NCLEX: Cardiovascular disorders

Cardiovascular disorders: Common cardiovascular disorders

Focus topic: Cardiovascular disorders

Cardiovascular disorders

Treatments include diuretics that reduce preload by decreasing total blood volume and circulatory congestion. ACE inhibitors dilate blood vessels and decrease systemic vascular resistance, reducing the heart’s workload. The patient who can’t tolerate ACE inhibitors can instead receive vasodilators. These increase cardiac output by reducing impedance to ventricular outflow, which decreases after load.


Strengthening medicine

Focus topic: Cardiovascular disorders

  • Digoxin may help strengthen myocardial contractility. Betaadrenergic blockers may prevent cardiac remodeling (left ventricular dilation and hypertrophy). Nesiritide (Natrecor), a human BNP, can augment diuresis and decrease after load. Positive inotropic agents, such as I.V. dopa mine or dobutamine, are reserved for those with end-stage heart failure or those awaiting heart transplantion.

Stop and go

Focus topic: Cardiovascular disorders

The patient must alternate periods of rest with periods of activity and follow a sodium-restricted diet with smaller, more frequent meals. He may have to wear antiembolism stockings to prevent venostasis and possible thromboembolism formation. The practitioner may also order oxygen therapy.
Although controversial, surgery may be performed if the patient’s heart failure doesn’t improve after therapy and lifestyle modifications. If the patient with valve dysfunction has recurrent acute heart failure, he may undergo surgical valve replacement. A patient with heart failure caused by ischemia may undergo CABG, PTCA, or stenting.

Remodeling show

Focus topic: Cardiovascular disorders

The Dor procedure, also called partial left ventriculectomy or ventricular remodeling, involves the removal of nonviable heart muscle to reduce the size of the hypertrophied ventricle, thereby allowing the heart to pump more efficiently. Patients with severe heart failure may benefit from a mechanical VAD or cardiac transplantation. A patient with life-threatening arrhythmias may have an internal cardioverter-defibrillator implanted. Insertion of a biventricular pacemaker can control ventricular dyssynchrony.

What to do

  • Frequently monitor BUN, serum creatinine, potassium, sodium, chloride, and magnesium levels.
  • Reinforce the importance of adhering to the prescribed diet. If fluid restrictions have been ordered, arrange a mutually acceptable schedule for allowable fluids.
  • Weigh the patient daily to assess for fluid overload.
  • To prevent deep vein thrombosis from vascular congestion, assist the patient with range-of-motion (ROM) exercises. Enforce bed rest, and apply antiembolism stockings. Watch for calf pain and tenderness and unilateral edema. Organize activities to provide periods of rest.
  • Evaluate the patient. Successful recovery should reveal clear lungs, normal heart sounds, adequate blood pressure, and absence of dyspnea or edema. The patient should be able to perform ADLs and maintain his normal weight.

Cardiovascular disorders

Cardiovascular disorders: Hypertension

Focus topic: Cardiovascular disorders

Hypertension refers to an intermittent or sustained elevation in diastolic or systolic blood pressure. Essential (idiopathic) hypertension is the most common form. Secondary hypertension results from a number of disorders. Malignant hypertension is a severe, fulminant form of hypertension common to both types. Hypertension represents a major cause of stroke, cardiac disease, and renal failure. Detecting and treating it before complications develop greatly improves the patient’s prognosis. Severely elevated blood pressure may become fatal.

What causes it

Scientists haven’t been able to identify a single cause for essential hypertension. The disorder probably reflects an interaction of multiple homeostatic forces, including changes in renal regulation of sodium and extracellular fluids, in aldosterone secretion and metabolism, and in norepinephrine secretion and metabolism.
Secondary hypertension may be caused by renal vascular disease, pheochromocytoma, primary hyperaldosteronism, Cushing’s syndrome, or dysfunction of the thyroid, pituitary, or parathyroid glands. It may also result from coarctation of the aorta, pregnancy, and neurologic disorders.
Certain risk factors appear to increase the likelihood of hypertension. These include:

  • family history of hypertension
  • race (more common in blacks)
  • gender (more common in men)
  • diabetes mellitus
  • stress
  • obesity
  • high dietary intake of saturated fats or sodium
  • tobacco use
  • hormonal contraceptive use
  • sedentary lifestyle
  • aging.

