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Diseases » Bradycardia » Causes
 

Causes of Bradycardia

Contents
  1. Bradycardia: Introduction
  2. List of Causes
  3. Drugs/substances (76 causes)
  4. Drug interaction (69 causes)
  5. Hidden causes
  6. Excerpts from book chapters
  7. Complication causes
  8. Causes of symptoms
  9. Related cause information

List of causes of Bradycardia

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Bradycardia) that could possibly cause Bradycardia includes:

More causes: see full list of causes for Bradycardia

Bradycardia Causes: Book Excerpts

Bradycardia as a complication of other conditions:

Other conditions that might have Bradycardia as a complication may, potentially, be an underlying cause of Bradycardia. Our database lists the following as having Bradycardia as a complication of that condition:

Bradycardia as a symptom:

Conditions listing Bradycardia as a symptom may also be potential underlying causes of Bradycardia. Our database lists the following as having Bradycardia as a symptom of that condition:

Medications or substances causing Bradycardia:

The following drugs, medications, substances or toxins are some of the possible causes of Bradycardia as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

See full list of 76 medications causing Bradycardia


Drug interactions causing Bradycardia:

When combined, certain drugs, medications, substances or toxins may react causing Bradycardia as a symptom.

The list below is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

  • Ibuprofen and Baclofen interaction
  • Timolol and Cordarone interaction
  • Apo-Timolol and Cordarone interaction
  • Apo-Timop and Cordarone interaction
  • Betimol and Cordarone interaction
  • more interactions...»

See full list of 69 drug interactions causing Bradycardia

Related information on causes of Bradycardia:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Bradycardia may be found in:

Causes of Bradycardia: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Bradycardia.

Bradycardia: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Sinus bradycardia
    –Heart rate <60 bpm with normal-appearing P waves before each QRS wave (narrow complex)
    –Most often due to increased vagal tone or medications (e.g., β-blockers)
    –Normally seen in healthy young adults and well-trained athletes
    –May occur with hypothermia, advanced liver disease, hypothyroidism, sinoatrial node disease, anorexia nervosa, sleep disorders, and increased intracranial pressure
  • Medications (e.g., β-blockers)
  • Sinus node dysfunction
    –May occur as result of sinus node fibrosis (e.g., aging) or infiltrative diseases (e.g., amyloidosis)
    –SSS: Symptomatic bradycardia with sinus node dysfunction
    –Tachycardia-bradycardia syndrome: SSS manifested by tachyarrhthymias alternating with bradyarrhthymias
  • Heart block
    –First-degree AV block: Fixed prolongation of PR interval (PR ≥200 msec); results from slowed conduction through AV node
    –Second-degree AV block, Mobitz I (Wenckebach): Results from delayed conduction through AV node; progressive prolongation of PR interval occurs until a QRS is dropped (typically benign)
    –Second-degree AV block, Mobitz II: Results from disease in the bundle of His; PR is constant, but sporadic P waves are not conducted (may be life threatening because of risk of complete heart block or ventricular asystole)
    –Complete heart block: Atrial impulses are not conducted to the ventricles; thus, atrial activity occurs independent of ventricular activity (AV dissociation, with atrial rate faster than ventricular rate)
  • Congenital heart block
  • Aortic stenosis
  • Myocardial infarction
    –More common with inferior wall MI
  • Atrial fibrillation/flutter with high-degree block
  • Infections (e.g., Lyme disease)
>

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Murmurs - Diastolic: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Aortic insufficiency
    –Decrescendo murmur heard best at the right second intercostal space
  • Austin Flint murmur
    –Late diastolic rumble of severe aortic regurgitation
    –A result of aortic regurgitation so severe that it causes diastolic mitral regurgitation
  • Mitral stenosis
    –Opening snap with mid-diastolic rumble, especially in the left lateral decubitus position
  • Pulmonary insufficiency
    –Accentuated P2 and decrescendo murmur at the left second/third intercostal spaces
  • Tricuspid stenosis
    –Mid-diastolic rumble at the left sternal border
    –Increases with inspiration
  • Cervical venous hum (disappears upon pressure to the jugular vein)
  • Hepatic venous hum (disappears with epigastric pressure)
  • Mammary souffle (in pregnancy; disappears on compressing breast)
  • PDA (continuous machinery sound)
  • Coronary or pulmonary arteriovenous fistula
  • Coarctation of the aorta
  • ASD with left-to-right shunt
  • Atrial myxoma (“tumor plop”)
  • Pericardial knock (constrictive pericarditis)
  • Bronchial collaterals (congenital heart disease)
  • Anomalous pulmonary venous drainage with left-to-right shunt
  • Pulmonary artery branch stenosis
  • Carey-Coombs murmur (mid-diastolic murmur that occurs in acute rheumatic fever)

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Murmurs - Systolic: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Innocent systolic murmur
    –Heard at left sternal border
    –Increased when supine
    –May be caused by increased flow states (e.g., anemia, hypovolemia, fever)
  • Still's murmur
  • Mitral valve prolapse
    –Midsystolic click with late systolic murmur that shifts with maneuvers
  • Aortic stenosis
    –Right side at second intercostal space
    –Radiates to carotid arteries
  • Aortic sclerosis
    –Right side at second intercostal space
    –Midsystole
  • Hyperthyroidism
  • Cervical venous hum
    –Disappears with jugular vein pressure
  • Hepatic venous hum
    –Disappears with epigastric pressure
  • Mammary souffle
    –Occurs in pregnancy
    –Disappears upon compression of breast
  • Bicuspid aortic valve
    –Right side at second intercostal space
    –Little radiation
    –Possible early diastolic aortic murmur
    –Opening sound of aortic valve heard in early systole (systolic ejection click)
  • Mitral insufficiency
    –Holosystolic murmur heard best in the left lateral decubitus position
    –S1 is usually diminished in intensity
  • Tricuspid insufficiency
    –Holosystolic murmur at second/third intercostal spaces
  • Endocarditis
    –Abrupt onset of new murmur
  • Peripheral pulmonary artery stenosis
  • Atrial or ventricular septal defect
  • Ventricular septal defect
  • Patent ductus arteriosus (continuous machinery sound, second left intercostal space)
  • Coarctation of the aorta
  • Left ventricular outflow tract obstruction
  • Pulmonary artery stenosis
  • Prosthetic valve noises
  • Pericardial friction rubs
  • Papillary muscle dysfunction
  • Pulmonic outflow obstruction
  • Coronary/pulmonary arteriovenous fistula

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Bradycardia: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

    • Vasovagal response
      –Defecation, yawning, rectal stimulation, placement of nasogastric tube, sight of blood, etc.
    • Drug reaction
      –β-blockers, calcium channel blockers (diltiazem, verapamil), carbamates, clonidine, digoxin, opiates, organophosphates, gamma-hydroxybutyrate (“date rape” drug), and plants (lily of the valley, foxglove, oleander)
  • Healthy athlete
    –Sinus bradycardia
  • Hypothermia
  • GER (in infants, especially premature)
  • Low birth weight infants: Sinus bradycardia (great variations in sinus rate, can have junctional escape beats)
  • Congenital complete heart block: Associated with maternal SLE
  • Congenital heart disease
  • Sepsis
  • Obstructive sleep apnea
    –Seen in children with obesity, tonsillar or adenoid hypertrophy, craniofacial anomalies, neuromuscular diseases
    –Hypoxia and hypercapnia lead to pulmonary hypertension and arrhythmia
  • Electrolyte abnormalities can lead to dysrhythmias
    • Anorexia nervosa
      –Prolonged QT syndrome and junctional arrhythmia
      –Associated hypokalemia may also cause ECG changes and life-threatening dysrhythmias
  • AV node blocks (second- and third-degree)
  • Idioventricular rhythm
  • Hypothyroidism (myxedema)
  • Allergic reaction/anaphylaxis
  • Increased intracranial pressure (IVH, extradural hemorrhage, trauma, etc.)
  • Sick sinus syndrome (tachy-brady syndrome)
  • Psittacosis, typhoid fever, Lassa fever
  • Myocardial infarction

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Pulse, absent or weak: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Aortic aneurysm (dissecting)

When a dissecting aneurysm affects circulation to the innominate, left common carotid, subclavian, or femoral artery, it causes weak or absent arterial pulses distal to the affected area. Absent or diminished pulses occur in 50% of patients with proximal dissection and usually involve the brachiocephalic vessels. Pulse deficits are much less common in patients with distal dissection and tend to involve the left subclavian and femoral arteries. Tearing pain usually develops suddenly in the chest and neck and may radiate to the upper and lower back and abdomen. Other findings include syncope, loss of consciousness, weakness or transient paralysis of the legs or arms, the diastolic murmur of aortic insufficiency, systemic hypotension, and mottled skin below the waist.

Aortic arch syndrome (Takayasu’s arteritis)

Aortic arch syndrome produces weak or abruptly absent carotid pulses and unequal or absent radial pulses. These signs are usually preceded by malaise, night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. Other findings include neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; dizziness; and syncope. If the carotid artery is involved, diplopia and transient blindness may occur.

Aortic bifurcation occlusion (acute)

Aortic bifurcation occlusion is a rare disorder that produces abrupt absence of all leg pulses. The patient reports moderate to severe pain in the legs and, less commonly, in the abdomen, lumbosacral area, or perineum. Also, his legs are cold, pale, numb, and flaccid.

Aortic stenosis

With aortic stenosis, the carotid pulse is sustained but weak. Dyspnea (especially on exertion or paroxysmal nocturnal), chest pain, and syncope dominate the clinical picture. The patient commonly has an atrial gallop. Other findings include a harsh systolic ejection murmur, crackles, palpitations, fatigue, and narrowed pulse pressure.

Arrhythmias

Cardiac arrhythmias may produce generalized weak pulses accompanied by cool, clammy skin. Other findings reflect the arrhythmia’s severity and may include hypotension, chest pain, dyspnea, dizziness, and a decreased level of consciousness (LOC).

