Chapter 4 - Cardiovascular System

CHAPTER 4 – CARDIOVASCULAR SYSTEM
First Nations and Inuit Health Branch (FNIHB) Clinical Practice Guidelines for Nurses in Primary Care.
The content of this chapter was reviewed August 2010.
Table of Contents
ASSESSMENT OF THE CARDIOVASCULAR SYSTEM..........................................4–1

History of Present Illness and Review of Systems..............................................4–1
Physical Examination..........................................................................................4–2
Differential Diagnoses of Cardinal Cardiovascular Symptoms............................4–4
COMMON PROBLEMS OF THE CARDIOVASCULAR SYSTEM.............................4–8
Aortic Aneurysm, Abdominal (Pulsatile Abdominal Mass)...................................4–8
Arrhythmias.........................................................................................................4–9
Arterial Peripheral Vascular Disease, Chronic..................................................4–11
Atrial Fibrillation................................................................................................4–13
Congestive Heart Failure..................................................................................4–14
Deep Vein Thrombosis......................................................................................4–19
Dyslipidemia (Hyperlipidemia)..........................................................................4–21
Hypertension.....................................................................................................4–24
Ischemic Heart Disease, Including Angina........................................................4–27
Pericarditis, Acute.............................................................................................4–32
Venous Insufficiency, Chronic...........................................................................4–33
EMERGENCIES OF THE CARDIOVASCULAR SYSTEM......................................4–34
Acute Arterial Occlusion of a Major Peripheral Artery.......................................4–34
Myocardial Infarction.........................................................................................4–35
Pulmonary Edema............................................................................................4–37
SOURCES...............................................................................................................4–39
Clinical Practice Guidelines for Nurses in Primary Care 2010

Cardiovascular System 4–1
ASSESSMENT OF THE CARDIOVASCULAR SYSTEM
HISTORY OF PRESENT ILLNESS Fainting or Syncope

AND REVIEW OF SYSTEMS –– Weakness, lightheadedness, loss of consciousness
–– Associated symptoms (for example, pain,
The following characteristics of each symptom
palpitations, shortness of breath, lightheadedness,
should be elicited and explored:
nausea, sweating)
–– Current situation (improving or deteriorating) –– Relation to postural changes, vertigo or neurologic
–– Location symptoms
–– Chronology
–– Onset (sudden or gradual) Palpitations
–– Precipitating and aggravating factors –– Description: fast or slow, irregular or regular
–– Quality –– Relation to exercise
–– Radiation –– Relation to anxiety or panic attack
–– Severity
Sputum
–– Timing (frequency, duration)
–– Relieving factors –– Colour, amount
–– Associated symptoms –– Consistency (for example, frothy white, pink)
–– Effects on daily activities
Cyanosis
–– Previous investigations and/or diagnosis
of similar episodes –– Observation of blue colour of the lips or fingers
–– Previous treatments (under what circumstances, when first noted, recent
–– Efficacy of previous treatments change in this characteristic)
CARDINAL SYMPTOMS Extremities
In addition to the general characteristics outlined –– Site of edema (for example, in dependent
above, additional characteristics of specific symptoms body parts)
should be elicited, as follows. –– Relation of edema to activity or time of day,
(for example, relieved by rest, elevation of legs)
Chest Pain –– Intermittent claudication (exercise-induced leg pain)
–– Associated symptoms (for example, faintness, –– Distance client can walk before onset of pain
syncope, shortness of breath, diaphoresis, nausea, related to claudication
vomiting) –– Time needed to rest to relieve claudication
–– Relation to effort, exercise, emotional state, meals, –– Temperature of affected tissue (warm, cool or cold)
bending over –– Tingling
–– Leg cramps or pain at rest
Shortness of Breath –– Presence of varicose veins
–– Relation to exercise (level ground, uphill, stairs)
–– Relation to posture
–– Orthopnea (number of pillows used for sleeping)
–– Paroxysmal nocturnal dyspnea
–– Associated swelling of ankles or recent weight gain

4–2 Cardiovascular System
MEDICAL HISTORY PHYSICAL EXAMINATION

–– Increased cholesterol level An examination of the cardiovascular system
–– Hypertension involves more than just examining the heart. The
–– Coronary artery disease (angina) examination generally covers two systems: the central
–– Myocardial infarction cardiovascular system (head, neck and precordium
–– Cardiac murmurs [anterior chest]) and the peripheral vascular system
–– Rheumatic fever (extremities). Examination of the cardiovascular
system must also include a full assessment of the
–– Valvular heart disease
lungs and neuromental status (for signs of confusion,
–– Diabetes mellitus
irritability or altered level of consciousness).
–– Thyroid disease
–– Chronic renal disease VITAL SIGNS
–– Chronic obstructive pulmonary disease (COPD) –– General appearance (for example, respiratory
–– Systemic lupus erythematosus distress, acute pain, diaphoretic, unwell)
–– Recent viral illness (for example, viral –– Temperature
cardiomyopathy) –– Pulse (regular, regularly irregular or irregularly
–– Previous cardiac investigations (for example, irregular)
echocardiogram, exercise stress test) –– Respiratory rate
FAMILY HISTORY –– Oxygen saturation
–– Blood pressure (lying and standing, in both arms)
–– Height, weight, BMI
–– Hypertension
–– Waist circumference
–– Coronary artery disease (ischemic) (especially
in family members < 50 years of age) HEAD AND NECK
–– Myocardial infarction (especially in family
–– Central cyanosis
members < 50 years of age)
–– Colour of lips
–– Sudden death from cardiac disease
–– Jugular venous pressure
–– Hypercholesterolemia
–– Carotid bruits
–– Hypertrophic cardiomyopathy
INSPECTION OF PRECORDIUM
PERSONAL AND SOCIAL HISTORY
(ANTERIOR CHEST)
–– Smoking
–– Look for visible pulsations of the chest wall
–– Exposure to second-hand smoke (point of maximal impulse)
–– Abdominal obesity (waist measurement > 100 cm –– Look for accessory muscle use
[40 in] in men, > 90 cm [35 in] in women)
–– Body mass index (BMI) > 25 PALPATION
–– Lack of physical activity (< 20 minutes of vigorous –– Location of apical beat (point of maximal
activity 3 times a week, or < 30 minutes of impulse [PMI]) (in adults, normal apical beat is
moderate activity per day) found in the 5th intercostal space, medial to the
–– High stress levels (personal or occupational) mid‑clavicular line)
–– Chronic abuse of cocaine, amphetamines, anabolic –– Quality and intensity of apical beat (normal,
steroids, solvents, ecstasy diffuse, weak, forceful)
–– Alcohol abuse –– Heave (abnormally forceful PMI)
–– Thrill (a palpable murmur that feels like a purr)
–– Identify and assess pulsations and thrills in aortic,
pulmonic, mitral and tricuspid areas, along left and
right sternal borders, in epigastrium and along left
anterior axillary line
2010 Clinical Practice Guidelines for Nurses in Primary Care

AUSCULTATION S4 (Pressure Overloaded Ventricle)

–– Listen to normal heart sounds before trying –– Ischemia
to identify murmurs and extra heart sounds –– Ventricular hypertrophy from systemic
–– Use diaphragm of stethoscope first, then bell hypertension, aortic stenosis, hypertrophic
of stethoscope, when listening to the heart cardiomyopathy
–– Listen at apex, in aortic and pulmonic areas –– Right ventricular S4 due to pulmonary hypertension
and along left sternal border or pulmonic stenosis
–– Listen at bilateral carotid arteries for bruits To hear an example of S4, refer to the 3M Heart and
Lung Sounds page at: http://solutions.3m.com/wps/
HEART SOUNDS
portal/3M/en_US/Littmann/stethoscope/education/
–– Determine rate and rhythm heart-lung-sounds/.
–– Determine if there is an underlying rhythm or
if rhythm is completely irregular (for example, Other Extra Sounds
regular, regularly irregular or irregularly irregular) –– Opening snaps (early diastolic sounds associated
–– Identify and describe intensity of first and second with mitral stenosis)
heart sounds –– Ejection clicks (associated with aortic stenosis,
–– Identify extra sounds (S3, S4, splitting of second pulmonic stenosis)
sound, rubs) –– Mid-systolic clicks (mitral valve prolapse,
tricuspid valve prolapse)
MURMURS
–– Pericardial fraction rubs (pericarditis)
–– Timing (in relation to the cardiac cycle,
To hear an example of an ejection click and opening
for example, systolic or diastolic)
snap refer to the 3M Heart and Lung Sounds page
–– Quality
at: http://solutions.3m.com/wps/portal/3M/en_US/
–– Intensity (loudness) Littmann/stethoscope/education/heart-lung-sounds/.
–– Location where murmurs sound loudest
–– Radiation Systolic “Ejection” Murmurs (Diamond
–– Pitch Shape, Crescendo-Decrescendo)
–– Murmur gets louder and then quieter during
DIFFERENTIAL DIAGNOSIS OF one cardiac cycle
ABNORMALITIES IN HEART SOUNDS
–– Outflow obstruction (aortic stenosis, pulmonic
S3 (Volume Overloaded Ventricle) stenosis, hypertrophic cardiomyopathy)
–– High output or “flow” murmurs (accompanying
–– May be normal in children and younger adults
anemia, pregnancy, thyrotoxicosis, fever,
(< 30 years), however, some may not be and
arteriovenous fistula and in young children)
should have further assessment and investigations
–– Left ventricular failure (due to systolic dysfunction, To hear an example of a systolic murmur (early and
acute myocardial infarction) late), refer to the 3M Heart and Lung Sounds page
–– Mitral regurgitation (rapid ventricular filling) at: http://solutions.3m.com/wps/portal/3M/en_US/
Littmann/stethoscope/education/heart-lung-sounds/.
–– Right ventricular S3 (due to tricuspid regurgitation,
mitral stenosis, right ventricular failure) Pansystolic Murmurs
To hear an example of S3, refer to the 3M Heart and –– Mitral regurgitation
Lung Sounds page at: http://solutions.3m.com/wps/
–– Tricuspid regurgitation
portal/3M/en_US/Littmann/stethoscope/education/
heart-lung-sounds/. –– Ventricular septal defect
To hear an example of a pansystolic murmur, refer
to the 3M Heart and Lung Sounds page at: http://
solutions.3m.com/wps/portal/3M/en_US/Littmann/
stethoscope/education/heart-lung-sounds/.

High-Pitched Diastolic Decrescendo Murmurs Legs

–– Aortic regurgitation –– Colour (pigmentation, discolouration), distribution
–– Pulmonic regurgitation of hair
–– Temperature, texture
Low-Pitched Diastolic Murmurs –– Capillary refilling time
(Mid-Diastolic Rumbles)
–– Changes in foot colour with changes in leg position
–– Mitral stenosis (for example, blanching with elevation, rubor with
–– Tricuspid stenosis dependency)
–– Continuous murmurs –– Ulcers (for example, venous stasis), varicose veins,
–– Patent ductus arteriosus pitting or nonpitting edema (check sacrum if client
–– Mammary souffle (goes away with pressure is bedridden)
on stethoscope) –– Presence and equality of pulses (femoral, popliteal,
–– Coronary arteriovenous fistula posterior tibial, dorsalis pedis)
–– Venous hum (due to high flow in jugular veins, OTHER ASSESSMENTS
high cardiac output states)
For a client whose condition is not of an urgent nature,
To hear an example of a diastolic rumble, refer assess the following:
to the 3M Heart and Lung Sounds page at: http://
solutions.3m.com/wps/portal/3M/en_US/Littmann/ –– Evidence of hypertensive or diabetic retinopathies
stethoscope/education/heart-lung-sounds/. (funduscopic exam)
–– Colour, temperature, rashes, lesions, xanthoma of skin
Bruits –– Abdominal bruits, enlargement of liver, tenderness
–– Carotid in right upper quadrant of abdomen
–– Abdominal
–– Iliac DIFFERENTIAL DIAGNOSES OF
–– Femoral CARDINAL CARDIOVASCULAR
SYMPTOMS
EXTREMITIES
CHEST PAIN
Hands
When assessing chest pain, it is important to consider
–– Colour of skin, nail beds
and rule out serious causes of chest pain. See Table 1,
–– Nicotine stains “Differential Diagnosis of Chest Pain.”
–– Clubbing of fingers
–– Temperature
–– Equality of pulses (brachial, radial)
–– Synchrony of radial and femoral pulses
–– Capillary refilling time

Table 1 – Differential Diagnosis of Chest Pain

Differential Diagnosis of Chest Pain+
Myocardial
Infarction or
Characteristic Acute Coronary Aortic Pulmonary
of Chest Pain Syndrome Angina Dissection1 Pneumonia Embolism*
Onset Sudden, patient With exertion Sudden Gradual or Sudden
at rest sudden
Location Retrosternal, Retrosternal, Retrosternal, Anterior, lateral Retrosternal, anterior
anterior chest anterior chest epigastric, back, and/or posterior chest, lateral chest
posterior and/or lung field(s)
anterior chest
Radiation Left arm, left Left arm, left Anywhere Anterior chest, Variable
shoulder, neck, shoulder, neck, in thorax or shoulder, neck
jaw, back, upper jaw, back, upper abdomen
abdomen abdomen
Duration > 20 min Usually <1–2 min > 20 min Hours Variable
Intensity Severe Mild to moderate Severe Moderate Absent or mild
to moderate
Quality Sensation of Sensation Tearing Constant ache, Dull ache; knife-like
squeezing, of tightness, or sharp with intermittent pain may also be
pressure pressure knife-like pain present
Relief May be relief Rapid relief None None None
with sublingual with rest and/
nitroglycerin2 or sublingual
nitroglycerin
Precipitating None may Exertion, heavy None Increased pain Immobilization,
or aggravating be obvious meal, walking with coughing or estrogen therapy,
factors uphill against deep inspiration; active cancer or
a cold wind, recently ill with a cancer treatment;4
occasionally cold none may be obvious;
from lying down3 pain may be worse
with deep inspiration
or coughing
Associated Nausea, sweating, Typically none Hypotension, Fever, cough, Shortness of breath,
signs and shortness of breath, shock, syncope, sputum, shortness sweating, hemoptysis,
symptoms anxiety, palpitations myocardial of breath, malaise, leg pain (rare), leg
infarction weakness or swelling or pitting
fatigue edema
+ other presentations are common among women (for example, epigastric pain or indigestion) and diabetics
(for example, may have silent symptoms)
* Chest pain may be absent in pulmonary embolism

