Cardiovascular System

Cardiac dysrhythmias
 Risk Factors: Acute MI, CHF, CAD, COPD, Electrolyte disturbances, HTN, Valve disorders, Drug
effects
 Symptoms: Irregular HR or rhythm, Hypotension, syncope, angina, SOB, agitation, restlessness,
weakness, fatigue, N/V, pallor
 Normal Sinus Rhythm: regular, rate = 60-100 bpm, one upright P wave in front of QRS, constant .
12-.20 sec PR interval, QRS less than .12 sec
1. Bradycardia
a. Risk factors.(Brady)
i. Occurs in response to
1. Carotid sinus massage
2. Valsalva maneuver
3. Hypothermia
4. Increased intraocular pressure
5. Vagal stimulation
6. Drugs such as beta blockers and calcium channel blockers
ii. Disease states commonly seen in
1. Hypothyroidism
2. Increased intracranial pressure
3. Inferior MI
iii. May be seen in aerobically-trained athletes
b. Pathophysiology.(Brady)
i. ECG rhythm is regular
ii. Rate is <60 BPM
c. Clinical manifestations(Brady)
i. Pale, cool skin
ii. Hypotension
iii. Weakness
iv. Angina
v. Dizziness/ syncope
vi. Confusion/ disorientation
vii. Shortness of breath
d. Collaborative (interprofessional) care (Brady)
i. Drugs
1. IV atropine
2. Dopamine
3. Epinephrine
ii. Transcutaneous pacing
iii. Permanent pacemaker therapy may be necessary
2. Tachycardia
a. Risk factors.(Tachy)
i. Stressors (physical and psychological)
1. Exercise
2. Fever
3. Pain
4. Hypotension
 5. Hypovolemia
6. Anemia
7. Hypoxia
8. Hypoglycemia
9. MI
10. Heart failure
11. Hyperthyroidism
12. Anxiety/ fear
ii. Drugs
1. Epinephrine
2. Norepinephrine
3. Atropine
4. Caffeine
5. Theophylline
6. Hydralazine
7. OTC drugs such as sudafed
b. Pathophysiology.(Tachy)
i. ECG rhythm is regular
ii. Rate is 101-200 BMP
iii. Cardiac output decreased
c. Clinical manifestations(Tachy)
i. Decreased CO may cause
1. Dizziness
2. Hypotension
3. Dyspnea
ii. Increased HR increases O2 demand, which can cause
1. Angina
2. MI
d. Collaborative (interprofessional) care (Tachy)
i. Treatment guided by underlying cause
1. Pain management
2. Vagal maneuvers
3. Drugs
a. Beta blockers
b. Adenosine
c. Calcium channel blockers
4. Synchronized cardioversion
3. Atrial dysrhythmias
a. Premature atrial contraction (PAC)
i. Risk factors.(PAC)
1. In healthy heart, caused by
a. Emotional stress
b. Physical fatigue
c. Substances such as alcohol, caffeine, tobacco
2. Unhealthy situations that can cause PAC
a. Hypoxia
b. Electrolyte imbalance
c. Hyperthyroidism
d. COPD
 e. Heart disease including CAD and valvular disease
ii. Pathophysiology.(PAC)
1. Location in atrium other than SA node sends signal to contract sooner
than the next sinus beat
2. AV node may stop it, delay it, or let it through
3. Conducted normally through ventricles in most cases
4. ECG
a. P wave is different shape than the sinus P wave
b. Rhythm is irregular
c. PR interval may be shorter or longer
d. QRS is usually normal
e. Abnormal or absent P wave
f. Atrial rate may be rapid, ventricular rate slow or fast
g. Loss of atrial filling decreases CO
h. Poor coronary perfusion > ischemia (restriction in blood supply to
tissues, causing a shortage of oxygen)
iii. Clinical manifestations(PAC) –
palpitations or feeling that heart skipped a beat
iv. Collaborative (interprofessional) care (PAC)
1. Treatment depends on patient’s symptoms.
2. May include withdrawal of stimulation sources such as caffeine or
sympathomimetic drugs
3. Beta blockers may be used
b. Paroxysmal supraventricular tachycardia (PSVT)
i. Risk factors (PSVT)
1. Overexertion
2. Emotional stress
3. Deep inspiration
4. Stimulants such as caffeine and tobacco
5. Rheumatic heart disease
6. Dig toxicity
7. CAD
8. Cor pulmonale
ii. Pathophysiology (PSVT)
1. Somewhere above bundle of His begins contraction pathway, resulting
in ventricles contracting sooner than they were going to if they were
waiting on the sinus-initiated contraction signal
2. Usually triggers a run of repeated premature beats, after which a brief
period of asystole (absence of all cardiac electrical activity) may follow
3. ECG
a. HR is 150-220
b. Rhythm may be regular or irregular
c. P wave often hidden in preceding T wave
d. PR interval may be normal or shortened
e. QRS usually normal
iii. Clinical manifestations (PSVT)
1. Hypotension
2. Palpitations
3. Dyspnea
 4. Angina
5. SOB
iv. Collaborative care (PSVT)
1. Vagal stimulation
a. Valsalva maneuver
b. Carotid massage
c. Coughing
2. Drugs
a. IV adenosine is drug of choice
b. Beta blockers
c. Calcium channel blockers
3. Synchronized cardioversion when above treatments are not working
c. Atrial flutter
i. Risk factors (A. flutter)
1. Rarely found in healthy hearts
2. Associated with
a. CAD
b. Hypertension
c. Mitral valve disorders
d. Pulmonary embolus
e. Chronic lung disease
f. Cor pulmonale
g. Cardiomyopathy
h. Hyperthyroidism
i. Drugs such as
i. Digoxin
ii. Quinidine
iii. Epinephrine
ii. Pathophysiology (A. flutter)
1. Ectopic focus in atrium causes repeated atrial contractions
2. ECG
a. Atrial rate 200-350 BPM
b. Regular, Sawtooth representing atrial flutter contractions
c. Ventricular rate varies based on how much is blocked by AV
node
d. PR interval varies and is not measurable
e. Loss of atrial filling decreases CO
f. Can precipitate heart failure
g. Increases risk for stroke
iii. Clinical manifestations (A. flutter)
1. Decreased cardiac output can cause serious consequences
a. HF
b. Stroke because of churning blood in atria may cause thrombus
iv. Collaborative care (A. flutter)
1. Primary treatment goal = slow ventricular response by increasing AV
block
 2. Drugs (A. flutter)
a. Calcium channel blockers
b. Beta blockers
c. Warfarin to reduce thrombus formation
3. Electrical cardioversion if necessary:
 Electrical therapy applied for hemodynamically unstable
ventricular rhythms or SVT
 Synchronized countershock delivered during the QRS complex
of the ECG
 Patient sedated, low energy, 50-100 joules
4. Radiofrequency catheter ablation if necessary, which obliterates ectopic
foci
d. Atrial fibrillation
i. Risk factors (A. fib)
1. Underlying heart conditions
a. CAD
b. Valvular heart disease
c. HF
d. Pericarditis
2. Acute conditions
a. Thyrotoxicosis
b. Alcohol intoxication
c. Caffeine
d. Electrolyte disturbances
e. Stress
f. Heart surgery
ii. Pathophysiology (A. fib)
1. Multiple foci are firing and conduct signal in many directions.
2. Atria contract in different places at different times, resulting in a quivering
of the muscle.