Arterial occlusion

With acute occlusion, arterial pulses distal to the obstruction are unilaterally weak and then absent. The affected limb is cool, pale, and cyanotic, with an increased capillary refill time, and the patient complains of moderate to severe pain and paresthesia. A line of color and temperature demarcation develops at the level of obstruction. Varying degrees of limb paralysis may also occur, along with intense intermittent claudication. With chronic occlusion, occurring with disorders such as arteriosclerosis and Buerger’s disease, pulses in the affected limb weaken gradually.

Cardiac tamponade

Life-threatening cardiac tamponade causes a weak, rapid pulse accompanied by these classic findings: paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds. Narrowed pulse pressure, pericardial friction rub, and hepatomegaly may also occur. The patient may appear anxious, restless, and cyanotic and may have chest pain, clammy skin, dyspnea, and tachypnea.

Coarctation of the aorta

Findings of coarctation of the aorta include bounding pulses in the arms and neck, with decreased pulsations and systolic pulse pressure in the lower extremities.

Peripheral vascular disease

Peripheral vascular disease causes a weakening and loss of peripheral pulses. The patient complains of aching pain distal to the occlusion that worsens with exercise and abates with rest. The skin feels cool and shows decreased hair growth. Impotence may occur in male patients with occlusion in the descending aorta or femoral areas.

Pulmonary embolism

Pulmonary embolism causes a generalized weak, rapid pulse. It may also cause an abrupt onset of chest pain, tachycardia, dyspnea, apprehension, syncope, diaphoresis, and cyanosis. Acute respiratory findings include tachypnea, dyspnea, decreased breath sounds, crackles, a pleural friction rub, and a cough — possibly with blood-tinged sputum.

Shock

With anaphylactic shock, pulses become rapid and weak and then uniformly absent within seconds or minutes after exposure to an allergen. This is preceded by hypotension, anxiety, restlessness, feelings of doom, intense itching, a pounding headache and, possibly, urticaria.

With cardiogenic shock, peripheral pulses are absent and central pulses are weak, depending on the degree of vascular collapse. Pulse pressure is narrow. A drop in systolic blood pressure to 30 mm Hg below baseline, or a sustained reading below 80 mm Hg, produces poor tissue perfusion. Resulting signs include cold, pale, clammy skin; tachycardia; rapid, shallow respirations; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, all pulses in the extremities become weak and then uniformly absent, depending on the severity of hypovolemia. As shock progresses, remaining pulses become thready and more rapid. Early signs of cardiogenic shock include restlessness, thirst, tachypnea, and cool, pale skin. Late signs include hypotension with narrowing pulse pressure, clammy skin, a drop in urine output to less than
25 ml/hour, confusion, a decreased LOC and, possibly, hypothermia.

With septic shock, all pulses in the extremities first become weak. Depending on the degree of vascular collapse, pulses may then become uniformly absent. Shock is heralded by chills, a sudden fever and, possibly, nausea, vomiting, and diarrhea. Typically, the patient experiences tachycardia, tachypnea, and flushed, warm, and dry skin. As shock progresses, he develops thirst, hypotension, anxiety, restlessness, and confusion. Then pulse pressure narrows and the skin becomes cold, clammy, and cyanotic. The patient experiences severe hypotension, oliguria or anuria, respiratory failure, and coma.

Thoracic outlet syndrome

A patient with thoracic outlet syndrome may develop gradual or abrupt weakness or loss of the pulses in the arms, depending on how quickly vessels in the neck compress. These pulse changes commonly occur after the patient works with his hands above his shoulders, lifts a weight, or abducts his arm. Paresthesia and pain occur along the ulnar distribution of the arm and disappear as soon as the patient returns his arm to a neutral position. The patient may also have asymmetrical blood pressure and cool, pale skin.

Other causes

Treatments

Localized absent pulse may occur distal to arteriovenous shunts for dialysis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Murmurs: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Aortic insufficiency

Acute aortic insufficiency typically produces a soft, short diastolic murmur over the left sternal border that’s best heard when the patient sits and leans forward and at the end of a forced held expiration. S2 may be soft or absent. Sometimes, a soft, short midsystolic murmur may also be heard over the second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein distention, crackles, increased fatigue, and pale, cool extremities.

Chronic aortic insufficiency causes a high-pitched, blowing, decrescendo diastolic murmur that’s best heard over the second or third right intercostal space or the left sternal border with the patient sitting, leaning forward, and holding his breath after deep expiration. An Austin Flint murmur — a rumbling, mid-to-late diastolic murmur best heard at the apex — may also occur. Complications may not develop until the patient is between ages 40 to 50; then, typical findings include palpitations, tachycardia, angina, increased fatigue, dyspnea, orthopnea, and crackles.

Aortic stenosis

With aortic stenosis, the murmur is systolic, beginning after S1 and ending at or before aortic valve closure. It’s harsh and grating, medium-pitched, and crescendo-decrescendo. Loudest over the second right intercostal space when the patient is sitting and leaning forward, this murmur may also be heard at the apex, at the suprasternal notch (Erb’s point), and over the carotid arteries.

If the patient has advanced disease, S2 may be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the apex is typical, but is absent when the valve is severely calcified. Associated signs and symptoms usually don’t appear until age 30 in congenital aortic stenosis, ages 30 to 65 in stenosis due to rheumatic disease, and after age 65 in calcific aortic stenosis. They may include dizziness, syncope, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and angina.

Cardiomyopathy (hypertrophic)

Hypertrophic cardiomyopathy generates a harsh late systolic murmur, ending at S2. Best heard over the left sternal border and at the apex, the murmur is commonly accompanied by an audible S3or S4. The murmur decreases with squatting and increases with sitting down. Major associated symptoms are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.

Mitral insufficiency

Acute mitral insufficiency is characterized by a medium-pitched blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a widely split S2 and commonly an S4. This murmur doesn’t get louder on inspiration as with tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.

Chronic mitral insufficiency produces a high-pitched, blowing, holosystolic plateau murmur that’s loudest at the apex and usually radiates to the axilla or back. Fatigue, dyspnea, and palpitations may also occur.

Mitral prolapse

Mitral prolapse generates a midsystolic to late-systolic click with a high-pitched late-systolic crescendo murmur, best heard at the apex. Occasionally, multiple clicks may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness, syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.

Mitral stenosis

With mitral stenosis, the murmur is soft, low-pitched, rumbling, crescendo-decrescendo, and diastolic, accompanied by a loud S1 or an opening snap — a cardinal sign. It’s best heard at the apex with the patient in the left lateral position. Mild exercise helps make this murmur audible.

With severe stenosis, the murmur of mitral regurgitation may also be heard. Other findings include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.

Myxomas

A left atrial myxoma (most common) usually produces a mid- diastolic murmur and a holosystolic murmur that’s loudest at the apex, with an S4, an early diastolic thudding sound (tumor plop), and a loud, widely split S1.Related features include dyspnea, orthopnea, chest pain, fatigue, weight loss, and syncope.

A right atrial myxoma causes a late diastolic rumbling murmur, a holosystolic crescendo murmur, and tumor plop, best heard at the lower left sternal border. Other findings include fatigue, peripheral edema, ascites, and hepatomegaly.

A left ventricular myxoma (rare) produces a systolic murmur, best heard at the lower left sternal border; arrhythmias; dyspnea; and syncope.

A right ventricular myxoma commonly generates a systolic ejection murmur with delayed S2 and a tumor plop, best heard at the left sternal border. It’s accompanied by peripheral edema, hepatomegaly, ascites, dyspnea, and syncope.

Papillary muscle rupture

With papillary muscle rupture — a life-threatening complication of an acute MI — a loud holosystolic murmur can be auscultated at the apex. Related findings include severe dyspnea, chest pain, syncope, hemoptysis, tachycardia, and hypotension.

Rheumatic fever with pericarditis

A pericardial friction rub along with murmurs and gallops are heard best with the patient leaning forward on his hands and knees during forced expiration. The most common murmurs heard are the systolic murmur of mitral regurgitation, a midsystolic murmur due to swelling of the mitral valve leaflet, and the diastolic murmur of aortic regurgitation. Other signs and symptoms include a fever, joint and sternal pain, edema, and tachypnea.

Tricuspid insufficiency

Tricuspid insufficiency is a valvular abnormality that’s characterized by a soft, high-pitched, holosystolic blowing murmur that increases with inspiration (Carvallo’s sign), decreases with exhalation and Valsalva’s maneuver, and is best heard over the lower left sternal border and the xiphoid area. Following a lengthy asymptomatic period, exertional dyspnea and orthopnea may develop, along with jugular vein distention, ascites, peripheral cyanosis and edema, muscle wasting, fatigue, weakness, and syncope.

Tricuspid stenosis

Tricuspid stenosis is a valvular disorder that produces a diastolic murmur similar to that of mitral stenosis, but louder with inspiration and decreased with exhalation and Valsalva’s maneuver. S1 may also be louder. Associated signs and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites, hepatomegaly, and dyspnea.

Other causes

Treatments

Prosthetic valve replacement may cause variable murmurs, depending on the location, valve composition, and method of operation.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse rhythm abnormality: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Arrhythmias

An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, a decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulsus paradoxus: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Cardiac tamponade

Pulsus paradoxus commonly occurs with cardiac tamponade, but it may be difficult to detect if intrapericardial pressure rises abruptly and profound hypotension occurs. With severe tamponade, assessment also reveals these classic findings: hypotension, diminished or muffled heart sounds, and jugular vein distention. Related findings include chest pain, a pericardial friction rub, narrowed pulse pressure, anxiety, restlessness, clammy skin, and hepatomegaly. Characteristic respiratory signs and symptoms include dyspnea, tachypnea, and cyanosis; the patient typically sits up and leans forward to facilitate breathing.

If cardiac tamponade develops gradually, pulsus paradoxus may be accompanied by weakness, anorexia, and weight loss. The patient may also report chest pain, but he won’t have muffled heart sounds or severe hypotension.

Chronic obstructive pulmonary disease (COPD)

The wide fluctuations in intrathoracic pressure that characterize COPD produce pulsus paradoxus and possibly tachycardia. Other findings vary, but may include dyspnea, tachypnea, wheezing, a productive or nonproductive cough, accessory muscle use, barrel chest, and clubbing. The patient may show labored, pursed-lip breathing after exertion or even at rest. He typically sits up and leans forward to facilitate breathing. Auscultation reveals decreased breath sounds, rhonchi, and crackles. Weight loss, cyanosis, and edema may occur.