Table 1 – Differential Diagnosis of Chest Pain (Continued)

Differential Diagnosis of Chest Pain+
Chest Wall Pain
Characteristic (for example, Esophageal, Gastric Stress or Emotional
of Chest Pain Pericarditis costochondritis) or Duodenal Disorder Disorder
Onset Gradual or sudden Gradual or sudden Gradual or sudden Gradual or sudden
Location Retrosternal, Anterior, lateral and/or Retrosternal, epigastric, Variable; anterior
anterior chest posterior chest wall left chest, left or right chest, left chest
upper quadrant
Radiation Variable: shoulder Arm, shoulder, neck, May be felt in back or Usually none
tip, neck back, abdomen arm
Duration Hours to days Minutes or hours Minutes or hours Minutes or hours
Intensity Usually moderate, Mild to moderate Moderate Mild to moderate
but may be severe
Quality Sharp Dull ache; sharp pain Burning (usually), Achy, stabbing
may also be present tightness
Relief Sitting up and Rest, mild analgesics Antacids, milk, Rest, relaxation,
leaning forward sitting up or distraction
often helps; other standing up
changes in position
may alter the pain
Precipitating Previous infection History of unaccustomed Certain foods, a large Stressful situations,
or aggravating of upper respiratory physical work; pain meal, bending over; fatigue
factors tract; pain worse with arm action pain may awaken
worse with deep person from sleep
inspiration and may occur when
or coughing stomach is empty
Associated signs Symptoms of Localized chest-wall Regurgitation of acid Tightness in neck and
and symptoms infection of upper tenderness, tender in mouth, belching, shoulder(s), headaches,
respiratory tract costochondral area difficulty swallowing, reduced appetite, mild
may be present; sticking sensation when weight loss, fatigue,
malaise; usually food swallowed, cough sleep disturbance,
occurs in younger (rare); test of stool for palpitations, dizziness,
adults occult blood may be hyperventilation
positive symptoms
+ other presentations are common among women (for example, epigastric pain or indigestion) and diabetics
(for example, may have silent symptoms)
* Chest pain may be absent in pulmonary embolism
DYSPNEA Pulmonary Causes
Cardiac Causes –– COPD/obstructive lung disease

–– Asthma
–– Congestive heart failure (right, left or biventricular)
–– Restrictive lung disorders, such as pulmonary
–– Coronary artery disease fibrosis
–– Myocardial infarction (recent or past history) –– Hereditary lung disorders
–– Cardiomyopathy –– Pneumothorax
–– Valvular dysfunction –– Primary pulmonary hypertension
–– Left ventricular hypertrophy –– Pulmonary embolus
–– Asymmetric septal hypertrophy –– Pneumonia
–– Pericarditis
–– Arrhythmias

Mixed Cardiac and Pulmonary Causes Other Causes

–– COPD with pulmonary hypertension –– Hypoglycemia
and cor pulmonale –– Hyperventilation (syncope rare, faintness common)
–– Deconditioning –– Hypoxia
–– Chronic pulmonary emboli
–– Trauma PALPITATIONS
Noncardiac or Nonpulmonary Causes Primary Arrhythmic Causes
–– Metabolic conditions (for example, acidosis) –– Sinus tachycardia or arrhythmia

–– Pain –– Premature supraventricular or ventricular ectopic
contractions
–– Neuromuscular disorders
–– Bradycardia-tachycardia syndrome
–– Otorhinolaryngeal disorders
(“sick sinus syndrome”)
Functional Causes –– Supraventricular tachycardia
–– Multifocal atrial tachycardia
–– Anxiety
–– Atrial fibrillation, flutter or tachycardia
–– Panic disorders
–– Atrioventricular nodal re-entrant tachycardia
–– Hyperventilation
–– Atrioventricular reciprocating tachycardia
FAINTNESS AND SYNCOPE (Wolff-Parkinson-White syndrome)
–– Accelerated junctional rhythm
Faintness (pre-syncope) is characterized by transient
symptoms of lack of strength associated with an –– Ventricular tachycardia
impending sense of loss of consciousness. Syncope is –– Bradycardia due to advanced atrioventricular
characterized by transient symptoms of generalized block or sinus node dysfunction
weakness associated with loss of consciousness and
loss of muscle tone. Symptoms are due to a temporary Extracardiac Causes
impairment of cerebral function and are usually –– Changes in contractility, heart rate or stroke
precipitated by a reduction in cerebral perfusion. volume
–– Fever
Vascular Causes –– Hypovolemia
–– Vasovagal hypotension (common faint) –– Anemia
–– Postural hypotension –– Hypoglycemia
–– Cerebrovascular disease (transient ischemic attack, –– Pulmonary disease
stroke, vertebral-basilar insufficiency, carotid –– Pheochromocytoma
insufficiency) is an uncommon cause of syncope –– Thyrotoxicosis
Neurological Causes –– Vasovagal episodes
–– Seizure Drug-Related Causes

–– Head trauma –– Vasodilators
Cardiac Causes –– Substance abuse (for example, cocaine,
alcohol, tobacco, caffeine)
–– Abnormally slow heart rate and rhythm –– Digoxin
–– Abnormally rapid heart rate and rhythm –– Phenothiazine
–– Reduced cardiac output –– Theophylline
–– Acute blood loss (gastrointestinal hemorrhage) –– Beta2-agonists
causing hypotension
–– Antiarrhythmics
–– Valvular heart disease (aortic or pulmonic stenosis,
hypertrophic cardiomyopathy) Psychiatric Causes
–– Pulmonary hypertension
–– Panic attack
–– Hyperventilation

Other Cardiac Causes –– Congenital heart disease

–– Changes in contractility or stroke volume –– Pericarditis
–– Valvular disease such as aortic insufficiency –– Pacemaker-mediated tachycardia
or stenosis –– Pacemaker syndrome
–– Atrial or ventricular septal defect
LEG EDEMA
–– Congestive heart failure
–– Cardiomyopathy See Table 2, “Differential Diagnosis of Leg Edema.”
Table 2 – Differential Diagnosis of Leg Edema

Mechanism Disease or Syndrome Usual Clinical Features
Increased capillary pressure Thrombosis, malignancy Bilateral, severe (may be mild if partial
Obstruction of inferior vena cava obstruction)
Deep venous obstruction in leg Thrombosis, extrinsic compression Unilateral, mild
Reduced venous channels or venous Coronary bypass grafting, stroke, Unilateral or bilateral, mild
valve incompetence varicosities
Right atrial hypertension Left ventricular dysfunction Bilateral
Pulmonary disease Bilateral
Valve disease Bilateral
Renal dysfunction Bilateral, mild
Reduced lymphatic clearance Lymphadenopathy, filariasis Unilateral or bilateral
(lymphatic obstruction)
Decreased capillary oncotic Severe malnutrition; liver, renal, Bilateral, mild or severe, generalized,
pressure (hypoalbuminemia) gastrointestinal disease poor prognosis
Increased capillary permeability Calcium channel blockers Bilateral, mild
Idiopathic cyclic edema Bilateral, mild, premenstrual female
COMMON PROBLEMS OF THE CARDIOVASCULAR SYSTEM
AORTIC ANEURYSM, ABDOMINAL –– History of atherosclerosis (for example,

(PULSATILE ABDOMINAL MASS) intermittent claudication)
–– Hypertension
A pulsatile abdominal mass is considered and treated
as an abdominal aortic aneurysm until proven HISTORY
otherwise. It may be asymptomatic and discovered
If an aneurysm is leaking:
by accident.
–– Sudden onset of pain in mid-abdomen or back
An aortic aneurysm is a dilation of a specific part
(or both)
of the aorta. This may be in the thorax or in the
–– Sudden weakness and faintness
abdomen.
PHYSICAL FINDINGS
RISK FACTORS5
–– Pulse rapid and weak
–– Age over 60 years
–– Blood pressure low-normal to low
–– Smoking
–– Blood pressure may drop with change in posture
–– Male
–– Pulsating mid- or upper-abdominal mass
–– Family history of aortic aneurysm

If an aneurysm has ruptured: –– Insert a nasogastric tube, if upon consultation

a physician supports its use (because paralytic
–– Shock (hypovolemia)
ileus is common)
–– In severe distress, client may be unconscious
–– Insert a urinary catheter (optional unless transfer
–– Pulse diminished or absent delayed)
–– Blood pressure low or cannot be determined
–– A pulsating abdominal or flank mass Nonpharmacologic Interventions
may be palpable –– Bed rest
–– Subcutaneous bruising may be present –– Maintain “nothing-by-mouth” order
–– Death usually occurs
Monitoring and Follow-Up
MANAGEMENT OF ASYMPTOMATIC CLIENT
–– Monitor ABC (airway, breathing and circulation)
Goals of Treatment and vital signs closely, including oxygen saturation
–– Aim for pulse < 100 bpm and systolic blood
–– Identify and monitor the asymptomatic abdominal
pressure (BP) > 100 mm Hg
aneurysm
–– Monitor urinary output
Appropriate Consultation
Referral
Consult a physician when an asymptomatic aortic
aneursym is suspected or detected. Medevac as soon as possible.
Monitoring and Follow-Up ARRHYTHMIAS

–– Annual follow-up by physician Abnormal heart rhythm. The following are the most
–– Annual abdominal ultrasonography to measure size common types.
Referral SINUS BRADYCARDIA

Referral for vascular surgery (depending on size of Heart rate < 60 bpm; impulse originates in sinoatrial
the aneurysm) will usually be done by a physician. (SA) node.
MANAGEMENT OF SYMPTOMATIC CLIENT BRADYCARDIA

This is a medical emergency. Multiple causes which may include high grade
atrioventricular blocks; junctional escape rhythms;
Goals of Treatment heightened vagal tone; hyperkalemia.
–– Replace blood loss
SINUS TACHYCARDIA
Appropriate Consultation Heart rate > 100–160 bpm; impulse originates
Consult a physician immediately after intravenous in SA node.
access is established and oxygen is started.
SUPRAVENTRICULAR
Adjuvant Therapy TACHYDYSRHYTHMIAS
–– Oxygen via non-rebreather mask; titrate Heart rate > 100 bpm; impulse originates above
flow to keep oxygen saturation ≥ 90% the ventricles. There are two major types:
–– IV (16- to 18-gauge) with normal saline –– Atrioventricular (AV) nodal re-entrant tachycardia
(or lactated Ringer’s solution) is intranodal re-entry by means of fast and slow
–– Insert the needle into the largest vein available conduction pathways within the AV junction
–– Start a second IV line for rapid fluid replacement –– Orthodromic AV re-entrant tachycardia is
if client is in shock (See section “Shock” in tachycardia across accessory pathways associated
Chapter 14, “General Emergencies and Major with pre-excitation
Trauma”)

ATRIAL FIBRILLATION Predisposing Factors for Atrial Fibrillation

Chaotic electrical activity caused by rapid discharges –– Myocardial ischemia
from numerous ectopic foci in the atria. Atrial rate –– Thyrotoxicosis
is difficult to count. There are two types of atrial
fibrillation: Predisposing Factors for Premature
Ventricular Contractions
–– Paroxysmal atrial fibrillation occurs in people
who usually have normal sinus rhythm –– The prevalence of PVC is higher in:8
–– Chronic atrial fibrillation occurs in people who –– Men than women
have a permanent fibrillation rather than brief –– African Americans than Whites
episodes of symptoms –– Patients with organic disease
–– Prevalence increases with age
PREMATURE VENTRICULAR
–– Prevalence increases with hypokalemia,
CONTRACTIONS6
hypomagnesemia, hypertension and in those
Extra impulses that form within the purkinje fibres with a faster sinus rate
and result in an extra heart beat. They are very –– Stress
common and usually benign. –– Fatigue
PREDISPOSING FACTORS HISTORY
Predisposing Factors for Bradycardia –– Symptoms may not be present; however, client may
note irregular heartbeat
–– Increased vagal tone
–– Palpitations
–– Decreased sympathetic drive
–– Chest discomfort
–– Ischemia to sinoatrial node
–– Shortness of breath
–– Drugs: digoxin, beta-blockers (atenolol,
metoprolol, propranolol), calcium channel –– Dizziness
blockers, amiodarone and other antiarrythmic drugs –– Diaphoresis
–– Alcohol consumption –– Weakness
–– Athletic activity (normal variant in athletes) –– Syncope
–– Injury or other insult (normal body response) –– Nausea
–– Atrial enlargement –– Drug history (with particular attention to those
–– Acute myocardial infarction that affect heart rate)
–– Congestive heart failure PHYSICAL FINDINGS
–– Rheumatic heat disease
–– Sinus bradycardia: pulse regular but decreased
–– Hypertensive heart disease
(< 60 beats per minute [bpm]); blood pressure
–– Hypothermia normal or low; sinus rhythm on ECG
–– Electrolyte abnormality (rate < 60 bpm)
–– Acidosis –– Sinus tachycardia: pulse regular but increased
–– Infection (> 100 bpm); systolic blood pressure may be
normal, low or elevated; sinus rhythm on ECG
Predisposing Factors for Tachycardia (rate >100 bpm)
–– Decreased vagal tone –– Atrial fibrillation: pulse irregularly irregular, rate
–– Increased sympathetic tone variable; systolic blood pressure variable; narrow
–– Myocardial infarction complex ECG (absent p waves, rate variable)
–– Drugs (caffeine, nicotine, illicit drugs)7 –– Atrial flutter: atrial waves present as “sawtooths”
most commonly at 300 bpm; may be a regular
Predisposing Factors for block present such as a 2:1 atrial ventricular block
Supraventricular Tachycardia so the ventricular rate is regular at 150 bpm
–– Digoxin toxicity
–– Catecholamines

–– Supraventricular tachycardia: pulse regular and Nonpharmacologic Interventions

fast; blood pressure normal to low; regular narrow
complex tachycardia on ECG (rate so rapid it is Client education
hard to see P waves) –– Teach client some relaxation techniques
–– Premature ventricular contractions and premature –– Teach client and family members the signs of
atrial contractions: pulse regular with occasional hemodynamic compromise, including rapid heart
extra beat and pauses; blood pressure unaffected; rate, unexplained weight gain, worsening dyspnea
ECG: sinus rhythm with extra narrow or wide on exertion, decreased exercise tolerance
complex beats –– Teach client about long-term medication and its
side effects
DIFFERENTIAL DIAGNOSIS –– Identify and remove any contributing factors
–– Multifocal atrial tachycardia (for example, reduce caffeinated beverages)
–– Sinus tachycardia with multiple premature
Pharmacologic Interventions
atrial contractions
–– Atrial flutter Initial treatment prescribed only by a physician.
–– Ventricular tachycardia Selection of treatment modality should be based
–– Atrioventricular block on underlying pathophysiology.
–– Wolff-Parkinson-White syndrome Chronic atrial fibrillation is associated with stroke and
clients should be offered treatment with anticoagulants
COMPLICATIONS
such as warfarin (Coumadin) if the benefits outweigh
–– Heart failure the increased risks.
–– Myocardial infarction
–– Cerebrovascular accident, stroke Monitoring and Follow-Up
–– Thromboembolism –– For clients taking antiarrhythmic agents, liver
–– Life-threatening arrhythmia enzyme levels should be measured during first
4–8 weeks of therapy
DIAGNOSTIC TESTS –– Clients with risk factors for cardiac complications
–– Obtain ECG of therapy should undergo ECG during first weeks
–– 24-hour Holter monitoring (must be ordered of therapy and every 3–6 months thereafter
by a physician) –– Clients taking digoxin should be monitored
–– Determine level of thyroid-stimulating hormone carefully for toxic effects
(TSH) –– Evaluate INR on a regular basis to monitor
–– Check digoxin level if patient is on digoxin therapeutic response to warfarin
–– Check electrolytes including magnesium Referral
–– Obtain complete blood count
Medevac clients with hemodynamic instability.
–– Determine international normalized ratio (INR),
partial thromboplastin time (PTT)
ARTERIAL PERIPHERAL
MANAGEMENT VASCULAR DISEASE, CHRONIC
Goals of Treatment Decreased blood flow to one or more extremities,
–– Treat underlying condition primarily lower, leading to ischemia of the leg
muscles.
–– Relieve symptoms
–– Prevent recurrence CAUSES
–– Prevent complications
–– Atherosclerotic narrowing of the aorta and larger
Appropriate Consultation arteries supplying the lower limb
Consult a physician if client has abnormal ECG
pattern, new or refractory atrial fibrillation, suspicion
of Wolff-Parkinson-White or “sick sinus” syndrome.