3. ECG
a. Atrial rate may be as high as 350-600bpm
b. Ventricular rate varies and is usually irregular based on when the
AV node will let an impulse through
c. Fibrillatory waves replace the p wave
d. Loss of atrial filling decreases CO
e. Blood stasis promotes clots and increases risk for strokes
iii. Clinical manifestations (A. fib)
1. Decreased CO as blood churns in the atria instead of being squeezed
into the ventricles
2. Thrombi can form as blood churns
iv. Collaborative care (A. fib)
1. Goals
a. Decrease ventricular response to <100bpm
b. Prevent stroke
c. Convert to sinus rhythm

2. Drugs (A. fib)

 a. For rate control
i. Calcium channel blockers
ii. Beta blockers
iii. Dronedarone
iv. Digoxin
b. Warfarin to prevent thrombus formation.
3. Electrical cardioversion may be necessary to return to sinus rhythm
4. Radiofrequency catheter ablation, AV nodal ablation, and Maze
procedure physically interfere with the source of the fibrillations.
v. Complications (A. fib)
1. Stroke if thrombus travels to brain
4. Ventricular dysrhythmias
 Abnormal QRS waveform
 Disorganized rhythm
 Loss of pumping effect>low cardiac output
a. Premature ventricular contractions (PVC)
i. Risk factors.(PVC)
1. Use of certain substances/ drugs
a. Stimulants such as caffeine
b. Alcohol
c. Nicotine
d. Aminophylline
e. Epinephrine
ii. Pathophysiology.(PVC)
1. Ectopic focus in ventricles results in contraction before the sinus rhythm
would have had them contract
2. Beats occur early during refraction
3. Wide, distorted QRS
4. May not perfuse, assess for pulse deficit
5. Can lead to ventricular tachycardia
6. Classification
a. Number of ectopic foci
i. Unifocal
1. PVCs are same shape
2. Come from one focus
ii. Multifocal
1. PVCs vary in shape
2. Come from different foci
b. How many beats between PVCs
i. Bigeminy - every other beat is PVC
ii. Trigeminy - every third beat is PVC
7. VTach results when there are three or more consecutive PVCs
iii. Clinical manifestations(PVC)
1. Usually ok in pt with otherwise healthy heart
2. In pt with heart disease
a. Angina from reduced CO
b. May cause HF depending on frequency
iv. Collaborative (interprofessional) care (PVC)
1. Treatment will depend on the cause
 a. O2 therapy for hypoxia
b. Electrolyte replacement
2. Drugs
a. Beta blockers
b. Procainamide
c. Amiodarone
b. Ventricular tachycardia (VT)
i. Risk factors. (VT)
1. MI
2. CAD
3. Electrolyte imbalances
4. Cardiomyopathy
5. Long QT syndrome
6. Drug toxicity
7. Central nervous system disorders
ii. Pathophysiology.(VT)
1. A run of three or more PVCs
2. Wide distorted QRS
3. Rate 150-250 bpm
4. No P or T visible
5. Severe loss of CO
6. Types
a. Monomorphic - QRS complexes are all same size and shape
b. Polymorphic aka Torsades de pointes - QRS complexes vary in
size and shape
7. Deadly due to decreased CO
iii. Clinical manifestations(VT)
1. Pt may or may not have pulse
2. Severely decreased CO leads to
a. Hypotension
b. Pulmonary edema
c. Decreases cerebral blood flow
d. Cardiopulmonary arrest
iv. Collaborative (interprofessional) care (VT)
1. Must be treated quickly, even if it appears and then goes away
2. Identify and treat precipitating causes, such as electrolyte imbalances.
3. For stable pt (has pulse) with monomorphic VT and preserved LV
function, treat with
a. Procainamide (Na channel blocker)
b. Sotatol (K channel blocker)
c. Amiodarone (K channel blocker)
4. For pulseless pt
a. Begin CPR
b. Rapid defibrillation
c. If defib is unsuccessful, administer
i. Vasopressors (e.g. epinephrine)
ii. Antidysrhythmics (e.g. amiodarone)
c. Ventricular fibrillation (VF)
i. Risk factors.(VF)
 1. Medical conditions
a. MI
b. Myocardial ischemia
c. HF
d. Cardiomyopathy
2. Procedures
a. Cardiac pacing
b. Cardiac cath
3. Coronary reperfusion due to thrombolytic therapy
4. Other
a. Electric shock
b. Hyperkalemia
c. Hypoxemia
d. Acidosis
e. Drug toxicity
ii. Pathophysiology.(VF)
1. Multiple ectopic foci firing in ventricles
2. Quivering with no adequate contractions
3. Irregular, chaotic rhythm
4. Cannot identify specific waveforms
5. Creates no cardiac output
iii. Clinical manifestations(VF)
1. Unresponsive
2. No pulse
3. Not breathing
iv. Collaborative (interprofessional) care (VF)
1. Must be treated immediately or pt will die
2. CPR/ ACLS begun immediately
3. Defibrillation
 Used to terminate ventricular fibrillation
 Unsynchronized shock delivered immediately
 CPR in progress, higher energy, 200-360 joules
 Simultaneously repolarizes all myocardial cells
4. Drug therapy (epinephrine, vasopressin)

5. Warning dysrhythmias
a. Bradycardia
b. Tachycardia
c. PVCs
d. Vtach
e. ST segment changes - indicates MI
f. Second degree AV block
i. Type I aka Mobitz I aka Wenckeback heart block
1. Risk factors. (2nd deg. Type I)
a. Certain drugs
i. Digoxin
ii. Beta blockers
b. Diseases such as CAD
c. MI or myocardial ischemia
2. Pathophysiology.(2nd deg. Type I)
a. Prolonged AV conduction time
b. Progressive lengthening of PR interval
c. Eventually a QRS complex is “skipped”
3. Clinical manifestations(2nd deg. Type I)
a. Usually transient and tolerated ok
b. Warning sign of more serious AV conduction problem that may
arise, such as complete heart block
4. Collaborative (interprofessional) care (2nd deg. Type I)
a. Symptomatic pt
i. Atropine to increase HR
ii. Temporary pacemaker, esp if pt has had MI