Pericarditis (chronic constrictive)

Pulsus paradoxus can occur in up to 50% of patients with pericarditis. Other findings include a pericardial friction rub, chest pain, exertional dyspnea, orthopnea, hepatomegaly, and ascites. Patients also exhibit peripheral edema and Kussmaul’s sign — jugular vein distention that becomes more prominent on inspiration.

Pulmonary embolism (massive)

Decreased left ventricular filling and stroke volume in massive pulmonary embolism produce pulsus paradoxus as well as syncope and severe apprehension, dyspnea, tachypnea, and pleuritic chest pain. The patient appears cyanotic, with jugular vein distention. He may succumb to circulatory collapse, with hypotension and a weak, rapid pulse. Pulmonary infarction may produce hemoptysis along with decreased breath sounds and a pleural friction rub over the affected area.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Bradycardia: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

❑ Cardiac arrhythmia. Depending on the type of arrhythmia and the patient's tolerance of it, bradycardia may be transient or sustained, benign or life-threatening. Related findings include hypotension, palpitations, dizziness, weakness, syncope, and fatigue.

❑ Cardiomyopathy. Cardiomyopathy is a potentially life-threatening disorder that may cause transient or sustained bradycardia. Other findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.

❑ Hypothermia. Bradycardia usually appears when the core temperature drops below 89.6° F (32° C). It's accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and confusion leading to stupor.

❑ Hypothyroidism. Hypothyroidism causes severe bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity to cold. Related signs include cool, dry, thick skin; sparse, dry hair; facial swelling; periorbital edema; thick, brittle nails; and confusion leading to stupor.

❑ Myocardial infarction (MI). Sinus bradycardia is the most common arrhythmia associated with an acute MI. Accompanying signs and symptoms of an MI include an aching, burning, or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric area; nausea and vomiting; cool, clammy, and pale or cyanotic skin; anxiety; and dyspnea. Blood pressure may be elevated or depressed. Auscultation may reveal abnormal heart sounds.

Other causes

❑ Diagnostic tests. Cardiac catheterization and electrophysiologic studies can induce temporary bradycardia.

❑ Drugs. Beta-adrenergic blockers and some calcium channel blockers, cardiac glycosides, topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics, and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may cause bradycardia.

❑ Invasive treatments. Suctioning can induce hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or damage to conduction tissues, causing bradycardia.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse, absent or weak: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Aortic aneurysm (dissecting)

When a dissecting aneurysm affects circulation to the innominate, left common carotid, subclavian, or femoral artery, it causes weak or absent arterial pulses distal to the affected area. Absent or diminished pulses occur in 50% of patients with proximal dissection and usually involve the brachiocephalic vessels. Pulse deficits are much less common in patients with distal dissection and tend to involve the left subclavian and femoral arteries. Tearing pain usually develops suddenly in the chest and neck and may radiate to the upper and lower back and abdomen. Other findings include syncope, loss of consciousness, weakness or transient paralysis of the legs or arms, the diastolic murmur of aortic insufficiency, systemic hypotension, and mottled skin below the waist.

Aortic arch syndrome (Takayasu’s arteritis)

This syndrome produces weak or abruptly absent carotid pulses and unequal or absent radial pulses. These signs are usually preceded by malaise, night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. Other findings include neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; dizziness; and syncope. If the carotid artery is involved, diplopia and transient blindness may occur.

Aortic bifurcation occlusion (acute)

This rare disorder produces abrupt absence of all leg pulses. The patient reports moderate to severe pain in the legs and, less commonly, in the abdomen, lumbosacral area, or perineum. Also, his legs are cold, pale, numb, and flaccid.

Aortic stenosis

With this disorder, the carotid pulse is sustained but weak. Dyspnea (especially on exertion or paroxysmal nocturnal), chest pain, and syncope dominate the clinical picture. The patient commonly has an atrial gallop. Other findings include a harsh systolic ejection murmur, crackles, palpitations, fatigue, and narrowed pulse pressure.

Arrhythmias

Cardiac arrhythmias may produce generalized weak pulses accompanied by cool, clammy skin. Other findings reflect the arrhythmia’s severity and may include hypotension, chest pain, dyspnea, dizziness, and decreased level of consciousness.

Arterial occlusion

With acute occlusion, arterial pulses distal to the obstruction are unilaterally weak and then absent. The affected limb is cool, pale, and cyanotic, with increased capillary refill time, and the patient complains of moderate to severe pain and paresthesia. A line of color and temperature demarcation develops at the level of obstruction. Varying degrees of limb paralysis may also occur, along with intense intermittent claudication. With chronic occlusion, occurring with disorders such as arteriosclerosis and Buerger’s disease, pulses in the affected limb weaken gradually.

Cardiac tamponade

Life-threatening cardiac tamponade causes a weak, rapid pulse accompanied by these classic findings: paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds. Narrowed pulse pressure, pericardial friction rub, and hepatomegaly may also occur. The patient may appear anxious, restless, and cyanotic and may have chest pain, clammy skin, dyspnea, and tachypnea.

Coarctation of the aorta

Findings of this disorder include bounding pulses in the arms and neck, with decreased pulsations and systolic pulse pressure in the lower extremities.

Peripheral vascular disease

This disorder causes a weakening and loss of peripheral pulses. The patient complains of aching pain distal to the occlusion that worsens with exercise and abates with rest. The skin feels cool and shows decreased hair growth. Impotence may occur in male patients with occlusion in the descending aorta or femoral areas.

Pulmonary embolism

This disorder causes a generalized weak, rapid pulse. It may also cause abrupt onset of chest pain, tachycardia, dyspnea, apprehension, syncope, diaphoresis, and cyanosis. Acute respiratory findings include tachypnea, dyspnea, decreased breath sounds, crackles, a pleural friction rub, and a cough—possibly with blood-tinged sputum.

Shock

With anaphylactic shock, pulses become rapid and weak and then uniformly absent within seconds or minutes after exposure to an allergen. This is preceded by hypotension, anxiety, restlessness, feelings of doom, intense itching, a pounding headache and, possibly, urticaria.

With cardiogenic shock, peripheral pulses are absent and central pulses are weak, depending on the degree of vascular collapse. Pulse pressure is narrow. A drop in systolic blood pressure to 30 mm Hg below baseline, or a sustained reading below 80 mm Hg, produces poor tissue perfusion. Resulting signs include cold, pale, clammy skin; tachycardia; rapid, shallow respirations; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, all pulses in the extremities become weak and then uniformly absent, depending on the severity of hypovolemia. As shock progresses, remaining pulses become thready and more rapid. Early signs of cardiogenic shock include restlessness, thirst, tachypnea, and cool, pale skin. Late signs include hypotension with narrowing pulse pressure, clammy skin, a drop in urine output to less than 25 ml/hour, confusion, decreased level of consciousness and, possibly, hypothermia.

With septic shock, all pulses in the extremities first become weak. Depending on the degree of vascular collapse, pulses may then become uniformly absent. Shock is heralded by chills, sudden fever and, possibly, nausea, vomiting, and diarrhea. Typically, the patient experiences tachycardia, tachypnea, and flushed, warm, and dry skin. As shock progresses, he develops thirst, hypotension, anxiety, restlessness, and confusion. Then pulse pressure narrows and the skin becomes cold, clammy, and cyanotic. The patient experiences severe hypotension, oliguria or anuria, respiratory failure, and coma.

Thoracic outlet syndrome

A patient with this syndrome may develop gradual or abrupt weakness or loss of the pulses in the arms, depending on how quickly vessels in the neck compress. These pulse changes commonly occur after the patient works with his hands above his shoulders, lifts a weight, or abducts his arm. Paresthesia and pain occur along the ulnar distribution of the arm and disappear as soon as the patient returns his arm to a neutral position. The patient may also have asymmetrical blood pressure and cool, pale skin.

Other causes

Treatments

Localized absent pulse may occur distal to arteriovenous shuntsfor dialysis.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Murmurs: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Aortic insufficiency

Acute aortic insufficiency typically produces a soft, short diastolic murmur over the left sternal border that’s best heard when the patient sits and leans forward and at the end of a forced held expiration. S2 may be soft or absent. Sometimes, a soft, short midsystolic murmur may also be heard over the second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein distention, crackles, increased fatigue, and pale, cool extremities.

Chronic aortic insufficiency causes a high-pitched, blowing, decrescendo diastolic murmur that’s best heard over the second or third right intercostal space or the left sternal border with the patient sitting, leaning forward, and holding his breath after deep expiration. An Austin Flint murmur—a rumbling, mid-to-late diastolic murmur best heard at the apex—may also occur. Complications may not develop until ages 40 to 50; then, typical findings include palpitations, tachycardia, angina, increased fatigue, dyspnea, orthopnea, and crackles.

Aortic stenosis

With this valvular disorder, the murmur is systolic, beginning after S1 and ending at or before aortic valve closure. It’s harsh and grating, medium-pitched, and crescendo-decrescendo. Loudest over the second right intercostal space when the patient is sitting and leaning forward, this murmur may also be heard at the apex, at the suprasternal notch (Erb’s point), and over the carotid arteries.

If the patient has advanced disease, S2 may be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the apex is typical but is absent when the valve is severely calcified. Associated signs and symptoms usually don’t appear until age 30 in congenital aortic stenosis, ages 30 to 65 in stenosis due to rheumatic disease, and after age 65 in calcific aortic stenosis. They may include dizziness, syncope, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and angina.

Cardiomyopathy (hypertrophic)

This disorder generates a harsh late systolic murmur, ending at S2. Best heard over the left sternal border and at the apex, the murmur is commonly accompanied by an audible S3or S4. The murmur decreases with squatting and increases with sitting down. Major associated symptoms are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.

Mitral insufficiency

Acute mitral insufficiency is characterized by a medium-pitched blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a widely split S2 and commonly an S4. This murmur doesn’t get louder on inspiration as with tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.

Chronic mitral insufficiency produces a high-pitched, blowing, holosystolic plateau murmur that’s loudest at the apex and usually radiates to the axilla or back. Fatigue, dyspnea, and palpitations may also occur.