RISK FACTORS DIFFERENTIAL DIAGNOSIS

–– Major: smoking, diabetes, –– Acute arterial occlusion
hyperchromocysteinemia –– Raynaud’s disease (Raynaud’s phenomenon)
–– Minor: hypertension, hyperlipidemia, obesity, –– Venous stasis (for example, varicose veins)
family history, sedentary lifestyle, male gender –– Osteoarthritis
–– Neurogenic claudication due to lumbar spinal
HISTORY
stenosis or spinal radiculopathy
–– Symptoms initially intermittent, reversible, –– Popliteal entrapment (for example, tumour,
reproducible Baker’s cyst)
–– Intermittent claudication: pain, ache, cramp located
in calf, instep, buttock, hip or thigh (rarely in an arm) COMPLICATIONS
–– Pain precipitated by exercise –– Ischemic ulcer
–– Discomfort quickly and consistently relieved –– Infection of ischemic ulcer
with rest (in 2–5 minutes) –– Loss of distal ischemic limb
–– Distance client can walk before experiencing –– Acute arterial occlusion
claudication (should be documented)
–– As disease progresses, symptoms occur with less DIAGNOSTIC TESTS
effort and last longer
–– Ankle-brachial index (ABI < 0.90 is abnormal)
–– With advanced disease, foot pain occurs at night
–– Arterial doppler
(nocturnal pain)
–– Arteriography (gold standard for diagnosis)
–– Nocturnal pain relieved by placing the leg into a
dependent position or by standing on a cold floor MANAGEMENT
–– With severe disease the involved area becomes
chronically ischemic, and pain is present during rest Goals of Treatment
–– Impotence may occur –– Slow progression of disease
–– Associated vascular disease of other target organs –– Identify, modify and treat risk factors (diabetes
may be present (angina, previous stroke or transient mellitus, hypertension, hyperlipidemia)
ischemic attacks)
–– Promote formation of collateral circulation
PHYSICAL FINDINGS –– Prevent complications
–– Hypertension Appropriate Consultation

–– Ischemic skin changes in foot and distal limb may
Consult a physician immediately if any of the
be present (thin, fragile skin; loss of hair on distal
following are present: ischemic ulcer, pain at rest,
leg; shiny and atrophic skin; leg muscle atrophy)
nocturnal pain, recent transient ischemic attack and/or
–– Arterial ulcers on toes or feet pulsatile abdominal mass.
–– Toenails may be hypertrophic
–– Rubor of foot with dependency, blanching Nonpharmacologic Interventions
of foot with elevation
Client education
–– Capillary refilling time slowed (> 2 seconds)
–– Recommend strongly that client stop smoking
–– Peripheral pulses decreased or absent
–– Recommend weight loss (if appropriate)
–– Pulsating abdominal mass may be present
(aortic aneurysm) –– Recommend daily exercise to improve fitness and
exercise tolerance of the leg muscles, which will
–– Arterial bruits may be present (abdominal
also help to improve collateral circulation (walking
aortic, iliac, femoral, popliteal)
is the best exercise)
–– Recommend that client elevate the head of the
bed (using 5- to 8-cm [2- to 3-in] wooden blocks)
–– Recommend that client keep feet and legs cool
while sleeping

–– To reduce skin irritation, client should put ASSOCIATED CONDITIONS9

sheepskin or bubble pads on the bed –– Hypertensive heart disease
–– Teach proper foot care: avoid clipping nails too –– Valvular or rheumatic heart disease
close to the skin, avoid tight-fitting shoes, keep feet
–– Coronary artery disease
dry and protected from injury (no slippers or bare
feet, even in the house) –– Acute myocardial infarction
–– For diabetic clients, teach proper foot care to a –– Pulmonary embolus
family member, if possible, so that this person can –– Cardiomyopathy
carry out the necessary tasks; alternatively, have –– Congestive heart failure
the client attend a clinic on a monthly basis for –– Infiltrative heart disease
care of nails and feet –– Pericarditis
–– Hyperthyroidism (uncontrolled)
–– Obstructive pulmonary disease
Consult a physician regarding an antiplatelet agent (for example, COPD)
(ASA or clopidogrel) and analgesia if there are –– Pulmonary hypertension
significant symptoms at time of diagnosis. –– Obesity
Monitoring and Follow-Up HISTORY
–– Recommend follow-up every 6 months to identify –– Palpitations
new symptoms or changes in existing symptoms
–– Lightheadedness
–– Advise client to return to the clinic if a leg/foot
–– Poor exercise capacity
injury occurs, no matter how small
–– Fatigue
–– With conservative therapy 60–80% will improve,
–– Dyspnea
20–30% will stay the same, 5–10% deteriorate,
5% will require intervention within 5 years, and –– Angina
< 4% will require amputation –– Syncope or near syncope
–– Stroke
Referral –– Arterial embolization
Refer to a physician as soon as feasible if there
is evidence of advanced disease (for example, PHYSICAL FINDINGS
intolerable pain, pain at rest, nocturnal pain, foot Do a complete cardiovascular and respiratory
ulcers and impending gangrene). A consult with a examination. Also assess the eyes for lid lag
vascular surgeon may be necessary. All patients with (hyperthyroid sign) and the neck for thyroid
risk factors and symptoms consistent with intermittent enlargement and elevated jugular venous pressure
claudication should be assessed by a physician for (JVP). The pulse should be irregularly irregular and
appropriate investigations. is usually tachycardic. The client may exhibit signs
of heart failure and/or hypotension.
ATRIAL FIBRILLATION
DIFFERENTIAL DIAGNOSIS
Atrial fibrillation is a cardiac arrhythmia in which –– Multifocal atrial tachycardia
chaotic electrical activity replaces the orderly
–– Sinus tachycardia with frequent atrial premature
activation sequence of normal sinus rhythm.
beats
–– Atrial flutter
COMPLICATIONS
–– Embolic stroke
–– Peripheral arterial embolization
–– Complications of pharmacologic therapy, including
bradycardic arrhythmias
–– Inherent risk of bleeding with anticoagulation

DIAGNOSTIC TESTS In clients with chronic atrial fibrillation, long-

For asymptomatic people: term anticoagulation may be advised to prevent
thromboembolic complications, depending on the
–– ECG (rapid, irregular, narrow QRS complexes with age of the patient and other comorbid conditions
no P waves) such as hypertension. Warfarin is usually used for
–– Thyroid-stimulating hormone (TSH) anticoagulation, but in some patients an antiplatelet
–– International normalized ratio (INR) and partial agent such as ASA may be sufficient or preferable.
thromboplastin time (PTT) Before any cardioversion with drugs or electricity,
–– Chest x-ray if there are concerns about heart failure a client must be adequately anticoagulated to prevent
or cardiomegaly a thromboembolic event.
–– Echocardiogram Counsel client about appropriate medication use,
–– Exercise tolerance test including side effects.
MANAGEMENT Monitoring and Follow-Up
Goals of Treatment –– Clients with stable atrial fibrillation should be

followed up regularly to assess for symptoms and
–– Search for and treat all predisposing factors (See signs of recurrence, complications, compliance
section “Associated Conditions” in this chapter) with therapy and side effects of medication
–– Reduce symptoms –– Clients on anticoagulation must have INR levels
–– Prevent complications monitored regularly (target INR level is usually
2–3; frequency of INR monitoring is individual,
Appropriate Consultation depending on response to drug)
Consult a physician for a symptomatic client as soon
as possible. Referral
Refer the stable symptomatic client to a physician for
NONPHARMACOLOGIC INTERVENTIONS thorough evaluation and initiation of therapy as soon
as possible.
Client education
–– Ensure that client understands disease process Medevac clients who are hemodynamically unstable.
and prognosis Electrical cardioversion in hospital is sometimes
–– Teach client signs and symptoms of complications necessary if symptoms are severe.
that require immediate follow-up (rapid heart
rate, palpitations, edema, shortness of breath CONGESTIVE HEART FAILURE
on exertion, chest pain)
–– Recommend avoidance of alcohol, caffeine A clinical syndrome caused by an accumulation
of fluid peripherally (right ventricular failure) or
–– Recommend smoking cessation (if applicable)
in the lungs (left ventricular failure), or both, from
–– Counsel client to avoid sleep deprivation
inadequate functioning of the heart. Congestive
Pharmacologic Interventions heart failure is a complication of an underlying
disease process.
Drug therapy is directed at controlling the ventricular
rate, and in some cases of new onset atrial fibrillation, Systolic heart failure (the more common form)
converting the client to sinus rhythm. A wide variety is due to impaired systolic pumping action of
of medications are used, such as beta-blockers (for the heart. Diastolic heart failure occurs when the
example, atenolol, metoprolol) or calcium channel systolic function is normal but the filling of the
blockers (for example, diltiazem, verapamil). These heart is impaired.
medications must be prescribed by a physician.

NEW YORK HEART ASSOCIATION –– Connective tissue disease

(NYHA) FUNCTIONAL CLASSIFICATION –– HIV infection
OF CHRONIC HEART FAILURE10 –– Hypertension
Clients with cardiac dysfunction (ejection fraction
< 40%, grade II-IV left ventricular dysfunction or CAUSES OF EXACERBATIONS
dilatation) and
Increased Myocardial Demand
Class I
–– Arrhythmias
–– No symptoms –– Infection or fever
–– No undue fatigue or shortness of breath with –– Anemia
ordinary physical activity, such as walking –– Hyperthyroidism
or climbing stairs –– Hypertension
Class II –– Pregnancy
–– Symptoms of heart failure occur with ordinary –– Stress (physical, environmental or emotional)
physical activity
Compliance and Lifestyle
–– Undue fatigue or shortness of breath with
emotional stress or on walking or climbing stairs –– Inadequate or improper medication intake
rapidly, walking uphill, walking or climbing stairs –– Dietary indiscretion (for example, excess
after meals or walking in cold air or wind consumption of salt or water in a client with
underlying cardiac or renal disease)
Class III
–– Heavy alcohol consumption
–– Symptoms of heart failure with less than ordinary
physical activity Salt and Water Retention
–– Undue fatigue and shortness of breath on walking –– Medications: nonsteroidal anti-inflammatory
one or two blocks on level ground, or climbing drugs (NSAIDs), steroids
more than one flight of stairs in normal conditions –– Renal disease
Class IV
Decreased Pump Function of the Ventricles
–– Symptoms of heart failure at rest
–– Negative inotropic medications: beta-blockers,
–– Inability to carry out any physical activity without
calcium channel blockers, antiarrhythmics, certain
fatigue, discomfort or shortness of breath
chemotherapeutic agents
CAUSES10 –– Arrhythmias
–– Myocardial ischemia or infarction (60–70%)
–– Drugs11
–– Valvular heart disease
–– Negative inotropic medications (for example,
beta-blockers, calcium channel blockers, –– Hereditary hypertrophic cardiomyopathy
antiarrhythmics) –– Pulmonary embolism
–– Drugs that cause sodium and water retention –– Radiation treatment
(for example, NSAIDs, corticosteroids, –– Chronic obstructive pulmonary disease
thiazolidinediones) –– Pulmonary hypertension
–– Cardiotoxic drugs (for example, alcohol, –– Infiltrative diseases (for example,
cocaine, certain chemotherapeutic agents) hemochromatosis)
–– Myocardial ischemia or infarction (60–70%)
–– Myocarditis HISTORY
–– Hereditary hypertrophic, hypertrophic obstructive, –– Shortness of breath (initially induced by exercise)
restrictive or peripartum cardiomyopathy –– Later progression to orthopnea, paroxysmal
–– Infiltrative diseases (for example, nocturnal dyspnea and dyspnea at rest
hemochromatosis) –– Nocturnal angina symptoms
–– Valvular disease –– Chronic, nonproductive cough, worse at night
–– Substance abuse or when lying down