b. Closely monitor asymptomatic pt and have transcutaneous
pacemaker handy
ii. Type II aka Mobitz II
1. Risk factors. (2nd deg type II)
a. Rheumatic heart disease
b. CAD
c. Anterior MI
d. Drug toxicity
2. Pathophysiology. (2nd deg type II)
a. No progressive lengthening of PR interval
b. Usually a bundle branch is blocked
c. More serious than type I
3. Clinical manifestations (2nd deg type II)
a. Decreased CO
b. Hypotension
c. Myocardial ischemia
4. Collaborative (interprofessional) care
a. Permanent pacemaker
5. Complications (2nd deg type II)
a. Often progresses to third-degree AV block (complete heart
block)
6. Deadly dysrhythmias
a. Extreme bradycardia
b. Ventricular tachycardia (VT)
c. Ventricular fibrillation (VF)
d. Pulseless electrical activity (PEA)
e. Asystole
f. Third degree AV block aka complete heart block
i. Risk factors. (complete heart block)
1. Severe heart disease
a. CAD
b. MI
c. Myocarditis
d. Cardiomyopathy
2. Systemic diseases
a. Amyloidosis
b. Progressive systemic sclerosis (scleroderma)
3. Drugs
a. Digoxin
b. Beta blockers
c. Calcium channel blockers
ii. Pathophysiology.(complete heart block)
1. No impulses from atria are conducted to ventricles
2. Only ventricular beats are “escape” beats initiated by conduction cells in
the ventricles
3. Ventricular beats are not frequent enough to provide adequate CO
4. ECG
a. Atrial rate is normal sinus rate 60-100 bpm
b. Ventricular rate will depend on location of block
i. AV node: 40-60 bpm
ii. His-purkinje system: 20-40 bpm
c. P wave is normal shape
d. QRS
i. Normal shape if escape is initiated at bundle of His or
above
ii. Widened if escape is initiated below bundle of His
iii. Clinical manifestations(complete heart block)
1. Reduced CO leads to
a. Ischemia
b. HF
c. Shock
d. Syncope
iv. Collaborative (interprofessional) care (complete heart block)
1. Pacemakers
a. First, transcutaneous pacemaker
b. Then temporary transcutaneous pacemaker
c. Permanent pacemaker needed ASAP
2. Drugs to increase HR and support BP until pacemaker is in use
a. Epinephrine
b. Dopamine
 v. Complications(complete heart block)
1. Severe bradycardia
2. Asystole
3. You die.
g. Pulseless electrical activity (PEA)
i. Risk factors. (PEA)
1. Commonly appears after defibrillation
2. Usually caused by
a. Hypoxia
b. Hypovolemia
c. Metabolic acidosis
d. Hyperkalemia
e. Hypokalemia
f. Hypoglycemia
g. Hypothermia
h. Toxins such as drug overdose
i. Cardiac tamponade
j. Thrombosis (MI, PE)
k. Tension pneumothorax
l. Trauma
ii. Pathophysiology.(PEA)
1. Electrical activity shows on ECG but there is no mechanical heart activity
(it’s not pumping)
iii. Clinical manifestations(PEA)
iv. Collaborative (interprofessional) care (PEA)
1. CPR
2. Drugs such as epinephrine
3. Intubation
v. Complications(PEA)
1. Leads to death if not fixed
h. Asystole
i. Risk factors.(asystole)
1. End-stage heart disease
2. Prolonged cardiac arrest
ii. Pathophysiology.(asystole)
1. Total absence of ventricular electrical activity
2. There may be an occasional P wave
3. Monitor may show “blips”
4. No pulse, patient unresponsive
iii. Clinical manifestations(asystole)
1. Unresponsive
2. No pulse
3. Not breathing
 iv. Collaborative (interprofessional) care (asystole)
1. Requires immediate treatment or pt will die
2. NOT a shockable rhythm
3. Begin CPR/ ACLS measures
a. Drug therapy
i. Epinephrine
ii. Vasopressin
b. Intubation
v. Complications(asystole)
1. Poor prognosis - often leads to death

 Pace Makers:
 Indications:
o Bradycardias
o Heart blocks
o Tachyarrhythmias
o Atrial fibrillation with slow ventricular response
 Types:
o Temporary
o Fixed
o Demand
o AICD(P)
 Safety Precautions:
o Incision care
o Limited postop activity
o Routine monitoring, pulse checks
o No MRI, microwave OK
o ID card
o Defib pad placement
o Avoid welding equipment
o Avoid working on a running engine
o No MRIs
o Caution around generators, radio towers, or power plants
 Symptoms of pacemaker failure:
o Slow, irregular, or weak pulse
o Low blood pressure
o Dizziness or fainting
o Palpitations
o Signs of heart failure
7. Hypertension
a. Definition
i. Any of the following
1. Persistent systolic BP of 140 mmHg or more
2. Diastolic BP of 90 or more
3. Current use of antihypertensives
b. Risk factors (HTN).
i. Age - SBP rises with age, DBP may decrease
 ii. Alcohol use
iii. Tobacco use
iv. Diabetes mellitus - target organ disease is especially severe
v. Elevated serum lipids - linked development of atherosclerosis which increases
systemic vascular resistance (SVR) in turn increasing BP
vi. Excess dietary sodium
vii. Gender
1. In young adulthood and middle age - men are more prone
2. After 64, women are more prone
viii. Family history
ix. Obesity
x. Ethnicity - 2x more african americans affected than whites
xi. Sedentary lifestyle
xii. Socioeconomic status - lower status more prone
xiii. Stress
c. Pathophysiology (HTN).
i. Persistently increased SVR, which can occur in several ways
1. Defects in mechanisms that maintain normal BP
a. Water/ sodium retention
b. RAAS mechanism
c. Sympathetic nervous system (SNS)
2. Defects in metabolism as it pertains to
a. Glucose
b. Lipoproteins
c. Insulin
3. Endothelial dysfunction
d. Clinical manifestations (HTN) - called the “silent killer” because it is often asymptomatic
until serious complications occur (see below section on complications).