Mitral prolapse

This disorder generates a midsystolic to late-systolic click with a high-pitched late-systolic crescendo murmur, best heard at the apex. Occasionally, multiple clicks may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness, syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.

Mitral stenosis

With this valvular disorder, the murmur is soft, low-pitched, rumbling, crescendo-decrescendo, and diastolic, accompanied by a loud S1 or an opening snap—a cardinal sign. It’s best heard at the apex with the patient in the left lateral position. Mild exercise will help make this murmur audible.

With severe stenosis, the murmur of mitral insufficiency may also be heard. Other findings include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.

Myxomas

A left atrial myxoma (most common) usually produces a middiastolic murmur and a holosystolic murmur that’s loudest at the apex, with an S4, an early diastolic thudding sound (tumor plop), and a loud, widely split S1.Related features include dyspnea, orthopnea, chest pain, fatigue, weight loss, and syncope.

A right atrial myxoma causes a late diastolic rumbling murmur, a holosystolic crescendo murmur, and tumor plop, best heard at the lower left sternal border. Other findings include fatigue, peripheral edema, ascites, and hepatomegaly.

A left ventricular myxoma (rare) produces a systolic murmur, best heard at the lower left sternal border, arrhythmias, dyspnea, and syncope.

A right ventricular myxoma commonly generates a systolic ejection murmur with delayed S2 and a tumor plop, best heard at the left sternal border. It’s accompanied by peripheral edema, hepatomegaly, ascites, dyspnea, and syncope.

Papillary muscle rupture

With this life-threatening complication of an acute MI, a loud holosystolic murmur can be auscultated at the apex. Related findings include severe dyspnea, chest pain, syncope, hemoptysis, tachycardia, and hypotension.

Rheumatic fever with pericarditis

A pericardial friction rub along with murmurs and gallops are heard best with the patient leaning forward on his hands and knees during forced expiration. The most common murmurs heard are the systolic murmur of mitral insufficiency, a midsystolic murmur due to swelling of the leaflet of the mitral valve, and the diastolic murmur of aortic insufficiency. Other signs and symptoms include fever, joint and sternal pain, edema, and tachypnea.

Tricuspid insufficiency

This valvular abnormality is characterized by a soft, high-pitched, holosystolic blowing murmur that increases with inspiration (Carvallo’s sign), decreases with exhalation and Valsalva’s maneuver, and is best heard over the lower left sternal border and the xiphoid area. Following a lengthy asymptomatic period, exertional dyspnea and orthopnea may develop, along with jugular vein distention, ascites, peripheral cyanosis and edema, muscle wasting, fatigue, weakness, and syncope.

Tricuspid stenosis

This valvular disorder produces a diastolic murmur similar to that of mitral stenosis, but louder with inspiration and decreased with exhalation and Valsalva’s maneuver. S1 may also be louder. Associated signs and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites, hepatomegaly, and dyspnea.

Other causes

Treatments

Prosthetic valve replacement may cause variable murmurs, depending on the location, valve composition, and method of operation.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulse rhythm abnormality: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Arrhythmias

An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulsus paradoxus: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Cardiac tamponade

Pulsus paradoxus commonly occurs with this disorder, but it may be difficult to detect if intrapericardial pressure rises abruptly and profound hypotension occurs. With severe tamponade, assessment also reveals these classic findings: hypotension, diminished or muffled heart sounds, and jugular vein distention. Related findings include chest pain, pericardial friction rub, narrowed pulse pressure, anxiety, restlessness, clammy skin, and hepatomegaly. Characteristic respiratory signs and symptoms include dyspnea, tachypnea, and cyanosis; the patient typically sits up and leans forward to facilitate breathing.

If cardiac tamponade develops gradually, pulsus paradoxus may be accompanied by weakness, anorexia, and weight loss. The patient may also report chest pain, but he won’t have muffled heart sounds or severe hypotension.

Chronic obstructive pulmonary disease (COPD)

The wide fluctuations in intrathoracic pressure that characterize this disorder produce pulsus paradoxus and possibly tachycardia. Other findings vary but may include dyspnea, tachypnea, wheezing, productive or nonproductive cough, accessory muscle use, barrel chest, and clubbing. The patient may show labored, pursed-lip breathing after exertion or even at rest. He typically sits up and leans forward to facilitate breathing. Auscultation reveals decreased breath sounds, rhonchi, and crackles. Weight loss, cyanosis, and edema may occur.

Pericarditis (chronic constrictive)

Pulsus paradoxus can occur in up to 50% of patients with this disorder. Other findings include pericardial friction rub, chest pain, exertional dyspnea, orthopnea, hepatomegaly, and ascites. The patient also exhibits peripheral edema and Kussmaul’s sign—jugular vein distention that becomes more prominent on inspiration.

Pulmonary embolism (massive)

Decreased left ventricular filling and stroke volume in massive pulmonary embolism produce pulsus paradoxus, as well as syncope and severe apprehension, dyspnea, tachypnea, and pleuritic chest pain. The patient appears cyanotic, with jugular vein distention. He may succumb to circulatory collapse, with hypotension and a weak, rapid pulse. Pulmonary infarction may produce hemoptysis along with decreased breath sounds and a pleural friction rub over the affected area.

Right ventricular infarction

This infarction may produce pulsus paradoxus and elevated jugular venous or central venous pressure. Other findings are similar to those of myocardial infarction.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Bradycardia: Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))

Cardiac arrhythmias

Depending on the type of arrhythmia and the patient’s tolerance of it, bradycardia may be transient or sustained and benign or life-threatening. Related findings include hypotension, palpitations, dizziness, weakness, syncope, and fatigue.

Cardiomyopathy

Cardiomyopathy is a potentially life-threatening disorder that may cause transient or sustained bradycardia. Other findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.

Cervical spinal injury

Bradycardia may be transient or sustained, depending on the severity of the injury. Its onset coincides with sympathetic denervation. Associated signs and symptoms include hypotension, decreased body temperature, slowed peristalsis, leg paralysis, and partial arm and respiratory muscle paralysis.

Hypothermia

Bradycardia usually appears when the core temperature drops below 89.6° F (32° C). It’s accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and confusion leading to stupor.

Hypothyroidism

Hypothyroidism causes severe bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity to cold. Related signs include cool, dry, thick skin; sparse, dry hair; facial swelling; periorbital edema; thick, brittle nails; and confusion leading to stupor.

Increased intracranial pressure (ICP)

Bradycardia occurs as a late sign of increased ICP along with rapid respiratory rate, elevated systolic pressure, decreased diastolic pressure, and widened pulse pressure. Associated signs and symptoms include persistent headache, projectile vomiting, decreased level of consciousness (LOC), and fixed, unequal, and possibly dilated pupils.

Myocardial infarction (MI)

Sinus bradycardia is the most common arrhythmia associated with an acute MI. Accompanying signs and symptoms of an MI include an aching, burning, or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric area; nausea and vomiting; cool, clammy, and pale or cyanotic skin; anxiety; and dyspnea. Blood pressure may be elevated or depressed. Auscultation may reveal abnormal heart sounds.

Other causes

Diagnostic tests

Cardiac catheterization and electrophysiologic studies can induce temporary bradycardia.

Drugs

Beta-adrenergic blockers, some calcium channel blockers, cardiac glycosides, topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics, and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may cause bradycardia.

Invasive treatments

Suctioning can induce hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or damage to conduction tissues, causing bradycardia.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Bradycardia: Differential Overview
(Field Guide to Bedside Diagnosis)

Sinus Bradycardia

❑ Hypothyroidism

❑ Hypervagotonia

❑ Hypersensitive carotid sinus

❑ Hypothermia

❑ Acute increased intracranial pressure

Complete Heart Block

❑ Inferior myocardial infarction

❑ Drugs

❑ Sick sinus syndrome

❑ Viral myocarditis

❑ Lyme disease

❑ Sarcoidosis

❑ Acute rheumatic fever

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Source: Field Guide to Bedside Diagnosis, 2007

Diastolic Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Aortic regurgitation

❑ Pulmonic regurgitation

❑ Mitral stenosis

❑ Tricuspid stenosis

❑ Atrial septal defect

❑ Left anterior descending artery stenosis

❑ Atrial myxoma

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Systolic Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Systolic ejection murmur

❑ Mitral regurgitation

❑ Mitral valve prolapse

❑ Aortic stenosis

❑ Aortic valve sclerosis

❑ Hypertrophic obstructive cardiomyopathy

❑ Atrial septal defect

❑ Pulmonic stenosis

❑ Tricuspid regurgitation

❑ Ventricular septal defect

❑ Aortic coarctation

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Source: Field Guide to Bedside Diagnosis, 2007

Continuous Murmur: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Aortic stenosis/aortic insufficiency

❑ Pericardial friction rub

❑ Pulmonary arteriovenous fistula

❑ Venous hum

❑ Mammary souffle

❑ Aortic coarctation

❑ Mediastinal air dissection

❑ Patent ductus arteriosis

❑ Ruptured sinus of Valsalva

❑ Coronary artery fistula

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Murmurs: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Aortic insufficiency

Acute aortic insufficiency typically produces a soft, short diastolic murmur over the left sternal border that’s best heard when the patient sits and leans forward and at the end of a forced held expiration. S2 may be soft or absent. Sometimes, a soft, short midsystolic murmur may also be heard over the second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein distention, crackles, increased fatigue, and pale, cool extremities.

Chronic aortic insufficiency causes a high-pitched, blowing, decrescendo diastolic murmur that’s best heard over the second or third right intercostal space or the left sternal border with the patient sitting, leaning forward, and holding his breath after deep expiration. An Austin Flint murmur — a rumbling, mid-to-late diastolic murmur best heard at the apex — may also occur. Complications may not develop until ages 40 to 50; then, typical findings include palpitations, tachycardia, angina, increased fatigue, dyspnea, orthopnea, and crackles.

Aortic stenosis

With aortic stenosis — avalvular disorder — the murmur is systolic, beginning after S1 and ending at or before aortic valve closure. It’s harsh and grating, medium-pitched, and crescendo-decrescendo. Loudest over the second right intercostal space when the patient is sitting and leaning forward, this murmur may also be heard at the apex, at the suprasternal notch (Erb’s point), and over the carotid arteries.

