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dilates veins causes venous pooling throughout the body with less blood return to the heart (less preload) to decrease stress to the heart and dilates the arteries leading to the heart which improves O2 supply. Sublingual or buccal. Carry medication at all times away from moisture, air and light and replace every 6 months. Take just before exercise. If pain persists after taking 3 doses 5 minutes apart, go to the ER. Side effets include flushing, throbbing HA, hypotension, tachycardia. (sit down after taking to prevent syncope.
blocks the sympathetic stimulation to the heart (blocking epinephrine and norepinephrine) at the bets-adrenergic receptors. Results in reduced heart rate, blood pressure and contractility. Side effects include hypotension, bradycardia, AV block, acute heart failure. Mask symptoms of hypoglycemia (careful evaluation of BS for DM patients on insulin.) Do not stop taking abruptly because angina may worsen and MI may develop (give to patient who is NPO prior to surgery)
Calcium Channel Blockers
Reduction in muscle contraction by blocking calcium channels in cardiac muscles and decreasing intracellular calcium. Slower heart rate from decreased SA and AV node conduction. Relaxation of blood vessels causing lower BP. Not a first line drug for Angina. Used as an adjunct if nitro and BB not effective or can not tolerate their side effects. Side effects include AV block, bradycardia, constipation and gastric distress.
Surgical interventions for CAD
PTCA - precutaneous transluminal coronary angioplasty, stents
CABG - coronary artery bypass graft
Death of myocardial tissue due to blockage of the oxygenated blood supply to the heart.
Severe, crushing or vice-like pain, often radiating to the jaw, arms or back, weakness, hypotension and tachycardia (or bradycardia), Nausea/vomiting, pallor; cool, clammy skin
treat ventricular arrhythmia by minimal depression of depolarization and shortened depolarizaiton. Symptoms of CNS changes such as bradycardia and GI distress.
Morphine for MI
IV bolus to reduce pain and anxiety. Relaxes bronchioles to enhance oxygenation. Symptoms include depressed respirations.
Vasodilators - Angiotensin-converting enzyme inhibitor (ACEI)
prevents conversion of angiotensin I to angiotension II which is a potent vaso constrictor, therefore the blood vessels dilate reducing blood pressure. Also causes the kidneys to excrete sodium and fluid (dieresis)
Used in acute MI to dissolve the thrombus or clot in the coronary artery. Patient will need to be put on bleed precaution. Indications, chest pain greater than 20 min not relieved with nitro, ST segment elevation, less than 6 hours from onset of pain.
Blood pressure HTN parameters
Normal less than or equal to 120 and less than or equal to 80
Prehypertension 120-139 or 80-89
HTN stage 1 140-159 or 90-99
HTN stage 2 greater than or equal to 160 or greater than or equal to 100
Essential hypertension or Primary hypertension
High BP from an unknown cause; 90-95% of people with HTN fall in this category
HTN is directly related to peripheral resistance (PR)
BP = CO (SV x HR) X peripheral resistance (PR)
Obesity - affects renin-angiotensin-aldosterone system which controls blood volume. More mass requires more blood vessels and the heart needs to pump harder. Lack of exercise.
Smoking - injures blood vessle walls and speeds up the process of hardening the arteries.
Stress - Sympathetic nervous system overactivity causes heart to increase rate and force of contraction and blood vessels to constrict
Arteriosclerosis and atherosclerosis - narrowing and hardening of arteries.
other risk factors HTN
family history, increased age - multiple changes to the heart and blood vessels as ppl age, race (AA) - genetic factors, diet high in salt and saturated fats - kidneys can not keep up with high salt levels and it ends up in the bloodstream and attracts water and increases volume. Saturated fats contribute to athrosclerosis.
Sympathetic nervous system from stress
Adrenal glands - cortex produces aldosterone which helps maintain salt and water
Underlying disease or abnormality
Renal abnormalities - many different abnormalities that can cause elevated BP and elevated BP can cause
Endocrine and Metabolic disorders -lack of insulin, too much epinephrine and aldosteron.
Metabolic syndrome (high blood pressure, high blood sugar, excess abdominal fat, high cholesterol levels)
CNS - regulates blood pressure
Coarctation of the aorta - congenital abnormality where the aorta narrows at the ductus arterioles
pheochromocytoma - tumor of the adrenal gland.
Systolic over 240
S/S CHF and CNS dysfunction
Tx: Nitroprusside & Diuretics
hypertensive emergency where the BP can result in target organ damage.
CNS - can lead to stroke, CV can lead to MI, renal - can lead to kidney damage.