e. Collaborative (interprofessional) care (HTN).
i. Goals of collaborative care
1. Achieving and maintaining goal BP
a. Lower than 140/90 for people younger than 60
b. Lower than 150/90 for people over 60
2. Reducing cardiovascular risk
3. Reducing target organ disease
ii. Means of achieving goals
1. Lifestyle modifications
a. Weight reduction - 22lb weight loss can reduce SBP 5-20 mmHg
b. DASH eating plan
i. Fruits
ii. Veggies
iii. Low-fat dairy
iv. Beans
v. Whole grains
vi. Seeds
vii. Nuts
viii. Poultry
c. Dietary sodium restriction - may be enough to control BP in salt-
sensitive patients
 d. Physical activity
i. Moderate intensity 30 mins 5x/week
ii. Or vigorous intensity 20 mins 3x/week
iii. Plus 2 days muscle strengthening
iv. Balance and flexibility exercise recommended, esp. for
elderly
e. Avoid tobacco
f. Manage psychosocial risk factors
2. Drug therapy
a. Two means of reducing BP
i. Decreasing circulating blood volume
ii. Reducing SVR
b. Types of drugs used to treat HTN
i. Diuretics
1. Promote sodium and water excretion, reducing
plasma volume
2. Reduce vascular response to catecholamines
ii. Adrenergic-inhibiting agents - diminish SNS effects
1. Centrally acting - act on vasomotor center to
inhibit norepinephrine release
2. Peripherally acting - block adrenergic receptors
in heart and vessels, resulting in reduced HR
and vasoconstriction
iii. Direct vasodilators
iv. Calcium channel blockers - prevent movement of
calcium into cells, resulting in vasodilation and
decreased HR
v. Angiotensin-converting enzyme (ACE) inhibitors -
prevent angiotensin II from forming, preventing
vasoconstriction and the release of aldosterone
vi. Angiotensin II receptor blockers (ARBs) - prevent
angiotensin II from binding to its target cells, reducing
vasoconstriction
c. Most patients require more than one drug to manage their HTN.
f. Explain nursing care (HTN).
i. RNs role in caring for patient with hypertension
1. Develop and conduct screening.
2. Assess for risk factors and develop risk modification plans.
3. Teach about lifestyle management and drug use.
4. Evaluate effectiveness of lifestyle management and drug use in
decreasing BP to acceptable levels.
5. Teach about home BP monitoring, including correct use of home
monitors.
6. Make appropriate referrals, such as to dietitian or smoking cessation
program.
7. Monitor for complications as described below.
8. Assess pt with hypertensive crisis for evidence of target organ disease,
such as encephalopathy, renal insufficiency, cardiac decompensation.
9. Manage hypertensive urgency/ emergency: administering drugs,
evaluation of crisis resolution.
g. Nursing diagnoses (HTN).
i. Possible nursing diagnoses for hypertension
1. Ineffective health management r/t lack of knowledge of pathology,
complications, and management of hypertension
2. Anxiety r/t complexity of management regimen
3. Sexual dysfunction r/t side effects of antihypertensive medication
4. Risk for decreased cardiac tissue perfusion
5. Risk for ineffective cerebral tissue perfusion
6. Risk for ineffective renal perfusion
h. Nursing interventions (HTN).
i. See above section on nursing care.
i. Complications (HTN).
i. Since HTN often goes untreated in its early stages, it can progress to cause
severe conditions in multiple systems.
1. Hypertensive heart disease
a. Coronary artery disease (CAD)
b. Left ventricular hypertrophy (LVH)
c. Heart failure
2. Cerebrovascular disease
a. Cerebral atherosclerosis
b. Transient ischemic attack (TIA)
c. Stroke
d. Hypertensive encephalopathy
3. Peripheral vascular disease (PVD)
4. Nephrosclerosis
a. Especially prevalent among African Americans
b. Some degree of renal disease present even in minimally
hypertensive patients
c. Eventually may lead to renal failure
d. Laboratory indications
i. Albuminuria
ii. Proteinuria
iii. Microscopic hematuria
iv. Elevated creatinine and BUN
 5. Retinal damage
a. Easier to assess than other systems
b. Damaged retinal vessels indicates damage to heart, brain, and
kidneys
c. Severe retinal damage can result in blurred vision, retinal
hemorrhage, vision loss
8. Coronary artery disease (CAD)
a. Definition
i. Blood vessel disorder that falls under the category of atherosclerosis, soft
deposits in blood vessels that harden over time
ii. Aka arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart
disease coronary heart disease
b. Risk factors. (CAD)
i. Nonmodifiable
1. Increasing age
2. Gender - more common in men until 75 years old
3. Ethnicity - more common in white men
4. Genetic predisposition/ family history of heart disease
ii. Modifiable
1. Major
a. Elevated serum lipids
i. Highest risks associated with
1. Total cholesterol > 200 mg
2. Fasting triglyceride > 150 mg
3. LDL > 160 mg
4. HDL < 40 mg men < 50 mg women
b. Hypertension
c. Tobacco use
d. Physical inactivity
e. Obesity
2. Contributing
a. Diabetes, even when well-managed
b. Metabolic syndrome
i. Central obesity (waists larger than a certain
circumference)
ii. Hypertension
iii. Abnormal serum lipids
iv. Elevated fasting blood glucose
c. Psychologic states, particularly stress and depression
d. Elevated homocysteine
e. Substance abuse - meth, cocaine
c. Pathophysiology.(CAD)
i. Four stages
1. Endothelial damage
a. Several factors contribute to chronic endothelial injury
i. Hypertension
ii. Diabetes mellitus
iii. Hyperhomocysteinemia
iv. Tobacco use
 v. Infections
vi. Toxins
vii. Hyperlipidemia
b. Fatty streak
i. Lipids seep into the damaged area and begin to fill
smooth muscle cells
ii. Can occur by age 20
iii. Yellow appearance
c. Fibrous plaque
i. LDLs and growth factors from platelets stimulate smooth
muscle proliferation
ii. Arterial wall thickens and more lipids accumulate
iii. Collagen covers fatty streak and takes on a white or
greyish appearance
iv. Vessel lumen narrows, diminishing blood flow to tissues
d. Complicated lesion
i. Fibrous plaque ruptures
ii. Thrombus forms, further occluding artery, possibly
completely
d. Clinical manifestations (CAD)
i. Clinical signs do not appear until late in the disease’s progression.
ii. First symptom may be fatigue.