If the patient has advanced disease, S2 may be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the apex is typical but is absent when the valve is severely calcified. Associated signs and symptoms usually don’t appear until age 30 in congenital aortic stenosis, ages 30 to 65 in stenosis due to rheumatic disease, and after age 65 in calcific aortic stenosis. They may include dizziness, syncope, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and angina.

Cardiomyopathy (hypertrophic)

Cardiomyopathy generates a harsh late systolic murmur, ending at S2. Best heard over the left sternal border and at the apex, the murmur is commonly accompanied by an audible S3or S4. The murmur decreases with squatting and increases with sitting down. Major associated symptoms are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.

Mitral insufficiency

Acute mitral insufficiency is characterized by a medium-pitched blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a widely split S2 and commonly an S4. This murmur doesn’t get louder on inspiration as with tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.

Chronic mitral insufficiency produces a high-pitched, blowing, holosystolic plateau murmur that’s loudest at the apex and usually radiates to the axilla or back. Fatigue, dyspnea, and palpitations may also occur.

Mitral prolapse

Mitral prolapse generates a midsystolic to late-systolic click with a high-pitched late-systolic crescendo murmur, best heard at the apex and left sternal border. Occasionally, multiple clicks may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness, syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.

Mitral stenosis

With mitral stenosis, the murmur is soft, low-pitched, rumbling, crescendo-decrescendo, and diastolic, accompanied by a loud S1 or an opening snap — a cardinal sign. It’s best heard at the apex with the patient in the left lateral position. Mild exercise will help make this murmur audible.

With severe stenosis, the murmur of mitral regurgitation may also be heard. Other findings include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.

Myxomas

A left atrial myxoma (most common) usually produces a middiastolic murmur and a holosystolic murmur that’s loudest at the apex, with an S4, an early diastolic thudding sound (tumor plop), and a loud, widely split S1.Related features include dyspnea, orthopnea, chest pain, fatigue, weight loss, and syncope.

A right atrial myxoma causes a late diastolic rumbling murmur, a holosystolic crescendo murmur, and tumor plop, best heard at the lower left sternal border. Other findings include fatigue, peripheral edema, ascites, and hepatomegaly.

A left ventricular myxoma (rare) produces a systolic murmur, best heard at the lower left sternal border, arrhythmias, dyspnea, and syncope.

A right ventricular myxoma commonly generates a systolic ejection murmur with delayed S2 and a tumor plop, best heard at the left sternal border. It’s accompanied by peripheral edema, hepatomegaly, ascites, dyspnea, and syncope.

Papillary muscle rupture

Papillary muscle rupture is a life-threatening complication of an acute MI, in which a loud holosystolic murmur can be auscultated at the apex. Related findings include severe dyspnea, chest pain, syncope, hemoptysis, tachycardia, and hypotension.

Rheumatic fever with pericarditis

A pericardial friction rub along with murmurs and gallops are heard best with the patient leaning forward on his hands and knees during forced expiration. The most common murmurs heard are the systolic murmur of mitral regurgitation, a midsystolic murmur due to swelling of the leaflet of the mitral valve, and the diastolic murmur of aortic regurgitation. Other signs and symptoms include fever, joint and sternal pain, edema, and tachypnea.

Tricuspid insufficiency

Tricuspid insufficiency is a valvular abnormality that’s characterized by a soft, high-pitched, holosystolic blowing murmur that increases with inspiration (Carvallo’s sign), decreases with exhalation and Valsalva’s maneuver, and is best heard over the lower left sternal border and the xiphoid area. Following a lengthy asymptomatic period, exertional dyspnea and orthopnea may develop, along with jugular vein distention, ascites, peripheral cyanosis and edema, muscle wasting, fatigue, weakness, and syncope.

Tricuspid stenosis

Tricuspid stenosis is a valvular disorder that produces a diastolic murmur similar to that of mitral stenosis, but louder with inspiration and decreased with exhalation and Valsalva’s maneuver. S1 may also be louder. Associated signs and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites, hepatomegaly, and dyspnea.

Other causes

Medical treatments

Prosthetic valve replacement may cause variable murmurs, depending on the location, valve composition, and method of operation.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Pulse rhythm abnormality: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Arrhythmias

An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, a decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Bradycardia: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Cardiac arrhythmias

Depending on the type of arrhythmia and the patient’s tolerance of it, bradycardia may be transient or sustained, benign, or life threatening. Related findings include hypotension, palpitations, dizziness, weakness, syncope, and fatigue.

Cardiomyopathy

Cardiomyopathy is a potentially life-threatening disorder that may cause transient or sustained bradycardia. Other findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.

Cervical spinal injury

Bradycardia may be transient or sustained, depending on the severity of the injury. Its onset coincides with sympathetic denervation. Associated signs and symptoms include hypotension, decreased body temperature, slowed peristalsis, leg paralysis, and partial arm and respiratory muscle paralysis.

Hypothermia

Bradycardia usually appears when the core temperature drops below 89.6° F (32° C). It’s accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and confusion leading to stupor.

Hypothyroidism

Hypothyroidism causes severe bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity to cold. Related signs include cool, dry, thick skin; sparse, dry hair; facial swelling; periorbital edema; thick, brittle nails; and confusion leading to stupor.

Increased intracranial pressure (ICP)

Bradycardia occurs as a late sign of increased ICP along with rapid respiratory rate, elevated systolic pressure, decreased diastolic pressure, and widened pulse pressure. Associated signs and symptoms include persistent headache, projectile vomiting, decreased LOC, and fixed, unequal and, possibly, dilated pupils.

Myocardial infarction (MI)

Sinus bradycardia is the most common arrhythmia associated with an acute MI. Accompanying signs and symptoms of an MI include an aching, burning, or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric area; nausea and vomiting; cool, clammy, and pale or cyanotic skin; anxiety; and dyspnea. Blood pressure may be elevated or depressed. Auscultation may reveal abnormal heart sounds.

Other causes

Diagnostic tests

Cardiac catheterization and electrophysiologic studies can induce temporary bradycardia.

Drugs

Beta-adrenergic blockers and some calcium channel blockers, cardiac glycosides, topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics, and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may also cause bradycardia.

Invasive treatments

Suctioning can induce hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or damage to conduction tissues, causing bradycardia.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Pulsus paradoxus [Paradoxical pulse]: Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

Cardiac tamponade

Pulsus paradoxus commonly occurs with cardiac tamponade, but it may be difficult to detect if intrapericardial pressure rises abruptly and profound hypotension occurs. With severe tamponade, assessment also reveals these classic findings: hypotension, diminished or muffled heart sounds, and jugular vein distention. Related findings include chest pain, pericardial friction rub, narrowed pulse pressure, anxiety, restlessness, clammy skin, and hepatomegaly. Characteristic respiratory signs and symptoms include dyspnea, tachypnea, and cyanosis; the patient typically sits up and leans forward to facilitate breathing.

If cardiac tamponade develops gradually, pulsus paradoxus may be accompanied by weakness, anorexia, and weight loss. The patient may also report chest pain, but he won’t have muffled heart sounds or severe hypotension.

Chronic obstructive pulmonary disease (COPD)

The wide fluctuations in intrathoracic pressure that characterize COPD produce pulsus paradoxus and possibly tachycardia. Other findings vary but may include dyspnea, tachypnea, wheezing, productive or nonproductive cough, accessory muscle use, barrel chest, and clubbing. The patient may show labored, pursed-lip breathing after exertion or even at rest. He typically sits up and leans forward to facilitate breathing. Auscultation reveals decreased breath sounds, rhonchi, and crackles. Weight loss, cyanosis, and edema may occur.

Pericarditis (chronic constrictive)

Pulsus paradoxus can occur in up to 50% of patients with chronic constrictive pericarditis. Other findings include pericardial friction rub, chest pain, exertional dyspnea, orthopnea, hepatomegaly, and ascites. Patients also exhibit peripheral edema and Kussmaul’s sign — jugular vein distention that becomes more prominent on inspiration.

Pulmonary embolism (massive)

Decreased left ventricular filling and stroke volume in massive pulmonary embolism produce pulsus paradoxus as well as syncope and severe apprehension, dyspnea, tachypnea, and pleuritic chest pain. The patient appears cyanotic, with jugular vein distention. He may succumb to circulatory collapse, with hypotension and a weak, rapid pulse. Pulmonary infarction may produce hemoptysis along with decreased breath sounds and a pleural friction rub over the affected area.

Right ventricular infarction

Infarction may produce pulsus paradoxus and elevated jugular venous or central venous pressure. Other findings are similar to those of myocardial infarction.

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Pulse, absent or weak: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Aortic aneurysm (dissecting)

When a dissecting aneurysm affects circulation to the innominate, left common carotid, subclavian, or femoral artery, it causes weak or absent arterial pulses distal to the affected area. Absent or diminished pulses occur in 50% of patients with proximal dissection and usually involve the brachiocephalic vessels. Pulse deficits are much less common in patients with distal dissection and tend to involve the left subclavian and femoral arteries. Tearing pain usually develops suddenly in the chest and neck and may radiate to the upper and lower back and abdomen. Other findings include syncope, loss of consciousness, weakness or transient paralysis of the legs or arms, the diastolic murmur of aortic insufficiency, systemic hypotension, and mottled skin below the waist.

Aortic stenosis

With aortic stenosis, the carotid pulse is sustained but weak. Dyspnea (especially paroxysmal dyspnea or dyspnea on exertion), chest pain, and syncope dominate the clinical picture. The patient commonly has an atrial gallop. Other findings include a harsh systolic ejection murmur, crackles, palpitations, fatigue, and narrowed pulse pressure.

Arterial occlusion

With acute occlusion, arterial pulses distal to the obstruction are unilaterally weak and then absent. The affected limb is cool, pale, and cyanotic, with increased capillary refill time, and the patient complains of moderate to severe pain and paresthesia. A line of color and temperature demarcation develops at the level of obstruction. Varying degrees of limb paralysis may also occur, along with intense intermittent claudication. With chronic occlusion, occurring with such disorders as arteriosclerosis and Buerger’s disease, pulses in the affected limb weaken gradually.