–– Ankle edema –– Angina or myocardial infarction

–– Recent weight gain –– Decreased renal function, decreased renal clearance
–– Nocturia of drugs that are renally eliminated (digoxin
–– Chronic fatigue toxicity if the dosage is not adjusted)
–– Palpitations –– Pulmonary embolism
–– Symptoms of intercurrent illness (for example, –– Side effects of medication
pneumonia)
DIAGNOSTIC TESTS
–– Anxiety may aggravate condition
–– Alterations of mental status in elderly clients Do the following diagnostic tests only if the person
may be present as chronic heart failure progresses is not ill enough to require hospitalization and if not
conducted within the past 3 months:
PHYSICAL FINDINGS –– Perform ECG and compare with any previous
–– There is a broad range in severity of findings tracings (look for signs of ischemia [depression
–– Heart rate elevated or elevation of ST segment, inversion of T wave],
–– Respiratory rate increased atrial fibrillation, bradycardia)
–– Hypoxia may be present –– Complete blood count
–– Blood pressure may be normal, elevated or low –– Blood glucose level
–– Weight increased (reflecting fluid retention) –– Lipids
–– Minimal to extreme distress when client lies down –– Thyroid function
–– Jugular venous distention may be present –– Liver function
–– Jugular venous pressure elevated (> 3 cm) –– Ferritin level
–– Edema may be present (pedal, ankle or tibial; –– Creatinine level
sacral if bedridden) –– Electrolyte levels
–– Hepatomegaly –– Digoxin level (if applicable)
–– Hepatojugular reflux –– Chest x-ray (for cardiomegaly, pulmonary edema,
–– Ascites (rare) pleural effusions), if available
–– Lung bases may be dull (pleural effusion) bilaterally, –– Echocardiogram
but only rarely. More commonly congestive heart –– Exercise tolerance test
failure causes a unilateral pleural effusion
–– Fine crackles in the bases of lungs MANAGEMENT
–– S3, S4 or gallop rhythm may be present; murmurs MANAGEMENT OF CHRONIC
may be present if there is associated valvular HEART FAILURE
dysfunction
Goals of Treatment
–– Control symptoms
–– See section “Causes of Exacerbations” –– Identify and manage underlying cause
–– Acute exacerbation of chronic obstructive –– Limit risk factors that precipitate or aggravate
pulmonary disease (COPD) or asthma condition
–– Other causes of edema (renal disease, liver –– Prevent progression
disease, local venous stasis, lymphedema)
–– Improve quality of life and survival
–– Pulmonary embolism
Because there is a broad range of severity (see section
COMPLICATIONS “NYHA Functional Classification of Chronic Heart
Failure” in this chapter), assessment of severity will
–– Arrhythmias
help guide management. Definitive and precise medical
–– Hepatomegaly
management depends on whether the failure is due to
–– Ascites systolic or diastolic dysfunction and the underlying or
–– Acute pulmonary edema precipitating cause (for example, atrial fibrillation).
–– Respiratory failure, respiratory arrest
–– Hypokalemia from use of diuretics

Appropriate Consultation –– Recommend weight loss, if applicable

Consult a physician as soon as possible. –– Recommend that client monitor weight at home,
and see the nurse if he or she gains more than
Adjuvant Therapy 1.5 kg (3 lb) in a day
–– Recommend rest after meals
–– Pneumococcal vaccine every 5 years
–– Encourage client to start an exercise program
–– Influenza vaccine annually
(walking) to improve exercise tolerance
Nonpharmacologic Interventions –– Stress the importance of long-term follow-up
(every 3–6 months when stable)
Client education –– Teach clients taking digoxin to monitor pulse
–– Ensure client understands disease process and
outcome (progressive, can be controlled but not Pharmacologic Interventions
cured)
Several classes of drugs are used to manage
–– Recommend dietary modifications: reduce sodium congestive heart failure (Table 3). Medications
(to 2 g/day), increase dietary potassium (if renal used depend on symptom level (see section “NYHA
function has been adequate in the past), reduce Functional Classification of Chronic Heart Failure”
fat and cholesterol in this chapter), left ventricular ejection fraction and
–– Recommend reduction in fluid intake to 1.5–2 L/day individual client variables. All of these medications
–– Recommend restriction of alcohol use must be prescribed by a physician.
Table 3 – Drugs to manage congestive heart failure11

Evidence-based drugs and oral doses as shown in large clinical trials
Drug Start dose Target dose
ACE inhibitor
Captopril 6.25 mg to 12.5 mg tid 25 mg to 50 mg tid
Enalapril 1.25 mg to 2.5 mg bid 10 mg bid
Ramipril 1.25 mg to 2.5 mg bid 5 mg bid*
Lisinopril 2.5 mg to 5 mg od 20 mg to 35 mg od
Beta-blocker
Carvedilol 3.125 mg bid 25 mg bid
Bisoprolol 1.25 mg od 10 mg od
Metoprolol CR/XL †
12.5 mg to 25 mg od 200 mg od
ARB
Candesartan 4 mg od 32 mg od
Valsartan 40 mg bid 160 mg bid
Aldosterone antagonist
Spironolactone 12.5 mg od 50 mg od
Eplerenone †
25 mg od 50 mg od
Vasodilator
Isosorbide dinitrate 20 mg tid 40 mg tid
Hydralazine 37.5 mg tid 75 mg tid
* The Healing and Early Afterload Reducing Therapy (HEART) trial (165) showed that 10 mg once a day (od)
was effective for attenuating left ventricular remodelling.
† Not available in Canada.
ACE Angiotensin-converting enzyme; ARB Angiotensin receptor blocker; bid Twice a day;
CR/XL Controlled release/extended release; tid Three times a day

All patients with a left ventricular ejection fraction Long-Term Monitoring and Follow-Up
≤ 40% should receive an ACE inhibitor and a beta- –– Review cardiac and respiratory systems for
blocker. They are first-line therapy for all patients symptoms and signs
with heart failure (NYHA class II-IV), unless
–– Weigh client and chart weight every visit
contraindicated or not tolerated.11
–– Monitor blood pressure, renal function and
ACE inhibitors (Table 3) reduce symptoms, improve serum potassium
quality of life, slow disease progression of heart –– Review current medications for use, dosage,
failure, reduce hospitalizations and decrease frequency, compliance, side effects, drugs with
mortality in patients with heart failure. When used sodium-retaining effects (for example, NSAIDs)
in combination with an ACE inhibitor, beta-blockers –– Instruct client to return to clinic if symptoms
reduce hospitalizations and decrease mortality. worsen or chest pain develops
ARBs are alternatives for clients who cannot tolerate –– Laboratory tests every 3–6 months: complete blood
ACE inhibitors. count, creatinine level, electrolyte levels, uric acid
level (if taking a thiazide diuretic), urinalysis for
Loop diuretics (for example, furosemide) are used
proteinuria, digoxin level
to control symptoms of congestive heart failure. Once
congestion has resolved the dose should be reduced to –– Annual screening of blood glucose and lipids, TSH
a level that results in stable symptom control (monitor
Referral
weight, serum potassium and renal function).
Refer client to a physician for a thorough evaluation
Aldosterone antagonists (for example, spironolactone) and tailoring of drug therapy regimen.
has been shown to reduce mortality in people with
severe heart failure receiving optimal therapy (for MANAGEMENT OF ACUTE
example, ACE inhibitors, ARBs, beta-blockers and/ DECOMPENSATED HEART FAILURE
or diuretics).12,13 Monitor serum potassium closely
in patients receiving spironolactone in combination Appropriate Consultation
with ACE inhibitors and/or ARBs because all of these
Consult a physician immediately.
drugs cause potassium retention.
The combination of hydralazine plus oral isosorbide Adjuvant Therapy
dinitrate (a nitrate) improves symptoms and may –– Oxygen via non-rebreather mask; titrate flow
reduce mortality. It is generally used only in African to keep oxygen saturation ≥ 90%
Americans and in those unable to tolerate standard
–– Start intravenous (IV) therapy with normal saline
therapy.11
to keep vein open
Nitrates in all forms (topical and oral) may be used as
an adjunct to the above therapies. They can improve Nonpharmacologic Interventions
symptoms and exercise tolerance and are useful Bed rest with head elevated and legs hanging down
for clients who have a component of myocardial (unless client is hypotensive).
ischemia. A nitrate-free period of 10–12 hours per
day is required to prevent loss of effect. Pharmacologic Interventions
Cardiac glycosides (for example, digoxin) are used Fluid removal with IV loop diuretics can relieve
to control ventricular rate in clients with atrial symptoms and improve oxygenation status.14
fibrillation. They can also improve symptoms and
Diuretics:
exercise tolerance and reduce hospital admissions,
especially in those with severe ventricular furosemide (Lasix), 40–80 mg IV
dysfunction. The dose may have to be higher in a person on an
Anticoagulation is strongly recommended for oral maintenance dose. It is reasonable to administer
all clients with heart failure and associated atrial an initial dose that is equivalent to the client’s usual
fibrillation. maintenance dose.14 Adjust the diuretic dose according
to client’s response (monitor urine output). Look for
Counsel client about appropriate use of medications improvement in respiratory status.
(dose, frequency, compliance, side effects).

Nitrates can relieve congestive symptoms in patients –– Drugs

without hypotension. Intravenous nitroglycerin is –– Oral and transdermal contraceptives
preferred because of its rapid onset of action and –– Hormone replacement therapy
the ability to rapidly titrate the dose,14 but may be –– Tamoxifen
impractical to administer in the nursing station. If it is
–– Bevacizumab (Avastin), an anticancer agent
used, it is to be ordered by a physician. For this reason
nitroglycerin patches (or ointment) may be used. –– Trauma
Nitroglycerin is rapidly absorbed after application of a –– Major surgery
patch (steady state is achieved within 30 minutes and –– Infection after orthopedic surgery
is maintained for 24 hours). The plasma concentration –– Acute myocardial infarction
decreases to zero within 2 hours of removal.15 –– Stroke
nitroglycerin (Nitro-Dur) transdermal patches, –– Old age (related to decreased activity)
0.2- 0.8 mg/h –– Hypercoagulable states (for example, chronic
Sublingual nitroglycerin may be useful for rapid relief infection, autoimmune disease, primary blood
of chest pain: diseases like antithrombin III deficiency)
sublingual nitroglycerin, 0.4 mg HISTORY
Monitoring and Follow-Up –– Symptoms may be subtle, variable or vague

–– Usually occurs in leg or deep pelvic veins
–– Monitor vital signs, pulse oximetry (if available) (popliteal, femoral, iliac)
–– Airway, breathing and circulation (ABC) –– Presence of one or more risk factors (see “Risk
–– Level of consciousness Factors” in this section)
–– Listen to heart and lung sounds –– Recent leg injury
–– Record intake and urinary output –– Leg pain may be mild or absent
–– Monitor response to therapy –– Pain described as a dull ache or tightness,
rarely severe
Referral
–– Leg discomfort worse when walking
Medevac as soon as possible. –– Swelling of lower leg
–– Fever
DEEP VEIN THROMBOSIS Symptoms may be absent or minimal until shortness
Acute formation of a blood clot or thrombus within a of breath and other pulmonary complaints appear
vein resulting in obstruction of venous return. because of embolism to the lungs. The risk of
pulmonary emboli is low when only the calf veins
CAUSES are involved but increases to 40% when the thigh
veins are involved.
Unknown, but the triad of venous stasis, injury to
vessel intima and altered blood coagulability are PHYSICAL FINDINGS
central to the process.
–– Variable; dependent on size and location of clot
Risk Factors and severity of venous obstruction
–– Heart rate may be elevated
–– Prolonged bed rest for any reason
–– Minimal to moderate distress
–– Recent prolonged air travel
–– Difficulty walking
–– Paralysis
–– Minimal to marked swelling of lower leg
–– Malignant disease
–– Redness of affected calf or leg may be present
–– Childbirth
–– Superficial leg veins may be distended
–– Pregnancy
–– Mild to moderate calf tenderness: flexion
of the ankle may increase pain
–– Localized warmth may be present
–– Peripheral pulses (compare sides for symmetry)

DIFFERENTIAL DIAGNOSIS Pharmacologic Interventions

–– Calf-muscle strain Consult a physician regarding initial anticoagulation
–– Trauma with hematoma with a low molecular weight heparin (LMWH). Doses
–– Thrombophlebitis for treatment of existing DVT may differ from those
–– Cellulitis for prevention of DVT.
–– Ruptured Baker’s cyst (popliteal cyst) enoxaparin (Lovenox), 1 mg/kg twice daily SC or
1.5 mg/kg once daily SC for treatment of acute DVT
COMPLICATIONS Administration should be alternated between the left
–– Pulmonary embolism and right front abdominal wall, towards the sides.
–– Chronic venous insufficiency Dosage reductions may be necessary for patients with
impaired kidney function.
DIAGNOSTIC TESTS
–– D-Dimer can be helpful to rule out diagnosis Antiplatelet drugs (ASA, clopidogrel) and NSAIDs
increase the risk of bleeding in patients receiving low
–– EKG if pulmonary embolus is suspected
molecular weight heparins.
–– CBC, renal function, INR and PTT
–– Ultrasound of lower limb(s) LMWH do not cross the placenta and there is no
–– CT scan or V/Q scan if pulmonary embolus evidence of teratogenicity or risk of fetal bleeding.
is suspected These drugs are preferred for the treatment of DVT
in pregnant women.16
MANAGEMENT Long-term anticoagulant therapy is recommended
for 3–6 months as prophylaxis against recurrence in
Goals of Treatment
nonpregnant patients. The duration of anticoagulation
–– Early detection depends on a variety of factors (for example, cause,
–– Prevent complications presence of pulmonary embolus and whether this
is a first occurrence or recurrence).
Consult a physician immediately if you have
any suspicion of this disorder. Acute symptoms:
–– Observe client for shortness of breath or
Nonpharmacologic Interventions
unexplained tachycardia (signs of pulmonary
for Acute Symptoms
embolism)
–– Bed rest
Long-term:
–– Elevation of leg above level of the heart
–– Follow up every 3–6 months once stable
–– Monitor vital signs closely
–– Review prevention strategies, medication use,
Nonpharmacologic Interventions side effects
Over the Long Term –– Regular INR to monitor warfarin (Coumadin)
therapy
Client education
–– Counsel client about appropriate use of Referral
medications (dose, frequency, side effects)
Medevac the acutely symptomatic client as soon
–– Recommend prophylactic use of anti-embolic as possible.
stockings
–– Recommend avoidance of restrictive clothing
around knees and ankles (for example, socks,
garters)
–– Ensure that bedridden clients are turned and
repositioned frequently (q2h)
–– Recommend active or passive leg exercises
while in bed

