems resulting from a scar in your heart’s muscle tissue from a previous heart attack.
  • Can be caused by a ventricular tachycardia (VT)
    *
275
Q

What are some characteristics of ventricular fibrillation?

A
  • The ventricular cells are excitable and depolarizing randomly.
  • Rapid drop in cardiac output and death occurs if not quickly reversed
  • Completely abnormal.

N3523 Adult and Older Adult Health Care II (9 decks)

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