iii. Other signs/ symptoms
1. Angina
2. Dyspnea
3. Palpitations
4. Tachycardia
5. Weakness
6. Diaphoresis
7. Syncope
8. Nausea
e. Collaborative (interprofessional) care.(CAD)
i. Identify and manage high-risk individuals - through reducing modifiable risk
factors, those with non-modifiable risk factors can reduce their chances of
developing CAD
ii. Develop physical activity program
iii. Nutritional therapy
iv. Lipid-lowering drug therapy
1. Three categories
a. Drugs that restrict lipoprotein production
i. HMG-CoA reductase inhibitors (statins)
1. Inhibit cholesterol synthesis in liver
2. Increase hepatic LDL receptors
3. Overall effect
a. Small increase in HDL
b. Lower LDL
c. Lower triglycerides
4. Examples
a. atorvastatin (Lipitor)
b. rosuvastatin (Crestor)
c. simvastatin – muscle pain
**rhabdomyolysis**
d. MONITOR LFTs
 ii. Niacin
1. Interferes with LDL and triglyceride synthesis
2. Unpleasant side effects, such as flushing, and
GI upset
3. Overall effect
a. Increase HDL (best drug at this)
b. Lower LDL
c. Lower triglycerides
4. Example: niacin (Niaspan)
iii. ***Fibric acid derivatives
1. Aid removal of VLDLs (triglycerides)
2. Increase production of apolipoproteins
3. Overall effect
a. Lower triglycerides (best drugs for
this)
b. Increasing HDL (also good at this
compared to other drugs)
c. No effect on LDL
d. RASH, GI UPSET
e. INCREASE EFFECT OF WARFARIN
4. Examples
a. fenofibrate (Tricor)
b. gemfibrozil (Lopid)
b. Drugs that increase lipoprotein removal
i. Bile acid sequestrants
1. Converting cholesterol into bile in the liver and
excreting it in feces
2. GI symptoms
3. Interfere with drugs: beta-blockers, thiazide
diuretics,thyroid hormones, warfarin, and others
4. Overall effect: lower LDL
5. Examples
a. cholestyramine (Prevalite)
b. colestipol (Colestid)
ii. Proprotein convertase subtilisin/ Kexin 9 (PCSK9)
Inhibitors
1. Makes more LDL receptors available on liver
2. Overall effect: lower LDL
3. Examples
a. evolocumab (Repatha)
b. alirocumab (Praluent)
c. Drugs that decrease cholesterol absorption
i. Inhibit intestinal absorption of cholesterol
ii. Overall effect:
1. Lower LDL
2. Raise HDL
iii. Example: ezetimibe (Zetia)
 f.Nursing care (CAD)
i. Nursing diagnoses (CAD)
1. Possible nursing diagnoses
a. Risk for injury, MI, r/t decreased myocardial tissue perfusion
b. Activity intolerance r/t decreased myocardial tissue perfusion
c. Risk for noncompliance r/t adverse effects of medication regimen
d. Deficient knowledge r/t disease, risk factors, treatment, and
home care
ii. Nursing interventions (CAD)
1. Until CAD progresses to angina or MI, the main interventions are patient
education.
a. Health-promoting factors to reduce modifiable risk factors.
b. What drug regimen entails - importance of adherence, side
effects etc.
g. Complications (CAD)
i. Activity intolerance
ii. MI
iii. Death from MI
9. Angina
a. Definition
i. Chest pain caused by myocardial ischemia - when the heart muscle isn’t getting
enough oxygen
ii. Types
1. Chronic stable angina
a. Chest pain occurs intermittently over long period of time with
similar onset, duration, intensity of symptoms
b. Provoked by physical exertion, stress, emotional upset
c. Relieved by rest or nitroglycerin
2. Prinzmetal's angina - coronary artery spasm
3. Microvascular angina - small distal vessels occluded by atherosclerosis
4. Unstable angina
a. Chest pain that is new in duration, onset, or frequency, or occurs
at rest
b. Requires emergency medical attention
b. Risk factors (Angina)
i. Chronic stable angina - atherosclerosis is the main cause, so the same risk
factors apply (see above)
ii. Prinzmetal’s - often seen in pt with history of migraines, Raynaud’s phenomenon,
heavy smoking
iii. Microvascular - occurs most commonly in postmenopausal women
c. Pathophysiology. (Angina)
i. Chronic stable
1. Atherosclerosis narrows the coronary arteries.
2. Heart muscle isn’t able to get enough oxygen when
a. Oxygen demand increases
b. Oxygen supply decreases
ii. Prinzmetal’s
1. Caused somewhat randomly by coronary artery spasm, not physical
activity etc.
 2. Can occur independently of CAD
iii. Microvascular - atherosclerosis or spasm occurs in small distal branch vessels of
coronary microcirculation
iv. Unstable - may arise in someone with previous chronic stable angina, or may be
the first sign that presents of CAD for a patient (usually women)
d. Clinical manifestations (Angina)
i. Chronic stable angina
1. Chest pain or pressure, may radiate from chest
2. Ischemia indicated on 12-lead EKG by
a. ST segment depression
b. T wave inversion
ii. Prinzmetal’s
1. Angina
2. Transient ST segment elevation
iii. Microvascular
1. Prolonged angina, brought on by physical exertion
2. Positive stress test
3. Inconsistent response to nitrates
iv. Unstable
1. In pt with previous chronic stable angina, unstable has increased
frequency and provoked by no exertion
2. In women, symptoms are not always as direct as chest pain, and can
also include
a. Fatigue
b. Shortness of breath
c. Indigestion
d. Anxiety
e. Collaborative (interprofessional) care (Angina)
i. Chronic stable
1. Treatment aims
a. Increase O2 supply
b. Decrease O2 demand
2. Treatment approach
a. ABCDEF
i. A
1. Antiplatelet/ anticoagulant therapy
2. Antianginal therapy
3. ACE inhibitor/ ARB
ii. B
1. Beta blocker
2. BP control
iii. C
1. Cigarette cessation
2. Cholesterol/ lipid management
3. Calcium channel blockers
4. Cardiac rehab
iv. D
1. Diet/ weight management
2. Diabetes management
3. Depression screening
v. E
1. Education
2. Exercise
vi. F - flu vaccine
3. In addition to treatments to manage CAD, these therapeutic agents are
used for chronic stable angina:
a. Nitrates
i. First line -therapy
1. Mechanisms of action
a. Dilate peripheral blood vessels -
reduces O2 demand by reducing SVR,
preload, and increasing venous pooling
b. Dilate coronary arteries - increases O2
availability, but not as effective in
atherosclerotic arteries
b. ACE inhibitors and ARBs
i. Vasodilate and reduce blood volume
ii. Should be taken indefinitely for certain patients with
chronic stable angina
1. 40% ejection fraction or less
2. Diabetes
3. Hypertension
4. Chronic kidney disease
5. Or >40% EF AND one of the above
comorbidities
iii. Prevent/ reverse ventricular remodeling in pt with MI
c. Beta blockers
i. Reduce O2 demand by decreasing
1. Myocardial contractility
2. HR
3. BP
4. SVR
ii. Taken indefinitely by patients with chronic stable angina
and
1. LV dysfunction
2. Elevated BP
3. Have had an MI
iii. Absolutely contraindicated for pt with
1. Severe bradycardia
2. Acute HF
iv. Cautiously used for diabetics as can mask hypoglycemia
symptoms
d. Calcium-channel blockers
i. Used for chronic stable angina when beta blockers are
not appropriate or not working.