DYSLIPIDEMIA (HYPERLIPIDEMIA) HISTORY
Elevation in serum lipoproteins are a major risk factor –– Ask about risk factors and possible causes of
for coronary artery disease. The two main lipids in secondary hyperlipidemia
blood are cholesterol and triglyceride. Cholesterol –– Previously identified hypercholesterolemia
is transported in the blood as a component of high- (total cholesterol > 5.2 mmol/L)
density lipoprotein (HDL), low-density lipoprotein –– Previously identified low levels of HDL cholesterol
(LDL) and very-low-density lipoprotein (VLDL). (< 0.9 mmol/L)
–– Smoking
Triglyceride is found in VLDL particles. Moderate
hypertriglyceridemia (1.7–5 mmol/L) is part of the –– Hypertension: blood pressure (BP) of 140/90 mm
“metabolic syndrome” of insulin resistance, elevated Hg confirmed on repeated determinations or while
triglycerides, elevated LDL and low HDL. The client is taking antihypertensive medication
metabolic syndrome is associated with a marked –– Antecedent cardiovascular disease or family
increase in cardiovascular risk. High triglyceride history of premature myocardial infarction (in
levels (>11 mmol/L) increase the risk for pancreatitis. people < 55 years of age)
–– Endocrine disease (diabetes mellitus or secondary
Dyslipidemia is one of the primary causes of
causes, including hypothyroidism, renal disease or
atherosclerotic plaque. Up to 75% of clients
medications) (note: clients > 35 years of age with
with coronary artery disease have dyslipidemia.
diabetes have a very high risk of cardiovascular
Normalization of lipid values lowers the rate of
disease)
symptomatic coronary artery disease and improves
–– Men > 45 years of age are at greater risk
overall survival. Dyslipidemia is strongly associated
with recurrence of symptomatic coronary artery –– Postmenopausal women (> 55 years of age) and
disease. younger women with artificial menopause and
no hormonal replacement are at greater risk
CAUSES
PHYSICAL FINDINGS
Primary Hyperlipidemia –– BP may be elevated
Primary (genetic) single-gene disorders are –– Arcus corneae (significant in a younger person)
transmitted by simple dominant or recessive –– Retinopathies (seen on funduscopy)
mechanism. –– Xanthomas (lipid deposits that occur as skin
eruptions or as lumps on tendons)
Secondary Hyperlipidemia
–– Arterial bruits may develop if atherosclerosis
Secondary hyperlipidemia occurs as part of a is present
constellation of abnormalities in certain metabolic –– Peripheral pulses may be diminished if
pathways. atherosclerosis is present
–– Diet –– Abdominal obesity (waist measurement > 100 cm
–– Diabetes [40 in] in men, > 90 cm [35 in] in women)
–– Hypothyroidism –– Body mass index (BMI) > 25
–– Pregnancy COMPLICATIONS
–– Obesity (high triglycerides)
–– Coronary artery disease (for example, angina,
–– Excess alcohol intake (high triglycerides)
myocardial infarction)
–– Liver disease (cholestatic, acute hepatitis)
–– Cerebrovascular disease
–– Renal disease (nephrotic syndrome, uremia)
–– Peripheral arterial disease
–– Medications (for example, thiazide diuretics, some
–– Pancreatitis (hypertriglyceridemia)
beta-blockers, oral contraceptives, corticosteroids,
antiretroviral therapy)

DIAGNOSTIC TESTS17 A person at high risk has a 10-year risk score of

greater than or equal to 20%, at moderate risk a
Guidelines for Lipid Screening risk score of 10–19% and at low risk a risk score
Fasting lipid profile (total cholesterol, HDL less than 10%.
cholesterol, LDL cholesterol and triglycerides)
is suggested for the following groups. MANAGEMENT
Every 5 years Goals of Treatment

–– Asymptomatic men > 40 years of age and women –– Decrease cardiovascular disease by modifying
> 50 years of age or postmenopausal with no other serum cholesterol according to client’s level of risk
risk factors –– Prevent pancreatitis from severe hypertriglyceridemia
Every 1–3 years
Nonpharmacologic Interventions18
–– Any adult with the following risk factors:
–– diabetes, cigarette smoking, hypertension, –– Dietary modification (decrease saturated fats
obesity (body mass index > 27 kg/m2), family [substitute unsaturated fats for saturated and
history of premature coronary artery disease, trans fats]; increase consumption of fruits and
clinical signs of hyperlipidemia (for example, vegetables; decrease consumption of sodium
xanthomas), evidence of atherosclerosis and simple sugars)
(clinical evidence of coronary artery disease, –– Weight reduction and maintenance
peripheral vascular disease or carotid vessel –– Smoking cessation
disease [transient ischemic attacks, carotid –– Increased physical activity (daily exercise)
bruits, carotid plaques on ultrasound, previous –– Stress management
cerebrovascular accident]), rheumatoid arthritis,
systemic lupus erythematosis, psoriasis, HIV Optimal control of other diseases related to the
infection on highly active antiretroviral therapy, development of heart disease:
estimated glomerular filtration rate of less than –– For hypertension, target BP: systolic < 140 mm
60 mL/min/1.73 m2 or erectile dysfunction Hg, diastolic < 90 mm Hg (130/80 mm Hg for
–– Any child with a family history of clients with diabetes, < 125/75 if diabetic with
hypercholesterolemia or chylomicronemia nephropathy)
Frequency of screening for the above groups is based –– For diabetes mellitus, aim for optimal, realistic
on clinical judgement regarding risk. More frequent blood glucose level
screening may be needed to monitor levels of those
under treatment. Pharmacologic Interventions19
See Table 4 for drugs and recommended dosage ranges.20
Lipid test results should be interpreted in light
of other risk factors for coronary artery disease.
A cardiovascular risk assessment like the Framingham
Risk Score helps one to determine an estimated
10‑year risk of cardiovascular disease for an
individual. It considers family history, age, HDL-C,
total cholesterol, systolic blood pressure, whether
patient’s hypertension is treated or not, smoking
status, sex and diabetes. See pages 575 to 577 of the
“Canadian Cholesterol Guidelines 2009” for how
to estimate 10-year risk of cardiovascular disease
(available at: http://www.ccs.ca/download/consensus_
conference/consensus_conference_archives/2009_
Dyslipidemia-Guidelines.pdf).

Table 4 – Lipid-lowering Medications

Recommended
Generic name Trade name (manufacturer) dose range (daily)
Statins
Atrovastatin Lipitor (Pfizer Canada Inc) 10 mg – 80 mg
Fluvastatin Lescol (Novartis Pharmaceuticals Canada Inc) 20 mg – 80 mg
Lovastatin Mevacor (Merck Frosst Canada Ltd) 20 mg – 80 mg
Pravastatin Pravachol (Bristol-Myers Squibb Canada) 10 mg – 40 mg
Rosuvastatin Crestor (AstraZeneca Canada) 5 mg – 40 mg
Simvastatin Zocor (Merck Frosst Canada Ltd) 10 mg – 80 mg*
Bile acid and/or cholesterol absorption inhibitors
Cholestyramine Questran (Bristol-Myers Squibb, USA) 2 g – 24 g
Colestipol Colestid (Pfizer Canada Inc) 5 g – 30 g
Ezetimibe Ezetrol (Merck Frosst/Schering Pharmaceuticals Canada) 10 mg
Fibrates
Bezafibrate Bezalip (Actavis Group PTC EHF, Iceland) 400 mg
†
Fenofibrate Lipidil Micro/Supra/EZ (Fournier Pharma Inc, Canada) 48 mg – 200 mg
Gemfibrozil†‡ Lopid (Pfizer Canada Inc) 600 mg – 1200 mg
Niacin
Nicotinic acid Generic crystalline niacina 1g–3g
Niaspan (Oryx Pharmaceuticals Inc, Canada) 0.5 g – 2 g
* Increased myopathy on 80 mg.
† Reduce dose or avoid in renal impairment.
‡ Should not be used with a statin because of an increased risk of rhabdomyolysis.
A baseline FBS, TSH, ALT, AST, creatinine, Frequency of testing to monitor treatment
creatinine kinase should be done to identify other of dyslipidemia:
causes of dyslipidemia and monitor potential side
Patients on diet therapy only:
effects prior to starting treatment.
Initiation: Every 3–6 months to 1 year
If clients experience unexplained muscle pain
or tenderness, advise them to discontinue statins Maintenance: Every 6–12 months
immediately and to see a nurse for a serum creatine Patients on diet and drug therapy:
kinase (CK) measurement. Contact the physician with
Initiation of drug therapy: Every 6–8 weeks to
CK level for suggestions on continued therapy.
6 months, depending on severity
Monitoring and Follow-Up Maintenance: Every 3 months in the first year,
every 6–12 months thereafter
Check the response to treatment within 6 weeks
(blood tests should be carried out early – see below) Referral
and, if the results are satisfactory, continue follow-up
at regular intervals thereafter (every 3–12 months). Refer all clients diagnosed with hyperlipidemia to
a physician so that they can be evaluated for risk of
Monitor liver function (ALT,AST), creatinine kinase, coronary artery disease and to determine whether
complete blood count and serum creatinine at 3, 6 and lipid-lowering medications are needed.
12 months after initiation of lipid-lowering drugs
and semi-annually thereafter, or with any changes PREVENTION21
in therapy. Clients on niacin also need a FBS and
Primary prevention is aimed at identifying
glycosylated hemoglobin done every 6–12 months.
dyslipidemia before complications occur. Target
levels of LDL cholesterol are based on individual
cardiovascular risk factors. Generally, any client with

LDL cholesterol > 5 mmol/L, even in the absence CAUSES

of other risk factors, is considered at high risk for Cause of essential hypertension (which accounts
developing cardiovascular disease. See section for 90% of cases of hypertension) is unknown.
“Guidelines for Lipid Screening” in this chapter
to calculate a risk score. Risk Factors for Primary
For anyone at high risk (10-year risk score of (Essential) Hypertension
≥ 20%), or men > 45 years and women > 50 years –– Heredity
with diabetes, or anyone with evidence of coronary –– Obesity
artery disease, peripheral vascular disease and/or
–– High salt intake
atherosclerosis:
–– Smoking
Target: LDL cholesterol < 2 mmol/L or a 50% –– High alcohol consumption
reduction from baseline LDL cholesterol
–– Chronic stress
For those at high risk, pharmacologic interventions –– Age
should be started as soon as possible, in conjunction –– Hyperlipidemia
with healthy lifestyle changes (for example, smoking
cessation, diet with reduced saturated fats and refined Risk Factors for Secondary
sugars, weight reduction and maintenance, exercise, Hypertension (10% of Cases)
stress management).
–– Renal disease
For clients at moderate risk (10-year risk score of –– Polycystic kidneys
10–19%), LDL-C > 3.5 mmol/L, TC/HDL-C > 5.0: –– Renal vascular disease
Target: LDL cholesterol < 2 mmol/L or a 50% –– Pregnancy
reduction in LDL cholesterol from baseline –– Hyperthyroidism
For those at moderate risk, healthy lifestyle changes –– Cushing’s syndrome
should be promoted; if target lipid levels are not –– Primary hyperaldosteronism
achieved in 3 months, drug therapy should be started, –– Pheochromocytoma
after consultation with a physician. –– Coarctation of aorta
For clients at low risk (10-year risk score of < 10%) –– Chronic alcohol abus
Target LDL cholesterol is a 50% reduction from
–– Drugs:
baseline –– NSAIDs
–– Corticosteroids
For those at low risk, healthy lifestyle changes should
be promoted; if target lipid levels are not achieved –– Oral contraceptives, sex hormones, anabolic
in 6 months, drug therapy should be considered in steroids
consultation with a physician. –– Cyclosporine, tacrolimus (to prevent transplant
rejection)
All risk factors should be treated, if possible, –– Erythropoietin
by nonpharmacologic means.
–– Monoamine oxidase inhibitors (for depression)
Secondary prevention is directed at reducing the –– Midodrine
impact of dyslipidemia on people with previous –– Stimulants including cocaine
cardiovascular disease. These targets are aimed
specifically at high-risk clients and are more stringent HISTORY
than those recommended for the general population.
–– Presence of one of the risk factors (see
Target: LDL cholesterol < 2 mmol/L section “Risk Factors for Primary (Essential)
Hypertension” in this chapter)
HYPERTENSION –– Client usually > 35 years of age
–– Condition usually discovered only on routine
Persistently elevated blood pressure from increased
screening of blood pressure; all adults over
peripheral arterial resistance related to salt or water
21 years of age should be screened at every
retention or endogenous pressure activity.
office visit22

–– Usually asymptomatic Other Findings (Target Organ Damage)

–– Headache on rising in the morning, gradually –– Ocular funduscopic exam may reveal retinal
subsiding during the day (rare) changes
–– Fatigue –– Augmented second aortic heart sound
–– Transient ischemic attack –– Enlarged heart (left ventricular hypertrophy)
–– Nausea or vomiting –– Bruits (carotid, abdominal aortic, renal and
–– Altered level of consciousness femoral)
–– Palpitations
–– Angina Differential Diagnosis
–– Symptoms of cardiac failure –– Essential hypertension
–– Epistaxis –– Secondary hypertension
PHYSICAL FINDINGS23 General Clues to Secondary Hypertension

When assessing for hypertension, if the systolic BP is –– Severity of high blood pressure: severe
≥ 140 mm Hg and/or the diastolic BP is ≥ 90 mm Hg hypertension is more likely secondary to a specific
take 2 more readings during the same visit. Discard underlying cause
the first reading and average the last two. –– Speed of onset: if hypertension develops rapidly,
Hypertension can be diagnosed immediately if there it should be considered secondary until proven
is evidence of urgency or emergency: otherwise
–– Age at onset: rapid onset in people younger than
–– Asymptomatic diastolic BP ≥ 130 mm Hg 25 years or older than 55 years should suggest
–– Hypertension compromising vital organ function secondary hypertension
(encephalopathy, left ventricular failure, acute –– Female sex: the presence of hypertension in a
myocardial ischemia) young woman in whom an abdominal bruit is
–– Hypertension and an acute aortic dissection. heard suggests stenosis of the renal arteries
Evidence of malignant hypertension (sufficient
elevation of blood pressure to cause papilledema COMPLICATIONS
and other manifestations of vascular damage, –– Congestive heart failure
such as retinal hemorrhages, bulging optic disks,
–– Angina
mental status changes)
–– Myocardial infarction
Hypertension can be diagnosed in 2 visits within –– Stroke or transient ischemic attacks
1 month if the BP is ≥ 180/110 mm Hg or BP is
–– Hypertensive crisis
140–179/90–109 mm Hg with target organ damage,
–– Kidney disease
diabetes or chronic kidney disease.
–– Retinal disease
Target organ damage can be initially established on –– Peripheral disease
the basis of a history of angina, myocardial infarction,
–– Complications related to therapy (for example,
transient ischemic attacks, cerebrovascular accident,
thiazide diuretics increase risk of gout)
peripheral ateriovascular insufficiency (claudication)
–– Poor response to therapy
or renal insufficiency.
Hypertension can be diagnosed in 3 visits if the DIAGNOSTIC TESTS
average across the visits is a systolic BP of ≥ 160 mm –– Urinalysis (routine and for microalbuminuria
Hg or a diastolic BP of ≥ 100 mm Hg. Hypertension in diabetic clients)
can be diagnosed in 5 visits if the average across the
–– Obtain complete blood count
visits is a systolic BP of ≥ 140 mm Hg or a diastolic
–– Determine blood glucose; total, LDL and HDL
BP of ≥ 90 mm Hg and there is no target organ
cholesterol; and triglyceride levels (while fasting)
dysfunction. If blood pressure is still elevated on the
third visit, baseline diagnostic investigations should –– Determine creatinine and electrolyte levels
be done. –– Obtain baseline electrocardiogram (ECG) and
chest x-ray (if available) if > 50 years of age