Pathophysiology

Essential hypertension usually begins insidiously as a benign disease, slowly progressing to a malignant state. If left untreated, even mild cases can cause major complications and death.

Why? Why? Why?

Focus topic: Cardiovascular disorders

Several theories help to explain the development of hypertension. It’s thought to arise from:

  • changes in the arteriolar bed that cause increased resistance
  • abnormally increased tone in the sensory nervous system that originates in the vasomotor system centers, causing increased peripheral vascular resistance
  • increased blood volume resulting from renal or hormonal dysfunction
  • increased arteriolar thickening caused by genetic factors, leading to increased peripheral vascular resistance
  • abnormal renin release, resulting in the formation of angiotensin II, which constricts the arterioles and increases blood volume.The domino effect

The pathophysiology of secondary hypertension is related to the underlying disease. The most common cause is chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal artery stenosis can interfere with sodium excretion, the renin-angiotensin-aldosterone system, or renal perfusion. This in turn causes blood pressure to rise.
Other diseases can also underlie secondary hypertension. In Cushing’s syndrome, increased cortisol levels raise blood pressure by increasing renal sodium retention, angiotensin II levels, and vascular response to norepinephrine. In primary aldosteronism, increased intravascular volume, altered sodium concentrations in vessel walls, or very high aldosterone levels cause vasoconstriction (increased resistance).
Pheochromocytoma is a secreting tumor of chromaffin cells, usually of the adrenal medulla. It causes hypertension by increasing epinephrine and norepinephrine secretion. Epinephrine functions mainly to increase cardiac contractility and rate; norepinephrine, mainly to increase peripheral vascular resistance.

Cardiovascular disorders

What to look for

Signs and symptoms may include:

  • blood pressure measurements of more than 140/90 mm Hg on two or more readings taken at two or more visits after an initial screening
  • throbbing occipital headaches upon waking
  • drowsiness
  • confusion
  • vision problems
  • nausea.

Expect a patient with secondary hypertension to have clinical manifestations of the primary disease. Other clinical effects don’t appear until complications develop as a result of vascular changes in target organs. These effects include:

  • left ventricular hypertrophy
  • angina
  • MI
  • heart failure
  • stroke
  • transient ischemic attack
  • nephropathy
  • peripheral arterial disease
  • retinopathy.

What tests tell you

  • In urinalysis, protein, red blood cell (RBC), and WBC levels may indicate glomerulonephritis.
  • Elevated blood glucose levels may indicate diabetes.
  • Complete blood count may reveal anemia (causes a high output state resulting in hypertension) or polycythemia (increases the risk of hypertension and stroke).
  • Lipid profile reveals elevated total cholesterol and low-density lipoprotein levels.
  • xcretory urography shows renal atrophy, indicating chronic renal disease; one kidney more than 5/8 (1.5 cm) shorter than the other suggests unilateral renal disease.

Cardiovascular disorders

  • Serum potassium levels are less than 3.5 mEq/L, indicating adrenal dysfunction (primary hyperaldosteronism).
  • BUN level is greater than 20 mg/dl and creatinine level is greater than 1.5 mg/dl, suggesting renal disease. Other tests help detect cardiovascular damage and other complications:
  • ECG may show left ventricular hypertrophy or ische mia.
  • Echocardiography may show left ventricular hypertrophy.
  • Chest X-ray may show cardiomegaly.

How it’s treated

Treatment of secondary hypertension includes correcting the underlying cause and controlling hypertensive effects. Although essential hypertension has no cure, lifestyle modifications along with drug therapy can control it. Lifestyle modifications for all patients may include changing diet (including restricting sodium and saturated fat intake), learning relaxation techniques, exercising regularly, quitting smoking, and limiting alcohol use.

Drugs can drop the pressure

Focus topic: Cardiovascular disorders

The need for drug therapy is determined by blood pressure and the presence of target organ damage or risk factors. Drug therapy for uncomplicated hypertension usually begins with a thiazide diuretic, an ACE inhibitor, or a beta-adrenergic blocker. Other anti hypertensive drugs include angiotensin II receptor blockers, alpha- receptor blockers, direct arteriole dilators, and calcium channel blockers.