Cardiac arrhythmias

Cardiac arrhythmias may produce generalized weak pulses accompanied by cool, clammy skin. Other findings reflect the arrhythmia’s severity and may include hypotension, chest pain, dyspnea, dizziness, and decreased level of consciousness (LOC).

Cardiac tamponade

Life-threatening cardiac tamponade causes a weak, rapid pulse accompanied by these classic findings: paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds. Narrowed pulse pressure, pericardial friction rub, and hepatomegaly may also occur. The patient may appear anxious, restless, and cyanotic and may have chest pain, clammy skin, dyspnea, and tachypnea.

Coarctation of the aorta

Findings of this disorder include bounding pulses in the arms and neck, with decreased pulsations and systolic pulse pressure in the lower extremities. Auscultation may reveal a systolic ejection click at the base and apex of the heart and, occasionally, over the carotid arteries that’s often accompanied by a systolic ejection murmur at the base.

Peripheral vascular disease

Peripheral vascular disease causes a weakening and loss of peripheral pulses. The patient complains of aching pain distal to the occlusion that worsens with exercise and abates with rest. The skin feels cool and shows decreased hair growth. Impotence may occur in male patients with occlusion in the descending aorta or femoral areas.

Pulmonary embolism

A pulmonary embolism causes a generalized weak, rapid pulse. It may also cause abrupt onset of chest pain, tachycardia, dyspnea, apprehension, syncope, diaphoresis, and cyanosis. Acute respiratory findings include tachypnea, dyspnea, decreased breath sounds, crackles, a pleural friction rub, and a cough — possibly with blood-tinged sputum.

Shock

With anaphylactic shock, pulses become rapid and weak and then uniformly absent within seconds or minutes after exposure to an allergen. This is preceded by hypotension, anxiety, restlessness, feelings of doom, intense itching, a pounding headache and, possibly, urticaria.

With cardiogenic shock, peripheral pulses are absent and central pulses are weak, depending on the degree of vascular collapse. Pulse pressure is narrow. Other signs include cold, pale, clammy skin; hypotension; tachycardia; rapid, shallow respirations; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, all peripheral pulses become weak and then uniformly absent, depending on the severity of hypovolemia. As shock progresses, remaining pulses become thready and more rapid. Early signs of hypovolemic shock include restlessness, thirst, tachypnea, and cool, pale skin. Late signs include hypotension with narrowing pulse pressure, clammy skin, a drop in urine output to less than 25 ml/hour, confusion, decreased LOC and, possibly, hypothermia.

With septic shock, all pulses in the extremities first become weak. Depending on the degree of vascular collapse, pulses may then become uniformly absent. Shock is heralded by chills, sudden fever and, possibly, nausea, vomiting, and diarrhea. Typically, the patient experiences tachycardia, tachypnea, and flushed, warm, and dry skin. As shock progresses, he develops thirst, hypotension, anxiety, restlessness, and confusion. Then pulse pressure narrows, and the skin becomes cold, clammy, and cyanotic. The patient experiences severe hypotension, oliguria or anuria, respiratory failure, and coma.

Thoracic outlet syndrome

In thoracic outlet syndrome, the patient may develop gradual or abrupt weakness or loss of the pulses in the arms, depending on how quickly vessels in the neck compress. These pulse changes commonly occur after the patient works with his hands above his shoulders, lifts a weight, or abducts his arm. Paresthesia and pain occur along the ulnar distribution of the arm and disappear as soon as the patient returns his arm to a neutral position. The patient may also have asymmetrical blood pressure and cool, pale skin.

Other causes

Treatments

Localized absent pulse may occur distal to arteriovenous shuntsfor dialysis.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Murmurs: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Aortic insufficiency

Acute aortic insufficiency typically produces a soft, short diastolic murmur over the left sternal border that’s best heard when the patient sits and leans forward and at the end of a forced held expiration. S2 may be soft or absent. Sometimes, a soft, short midsystolic murmur may also be heard over the second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein distention, crackles, increased fatigue, and pale, cool extremities.

Chronic aortic insufficiency causes a high-pitched, blowing, decrescendo diastolic murmur that’s best heard over the second or third right intercostal space or the left sternal border with the patient sitting, leaning forward, and holding his breath after deep expiration. An Austin Flint murmur — a rumbling, mid-to-late diastolic murmur best heard at the apex — may also occur. Findings include palpitations, tachycardia, angina, increased fatigue, dyspnea, orthopnea, and crackles.

Aortic stenosis

With aortic stenosis, the murmur is systolic, beginning after S1 and ending at or before aortic valve closure. It’s harsh and grating, medium-pitched, and crescendo-decrescendo. Loudest over the second right intercostal space when the patient is sitting and leaning forward, this murmur may also be heard at the apex, at the suprasternal notch (Erb’s point), and over the carotid arteries.

If the patient has advanced disease, S2 may be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the apex is typical but is absent when the valve is severely calcified. Associated signs and symptoms may include dizziness, syncope, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and angina.

Cardiomyopathy (hypertrophic)

Hypertrophic cardiomyopathy generates a harsh late systolic murmur, ending at S2. Best heard over the left sternal border and at the apex, the murmur is commonly accompanied by an audible S3or S4. The murmur decreases with squatting and increases with sitting down. Major associated symptoms are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.

Mitral insufficiency

Acute mitral insufficiency is characterized by a medium-pitched blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a widely split S2 and commonly an S4. This murmur doesn’t get louder on inspiration as with tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.

Chronic mitral insufficiency produces a high-pitched, blowing, holosystolic plateau murmur that’s loudest at the apex and usually radiates to the axilla or back. Fatigue, dyspnea, and palpitations may also occur.

Mitral prolapse

Mitral prolapse generates a midsystolic to late-systolic click with a high-pitched late-systolic crescendo murmur, best heard at the apex. Occasionally, multiple clicks may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness, syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.

Mitral stenosis

With mitral stenosis, the murmur is soft, low-pitched, rumbling, crescendo-decrescendo, and diastolic, accompanied by a loud S1 or an opening snap — a cardinal sign. It’s best heard at the apex with the patient in the left lateral position. Mild exercise will help make this murmur audible.

With severe stenosis, the murmur of mitral insufficiency may also be heard. Other findings include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.

Papillary muscle rupture

Papillary muscle rupture, a life-threatening complication of an acute MI, produces a loud holosystolic murmur that can be auscultated at the apex. Related findings include severe dyspnea, chest pain, syncope, hemoptysis, tachycardia, and hypotension.

Rheumatic fever with pericarditis

A pericardial friction rub along with murmurs and gallops is heard best with the patient leaning forward on his hands and knees during forced expiration. The most common murmurs heard in patients with rheumatic fever are the systolic murmur of mitral insufficiency, a midsystolic murmur due to swelling of the leaflet of the mitral valve, and the diastolic murmur of aortic insufficiency. Other signs and symptoms include fever, joint and sternal pain, edema, and tachypnea.

Tricuspid insufficiency

Tricuspid insufficiency is a valvular abnormality that’s characterized by a soft, high-pitched, holosystolic blowing murmur that increases with inspiration (Carvallo’s sign) and decreases with exhalation and Valsalva’s maneuver. This murmur is best heard over the lower left sternal border and the xiphoid area. Following a lengthy period without symptoms, exertional dyspnea and orthopnea may develop, along with jugular vein distention, ascites, peripheral cyanosis and edema, muscle wasting, fatigue, weakness, and syncope.

Tricuspid stenosis

Tricuspid stenosis is a valvular disorder that produces a diastolic murmur similar to that of mitral stenosis, but louder with inspiration and decreased with exhalation and Valsalva’s maneuver. S1 may also be louder. Associated signs and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites, hepatomegaly, and dyspnea.

Other causes

Treatments

Prosthetic valve replacement may cause variable murmurs, depending on the location, valve composition, and method of operation.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Pulse rhythm abnormality: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Cardiac arrhythmias

An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Pulsus paradoxus: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Cardiac tamponade

Pulsus paradoxus commonly occurs with cardiac tamponade, but it may be difficult to detect if intrapericardial pressure rises abruptly and profound hypotension occurs. With severe tamponade, assessment also reveals these classic findings: hypotension, diminished or muffled heart sounds, and jugular vein distention. Related findings include chest pain, pericardial friction rub, narrowed pulse pressure, anxiety, restlessness, clammy skin, and hepatomegaly. Characteristic respiratory signs and symptoms include dyspnea, tachypnea, and cyanosis; the patient typically sits up and leans forward to facilitate breathing.

If cardiac tamponade develops gradually, pulsus paradoxus may be accompanied by weakness, anorexia, and weight loss. The patient may also report chest pain, but he won’t have muffled heart sounds or severe hypotension.

Chronic obstructive pulmonary disease

The wide fluctuations in intrathoracic pressure that characterize chronic obstructive pulmonary disease (COPD) produce pulsus paradoxus and possibly tachycardia. Other findings vary but may include dyspnea, tachypnea, wheezing, productive or nonproductive cough, accessory muscle use, barrel chest, and clubbing. The patient may show labored, pursed-lip breathing after exertion or even at rest. Auscultation reveals decreased breath sounds, rhonchi, and crackles. Weight loss, cyanosis, and edema may occur.

Pericarditis (chronic constrictive)

Pulsus paradoxus can occur in up to 50% of patients with chronic constrictive pericarditis. Other findings include pericardial friction rub, chest pain, exertional dyspnea, orthopnea, hepatomegaly, and ascites. The patient also exhibits peripheral edema and Kussmaul’s sign — jugular vein distention that becomes more prominent on inspiration.

Pulmonary embolism (massive)

Decreased left ventricular filling and stroke volume in massive pulmonary embolism produce pulsus paradoxus as well as syncope and severe apprehension, dyspnea, tachypnea, and pleuritic chest pain. The patient appears cyanotic, with jugular vein distention. He may succumb to circulatory collapse, with hypotension and a weak, rapid pulse. Pulmonary infarction may produce hemoptysis along with decreased breath sounds and a pleural friction rub over the affected area.