ii. Effects
1. Systemic vasodilation - reduces SVR
2. Decreased myocardial contractility
3. Coronary vasodilation
4. Decreased HR
iii. Potentiate digoxin - closely monitor serum levels when
both are prescribed
e. Sodium current inhibitor - ranolazine (Renexa)
 f. Drugs to prevent platelet aggregation are given for those with
stents
i. Unfractionated heparin (UH)
ii. Low-molecular weight (LMWH)
iii. Direct thrombin inhibitors
iv. Glycoprotein IIb/IIIa inhibitors
v. After PCI, pt treated indefinitely with aspirin (indefinitely)
and clopidogrel for at least 12 months until intima grows
over stent
4. Diagnostic tests
a. Certain studies are implemented in patients with suspected CAD
and chronic stable angina patients with changes in their angina
i. Chest x-ray to reveal
1. Cardiac enlargement
2. Aortic calcifications
3. Pulmonary congestion
ii. 12-lead ECG
iii. Lab tests such as CRP, lipid profile
iv. Echocardiogram can detect resting LV wall abnormalities
v. Exercise stress (w/ or w/out echo)
vi. Pharmacologic stress test may be used for pt with
physical limitations
vii. Nuclear imaging
viii. Cardiac catheterization can determine if blockage is
amenable, resulting in subsequent procedures
1. Coronary revascularization
2. Percutaneous coronary intervention (PCI)
a. Balloon angioplasty - a balloon is
inflated in the middle of a blockage,
compressing it against the artery wall
and opening up the area for increased
bloodflow
b. Stent - mesh placed inside vessel to
keep it patent after balloon pushes all
the gunk to the sides
ii. Prinzmetal’s - controlled with SL NTG and calcium-channel blockers
f. Nursing care. (Angina)
i. Assessment of pt with chest pain
1. PQRST
a. P - precipitating events: what actions or activities brought on the
pain/ discomfort?
b. Q - quality of pain: What does it feel like? Ex. pressure, dull,
aching, tight, squeezing, heaviness
c. R - region and radiation: Where is the pain located, and does it
radiate to other areas?
d. S - severity of pain: 10 scale
e. T - timing: When did it first begin? Has it changed since the first
event?
ii. Nursing diagnoses. (Angina)
 iii. Nursing interventions. (Angina)
1. Teach risk reduction.
2. Drug teaching
a. Nitroglycerin use
i. Treat stable angina with 1 tablet or spray every 5 mins.
If it does not subside, seek emergency medical attention.
ii. Store pills in dark container away from light and heat
iii. Replace pills every 6 months once opened
iv. May cause hypotension
v. Can take prophylactically before activity
vi. Report increase in frequency or intensity of angina to
HCP
vii. Can cause headache - tylenol is ok to treat
b. Calcium channel blocker - teach dig. toxicity s/s in pt taking both
3. When pt presents with angina
a. Position pt upright
b. Apply supplemental O2
c. Take vitals
d. Obtain 12-lead ECG
e. Provide pain relief with NTG and opioids if necessary
f. Asses heart and lung sounds
g. Provide calm caring approach to reduce anxiety
h. Have pt rate and describe pain before and after treatment
measures
4. Cardiac cath
a. Pt allergic to iodine needs pre-procedure cortisol
b. Chronic kidney disease patients need lots of hydration pre- and
post-procedure
c. Monitor kidney function closely after procedure.
iv. Complications (Angina)
10. Myocardial infarction (MI)
a. Definition - abrupt blockage of blood flow through a coronary artery by platelet
aggregation leads to irreversible necrosis (after 20 minutes of ischemia) of the heart
muscle
b. Risk factors (MI) - almost always linked with CAD
c. Pathophysiology. (MI)
i. A coronary artery becomes blocked by an aggregation of platelets, related to
atherosclerosis
ii. Blood flow is occluded and the distal tissues are starved of oxygen and begin to
necrose.
iii. Usually occurs in left ventricle, and affected area depends on which coronary
artery was blocked
iv. Post MI event
1. Inflammatory processes kick in to help clean up necrotic tissue
2. In 10-14 days, necrotic debris is cleared and scar tissue is formed, but
still weak
d. Clinical manifestations (MI)
i. ECG changes in STEMI MI
1. Elevated S-T interval
 2. T-wave inversion
ii. Pain
1. Unlike any other pain
2. Can be described as crushing, constricting, burning, tight, heavy,
pressure
3. Usually occurs substernally or epigastric and may radiate to jaw and arm
 iii. SNS symptoms from catecholamines released from dying heart muscle
1. Diaphoresis
2. Increased BP and HR
3. Vasoconstriction of peripheral blood vessels
4. Skin may be ashen, cool, and clammy
iv. Nausea/ vomiting
v. Fever due to increased systemic inflammatory process caused by death of heart
cells
e. Collaborative (interprofessional) care (MI)
i. Diagnostic tests
1. ECG
a. Differentiates between STEMI and NSTEMI
i. STEMI (complete blockage)
1. Elevated ST interval
2. Inverted T wave
3. Q wave pathology
ii. NSTEMI (incomplete blockage)
1. No elevated ST interval, instead may have ST
depression
2. T wave inversion
3. No pathologic Q waves
b. Serum cardiac biomarkers
i. Troponins (I and T)
1. Best cardiac-specific biomarkers to indicate MI
2. Start to elevate 4-6 hours after onset
3. Peak at 10-24 hours
ii. CK-MB
1. Cardiac specific
2. Helps quantify myocardial damage
3. Starts to elevate 6 hours after MI
4. Peaks at 18 hours
5. Returns to normal with 24 hours
iii. Myoglobin
1. Increases, peaks, and returns to normal within
3-15 hours
2. Released by damages cardiac cells but not
specific enough to heart to be much use
2. Coronary angiography
a. STEMI pt must undergo within 90 minutes of MI (or receive
thrombolytics in 30 minutes if PCI not available)
b. UA and NSTEMI pt should undergo within 12-72 hours
3. If ECG and biomarkers are not confirming MI, pharmacologic stress may
be done.