What to do

  • If a patient enters the hospital with hypertension, find out if he was taking his prescribed medication. If not, help the patient to identify reasons for noncompliance. If the patient can’t afford the medication, refer him to an appropriate social service agency. If he suffered severe adverse effects, he may need different medication.
  • Routinely screen all patients for hypertension, especially those at high risk.
  • Evaluate the patient. After successful treatment for hypertension, the patient will have a blood pressure under 140/90 mm Hg at rest, the ability to tolerate activity, and the absence of enlargement of the left ventricle (as revealed by ECG or chest X-ray).

Cardiovascular disorders

Cardiovascular disorders: Hypertrophic cardiomyopathy

Focus topic: Cardiovascular disorders

Hypertrophic cardiomyopathy is a primary disease of the cardiac muscle characterized by disproportionate, asymmetrical thickening of the interventricular septum, particularly in the anteriorsuperior part. It affects both diastolic and systolic function. As the septum hypertrophies, blood flow through the aortic valve becomes obstructed. Mitral insufficiency develops as the papillary muscles become affected. The course of illness varies; some patients demonstrate progressive deterioration. Others remain stable for several years. Sudden cardiac death may also occur.

What causes it

Almost all patients inherit hypertrophic cardiomyopathy as a non– sex-linked autosomal dominant trait.

Pathophysiology

In hypertrophic cardiomyopathy, hypertrophy of the left ventricle and interventricular septum obstruct left ventricular outflow. The heart compensates for the resulting decreased cardiac output by increasing the rate and force of contractions. The hypertrophied ventricle becomes stiff and unable to relax and fill during diastole. As left ventricular volume diminishes and filling pressure rises, pulmonary venous pressure also rises, leading to venous congestion and dyspnea.

What to look for

Clinical features of hypertrophic cardiomyopathy include:

  • angina pectoris
  • arrhythmias
  • dyspnea
  • syncope
  • heart failure
  • systolic ejection murmur (of medium pitch, heard along the left sternal border and at the apex)
  • pulsus bisferiens
  • irregular pulse (with atrial fibrillation).

What tests tell you

  • Echocardiography shows increased thickness of the interventricular septum and abnormal motion of the anterior mitral leaflet during systole.
  • Cardiac catheterization reveals elevated left ventricular enddiastolic pressure and possibly mitral insufficiency.
  • ECG may demonstrate left ventricular hypertrophy, ST-s egment and T-wave abnormalities, deep waves (from hypertrophy, not infarction), left anterior hemiblock, ventricular arrhythmias and, possibly, atrial fibrillation.
  • Phonocardiography confirms an early systolic murmur.

How it’s treated

Treatment seeks to relax the ventricle and to relieve outflow tract obstruction. Propranolol (Inderal), a beta-adrenergic blocker, slows heart rate and increases ventricular filling by relaxing the obstructing muscle, thereby reducing angina, syncope, dyspnea, and arrhythmias. However, propranolol may aggravate symptoms of cardiac decompensation. Calcium channel blockers may be prescribed to relax the heart muscle and improve ventricular filling. Antiarrhythmic drugs may be prescribed to treat arrhythmias. Atrial fibrillation calls for cardioversion to treat the arrhythmia and, because of the high risk of systemic embolism, anticoagulant therapy until fibrillation subsides.

When drugs don’t do it

Focus topic: Cardiovascular disorders

If drug therapy fails, the patient may undergo surgery. Septal myectomy (resection of the hypertrophied septum) alone or combined with mitral valve replacement may ease outflow tract obstruction and relieve symptoms. However, this is an experimental procedure and can cause complications, such as complete heart block and ventricular septal defect. Dual-chamber pacing can prevent progression of hypertrophy and obstruction. Implantable defibrillators may be used in patients with ventricular arrhythmias.