Acute can cause HA, N/T, SOA, nose bleeds and anxiety
Systolic greater than 220
Diastolic greater than 115
the amount of blood presented to the ventricle just before systole.
the amount of resistance to ejection of blood from a ventricle
the percentage of blood volume in the ventricles at the end of diastole that is ejected during systole.
the amount of blood pumped out of the ventricle with each contraction.
Symptoms of venous insufficiency ulcers
present pedal pulses, edema, pigmentation changes of a reddish blue color. Ulcers caused by venous insufficiency will be irregular in shape and usually located around the ankles or the anterior tibial area.
Characteristics of arterial insufficiency ulcers
include location at the tips of the toes, great pain, and circular shape with a pale to black ulcer base.
A nurse is instructing a client about using antiembolism stockings. Antiembolism stockings help prevent deep vein thrombosis (DVT) by:
forcing blood into the deep venous system
is considered a thrombolytic, which lyses and dissolves thrombi. Thrombolytic therapy is most effective when given within the first 3 days after acute thrombosis. Heparin, Coumadin, and Lovenox do not lyse clots
Hardening and loss of elasticity.
The most important reason for a nurse to encourage a client with peripheral vascular disease to initiate a walking program is that this form of exercise:
it decreases venous congestion
Stable angina has predictable and consistent pain that occurs on exertion and it relieved by rest
Preinfarction angina is also known as unstable angina.
is exhibited by pain at rest with reversible ST-segment elevation.
antidote to heparin
Protamine sulfate is known as the antagonist to heparin.
Which chamber of the heart is responsible for pumping blood to all the cells and tissues of the body?
The left ventricle pumps that blood to all the cells and tissues of the body.
Which chamber of the heart is responsible for receiving oxygenated blood from the lungs?
The left atrium receives oxygenated blood from the lungs
the ability of the cardiac muscle to shorten in response to an electrical impulse.
the electrical activation of a cell caused by the influx of sodium into the cell while potassium exits the cell
the return of the cell to the resting state, caused by reentry of potassium into the cell while sodium exits the cell.
Which chamber of the heart is responsible for receiving deoxygenated blood from the venous system?
The right atrium receives deoxygenated blood from the venous system.
It is important for the nurse to encourage the patient to rise slowly from a sitting or lying position because
gradual changes in position provide time for the heart to increase its rate of contraction to resupply oxygen to the brain and not blood pressure or heart rate.
loop diuretics: action
inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle
a preparation of human BNP that mimics the action of endogenous BNP, causing dieresis and vasodilation, reducing blood pressure, and improving cardiac output. It is a preload and afterload reducer.
an MI without signs or symptoms
Conditions that mimic the signs and symptoms of an MI - spontaneous pneumothorax, pulmonary embolism, perferrated peptic ulcer, pancreatitis, cholecystitis.
1st layer, this is the inner layer consisting of endothelial tissue lining the cavity and covering the flaps of the valves.
2nd layer; this is the heart muscle. The cells of the myocardium differ from skeletal and smooth muscles.
3rd layer; this is the outer layer of the heart.
4th layer; this is a thin sac surrounding the heart.
The ionic movement within a single cell is referred to as the..
cardiac action potential.
Cardiac output =
stroke volume X heart rate. The amount of blood with each heartbeat X heart rate per minute.
what is left in the ventricle at the end of contraction.
Normal left ventricle ejection fraction is 55-65%. This is how much blood is left in the ventrical after the contraction.
The more blood left in the ventricle after the contraction, the higher the risk for heart failure.
the sound of tricuspid and mitral valve closure at the same time. (Heard best at the apex)Two phases of the cardiac cycle:
Systole: The time between S1 and S2
SI heart sound
the sound of pulmonic and aortic valves closing at the same time. (Heard best at the base of the heart)
Diastole: The time between S2 and repeat of S1S
S2 heart sound
CK - creatine kinase
used to suggest infarct right after and just hours after the infarct.
The most sensitive test for MI
Troponin T & I, released after 2-4 hours and lasts up to 7 days
High when muscle tissue is damaged but it lacks specificity the advantage is responding very rapidly.
Other lab tests
Lipid profile - Risk factor for heart disease.
BNP - Increased with heart failure.
C-reactive protein - Rise in response to inflammation.
Homocysteine - high levels related to development of heart and blood vessel disease.
A common complication of CHF. The accumulation of fluid in the lungs - causing crackles.
Results from any type of chronic heart disease (i.e: valvular, myopathy) that causes a strain on the left ventricle which in turns creates high pressure in the pulmonary vascular bed and forcing fluid from the intravascular compartment into the lung tissue.