ii. Emergency care
1. STEMI pt
a. Reperfusion therapy started ASAP
i. Emergent PCI (preferred)
1. Should undergo w/in 90 mins
2. Stent inserted
3. IABP implemented in cases of severe LV
dysfunction
4. Prevents need for CABG in most patients
 5. Advantages over CABG
a. Not a surgical intervention
b. Only local anaesthesia used
c. Pt ambulatory shortly after procedure
d. Shorter hospital stay
e. Shorter recovery time
ii. Thrombolytic therapy
1. Administered in facilities that lack PCI
capabilities
2. Goal is to administer w/in 30 mins
3. All thrombolytics given IV
4. Agents break up clot causing blockage and
restore bloodflow to distal tissues
5. Condraindicated for many pt due to high risk of
bleeding. Some examples
a. Recent major surgery
b. Stroke w/in 3 months
c. Severe hypertension
d. Pregnancy
e. Suspected aortic dissection
f. Other cerebral/ intracranial conditions
such as neoplasm, hemorrhage, etc.
6. Indicate effectiveness when
a. ECG returns to normal (no elevated ST
interval)
b. Chest pain resolved
c. Presence of serum biomarkers as
circulation is restored to necrotic tissue
b. Dual antiplatelet therapy
i. Aspirin
ii. Clopidogrel (Plavix)
c. Heparin
2. UA/ NSTEMI pt
a. Dual antiplatelet therapy and heparin, as described above
b. Cardiac cath/ PCI once pt is stable
iii. Coronary surgical revascularization
1. For patients that have contraindications to PCI and thrombolytics or
didn’t respond well
2. Can be emergency or scheduled
3. Types
a. Traditional coronary artery bypass graft (CABG)
i. Artery or vein “harvested” from elsewhere in the body is
attached to aorta and connects to area beyond blockage
to restore bloodflow
1. Internal mammary/ thoracic artery (IMA/ ITA)
a. Most common and most successful
choice
b. Already attached to left subclavian
artery so only needs to be clipped on
one end and reattached to the coronary
circulation
 2. Saphenous veins from leg
a. Not as successful
b. Prone to diffuse intimal hyperplasia,
contributing to future stenosis and
occlusion
c. Use of antiplatelet and statins after
surgery improves patency
3. Radial artery
a. Muscular and prone to spasm - treated
with calcium channel blockers and
nitrates perioperatively to control
b. Common side effects - paresthesia,
impaired sensation
c. Rare but serious side effects - hand
ischemia, wound infection
ii. Surgical procedure requires
1. Sternotomy - opening of chest cavity
2. Cardiopulmonary bypass (CPB) - machine that
diverts blood from heart, oxygenates it and
returns it to body
b. Minimally invasive direct coronary bypass (MIDCAB)
i. Does not require sternotomy and bypass machine
ii. Several small incisions are made through the intercostal
spaces.
iii. Scopes and robots stabilize the operative site of the
heart and clip and reattach the IMA.
c. Off-pump coronary artery bypass (OPCAB)
i. Requires sternotomy
ii. Does not use bypass; heart is stabilized mechanically
iii. Results in less blood loss, less renal dysfunction, less
post op afib, fewer neurologic complications
iv. For pt with multiple comorbidities who must avoid CABG
d. Robotic or totally endoscopic coronary artery bypass
(TECAB)
i. Can be done with or without CPB
ii. Used for limited bypass grafting
iii. Benefits
1. Increased precision
2. Small incisions
3. Decreased blood loss
4. Less pain
5. Shorter recovery time
e. Transmyocardial laser revascularization
i. For pt with advanced CAD who are not candidates for
CABG and who have persistent angina even with
maximum meds
ii. High-energy laser creates channels in heart muscle to
bring bloodflow to ischemic areas
4. Drugs used specifically to treat acute coronary syndrome
a. IV nitroglycerin
i. Initial treatment for pt with ACS
ii. Dilates vessels, reducing preload and afterload and
increasing O2 supply to heart
 b. Morphine
i. For pain unrelieved by NTG
ii. Vasodilates and decreases cardiac workload - reduces
contractility, BP, and HR
iii. Can reduce anxiety and fear
c. Beta blockers - decrease myocardial O2 demand by reducing
HR, BP, contractility
d. ACE inhibitors and ARBs
i. Started w/in 24 hours and continued indefinitely for pt
with MI, HF, or EF <40%
ii. Help prevent ventricular remodeling
iii. Help slow progression of HF
e. Antidysrhythmic drugs
f. Lipid-lowering drugs - ACS pt should receive lipid-lowering
therapy indefinitely
g. Stool softeners - for MI patients to prevent straining and vagal
stimulation which can result in bradycardia and provoke
dysrhythmias
5. Nutritional therapy
a. NPO until stable
b. Advance as tolerated to low-salt, low-cholesterol, low-fat diet
f. Nursing care. (MI)
i. Nursing diagnoses. (MI)
1. Decreased cardiac output r/t altered contractility and altered heart rate
and rhythm
2. Acute pain r/t an imbalance between myocardial O2 supply and demand
3. Anxiety r/t perceived or actual threat of death, pain, and/or lifestyle
change
4. Activity intolerance r/t general weakness secondary to decreased cardiac
output and poor lung and tissue perfusion
5. Ineffective health management r/t lack of knowledge of disease
processes, risk factor reduction, rehabilitation, home activities, and
medications
ii. Nursing interventions. (MI)
1. When pt first presents to emergency department (ED)
a. 12-lead ECG
b. O2 by nasal cannula or non-rebreather
c. IV access
d. SL NTG if not previously administered
e. 162-325mg aspirin if not previously administered
f. High-dose atorvastatin (Lipitor)
2. PCI pt
a. Before procedure
i. Check sensitivity to contrast media
ii. NPO 6-12 hours before procedure
iii. Explain the procedure
1. Local anaesthesia at insertion site
2. Catheter placement
3. Flushed feeling due to dye
 4. Fluttering of heart when catheter enters
5. Possible need to cough or deep breathe at
points during the procedure
6. ECG monitoring
iv. Give sedative and other ordered drugs
b. After procedure
i. Monitor for recurrent angina
ii. Frequently assess circulation to extremity used for
catheter insertion.