What to do

  • Administer medication as ordered. Warn the patient not to stop taking propranolol abruptly because doing so may cause rebound effects, resulting in MI or sudden death. Before surgery, administer prophylaxis for subacute bacterial endocarditis; tell the patient he’ll also need prophylactic antibiotics before dental work.
  • Provide psychological support. Refer the patient for psychosocial counseling to help him and his family accept his restricted lifestyle and cope with his poor prognosis. Urge parents of a school-age child to arrange for continuation of studies in the hospital.
  • Evaluate the patient. If treatment proves successful, the patient will show adequate tissue perfusion, clear lungs, and absence of edema and syncopal episodes. He’ll be able to maintain his weight, tolerate activity, and maintain adequate blood pressure.

Cardiovascular disorders

Cardiovascular disorders: Myocardial infarction

Focus topic: Cardiovascular disorders

An occlusion of a coronary artery, MI leads to oxygen deprivation, myocardial ischemia, and eventual necrosis. It’s one component of acute coronary syndrome.
The extent of functional impairment and the patient’s prognosis depend on the size and location of the infarct, the condition of the uninvolved myocardium, the potential for collateral circulation, and the effectiveness of compensatory mechanisms. In the United States, MI is the leading cause of death in adults.

What causes it

MI can arise from any condition in which the myocardial oxygen supply can’t keep pace with demand, including:

  • CAD
  • coronary artery emboli
  • thrombus
  • coronary artery spasm
  • severe hematologic and coagulation disorders
  • myocardial contusion
  • congenital coronary artery anomalies.

Certain risk factors increase a patient’s vulnerability to MI. These factors include family history of MI, gender (men are more susceptible), hypertension, smoking, diabetes mellitus, obesity, sedentary lifestyle, aging, stress, meno pause, elevated serum triglyceride, cholesterol, and low-density lipoprotein (LDL) levels.

Pathophysiology

MI results from prolonged ischemia to the myocardium with irreversible cell damage and muscle death. Functionally, MI causes:

  • reduced contractility with abnormal wall motion
  • altered left ventricular compliance
  • reduced stroke volume
  • reduced ejection fraction
  • elevated left ventricular end-diastolic pressure.

What to look for
The patient experiences severe, persistent chest pain that’s unrelieved by rest or nitroglycerin. He may describe the pain as crushing or squeezing. Usually substernal, pain may radiate to the left arm, jaw, neck, or shoulder blades. Other signs and symptoms include a feeling of impending doom, fatigue, nausea and vomiting, shortness of breath, cool extremities, perspiration, anxiety, hypotension or hypertension, palpable precordial pulse and, possibly, muffled heart sounds.

Cardiovascular disorders

Cardiovascular disorders

What tests tell you

  • Serial 12-lead ECG may show no abnormalities or may prove inconclusive during the first few hours after MI. When present, characteristic abnormalities on the ECG can help pinpoint the location of the MI.
  • ST-segment monitoring tracks the heart’s response to MI. Continuous monitoring can immediately detect ischemic episodes. During an MI, monitoring can help differentiate between an STsegment elevated MI (STEMI) and a non ST-segment elevated MI (NSTEMI); differentiating between a STEMI and NSTEMI helps the practitioner better guide treatment. ST-segment monitoring can also identify patients at high risk for reocclusion after PTCA or MI and permits prompt intervention if reocclusion occurs. After MI, monitoring may reduce or eliminate the need for angiography in patients receiving thrombolytic drugs by gauging the efficacy of the drugs.
  • Serial serum cardiac marker measurements show elevated CK, especially the CK-MB isoenzyme (the cardiac muscle fraction of CK), troponin I and T, and myoglobin.
  • Echocardiography shows ventricular wall dyskinesia (with transmural MI).

Cardiovascular disorders

[sociallocker]

How it’s treated

Primary treatment for MI seeks to relieve pain, stabilize heart rhythm, revascularize the coronary artery, preserve myocardial tissue, and reduce cardiac workload. These treatments include thrombolytic therapy and PTCA.

Thrombolytic thrill

Focus topic: Cardiovascular disorders

To preserve myocardial tissue, thrombolytic therapy should start within 3 hours of the onset of symptoms. This therapy involves administrating medications such as alteplase (Activase) or reteplase (Retavase). However, because of the nature of thrombolytic drugs, they carry many precautions and contraindications.

PTCA, please!

Focus topic: Cardiovascular disorders

PTCA is another option for opening blocked or narrowed arteries. If PTCA is performed soon after the onset of symptoms, the thrombolytic agent can be administered directly into the coronary artery.