Causes of Pulmonary Edema
Congestive heart failure
Chronic heart disease
Non cardiac causes:
Toxins (i.e. From severe infection or inhalants)
Drug overdose- prescribed & street drugs
Pulmonary disease (i.e: pulmonary embolism)
IV fluid therapy (Rapid infusion of if fluids or blood products).
Pathophysiology of Pulmonary edema
Fluid moves OUT of the Vascular space -
ENTERS the Interstitial Lung tissue -
moves INTO the Alveolar spaces and finally INTO the Bronchi.
This leads to -
Decreased diffusion of oxygen
Asphyxia (A condition of severely deficient supply of oxygen to the body that arises from being unable to breathe normally. An example of asphyxia is choking)
First the fluids leave the vascular space and enters the interstitial lung tissue.
Second the fluid moves into the alveolar spaces which is a gas blood barrier between the alveolar space and the pulmonary capillaries allows for rapid gas exchange. This causes crackles upon auscultation.
Third fluid enters the bronchioles/bronchi
Results in low diffusion of oxygen due to fluids in the way, tissue hypoxia or lack of oxygen and asphyxia which is extreme decrease in the amount of oxygen and increase of carbon dioxide leads to loss of consciousness or death.
I. Initial (Interstitial) state of PulmEdema s/s
SOB on exertion (i.e., when climbing stairs or walking)
Nocturnal dyspnea (i.e., when lying down or sleeping)
Increased respiratory rate (Even at rest)
Cough (Which may be frothy and tinged with blood)
Restlessness & anxiety from feeling of suffocating
III. Acute (Bronchial) stage of PulmEdema
Wheezing to diminished (from the small bronchioles retaining fluid)
Blood tinged sputum that is frothy
Metabolic acidosis (results because of lactic acid buildup. The lactic acid is a by product of anaerobic metabolism which happens when there is not enough oxygen for aerobic metabolism)
Diminished breath sounds
II. Advanced (Alveolar) stage of PulmEdema
Increased respiratory rate/SOB (even at rest)
Use of accessory muscles to inflate lungs
Adventitious lung sounds (crackles and wheezing)
Cyanosis (bluish grey tint to skin)
Diaphoresis (cool and clammy)
Arrythmias/Decreased BP (the heart is overloaded and not working effectively)
Confusion (from low oxygen and increased CO2 - respiratory alkalosis)
Lungs become stiff and can not expand.
Medical Management of Pulmonary Edema
Oxygen - Monitoring of O2 Sats
Low sodium diet
Medical management of pulmonary edema depends on stage.
O2 - monitor blood gases and O2 saturation. May need to be on 100% O2 facemask
Diuretics such as loop diuretic (lasix) peaks ½ hour with a duration of 2 hours.
Digoxin and other cardiac meds discussed earlier
Bronchodilators to keep open
Morphine to reduce anxiety and heart workload. Keep narcan nearby to reverse the drug if respiratory rate drops or becomes unresponsive.
Fluid restrictions for example less than 500ml/day
Low sodium diet
Positioning with HOB elevated or reverse trendelberg.
Nursing Diagnosis for Pulmonary Edema
Fluid volume excess R/T . . .
Ineffective breathing pattern R/T . .
Ineffective airway clearance R/T . . .
Impaired gas exchange R/T . . .
Activity intolerance R/T . . .
Fatigue R/T . . .
Anxiety R/T . . .
Alteration in thought process R/T. . .
Risk for injury; arrythmias R/T . . .
Risk for infection;bronchopulmonary R/T . . .
Knowledge deficit R/T . . .
Left Sided Heart Failure
Left ventricle becomes stiff and resistant to filling.
Uncontrolled left-sided heart failure can lead to right-sided heart failure.
Signs/Symptoms of left-sided failure:
Shortness of breath
Paroxysmal nocturnal dyspnea
Left Sided Heart Failure Cont....
Most common cause of MI - portion of the myocardium that does not get oxygen has died and becomes stiff. Loss of elasticity and resists filling
Uncontrolled left side heart failure leads to right side heart failure. LSHF - blood backs up into the lungs and right ventricle fights to pump blood into the lungs. This extra force from the right ventricle and once again, over time the heart enlarges as the workload increases, the walls of the chamber grow thicker.
Shortness of breath from left side backing up into the lungs. Impaired gas exchange related to pulmonary congestion. Very important to assess for lung sounds when a patient states that they are short of air and have a cough.
Edema from the right side backing up into the peripheral. Fluid volume excess
Fatigue from lack of oxygen delivered to the brain and tissues. Activity intolerance related to decreased oxygenation / tissue perfusion
Nursing Diagnosis for Left Sided CHF
Alteration in cardiac output R/T . . .