Right ventricular infarction

Right ventricular infarction may produce pulsus paradoxus and elevated jugular venous or central venous pressure. Other findings are similar to those of myocardial infarction. Signs of right-sided heart failure may occur, such as distended neck veins, hepatomegaly, and peripheral edema.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Bradycardia: Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Cardiac arrhythmia

Depending on the type of cardiac arrhythmia and the patient’s tolerance of it, bradycardia may be transient or sustained, benign, or life-threatening. Related findings result from reduced cardiac output and include hypotension, palpitations, dizziness, weakness, dyspnea, chest pain, decreased urine output, altered level of consciousness (LOC), syncope, and fatigue.

Cardiomyopathy

Cardiomyopathy, a potentially life-threatening disorder, may cause transient or sustained bradycardia. Other findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.

Cervical spinal injury

Bradycardia associated with a cervical spinal injury may be transient or sustained, depending on the severity of the injury. Its onset coincides with sympathetic denervation. Associated signs and symptoms of cervical spinal injury include hypotension, decreased body temperature, slowed peristalsis, leg paralysis, and partial arm and respiratory muscle paralysis.

Hypothermia

When core body temperature drops below 89.6° F (32° C), causing hypothermia, bradycardia usually appears. It’s accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and confusion leading to stupor. If the core temperature drops below 86° F (30° C), the patient may appear dead (in a state of rigor mortis) with no palpable pulse or audible heart sounds.

Hypothyroidism

Hypothyroidism causes severe bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity to cold. Related signs include cool, dry, thick skin; sparse, dry hair; facial swelling; periorbital edema; thick, brittle nails; and confusion leading to stupor.

Myocardial infarction

Sinus bradycardia is the arrhythmia most commonly associated with acute myocardial infarction (MI). Accompanying signs and symptoms of an MI include an aching, burning, or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric area; nausea and vomiting; cool, clammy, and pale or cyanotic skin; anxiety; and dyspnea. Blood pressure may be elevated or depressed. Auscultation may reveal abnormal heart sounds.

Other causes

Diagnostic tests

Cardiac catheterization and electrophysiologic studies can induce temporary bradycardia.

Drugs

Beta-adrenergic blockers and some calcium channel blockers, cardiac glycosides, topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics, and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may cause bradycardia.

Invasive treatments

Suctioning can induce hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or damage to conduction tissues, causing bradycardia.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Heart Murmurs (Asymptomatic): Principal Causes of Heart Murmurs (Asymptomatic)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

  1. Normalmurmurs
    1. Systolicejection murmurs
      1. Vibratory systolic murmur
      2. Pulmonary systolic murmur (pulmonarytrunk)
      3. Physiologic peripheral pulmonary systolicmurmur (pulmonary branches)
      4. Supraclavicular or brachiocephalicmurmur
    2. Continuous murmurs
      1. Venoushum
  2. Pathologic murmurs
    1. Systolicmurmurs
      1. Maximalintensity at the upper right sternal border
        1. Valvaraortic stenosis
      2. Maximal intensity at the upper leftsternal border
        1. Valvar pulmonic stenosis
        2. Atrial septal defects
        3. Mild-to-moderate coarctation of theaorta
        4. Small patent ductus arteriosus
      3. Maximal intensity at the lower leftsternal border
        1. Ventricular septal defect
        2. Tricuspid incompetence
      4. Maximal intensity at the apex
        1. Mitralincompetence
        2. Mitral valve prolapse
    2. Diastolic murmurs
      1. Maximalintensity at the upper right sternal border
        1. Aorticvalve incompetence
      2. Maximal intensity at the upper leftsternal border
        1. Pulmonic valve incompetence
      3. Maximal intensity at the lower leftsternal border
        1. Atrial septal defects
        2. Tricuspid stenosis
        3. Moderate-to-severe tricuspid incompetence
      4. Maximal intensity at the apex
        1. Mitralstenosis
        2. Moderate-to-severe mitral incompetence
        3. Moderate left-to-right shunt lesions
    3. Continuous murmurs
      1. Maximalintensity at the upper left sternal border
        1. Moderate patent ductus arteriosus
      2. Maximal intensity at the left mid sternalborder
        1. Aorticpulmonary window
      3. Maximal intensity with variable location
        1. Coronaryarteriovenous fistula
        2. Systemic arteriovenous fistula

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Pulse, absent or weak: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Aortic aneurysm (dissecting).When a dissecting aneurysm affects circulation to the innominate, left common carotid, subclavian, or femoral artery, it causes weak or absent arterial pulses distal to the affected area. Absent or diminished pulses occur in 50% of patients with proximal dissection and usually involve the brachiocephalic vessels. Pulse deficits are much less common in patients with distal dissection and tend to involve the left subclavian and femoral arteries. Tearing pain usually develops suddenly in the chest and neck and may radiate to the upper and lower back and abdomen. Other findings include syncope, loss of consciousness, weakness or transient paralysis of the legs or arms, the diastolic murmur of aortic insufficiency, systemic hypotension, and mottled skin below the waist.

Aortic arch syndrome (Takayasu's arteritis).Aortic arch syndrome produces weak or abruptly absent carotid pulses and unequal or absent radial pulses. These signs are usually preceded by malaise, night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud's phenomenon. Other findings include neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; dizziness; and syncope. If the carotid artery is involved, diplopia and transient blindness may occur.

Aortic bifurcation occlusion (acute).Aortic bifurcation occlusionproduces abrupt absence of all leg pulses. The patient reports moderate to severe pain in the legs and, less commonly, in the abdomen, lumbosacral area, or perineum. Also, his legs are cold, pale, numb, and flaccid.

Aortic stenosis.With aortic stenosis, the carotid pulse is sustained but weak. Dyspnea (especially on exertion or paroxysmal nocturnal), chest pain, and syncope dominate the clinical picture. The patient commonly has an atrial gallop. Other findings include a harsh systolic ejection murmur, crackles, palpitations, fatigue, and narrowed pulse pressure.

Arrhythmias.Cardiac arrhythmias may produce generalized weak pulses accompanied by cool, clammy skin. Other findings reflect the arrhythmia's severity and may include hypotension, chest pain, dyspnea, dizziness, and decreased level of consciousness (LOC).

Arterial occlusion.Withacute occlusion, arterial pulses distal to the obstruction are unilaterally weak and then absent. The affected limb is cool, pale, and cyanotic, with an increased capillary refill time, and the patient complains of moderate to severe pain and paresthesia. A line of color and temperature demarcation develops at the level of obstruction. Varying degrees of limb paralysis may also occur, along with intense intermittent claudication. With chronic occlusion, occurring with disorders such as arteriosclerosis and Buerger's disease, pulses in the affected limb weaken gradually.

Cardiac tamponade.Life-threatening cardiac tamponade causes a weak, rapid pulse accompanied by these classic findings: paradoxical pulse, jugular vein distention, hypotension, and muffled heart sounds. Narrowed pulse pressure, pericardial friction rub, and hepatomegaly may also occur. The patient may appear anxious, restless, and cyanotic and may have chest pain, clammy skin, dyspnea, and tachypnea.

Coarctation of the aorta.Findings of coarctation of the aorta include bounding pulses in the arms and neck, with decreased pulsations and systolic pulse pressure in the lower extremities.

Peripheral vascular disease.Peripheral vascular disease causes a weakening and loss of peripheral pulses. The patient complains of aching pain distal to the occlusion that worsens with exercise and abates with rest. The skin feels cool and shows decreased hair growth. Impotence may occur in male patients with occlusion in the descending aorta or femoral areas.

Pulmonary embolism.Pulmonary embolism causes a generalized weak, rapid pulse. It may also cause an abrupt onset of chest pain, tachycardia, dyspnea, apprehension, syncope, diaphoresis, and cyanosis. Acute respiratory findings include tachypnea, dyspnea, decreased breath sounds, crackles, a pleural friction rub, and a cough—possibly with blood-tinged sputum.

Shock.With anaphylactic shock, pulses become rapid and weak and then uniformly absent within seconds or minutes after exposure to an allergen. This is preceded by hypotension, anxiety, restlessness, feelings of doom, intense itching, a pounding headache and, possibly, urticaria.

With cardiogenic shock, peripheral pulses are absent and central pulses are weak, depending on the degree of vascular collapse. Pulse pressure is narrow. A drop in systolic blood pressure to 30 mm Hg below baseline, or a sustained reading below 80 mm Hg, produces poor tissue perfusion. Resulting signs include cold, pale, clammy skin; tachycardia; rapid, shallow respirations; oliguria; restlessness; confusion; and obtundation.

With hypovolemic shock, all pulses in the extremities become weak and then uniformly absent, depending on the severity of hypovolemia. As shock progresses, remaining pulses become thready and more rapid. Early signs of hypovolemic shock include restlessness, thirst, tachypnea, and cool, pale skin. Late signs include hypotension with narrowing pulse pressure, clammy skin, a drop in urine output to less than 25 ml/hour, confusion, decreased LOC and, possibly, hypothermia.

With septic shock, all pulses in the extremities first become weak. Depending on the degree of vascular collapse, pulses may then become uniformly absent. Shock is heralded by chills, a sudden fever and, possibly, nausea, vomiting, and diarrhea. Typically, the patient experiences tachycardia, tachypnea, and flushed, warm, and dry skin. As shock progresses, he develops thirst, hypotension, anxiety, restlessness, and confusion. Then pulse pressure narrows and the skin becomes cold, clammy, and cyanotic. The patient experiences severe hypotension, oliguria or anuria, respiratory failure, and coma.

Thoracic outlet syndrome.A patient with thoracic outletsyndrome may develop gradual or abrupt weakness or loss of the pulses in the arms, depending on how quickly vessels in the neck compress. These pulse changes commonly occur after the patient works with his hands above his shoulders, lifts a weight, or abducts his arm. Paresthesia and pain occur along the ulnar distribution of the arm and disappear as soon as the patient returns his arm to a neutral position. The patient may also have asymmetrical blood pressure and cool, pale skin.