Other options

Focus topic: Cardiovascular disorders

Other treatments include:

  • delivering oxygen to increase oxygenation of the blood
  • administering sublingual or I.V. nitroglycerin to relieve chest pain, unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 or greater than 100 beats/minute
  • administering morphine for analgesia (because pain stimulates the sympathetic nervous system, leading to an increase in heart rate and vasoconstriction)
  • administering aspirin to inhibit platelet aggregation
  • administering I.V. heparin for patients who have received tissue plasminogen activator to increase the chances of patency in the affected coronary artery
  • limiting physical activity for the first 12 hours to reduce cardiac workload, which should limit the area of necrosis
  • administering atropine or lidocaine as appropriate
  • administering I.V. nitroglycerin for 24 to 48 hours in patients without hypotension, bradycardia, or excessive tachycardia to reduce afterload and preload and relieve chest pain
  • administering glycoprotein IIb/IIIa inhibitors to patients with continued unstable angina, acute chest pain, or following invasive cardiac procedures, to reduce platelet aggregation
  • providing an early I.V. beta-adrenergic blocker to patients with evolving acute MI, followed by oral therapy (if no contraindications exist) to reduce heart rate and myocardial contractile force, which should reduce myocardial oxygen requirements
  • administering an ACE inhibitor to those with evolving MI with ST-segment elevation or left bundle-branch block but without hypotension or other contraindications to reduce after load and preload and prevent remodeling
  • performing laser angioplasty, atherectomy, stent placement, or transmyocardial revascularization
  • administering lipid-lowering drugs to patients with elevated LDL and cholesterol levels
  • transcutaneous or transvenous pacing
  • emergency interventions for cardiac arrest.

What to do

  • When caring for the post-MI patient, direct your efforts toward detecting complications, preventing further myocardial damage, and promoting comfort, rest, and emotional well-being. Many patients with MI receive treatment in the ICU, under constant observation for complications.
  • Monitor and record ECG readings, blood pressure, temperature, and heart and breath sounds.
  • Assess pain and administer analgesics, as ordered. Always record the severity and duration of pain. Don’t give I.M. injections because absorption from the muscle is unpredictable. Also, muscle damage increases CK, myoglobin, and LD levels, making diagnosis of MI more difficult.
  • Check the patient’s blood pressure after giving nitroglycerin, especially the first dose.
  • Frequently monitor the ECG to detect rate changes or arrhythmias.
  • During episodes of chest pain, obtain ECG, blood pressure, and pulmonary artery catheter measurements to determine changes.
  • Watch for signs and symptoms of fluid retention (crackles, cough, tachypnea, and edema), which may indicate impending heart failure. Carefully monitor daily weight, intake and output, respirations, serum enzyme levels, and blood pressure. Auscultate for adventitious breath sounds periodically (patients on bed rest commonly have atelectatic crackles) and for S3 or S4 gallops.

Do not disturb

Focus topic: Cardiovascular disorders

  • Organize patient care and activities to maximize periods of uninterrupted rest.
  • Ask the dietary department to provide a clear liquid diet until nausea subsides. A low-cholesterol, low-sodium diet may be ordered.
  • Provide a stool softener to prevent straining, which causes vagal stimulation and may slow heart rate. Allow the patient to use a bedside commode, and provide as much privacy as possible.
  • Administer a histamine2 receptor blocker to help prevent stress ulcers from forming.
  • Assist with ROM exercises and ambulation as allowed. If the patient is completely immobilized by a severe MI, turn him often. Antiembolism stockings help prevent venostasis and thrombophlebitis in patients on prolonged bed rest.
  • Provide emotional support, and help reduce stress and anxiety; administer tranquilizers, as needed. Involve his family as much as possible in his care.
  • Evaluate the patient. When assessing treatment outcomes, look for clear breath sounds; normal heart sounds and blood pressure; absence of arrhythmias, chest pain, shortness of breath, fatigue, and edema; and evidence of ability to tolerate exercise. The patient should also have adequate cardiac output, as shown by a normal LOC; warm, dry skin; and no dizziness.

Cardiovascular disorders

[/sociallocker]

FURTHER READING/STUDY:

Resources:

 

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.