Impaired gas exchange R/T . . .
Fluid volume excess R/T . . .
Activity intolerance R/T . . .
Alteration in tissue perfusion R/T . . .
Self Care deficits R/T . . .
Knowledge deficit R/T . . .
Anxiety R/T . . .
Risk for injury; digoxin toxicity R/T . . .
Risk for fluild/electrolyte imbalance R/T . . .
Potential for complications R/T . . .
Ride Sided Heart Failure s/s
Jugular vein distention (JVD)
Edema (Sacral area if pt. in bed)
Liver enlargement (Hepatomegaly)
Anorexia & Nausea
medical treatment for heart CHF
Reduce cardiac workload.
Strengthen myocardial contractility.
Eliminate excess fluids.
Low sodium diet.
Detect and relieve underlying cause.
Side effects of medical treatment of CHF
Nausea and vomiting
Visual disturbances (yellow green halos) - biggest hint of toxicity!!
Digitalis - Digoxin
Digitalis - Digoxin
Increases force of contractions.
Increases cardiac output.
Increases circulation and tissue perfusion- should increase the cap refill quickly - should be able to assess quickly after giving.
Increases renal blood flow
Therapeutic levels = 0.9 to 2.0
STOP if levels above and pt having S/S & contact the Dr.
Nursing responsibilities with Digoxin
Assess vital signs.
Assess therapeutic response- Therapeutic response would include a decrease of SOA, edema, fatigue and normal pulse.
Assess for signs./symptoms of toxicity.
Check lab results- digoxin level and electrolytes including K+
Checking pulse- apical heart rate for one minute. If less than 60 bpm, or irregular rhythm then hold digoxin.
Signs/symptoms to report
Over the counter drugs
Do not stop abruptly
Warfarin (coumadin) is the antagonist of...
Vitamin K. Vitamin K is a clotting factor which makes warfarin an anticoagulant.
Used for patients with atria arrhythmias.
Avoid foods high in vitamin K
Atria arrhythmias cause..
Stasis of blood in the atria which allow the platelets and other products in the blood to form a thrombus. A thrombus when pumped into the body can cause a stroke from cerebreal blockage, heart attack from coronary artery blockage or a pulmonary embolism from pulmonary artery blockage.
Decreases blood pressure-Inhibits the conversion of angiotensin I to angiotensin II which is a potent vaso constrictor.
Blocks release of aldosterone (aldosterone increases the retention of Na+). With aldosterone blocked there is increased excretion of Na+ and water which lowers blood pressure.
Decreases systemic vascular resistance (decrease preload pressure and decrease afterload resistance)
leading to -
Improved cardiac output
Improved tissue perfusion
Angiotensin Converting Enzyme Inhibitors suffix pril
Catopril (Capoten), enalapril (Vasotec), and lisinopril (Zestril)
Side effect - angioedema rapid swelling ( edema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues. ACE cough.
Angiotensin Receptor Blockers
ARBS- sartan suffix
Block the activation of angiotensin II
Valsartan and losartan are some examples.
Give an angiotensin II receptor blocker if the patient has tried an ACE inhibitor but can not tolorate it because of the ACE cough.
Blocks beta receptors in the SNS. Lowers cardiac workload.
Suffix is -lol. Metoprolol and propanolol.
Lowers cardiac workload.
A nurse suspects that a client has digoxin toxicity. The nurse should assess for:
Vision changes, such as halos around objects, are signs of digoxin toxicity.
Which of the following is an important assessment parameter for the patient diagnosed with congestive heart failure?
Explanation: During a head-to-toe assessment of a patient with congestive heart failure, the nurse checks for dyspnea, auscultates apical heart rate, counts radial heart rate, measures BP, checks for distended neck veins, and documents any signs of peripheral edema, lethargy, or confusion.
A nurse is caring for a client with left-sided heart failure. To reduce fluid volume excess, the nurse should anticipate using:
Explanation: Diuretics, such as furosemide (Lasix), reduce total blood volume and circulatory congestion. Antiembolism stockings prevent venostasis and thromboembolism formation. Oxygen administration increases oxygen delivery to the myocardium and other vital organs. Anticoagulants prevent clot formation but don't decrease fluid volume excess.
A patient has been diagnosed with systolic heart failure. The nurse would expect the patient's ejection fraction to be at which level?
Answer: Severely reduced Ex.>
Explanation: The ejection fraction is normal in diastolic heart failure, but severely reduced in systolic heart failure.
A patient is prescribed digitalis preparations. Which of the following conditions should the nurse closely monitor when caring for the patient?