MANAGEMENT Pharmacologic Interventions26
Goals of Treatment All pharmacotherapy must be initiated only after

consultation with a physician.
–– Decrease morbidity and mortality associated with
high blood pressure Pharmacotherapy should be initiated in the following
instance:
–– Optimal control of blood pressure with an
effective, well-tolerated treatment regimen –– Diastolic BP ≥ 100 mm Hg or systolic BP
Target BP levels are: 24 ≥ 160 mm Hg in the client who does not have
cardiovascular disease, cardiovascular risk factors
–– 140/90 mm Hg in the general population or target organ damage
–– 130/80 mm Hg in clients with diabetes or renal
Pharmacotherapy should be strongly considered in
dysfunction
the following instance:
Appropriate Consultation –– Diastolic BP ≥ 90 mm Hg or systolic BP ≥ 140 mm
Consult a physician if there is a need to treat Hg in the client with cardiovascular disease,
hypertension with medications. cardiovascular risk factors or target organ damage
The following classes of drugs are used in the
Nonpharmacologic Interventions25 treatment of hypertension:
Lifestyle modifications are first-line therapy for mild
elevation of blood pressure. –– Beta-blockers
–– Angiotensin-converting enzyme (ACE) inhibitors
Client education –– Angiotensin receptor blockers (ARBs)
–– Ensure that client understands disease process and –– Diuretics
prognosis –– Calcium channel blockers (CCBs)
–– Encourage client to lose weight if appropriate –– Alpha blockers (not commonly used)
(aim for a loss of 10% of current body weight, or
at least 4.5 kg [10 lb ]); maintain BMI of 20–25 The majority of patients will require combination
–– Encourage client to achieve and maintain a waist therapy to achieve recommended blood pressure
circumference < 102 cm for men and < 88 cm goals. Many antihypertensive medications are
for women available in combination products that can simplify
the regimen and may improve compliance.27 Consult
–– Recommend dietary modifications (for example,
a pharmacist to discuss availability of specific
avoid high-salt foods, avoid adding salt in cooking
combinations. Depending on the clinical situation,
or at table; adhere to diet high in fresh fruits and
these drugs can be used in combination. The selection
vegetables, high in soluble fibre and low fat dairy
of agent is made on the basis of the client’s age,
products, low in saturated fats)
coexisting medical conditions and risk factors.
–– Recommend smoking cessation
–– Recommend restriction of alcohol consumption Hypertension in pregnancy requires assessment and
(0–2 drinks per day – ≤ 14 drinks per week for treatment by a physician. Not all of the above drugs
men and ≤ 9 for women) are safe in pregnancy.
–– Recommend regular exercise, especially if
Hypertension Treatment Strategies
sedentary (30–60 minutes of moderate physical
According to Comorbidities
activity on most days, for example, a brisk walk
4–5 times a week) The Canadian Hypertension Education Program
–– Counsel client about appropriate use of (CHEP) Web site offers recommendations for the
medications (dose, frequency, side effects and management of hypertension in the presence of
importance of compliance) comorbidities (such as ischemic heart disease,
–– Ask client to return to clinic if any unusual non-diabetic chronic kidney disease or diabetes
symptoms occur or there is a change in status mellitus).27 Information can be accessed at: http://
hypertension.ca/chep/wp-content/uploads/2010/04/
FullRecommendations2010.pdf.

Monitoring and Follow-Up Referral

For clients on nonpharmacolgic therapy, follow up Arrange follow-up with physician at least yearly if the
every 3–4 months. client’s hypertension is stable or as soon as possible
if poorly controlled.
For clients on antihypertensive drug therapy, follow
up every month until 2 successive blood pressure Repeat physician consultation is necessary for
readings are at target level. Once blood pressure has chronically hypertensive clients if any of the
reached target level, follow up every 3–6 months. following situations apply:
More frequent follow-up is recommended for clients –– Client is not responding to therapy
with symptomatic hypertension, severe hypertension, –– Target organ damage caused by poorly controlled
antihypertensive drug intolerance or target organ blood pressure
damage. –– Signs and symptoms of complications
Routine Follow-up Assessment PREVENTION28

Related to Hypertension
Maintaining a healthy body weight (BMI 18.5–24.9 kg/m2
Determine history related to the following: and a waist circumference < 102 cm for men and < 88
–– Headaches cm for women is recommended.
–– Dizziness
–– Angina ISCHEMIC HEART DISEASE,
–– Congestive heart failure INCLUDING ANGINA
–– Transient ischemic attack
Ischemic heart disease (IHD) is a symptom complex
–– Stroke that is a result of an imbalance between oxygen supply
–– Nausea and vomiting and demand in the myocardium.
–– Vision changes
–– Medication compliance SPECTRUM OF IHD
–– Drug side effects The spectrum of ischemic heart diseases ranges
The physical examination should include the from asymptomatic disease to sudden death from
following: myocardial infarction or arrhythmia.
–– Blood pressure (supine and standing) ANGINA PECTORIS

–– Funduscopy (dilated) The result of myocardial ischemia, which occurs when
–– Neck examination (carotid artery for bruits, JVP the cardiac workload and myocardial oxygen demands
[jugular venous pressure] for congestive heart exceed the ability of the coronary arteries to supply
failure) oxygenated blood. It is the main clinical expression
–– Cardiovascular examination of coronary artery disease (subintimal deposition of
–– Respiratory examination atheromas in the large- and medium-sized arteries
–– ECG (annually) serving the heart).
–– Chest x-ray (annually) if cardiomegaly documented
CHRONIC STABLE ANGINA
–– Ophthalmologic exam (if funduscopic changes
have been documented) Most often due to a fixed stenosis caused by an
–– Blood work q3-6 months: complete blood count, atheroma. It is characterized by a predictable pattern
blood glucose level, creatinine level, electrolyte of pressure sensation in the anterior chest precipitated
levels, uric acid level (if client is taking thiazide by exertion, emotion and eating. Typically is of brief
diuretics) duration < 10–15 minutes and is relieved by rest or
–– Urinalysis (for protein) nitroglycerin. Alternative presentations should be
considered particularly in women and diabetics (for
example, different types of chest pain or primary
complaint of episodic shortness of breath).

UNSTABLE ANGINA MYOCARDIAL INFARCTION

A syndrome of acute plaque rupture with incomplete A syndrome of acute plaque rupture and thrombosis
or transient vessel occlusion. A client with new onset with total coronary occlusion resulting in myocardial
of undiagnosed ischemic pain is considered to have necrosis. For details, see section “Emergencies of the
unstable angina. In a previously diagnosed client, it is Cardiovascular System” later in this chapter.
characterized by an accelerating pattern of pain (for
example, increased frequency, severity or duration Causes
[more than 30 minutes, occurring with less exertion, –– The main pathogenetic mechanisms are
occurring at rest or decreased response to current atherosclerosis and thrombus formation
treatment]). It can also be present if never diagnosed
–– A less common cause is coronary artery vasospasm
previously. Pain on presentation at the clinic in anyone
with a history of recent onset angina or anginal Risk Factors
symptoms at rest, and anyone with known heart
disease and an increase or change in anginal pattern See Table 5, “Gender-Specific Risk Factors for
and ECG changes may be unstable angina. However, Cardiac Disease.”
ECG changes do not need to present in unstable
angina, particularly if the person is pain free when the
ECG is done. Anyone presenting with acute chest pain
should be treated as potentially having a myocardial
infarction until it is ruled out.
Table 5 – Gender-Specific Risk Factors for Cardiac Disease

Risk Factor Women Men
CAD = coronary artery disease, HDL = high-density lipoprotein, LDL = low-density lipoprotein, MI = myocardial
infarction
Family history Premature MI in parent Premature MI in parent increases
increases risk 2.8 times risk 3 to 5 times
Obesity 3 times greater risk of CAD 2 times greater risk of CAD
Smoking MI occurs 19 years earlier than in nonsmokers MI occurs 7 years earlier than in nonsmokers
Lipids High levels of triglycerides and low levels of High levels of total cholesterol and high levels of
HDL cholesterol are better predictors of CAD HDL cholesterol are better predictors of CAD
Hypertension Higher prevalence in older women Higher prevalence in middle age
Diabetes Risk of CAD increases 7 times Risk of CAD increases 3 times
Menopause Increases LDL, decreases HDL cholesterol
Male:female ratio = 2:1 for all age groups, 8:1 for age under 40 years and 1:1 for age over 70 years.
Peak incidence of symptomatic IHD is age 50–60 years for men and 60–70 years for women
Other associated risk factors: –– A prodrome of fatigue and a nonspecific feeling

of unwellness for weeks before a cardiac event
–– Sedentary lifestyle
–– Chronic fatigue, dizziness, ankle swelling, nausea,
–– Hyperhomocysteinemia
indigestion, change in chronic headache pattern
–– Hormone replacement therapy (in some women) and hot and flushed feelings
–– Chronic autoimmune diseases (for example, lupus) –– Pain in the back, neck or throat
Clinical Presentation in Women –– Shortness of breath, fatigue, flushing, nausea,
jaw pain and abdominal pain, which occur over
Women with coronary artery disease or coronary hours rather than minutes
heart disease experience more noncardiac chest pain –– No Q waves on ECG during myocardial infarction
than men. They are more likely to have atypical
–– Nondiagnostic, reversible ST segment elevations
manifestations such as:
or T wave abnormalities
–– Chest pain at rest or during sleep or with mental
stress

Young premenopausal women who have had a Differential Diagnosis

myocardial infarction have significantly higher –– Chest-wall pain (costochondritis)
mortality rates than men who have had a myocardial
–– Other musculoskeletal discomfort (rib fracture)
infarction at the same age. One possible explanation
for this may be the difference in primary prevention –– Peptic ulcer disease
strategies applied to women; management of early –– Gastroesophageal reflux
symptoms is often less aggressive. –– Esophageal spasm
–– Indigestion
History –– Anxiety attack
Chest pain described as tightness, pressure or –– Pulmonary emboli
aching that is typically located in the substernal –– Pericarditis
area, may radiate to neck, jaw and/or one or both –– Aortic dissection
shoulders/arms. Duration is brief – < 10–15 minutes. –– Pneumothorax (spontaneous)
Precipitated by exercise or emotional stress or eating.
–– Pneumonia
Typically relieved by rest and/or nitroglycerin.
Dyspnea or fatigue may present as “chest pain Complications
equivalents,” especially in post menopausal women. –– Unstable angina
–– Future myocardial infarction
Associated Symptoms
–– Dyspnea Diagnostic Tests
–– Nausea or vomiting –– ECG tracing – compare with previous one, if
–– Sweating available; look for signs of ischemia (depression
–– Weakness of ST segment, ST segment elevation, inversion
–– Palpitations of T wave, new changes)
–– Obtain complete blood count, fasting blood
Physical Findings glucose, creatinine, electrolytes and fasting
–– Diaphoresis cholesterol panel and TSH if this is the first
presentation or it has not been done recently
–– Apprehension
–– Oxygen saturation (usually normal unless MANAGEMENT
complications present )
–– Blood pressure (may be elevated if hypertension) Management of Stable Angina
–– Tachycardia – assess for arrhythmias
Goals of Treatment
–– Arterial bruits (carotid, aortic, femoral arteries)
–– S4 gallop –– Decrease or prevent recurrence of pain
–– Murmurs (aortic stenosis) –– Identify and manage cardiac risk factors
–– Hypertrophic cardiomyopathy to slow progression of disease
–– ECG changes (elevation or depression –– Improve exercise tolerance
of ST segment, inversion of T wave) –– Minimize the risk of nonfatal MI and
cardiovascular death
Physical findings are transient in stable angina and
disappear when the pain resolves. People with stable Appropriate Consultation
angina are usually seen in a clinic after an attack
Consult a physician as soon as possible if you suspect
because of the mild, short, episodic nature of the
this diagnosis.
discomfort. After an episode there are usually no
significant physical findings and no ECG changes.
There may be signs of underlying atherosclerotic
disease (for example, arterial bruits, heart murmurs,
hypertension).