Other causes

Treatments.Localized absent pulse may occur distal to arteriovenous shunts for dialysis or following orthopedic injury or repair.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Murmurs: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Aortic insufficiency.Acute aortic insufficiency typically produces a soft, short diastolic murmur over the left sternal border that's best heard when the patient sits and leans forward and at the end of a forced held expiration. S2 may be soft or absent. Sometimes, a soft, short midsystolic murmur may also be heard over the second right intercostal space. Associated findings include tachycardia, dyspnea, jugular vein distention, crackles, increased fatigue, and pale, cool extremities.

Chronic aortic insufficiency causes a high-pitched, blowing, decrescendo diastolic murmur that's best heard over the second or third right intercostal space or the left sternal border with the patient sitting, leaning forward, and holding his breath after deep expiration. An Austin Flint murmur—a rumbling, mid-to-late diastolic murmur best heard at the apex—may also occur. Complications may not develop until the patient is between ages 40 and 50; then, typical findings include palpitations, tachycardia, angina, increased fatigue, dyspnea, orthopnea, and crackles.

Aortic stenosis.With aortic stenosis, the murmur is systolic, beginning after S1 and ending at or before aortic valve closure. It's harsh and grating, medium-pitched, and crescendo-decrescendo. Loudest over the second right intercostal space when the patient is sitting and leaning forward, this murmur may also be heard at the apex, at the suprasternal notch (Erb's point), and over the carotid arteries.

If the patient has advanced disease, S2 may be heard as a single sound, with inaudible aortic closure. An early systolic ejection click at the apex is typical, but is absent when the valve is severely calcified. Associated signs and symptoms usually don't appear until age 30 in congenital aortic stenosis, ages 30 to 65 in stenosis due to rheumatic disease, and after age 65 in calcific aortic stenosis. They may include dizziness, syncope, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and angina.

Cardiomyopathy (hypertrophic).Hypertrophic cardiomyopathygenerates a harsh late-systolic murmur, ending at S2. Best heard over the left sternal border and at the apex, the murmur is commonly accompanied by an audible S3 or S4. The murmur decreases with squatting and increases with sitting down. Major associated symptoms are dyspnea and chest pain; palpitations, dizziness, and syncope may also occur.

Mitral insufficiency.Acute mitral insufficiency is characterized by a medium-pitched blowing, early systolic or holosystolic decrescendo murmur at the apex, along with a widely split S2 and commonly an S4. This murmur doesn't get louder on inspiration as with tricuspid insufficiency. Associated findings typically include tachycardia and signs of acute pulmonary edema.

Chronic mitral insufficiency produces a high-pitched, blowing, holosystolic plateau murmur that's loudest at the apex and usually radiates to the axilla or back. Fatigue, dyspnea, and palpitations may also occur.

Mitral prolapse.Mitral prolapse generates a midsystolic to late-systolic click with a high-pitched late-systolic crescendo murmur, best heard at the apex. Occasionally, multiple clicks may be heard, with or without a systolic murmur. Associated findings include cardiac awareness, migraine headaches, dizziness, weakness, syncope, palpitations, chest pain, dyspnea, severe episodic fatigue, mood swings, and anxiety.

Mitral stenosis.With mitral stenosis, the murmur is soft, low-pitched, rumbling, crescendo-decrescendo, and diastolic, accompanied by a loud S1 or an opening snap—a cardinal sign. It's best heard at the apex with the patient in the left lateral position. Mild exercise helps make this murmur audible.

With severe stenosis, the murmur of mitral insufficiency may also be heard. Other findings include hemoptysis, exertional dyspnea and fatigue, and signs of acute pulmonary edema.

Myxomas.A left atrial myxoma (most common) usually produces a mid-diastolic murmur and a holosystolic murmur that's loudest at the apex, with an S4, an early diastolic thudding sound (tumor plop), and a loud, widely split S1.Related features include dyspnea, orthopnea, chest pain, fatigue, weight loss, and syncope.

A right atrial myxoma causes a late-diastolic rumbling murmur, a holosystolic crescendo murmur, and tumor plop, best heard at the lower left sternal border. Other findings include fatigue, peripheral edema, ascites, and hepatomegaly.

A left ventricular myxoma (rare) produces a systolic murmur, best heard at the lower left sternal border; arrhythmias; dyspnea; and syncope.

A right ventricular myxoma commonly generates a systolic ejection murmur with delayed S2 and a tumor plop, best heard at the left sternal border. It's accompanied by peripheral edema, hepatomegaly, ascites, dyspnea, and syncope.

Papillary muscle rupture.With papillary muscle rupture—a life-threatening complication of an acute MI—a loud holosystolic murmur can be auscultated at the apex. Related findings include severe dyspnea, chest pain, syncope, hemoptysis, tachycardia, and hypotension.

Rheumatic fever with pericarditis.With rheumatic fever, a pericardial friction rub along with murmurs and gallops are heard best with the patient leaning forward on his hands and knees during forced expiration. The most common murmurs heard are the systolic murmur of mitral insufficiency, a midsystolic murmur due to swelling of the mitral valve leaflet, and the diastolic murmur of aortic insufficiency. Other signs and symptoms include fever, joint and sternal pain, edema, and tachypnea.

Tricuspid insufficiency.Tricuspid insufficiency is characterized by a soft, high-pitched, holosystolic blowing murmur that increases with inspiration (Carvallo's sign), decreases with exhalation and Valsalva's maneuver, and is best heard over the lower left sternal border and the xiphoid area. Following a lengthy period without symptoms, exertional dyspnea and orthopnea may develop, along with jugular vein distention, ascites, peripheral cyanosis and edema, muscle wasting, fatigue, weakness, and syncope.

Tricuspid stenosis.Tricuspid stenosis produces a diastolic murmur similar to that of mitral stenosis, but louder with inspiration and decreased with exhalation and Valsalva's maneuver. S1 may also be louder. Associated signs and symptoms include fatigue, syncope, peripheral edema, jugular vein distention, ascites, hepatomegaly, and dyspnea.

Other causes

Treatments.Prosthetic valve replacement may cause variable murmurs, depending on the location, valve composition, and method of operation.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse rhythm abnormality: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Arrhythmias.An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulsus paradoxus: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Cardiac tamponade.Pulsus paradoxus commonly occurs with cardiac tamponade, but it may be difficult to detect if intrapericardial pressure rises abruptly and profound hypotension occurs. With severe tamponade, assessment also reveals these classic findings: hypotension, diminished or muffled heart sounds, and jugular vein distention. Related findings include chest pain, a pericardial friction rub, narrowed pulse pressure, anxiety, restlessness, clammy skin, and hepatomegaly. Characteristic respiratory signs and symptoms include dyspnea, tachypnea, and cyanosis; the patient typically sits up and leans forward to facilitate breathing.

If cardiac tamponade develops gradually, pulsus paradoxus may be accompanied by weakness, anorexia, and weight loss. The patient may also report chest pain, but he won't have muffled heart sounds or severe hypotension.

Chronic obstructive pulmonary disease (COPD).The wide fluctuations in intrathoracic pressure that characterize COPD produce pulsus paradoxus and possibly tachycardia. Other findings vary, but may include dyspnea, tachypnea, wheezing, a productive or nonproductive cough, accessory muscle use, barrel chest, and clubbing. The patient may show labored, pursed-lip breathing after exertion or even at rest. He typically sits up and leans forward to facilitate breathing. Auscultation reveals decreased breath sounds, rhonchi, and crackles. Weight loss, cyanosis, and edema may occur.

Pericarditis (chronic constrictive).Pulsus paradoxus can occur in up to 50% of patients with pericarditis. Other findings include a pericardial friction rub, chest pain, exertional dyspnea, orthopnea, hepatomegaly, and ascites. Patients also exhibit peripheral edema and Kussmaul's sign—jugular vein distention that becomes more prominent on inspiration.

Pulmonary embolism (massive).Decreased left ventricular filling and stroke volume with massive pulmonary embolism produce pulsus paradoxus as well as syncope and severe apprehension, dyspnea, tachypnea, and pleuritic chest pain. The patient appears cyanotic, with jugular vein distention. He may succumb to circulatory collapse, with hypotension and a weak, rapid pulse. Pulmonary infarction may produce hemoptysis along with decreased breath sounds and a pleural friction rub over the affected area.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Bradycardia: Medical causes
(Nursing: Interpreting Signs and Symptoms)

Cardiac arrhythmia.Depending on the type of arrhythmia and the patient's tolerance of it, bradycardia may be transient or sustained, benign or life-threatening. Related findings may include hypotension, palpitations, dizziness, weakness, syncope, and fatigue.

Cardiomyopathy.Cardiomyopathy is a potentially life-threatening disorder that may cause transient or sustained bradycardia. Other findings include dizziness, syncope, edema, fatigue, jugular vein distention, orthopnea, dyspnea, and peripheral cyanosis.

Hypothermia.Bradycardia usually appears when the core temperature drops below 89.6° F (32° C). It's accompanied by shivering, peripheral cyanosis, muscle rigidity, bradypnea, and confusion leading to stupor.

Hypothyroidism.Hypothyroidism causes severe bradycardia in addition to fatigue, constipation, unexplained weight gain, and sensitivity to cold. Related signs include cool, dry, thick skin; sparse, dry hair; facial swelling; periorbital edema; thick, brittle nails; and confusion leading to stupor.

Myocardial infarction (MI).Sinus bradycardia is the most common arrhythmia associated with an acute MI. Accompanying signs and symptoms of an MI include an aching, burning, or viselike pressure in the chest that may radiate to the jaw, shoulder, arm, back, or epigastric area; nausea and vomiting; cool, clammy, and pale or cyanotic skin; anxiety; and dyspnea. Blood pressure may be elevated or decreased. Auscultation may reveal abnormal heart sounds.

Other causes

Diagnostic tests.Cardiac catheterization and electrophysiologic studies can induce temporary bradycardia.

Drugs.Beta-adrenergic blockers and some calcium channel blockers, cardiac glycosides, topical miotics (such as pilocarpine), protamine, quinidine and other antiarrhythmics, and sympatholytics may cause transient bradycardia. Failure to take thyroid replacements may cause bradycardia.

Invasive treatments.Suctioning can induce hypoxia and vagal stimulation, causing bradycardia. Cardiac surgery can cause edema or damage to conduction tissues, causing bradycardia.

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Source: Nursing: Interpreting Signs and Symptoms, 2007


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