Answer: Electrolyte and water loss Ex.>
Explanation: The nurse should closely monitor a patient being administered diuretics for electrolyte and water loss. Digitalis preparations (not diuretics) are potent and may cause various toxic effects. The nurse should monitor the patient for signs of digitalis toxicity, not just during the initial period of therapy, but throughout care management.
Antidote to Digoxin
Digoxin immune FAB (Digibind)
Digibind binds with digoxin and makes it unavailable for use. The Digibind dosage is based on the digoxin level and the patient's weight.
A client is admitted to the hospital with systolic left-sided heart failure. The nurse knows to look for which of the following assessment findings for this client?
Answer: Pulmonary congestion Ex.>
Explanation: When the left ventricle cannot effectively pump blood out of the ventricle into the aorta, the blood backs up into the pulmonary system and causes congestion, dyspnea, and shortness of breath.
A 73-year-old client has been admitted to the cardiac step-down unit where you practice nursing. After diagnostics, she was brought to your unit with acute pulmonary edema. What kind of symptoms would you expect to find during your assessment?
Answer: Moist, gurgling respirations
Explanation: Clients with acute pulmonary edema experience sudden dyspnea, wheezing, orthopnea, cough, cyanosis, and tachycardia. Respirations sound moist or gurgling.
While auscultating the heart sounds of a client with heart failure, the nurse hears an extra heart sound immediately after the second heart sound (S2). The nurse should document this as:
Answer: a third heart sound (S3).
Explanation: An S3 is heard following an S2, which commonly occurs in clients experiencing heart failure and results from increased filling pressures. An S1 is a normal heart sound made by the closing of the mitral and tricuspid valves. An S4 is heard before an S1 and is caused by resistance to ventricular filling. A murmur is heard when there is turbulent blood flow across the valves
Frequently, what is the earliest symptom of left-sided heart failure?
Dyspnea on exertion is often the earliest symptom of left-sided heart failure.
Deposit of fatty streaks leading to irregular thickening and plaque formation. The plaque may rupture and a thrombus might form, obstructing blood flow in the coronary artery.
The sinoatrial or SA node gives rise to the self-generating impulse known as the heartbeat. It is located at the boarder of the superior vena cava and the right atrium. it is the primary pacemaker of the heart which generates electrical impulses at a rate of 60 - 100 per minute.
The SA node is innervated by the sympathetic (increased rate) and parasympathetic (decreased rate) nerve fibers.
Rate changes in response to body's needs.
Impulse travels via specialized fibers through the right atrium to the AV node which is located near the tricuspid valve.
The impulse is relayed to the ventricles via the bundle of His which is separated into the left and right bundle branches. These impulses are located in the ventricle septum. The impulse ends at the purkinje fibers within the ventricle walls.
A nurse is reviewing laboratory values for a client diagnosed with hyperlipidemia 6 months ago. Which results indicate that the client has been following his therapeutic regimen?
a) High density lipoproteins (HDL) increase from 25 mg/dl to 40 mg/dl.
b) Total cholesterol level increases from 250 mg/dl to 275 mg/dl.
c) Triglycerides increase from 225 mg/dl to 250 mg/dl.
d) Low density lipoproteins (LDL) increase from 180 mg/dl to 190 mg/dl.
Correct response: High density lipoproteins (HDL) increase from 25 mg/dl to 40 mg/dl.
Explanation: The goal of treating hyperlipidemia is to decrease total cholesterol and LDL levels while increasing HDL levels. HDL levels should be greater than 35 mg/dl. This client's increased HDL levels indicate that he's followed his therapeutic regimen. Recommended total cholesterol levels are below 200 mg/dl. LDL levels should be less than 160 mg/dl, or, in clients with known coronary artery disease (CAD) or diabetes mellitus, less than 70 mg/dl. Triglyceride levels should be between 100 and 200 mg/d
Hyperlipidemia Goal of treatment
The goal of treating hyperlipidemia is to decrease total cholesterol and LDL levels while increasing HDL levels. HDL levels should be greater than 35 mg/dl. This client's increased HDL levels indicate that he's followed his therapeutic regimen. Recommended total cholesterol levels are below 200 mg/dl. LDL levels should be less than 160 mg/dl, or, in clients with known coronary artery disease (CAD) or diabetes mellitus, less than 70 mg/dl. Triglyceride levels should be between 100 and 200 mg/d.
the period of ventricular relaxation resulting in ventricular filling.
What is the management of ADHF?
What is hemodynamic monitoring used for?
If the SA node fails, what takes over as the backup pacemaker and what is the rate?
What is the purpose of Right Heart Catheterization?
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