Nonpharmacologic Interventions Calcium channel blockers (CCB) (for example,

–– Ensure that client understands disease process diltiazem, verapamil) are used for treatment of angina,
especially when there are contraindications to the
–– Encourage client to make lifestyle changes (for
above therapies, or if nitrates or beta-blockers are not
example, dietary modifications to reduce saturated
adequate. CCBs are not usually a first-line therapy but
fat and cholesterol, salt use and alcohol use)
may be a treatment of choice for clients with coronary
–– Encourage client to reduce weight, stop smoking, arterial spasm.31
avoid strenuous exercise but increase moderate
exercise (for example, walking, cycling, swimming) ACE inhibitors (ACEI) (for example, ramipril) reduce
the risk of death in patients with stable heart disease
Pharmacologic Interventions including chronic stable angina.32
For acute symptom relief: All clients with angina should receive secondary
nitroglycerin, 0.4 mg sublingual (SL) spray prophylaxis with an antiplatelet agent (for example,
q5min X 3 doses prn ASA 81 mg/day) and a statin30 (see section
“Dislipidemia (Hyperlipidemia)” in this chapter).
If pain not relieved with 3 doses proceed to treat as
possible acute myocardial infarction (See “Myocardial Monitoring and Follow-Up
Infarction” under the section “Emergencies of the
Cardiovascular System”). –– Follow up every 6 months once client’s symptoms
are stable
For longer-term symptom prophylaxis: –– Monitor symptoms and identify any changes,
Beta-blockers, calcium channel blockers and long- especially increases
acting nitrate preparations are used to prevent –– Monitor weight and smoking
recurrent attacks. The choice of agent depends on the –– Monitor blood pressure and pulse
presence of other comorbid illnesses. A combination –– Obtain regular blood work as directed
of agents may be used to control symptoms.29 –– Monitor adherence and response to long-term
Beta-blockers relieve anginal symptoms by decreasing lifestyle modifications and medications
the heart rate and contractility and reducing blood (for example, beta-blockers)
pressure.29 They should be used cautiously in clients
with diabetes if there is a concern about possible Referral
hypoglycemic episodes (they impair awareness Refer all previously undiagnosed clients and any
of hyperglycemia). They should also be used with clients whose symptoms are not controlled on current
caution in patients with bronchospastic disease but therapy to a physician for a thorough evaluation. Once
are sometimes used in patients who are not receiving the condition has been stabilized, the client should be
beta-agonists. The goal is achievement of a resting assessed by a physician at least twice annually.
heart rate of 50–60 beats/minute.
Management of Unstable Angina
Oral, spray or transdermal nitrates can be used for
prophylaxis (acute attack or prior to activities known Anyone presenting with chest pain should be treated
to exacerbate angina) or chronic therapy. Nitrate as possibly having an acute myocardial infarction.
tolerance is known to occur with continuous use.
With any nitrate preparation it is essential to ensure Goals of Treatment
a 10–12 hour30 nitrate-free interval to prevent loss –– To relieve chest pain and other symptoms of
of effect over time. The presenting symptoms will myocardial ischemia
influence the timing of the nitrate-free period, for –– To prevent further myocardial injury
example, a primarily exertional angina will be treated
–– To reduce the severity of or eliminate episodes
with a daytime nitrate dose while congested heart
of ischemia
failure and nocturnal angina may be managed with an
evening nitrate dose. Nitroglycerin preparations can Appropriate Consultation
be used in combination with beta-blockers or calcium
channel blockers.31 Consult a physician as soon possible.

Adjuvant Therapy Primary Prevention

If chest pain is present at the time of presentation: The Web site Hypertension.ca, Hypertension Canada
presents information from the Canadian Hypertension
–– Oxygen may be administered by nasal canula;
Society (CHS), the Canadian Hypertension Education
titrate flow to keep oxygen saturation ≥ 94%33
Program (CHEP) and Blood Pressure Canada (BPC).
–– Start intravenous (IV) therapy with normal saline In Part 2 of the recommendations from CHEP, you
to keep vein open will find information on modifiable lifestyle factors
for the prevention of vascular events through the
prevention of specifically hypertension. A summary
Bed rest for clients experiencing pain on presentation. of other risk factors and preventive measures are
presented below.
Nutritional strategies including:
nitroglycerin sublingual spray (0.4 mg)
q5min X 3 doses prn –– Fat intake: < 30% of total caloric intake with
< 10% of calories from saturated fats
If the client is hypotensive or has bradycardia on
presentation, do not give nitroglycerin without first –– Omega-3 fatty acid rich foods: 2 or more servings
consulting a physician. If pain is not relieved, treat of either fish (for example, salmon) or omega -3
as myocardial infarction (see “Myocardial Infarction” rich plant foods (for example, flaxseed, canola oil,
under the section “Emergencies of the Cardiovascular soybean oil or nuts)
System” later in this chapter). –– 7–8 servings of fruits and vegetables daily
–– Whole grain and high-fibre foods
If no contraindications, give:
–– Low salt intake:36
Uncoated ASA 162–325 mg as soon as possible –– Adults age 50 or less: 1500 mg (65 mmol) per day
(chew and swallow)34
–– Adults 51–70 years: 1300 mg (57 mmol) per day
Consult a physician regarding initial anticoagulation –– Adults > 70 years: 1200 mg (52 mmol) per day
with a therapeutic dose of low molecular weight
heparin while awaiting transfer. Alcohol: 2 or fewer drinks per day, not exceeding
14 standard drinks per week for men and 9 standard
Monitoring and Follow-Up drinks per week for women.36
Continue to closely monitor pain, vital signs Weight management: BMI within normal range of
(including oxygen saturation), heart and lung sounds 18.5–24.9 kg/m2 and waist circumference less than
and ECG results. 102 cm for men and 88 cm for women.36
Exercise program: Most guidelines recommend
Referral 30–60 minutes of moderate intensity exercise (such
Medevac as soon as possible. as walking, jogging, cycling or swimming) 4–7 days
a week.37
Revascularization procedures such as coronary
angioplasty, stenting or bypass surgery may be Smoking cessation counselling; minimize exposure
indicated for any client who continues to have to second-hand smoke.
significant symptoms despite medical therapy.
Oral Contraceptives: Use the lowest effective dose
Prevention of estrogen and progesterone to prevent pregnancy.
Avoid use in women who smoke, those with
Prevention of morbidity and mortality from vascular uncontrolled hypertension and/or a history of stroke,
disease requires recognition and management of ischemic heart disease or venous thromboembolism.38
modifiable risk factors. Primary prevention involves
management of risk factors before the patient
suffers a vascular event such as a stroke, myocardial
infarction or amputation. Secondary prevention
involves management of risks after the patient
suffered a vascular event.35

Secondary Prevention39 –– Hypothyroidism (myxedema)

Blood Pressure: Achieve and maintain a BP of –– Aortic dissection
< 140/90 mm Hg (130/80 mm Hg for clients with –– Sarcoidosis
diabetes). –– Pancreatitis
Diabetes: For type 1 or 2, maintain tight glycemic –– Inflammatory bowel disease
control (hemoglobin HbA1c ≤ 7%). –– AIDS
Lipids: HISTORY
–– Achieve and maintain optimal lipid level for age, –– Chest pain, typically sharp; retrosternal with
sex and cardiovascular risk status radiation to the trapezial ridge
–– Target LDL cholesterol < 2 mmol/L –– Pain, frequently sudden in onset
–– Pain reduced by leaning forward and sitting up
PERICARDITIS, ACUTE –– Splinted breathing
–– Odynophagia
An inflammation of the pericardium surrounding
–– Fever
the heart muscle. It may occur with or without an
effusion. The most common type is idiopathic or –– Myalgias
nonspecific pericarditis. –– Anorexia
CAUSES PHYSICAL FINDINGS
–– Idiopathic (unknown) –– Temperature may be elevated (low-grade fever)

–– Viral infection (for example, coxsackievirus, –– Respiration fast and shallow
ECHO virus, adenovirus, Epstein-Barr virus, –– Sinus tachycardia
mumps) –– A narrow pulse pressure (hypotension-elevated
–– Bacterial infection (for example, Streptococcus neck veins may indicate a restrictive pericarditis
pneumoniae and other Streptococcus species or that requires urgent decompression)
Staphylococcus species. Isolated gram-negative –– Pulsus paradoxus – weakening or disappearance
bacteria include Proteus species, Escherichia of the radial, brachial or femoral pulse during
coli, Pseudomonas species, Klebsiella species, inspiration (urgent decompression may be required
Salmonella species, Shigella, Neisseria if the difference in arterial pressure is greater than
meningitidis and Haemophilus influenza, 10 mm Hg between the first Korotkoff sounds
Nocardia species) heard only during expiration and the Korotkoff
–– Fungal infection (for example, aspergillosis, sounds first heard throughout inspiration and
candidiasis, histoplasmosis) expiration)
–– Mycobacterial infection (for example, –– Electrocardiogram (ECG) initially diffuse ST
Mycobacterium tuberculosis) segment elevation +/- depressed PR segment,
–– Parasites: protozoa 2–5 days later ST isoelectric with T wave flattening
–– Neoplasm: breast, lung, lymphoma, renal cell, and inversion
melanoma –– Anxiety
–– Drug-induced: isoniazid, phenytoin, procainamide, –– Mild distress
hydralazine, among others –– Flushing
–– Connective-tissue disease: systemic lupus –– Splinted breathing
erythematosus, rheumatoid arthritis, scleroderma, –– Shortness of breath (only in cases of pericardial
acute rheumatic fever tamponade or constrictive pericarditis)
–– Radiation therapy –– Pericardial friction rub
–– Post-myocardial infarction (Dressler’s syndrome) –– Localized lung crackles may be present
–– Chest trauma
–– Uremia

DIFFERENTIAL DIAGNOSIS Pharmacologic Interventions

–– Acute myocardial infarction Drugs are mainly used in cases of idiopathic
–– Pneumonia with pleurisy pericarditis. In other cases, underlying causes must
–– Pulmonary emboli be treated appropriately.
–– Aortic dissection NSAIDs40: acetylsalicylic acid (ASA), 650 mg q4-6h
–– Pneumothorax initially, then taper the dose over three to four weeks
(to reduce the likelihood of recurrence)
–– Mediastinal emphysema
–– Cholecystitis or
–– Pancreatitis ibuprofen (Motrin), 400–800 mg, q6-8h initially,
then taper the dose
COMPLICATIONS
In some clients, the condition becomes refractory and
–– Pericardial tamponade corticosteroids or pericardiectomy may be required.
–– Recurrence of pericarditis
–– Noncompressive effusion Monitoring and Follow-Up
–– Chronic constrictive pericarditis –– Follow up in 2 or 3 days, to make sure no
–– Atrial arrhythmia complications develop, and then again in 2 weeks
–– Repeat ECG and chest x-ray should be considered
DIAGNOSTIC TESTS at about 4 weeks
–– ECG –– In most clients complete resolution occurs after
–– Chest x-ray (if available), to rule out complications 2 weeks of therapy
such as pleural effusion or enlarged heart –– 15% of clients will have at least one recurrence
within the first few months
MANAGEMENT
Goals of Treatment VENOUS INSUFFICIENCY, CHRONIC

–– Prevent complications Impairment of the venous system that inhibits normal
–– Identify underlying treatable causes return of blood from the legs to the heart.
Appropriate Consultation CAUSES
Consult a physician if you suspect this diagnosis. Incompetent valves in veins of the legs.
The otherwise healthy client can often be safely Risk Factors

treated on an outpatient basis.
–– Familial predisposition
Nonpharmacologic Interventions –– Prolonged standing
–– Pregnancy
Client education –– Obesity
–– Ensure that client understands disease process –– Constricting garments worn over a long period
and prognosis of time
–– Counsel client about appropriate medication
use and side effects HISTORY
–– Recommend avoidance of heavy physical labour –– Dull aching heaviness or fatigue in legs, often
–– Teach client about symptoms and signs of occurring at the end of the day and relieved by
complications, and instruct client to report any elevation of the legs
that occur –– Mild edema at end of day
–– Stress the importance of follow-up –– Cramps in legs at night
–– Itching may be present (due to stasis dermatitis)
–– Stasis dermatitis, brownish red discolouration

PHYSICAL FINDINGS Nonpharmacologic Interventions

–– Dilated, tortuous, elongated varicose veins in foot, Client education
lower leg, medial thigh or behind knee –– Teach client proper skin hygiene and care of
–– Varicose veins seen more readily when person is lesions
standing –– Recommend support hose or support stockings
–– Skin changes may be present (erythema, brownish (compression stockings should exert a minimum
pigmentation, flaking and scaling, skin breakdown) of 20–30 mm Hg pressure at the ankle to be
–– Venous ulcers may be present on medial side of effective for moderate to severe varicose veins)41
lower leg just above medial malleolus or on medial –– Recommend elevation of legs above the level of
aspect of ankle the hip when sitting
–– Edema of foot and ankle may be present –– Recommend avoidance of prolonged standing
–– Dilated veins easily palpable when person (client should sit with legs elevated whenever
is standing possible and should avoid crossing legs)
–– Recommend avoidance of restrictive clothing
around the knees (for example, knee socks, garters)
–– Chronic occlusive arterial disease with arterial –– Recommend weight loss (if appropriate)
ulcers –– Recommend smoking cessation (if appropriate)
–– Orthopedic problems –– Instruct client to return to clinic if signs of skin
breakdown or skin irritation occur, or if a vein
COMPLICATIONS
becomes sore and tender
–– Stasis dermatitis –– Instruct client to do leg exercises qid in bed
–– Cellulitis to prevent deep vein thrombosis
–– Stasis ulcer
–– Thrombophlebitis Monitoring and Follow-Up
–– Deep vein thrombosis (if deep veins involved) Arrange follow-up in 1 month to assess adherence
to and efficacy of interventions.
DIAGNOSTIC TESTS
Referral
None.
Refer to a physician if condition does not improve
MANAGEMENT with conservative treatment or if complications arise.
Goals of Treatment
–– Facilitate venous return
EMERGENCIES OF THE CARDIOVASCULAR SYSTEM
ACUTE ARTERIAL OCCLUSION OF CAUSES

A MAJOR PERIPHERAL ARTERY –– Thrombus
–– Embolus
Sudden occlusion of a peripheral artery with resultant
acute ischemia in the distal limb. –– Trauma
–– Idiopathic
–– Predisposing factors: peripheral vascular disease,
atrial fibrillation, recent myocardial infarction,
prosthetic heart valve, oral contraceptive use,
history of TIA/stroke, antiphospholipid syndrome
or other hypercoagulable states

HISTORY Nonpharmacologic Interventions

–– Sudden onset of severe pain in distal part of a limb –– Bed rest
–– Paresthesia, coldness and pallor in distal limb –– Prevent injury to limb: handle carefully, protect
follow later from pressure or injury
–– Previous symptoms of intermittent claudication –– Do not elevate ischemic limb (keep horizontal
may be present or slightly dependent)
–– History of cardiac disease may be present
Adjuvant Therapy
PHYSICAL FINDINGS –– Start IV therapy with normal saline to keep vein
–– Heart rate elevated, pulse may be irregular open
–– Respiratory rate normal or increased –– Oxygen may be needed if there is evidence of
underlying cardiorespiratory compromise
–– Blood pressure normal or increased
–– Anxious, in acute distress Pharmacologic Interventions
–– Signs of longstanding peripheral vascular disease
Analgesia for pain:
in the opposite limb
–– Colour of limb normal initially, becomes pale later morphine, 2–5 mg IV prn (maximum 10 mg/h or
10 mg IM)
–– Skin temperature may be normal initially, becomes
cool or cold later Consult a physician regarding initial anticoagulation
–– Peripheral pulses lower than in opposite limb before transfer.
or absent altogether
–– Cutaneous sensation decreased or absent Monitoring and Follow-Up
–– Tenderness in calf on dorsiflexion of foot Monitor vital signs, general condition, cardiac and
–– Arterial bruits may be present (aortic, iliac, respiratory status frequently.
femoral, popliteal)
Referral
The 6 Ps of acute arterial occlusion are: pain, pallor,
Medevac as soon as possible. There is only a 4- to
polar (cold), pulseless, paresthesia and paralysis.
6-hour window of opportunity to perform surgical
DIFFERENTIAL DIAGNOSIS intervention to save limb from irreparable damage.
–– Compartment syndrome if trauma has been

involved MYOCARDIAL INFARCTION
Interruption of blood flow through the coronary
COMPLICATIONS arteries, resulting in ischemic injury and necrosis of a
–– Ischemic muscular contracture portion of the myocardium. As many as 15% to 25%
–– Loss of limb of cases are silent or atypical in presentation.
MANAGEMENT CAUSES
–– Acute thrombosis within a coronary artery with
Goals of Treatment underlying atherosclerosis
–– Improve oxygenation of the limb –– Coronary artery spasm
–– Prevent injury to or loss of limb
Risk Factors
Appropriate Consultation –– Smoking
Consult a physician immediately. –– Family history of heart disease
–– Hypertension
–– Dyslipidemia
–– Obesity
–– Sedentary lifestyle
–– Cocaine use42

HISTORY –– Dissecting aortic aneurysm

–– Acute retrosternal chest pain (heaviness, aching, –– Spontaneous pneumothorax
squeezing, typical pain of myocardial infarction)
COMPLICATIONS
–– Pain may radiate into left arm, neck, fingers,
shoulders, epigastrium, right chest, right upper –– Arrhythmias and conductive disturbances
quadrant, right arm or upper back –– Hypotension
–– Pain usually occurs at rest, with gradual or –– Congestive heart failure
sudden onset, and can be precipitated by stress –– Pericarditis
–– Pain not relieved by nitroglycerin –– Thromboembolism
–– Pain lasts longer than 30 minutes –– Cardiogenic shock
–– Shortness of breath –– Cardiac arrest
–– Nausea and vomiting –– Rupture of the heart
–– Diaphoresis –– Death
–– Weakness
Young premenopausal women who have had a
–– Loss of consciousness may occur myocardial infarction have significantly higher
In women, myocardial infarction tends to present mortality rates than men who have had a myocardial
atypically as shortness of breath, fatigue, flushing, infarction at the same age. One possible explanation
nausea, jaw pain and abdominal pain, with these for this may be the difference in primary prevention
symptoms occurring over hours rather than minutes. strategies applied to women. Management of early
symptoms is often less aggressive.
PHYSICAL FINDINGS
DIAGNOSTIC TESTS
–– Respiration rapid and shallow
–– Pulse variable (rapid or slow, regular or irregular, –– Obtain a 12-lead electrocardiogram (ECG) tracing;
full volume, “thready”) compare with a previous tracing, if available
–– Blood pressure increased, decreased or normal –– Identify new changes if possible; check for Q
–– Oxygen saturation may be abnormal if client waves, elevation of ST segment and inversion
is in shock or has congestive heart failure of T wave (signs of myocardial infarction)
–– Acute distress –– Check for depression of ST segment, inversion
of T wave (angina)
–– Pale
–– Diaphoresis During myocardial infarction in women, Q waves
–– Cyanosis (central or peripheral, or both) may not be present on ECG. Women are more likely
–– Client may be unconscious than men to demonstrate nondiagnostic, reversible
ST segment elevations or T wave abnormalities.
–– Skin may be cool and clammy
–– Lungs are usually clear; crackles present if –– If the patient has continuing pain, repeat 12-lead
congestive heart failure develops ECG twice more at 30-minute intervals, noting
–– S1, S2 normal; S3 and/or S4, murmurs, pericardial any evolving changes
friction rub may be present if there are –– Blood may need to be drawn for baseline cardiac
complications enzymes (CK, troponin) before transferring client
DIFFERENTIAL DIAGNOSIS MANAGEMENT

–– Peptic ulcer disease Goals of Treatment
–– Esophageal spasm or esophagitis
–– Improve oxygenation of myocardium
–– Gallbladder disease
–– Large pulmonary embolism
–– Keep infarct from extending
–– Indigestion
–– Pancreatitis Appropriate Consultation
–– Acute anxiety attack Consult a physician urgently.
–– Acute pericarditis

Adjuvant Therapy Beta-blockers should not be used if heart rate is

–– Oxygen via nasal prongs; titrate flow to keep < 60 bpm, systolic BP is < 100 mm Hg, congestive
oxygen saturation ≥ 94%43 heart failure or atrioventricular (AV) block is present,
or if there is a history of asthma. Use of beta-blockers
–– Start intravenous (IV) therapy with normal saline
is not recommended in patients with cocaine-associated
to keep vein open
myocardial infarction.42
Nonpharmacologic Interventions Other drugs may be ordered by a physician. Access
–– Bed rest with head elevated (unless hypotensive) to a cardiac monitor or defibrillator will influence
–– Offer support and reassurance to reduce anxiety therapeutic choices.
Ultimately, a thrombolytic medication (for example,
Pharmacologic Interventions streptokinase, tissue plasminogen activator [tPA])
Nitrates: might be required, if it can be given within the first
few hours of the onset of chest pain. Tenecteplase
sublingual nitroglycerin 0.4 mg spray prn but only
is generally the easiest to administer. Clients treated
if systolic blood pressure (BP) > 100 mm Hg
with these agents also need LMWH (for example,
Observe response and monitor severity of pain; enoxaparin) or unfractionated heparin.45,46
if pain not relieved, repeat:
0.4 mg q5min for another 2 doses, but only if systolic
BP remains > 100 mm Hg –– Monitor vital signs (including pulse oximetry)
Nitroglycerin can cause headache, hypotension and –– Repeat ECG (to check for arrhythmias)
tachycardia. Nitrates are contraindicated in patients –– Monitor lungs and heart sounds frequently
who have taken sildenafil (Viagra, Revatio), tadalafil for signs of heart failure
(Cialis) or vardenafil (Levitra).
Referral
Then give:
Medevac as soon as possible.
uncoated acetylsalicylic acid (ASA), 162–325 mg44,45
stat PO chewed, unless contraindicated (for example,
allergy to ASA or NSAIDs, active peptic ulcer) PULMONARY EDEMA
Patients hypersensitive to ASA or with major Accumulation of fluid within the lungs that interferes
gastrointestinal intolerance to ASA should receive with ventilation and oxygenation.
clopidogrel on physician consult.
CAUSES
If pain unrelieved by nitrates, administer analgesia:
Acute left-heart failure, with or without right-
morphine, 2–5 mg IV; repeat dose only under the
heart failure (see “Differential Diagnosis”). Adult
direction of a physician
respiratory distress syndrome or non-cardiogenic
Other pharmacologic measures, as prescribed by pulmonary edema can occur with severe infections,
a physician: malignancies and with some medications.
Beta-blockers are routinely used unless
HISTORY
contraindicated (see below). Initial oral dose
(example): –– Severe shortness of breath
metoprolol 50 mg PO BID (range 50–200 mg bid) –– Orthopnea, paroxysmal nocturnal dyspnea
(left ventricular failure)
Oral administration is preferred. IV administration is –– Fluid retention peripherally and weight gain
associated with an increased risk of cardiogenic shock (right heart failure) may also be present
and is not warranted unless there is ongoing pain at
–– Cough productive of frothy pink sputum
rest especially with tachycardia or hypertension in the
may be present
absence of contraindications.

PHYSICAL FINDINGS Adjuvant Therapy

–– Pulse rapid and may be “thready” or weak –– Oxygen via non-rebreather mask; titrate flow
–– Respiratory rate elevated to keep oxygen saturation ≥ 90%
–– Blood pressure normal, elevated or decreased –– Start IV therapy with normal saline to keep
–– Acute respiratory distress vein open
–– Diaphoresis
–– Central cyanosis may be present
–– Peripheral cyanosis with cool, mottled extremities –– Bed rest with head elevated
–– Swelling of ankles may be present –– Insert an indwelling urinary catheter
(monitor input and output)
–– Jugular venous pressure (JVP) may be elevated
–– Hepatojugular reflux and hepatomegaly Pharmacologic Interventions
may be present
IV loop diuretics:
–– Peripheral pitting edema may be present
–– Crackles and wheezes in lower half of lung fields furosemide (Lasix), 40–80 mg IV push
–– S3 gallop rhythm in the heart The dose may have to be higher in persons on an
oral maintenance dose. It is reasonable to administer
DIFFERENTIAL DIAGNOSIS an initial dose that is equivalent to the client’s usual
–– Chronic congestive heart failure maintenance dose.14 Adjust the diuretic dose according
–– Acute myocardial infarction to client’s response (monitor urine output). Look for
–– Acute pulmonary embolism improvement in respiratory status.
–– Atrial fibrillation To reduce venous return and workload on the heart,
–– Valvular heart disease the physician may order nitrates. All forms of nitrates
–– Adult respiratory distress syndrome are effective.
–– Acute exacerbation of COPD Nitrates:
COMPLICATIONS sublingual nitroglycerin 0.4 mg spray prn

or
–– Dependent on underlying disease process
–– Angina transdermal nitroglycerin 0.2 mg/hour patch
–– Hypotension, shock but only if systolic blood pressure (BP) > 100 mm Hg.
–– Respiratory failure
Nitroglycerin can cause headache, hypotension and
DIAGNOSTIC TESTS tachycardia. Nitrates are contraindicated in patients
who have taken sildenafil (Viagra, Revatio), tadalafil
–– Obtain ECG: look for signs of myocardial ischemia (Cialis) or vardenafil (Levitra).
or infarction
–– CBC, electrolytes, renal function Monitoring and Follow-up
MANAGEMENT –– Monitor vital signs (watch for hypotension)

and ABCs (airway, breathing and circulation)
Goals of Treatment frequently, including oxygen saturation
–– Monitor urine output hourly (if not diuresing, the
–– Improve oxygenation
client requires more IV diuretics)
–– Promote diuresis of accumulated fluids
–– Reduce venous return to the heart Referral
–– Treat any reversible precipitants (for example, Medevac as soon as possible.
cardiac ischemia, hypertension, arrhythmia)
Consult a physician immediately.

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Chapter 4 - Cardiovascular System

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CHAPTER 4 – CARDIOVASCULAR SYSTEM

ASSESSMENT OF THE CARDIOVASCULAR SYSTEM..........................................4–1

Clinical Practice Guidelines for Nurses in Primary Care 2010

ASSESSMENT OF THE CARDIOVASCULAR SYSTEM

HISTORY OF PRESENT ILLNESS Fainting or Syncope

CARDINAL SYMPTOMS Extremities

Clinical Practice Guidelines for Nurses in Primary Care 2010

MEDICAL HISTORY PHYSICAL EXAMINATION

2010 Clinical Practice Guidelines for Nurses in Primary Care

AUSCULTATION S4 (Pressure Overloaded Ventricle)

Clinical Practice Guidelines for Nurses in Primary Care 2010

High-Pitched Diastolic Decrescendo Murmurs Legs

2010 Clinical Practice Guidelines for Nurses in Primary Care

Table 1 – Differential Diagnosis of Chest Pain

Clinical Practice Guidelines for Nurses in Primary Care 2010

Table 1 – Differential Diagnosis of Chest Pain (Continued)

DYSPNEA Pulmonary Causes

Cardiac Causes –– COPD/obstructive lung disease

2010 Clinical Practice Guidelines for Nurses in Primary Care

Mixed Cardiac and Pulmonary Causes Other Causes

Noncardiac or Nonpulmonary Causes Primary Arrhythmic Causes

–– Metabolic conditions (for example, acidosis) –– Sinus tachycardia or arrhythmia

–– Seizure Drug-Related Causes

Clinical Practice Guidelines for Nurses in Primary Care 2010

Other Cardiac Causes –– Congenital heart disease

Table 2 – Differential Diagnosis of Leg Edema

COMMON PROBLEMS OF THE CARDIOVASCULAR SYSTEM

AORTIC ANEURYSM, ABDOMINAL –– History of atherosclerosis (for example,

2010 Clinical Practice Guidelines for Nurses in Primary Care

If an aneurysm has ruptured: –– Insert a nasogastric tube, if upon consultation

Monitoring and Follow-Up ARRHYTHMIAS

Referral SINUS BRADYCARDIA

MANAGEMENT OF SYMPTOMATIC CLIENT BRADYCARDIA

Clinical Practice Guidelines for Nurses in Primary Care 2010

ATRIAL FIBRILLATION Predisposing Factors for Atrial Fibrillation

2010 Clinical Practice Guidelines for Nurses in Primary Care

–– Supraventricular tachycardia: pulse regular and Nonpharmacologic Interventions

Clinical Practice Guidelines for Nurses in Primary Care 2010

RISK FACTORS DIFFERENTIAL DIAGNOSIS

–– Hypertension Appropriate Consultation

2010 Clinical Practice Guidelines for Nurses in Primary Care

–– To reduce skin irritation, client should put ASSOCIATED CONDITIONS9

Clinical Practice Guidelines for Nurses in Primary Care 2010

DIAGNOSTIC TESTS In clients with chronic atrial fibrillation, long-

MANAGEMENT Monitoring and Follow-Up

Goals of Treatment –– Clients with stable atrial fibrillation should be

2010 Clinical Practice Guidelines for Nurses in Primary Care

NEW YORK HEART ASSOCIATION –– Connective tissue disease

Clinical Practice Guidelines for Nurses in Primary Care 2010

–– Ankle edema –– Angina or myocardial infarction

2010 Clinical Practice Guidelines for Nurses in Primary Care

Appropriate Consultation –– Recommend weight loss, if applicable

Table 3 – Drugs to manage congestive heart failure11

Clinical Practice Guidelines for Nurses in Primary Care 2010

2010 Clinical Practice Guidelines for Nurses in Primary Care

Nitrates can relieve congestive symptoms in patients –– Drugs

sublingual nitroglycerin, 0.4 mg HISTORY

Monitoring and Follow-Up –– Symptoms may be subtle, variable or vague

Clinical Practice Guidelines for Nurses in Primary Care 2010

DIFFERENTIAL DIAGNOSIS Pharmacologic Interventions

2010 Clinical Practice Guidelines for Nurses in Primary Care

DYSLIPIDEMIA (HYPERLIPIDEMIA) HISTORY

Clinical Practice Guidelines for Nurses in Primary Care 2010