1. Peripheral pulses
2. Color
3. Sensation
iii. Observe insertion site for hematoma/ bleeding.
iv. Use compression device on insertion site if necessary to
stop bleeding.
v. Monitor vitals and ECG for
1. Hypo/hypertension
2. Dysrhythmias
3. Signs of pulmonary emboli (e.g. difficulty
breathing)
vi. Make sure pt is following rest orders.
3. CABG pt
a. Ongoing, intensive post-procedure monitoring in ICU via
i. Pulmonary artery catheter - hemodynamic monitoring
(ex. CO2)
ii. Arterial line - continuous BP monitoring
iii. Pleural and mediastinal chest tubes - chest drainage
iv. Continuous ECG monitoring
v. Endotracheal tube connected to vent
vi. Epicardial pacing wires - emergency pacing of heart
vii. Urinary catheter - monitor output
viii. NG tube - gastric decompression
b. Focus care on
i. Assess for bleeding such as at chest tube and incision
sites
ii. Hemodynamic monitoring
iii. Checking fluid status
iv. Replacing blood and electrolytes as needed
v. Restoring temperature such as with warm blankets
vi. Surgical site care (e.g. radial artery harvest site)
vii. Preventing DVT
viii. Preventing respiratory complications - e.g. use
spirometer, splint while coughing etc.
ix.
4. Thrombolytic therapy
a. Start several IVs prior to administering, as well as other invasive
procedures if they are indicated
b. Note time that therapy begins and monitor pt during and after
c. Assess
 i. Heart rhythm
ii. Vitals
iii. Pulse ox
iv. Heart and lung sounds
v. Changes in neuro status as can indicate cerebral
bleeding
vi. IV and other sites that may have increased bleeding and
need pressure dressing or ice packs
 vii. S/s of major bleeding
1. Drop in BP
2. Increase in HR
3. Sudden mental status change
4. Blood in urine or stool
5. Administering drugs for ACS
a. IV nitroglycerin - monitor BP closely for hypotension
b. Morphine - monitor for bradypnea and hypotension which are
especially harmful in cases of ischemia and infarction
6. Once pt is stable, priority interventions focus on
a. Pain assessment and relief
b. Physiologic monitoring - ECG
c. Promoting rest and comfort
d. Reducing anxiety and stress
e. Understanding emotional and behavioral reactions
7. Teaching for pt when the leave hospital should include
a. Most importantly
i. S/s of angina and
ii. MI and what to do when they occur (NTG, call 911)
iii. Importance of gradual, progressive resumption of activity
b. Also
i. Identification of risk factors and plan to reduce them
ii. A&P of heart
iii. Cause and effect of CAD
iv. Definition of terms such as CAD, angina, MI, heart
failure
v. Reasons for tests and treatments
vi. Anticipatory guidance - what to expect for the recovery
process
vii. Resumption of work, physical and sexual activity
viii. Measures to promote recovery and health such as
cardiac rehab program
g. Complications (MI)
i. Ventricular remodeling
1. Scarred area cannot pump the same way healthy tissue can, so the heart
tries to compensate by growing larger in other areas
2. Can lead to development of HF, esp in pt with atherosclerosis in other
coronary arteries or anterior MI
3. ACE inhibitors limit this process.
ii. Dysryhmias
1. Occur in 80-90% of patients with MI
2. Most common causes of death before patient gets to hospital
a. Ventricular tachycardia (VT)
b. Ventricular fibrillation (VF)
iii. Heart failure
1. Right or left side of the heart fails to pump effectively so that all the blood
gets where it needs to go
2. Signs/ symptoms
a. Left-sided HF
i. Dyspnea
ii. Restlessness
iii. Agitation
iv. Slight tachycardia
v. Pulmonary congestion as seen on chest x-ray
vi. S3 or S4 heart sounds
vii. Crackles in lungs
viii. Paroxysmal nocturnal dyspnea (PND)
ix. Orthopnea
b. Right-sided HF
i. Jugular vein distention
ii. Hepatic congestion
iii. Lower-extremity edema
iv. Cardiogenic shock
1. Inadequate supply of O2 and nutrients to tissues resulting from
a. Severe LV failure
b. Papillary muscle rupture
c. Ventricular septal rupture
d. LV free wall rupture
e. Right ventricular infarction
2. Often results in death
3. Treated aggressively
a. Control dysrhythmias
b. Intraaortic balloon pump (IABP) therapy
c. Vasoactive drugs to support contractility
v. Papillary muscle dysfunction or rupture
1. Infarcted area includes papillary muscle
2. Causes immediate and massive mitral regurgitation
3. Already-damaged LV further stressed as blood fills ventricle
4. CO plummets
5. Requires rapid treatment
a. Nitroprusside to reduce afterload
b. Emergency surgery to repair or replace mitral valve
vi. Left ventricular aneurysm
1. Part of infarcted heart wall becomes thin and bulges out
2. Can result in HF, dysrhythmias, angina
3. Can rupture and kill the person, or can hide emboli for later
4. Anticoagulation therapy in store if not contraindicated
vii. Ventricular septal well rupture and left ventricular free wall rupture
1. Both rare but super deadly
2. Ruptures cause HF and cardiogenic shock
3. Requires immediate treatment
4. More frequently seen in patients with first MI, pt with anterior MI, older
adults, and women
 viii. Pericarditis
1. Inflammation of pericardium
2. Causes pain distinct from MI pain
3. Can auscultate friction rub
4. Treated with high doses of aspirin
ix. Dressler syndrome
1. Pericarditis and fever that develop 1-8 weeks after MI
2. Possible autoimmune reaction to necrotic heart muscle
3. Chest pain, fever, malaise, pericardial friction rub, arthralgia
4. Treated with high-dose aspirin
x. Complications that can result from PCI
1. Abrupt closure from coronary artery dissection
2. Vascular injury at insertion site
3. Acute MI
4. Stent embolization
5. Coronary spasm
6. Dye allergy
7. Renal compromise
8. Bleeding
9. Infection
10. Stroke
11. Emergent CABG
xi. Post-CABG complications
1. Systemic inflammation
2. Bleeding and anemia from RBC and platelet damage
3. Fluid and electrolyte imbalances
4. Hypothermia
5. Infection
11. Congestive heart failure (CHF)
a. Definition - heart is unable to provide sufficient blood to meet O2 needs of tissues and
organs
b. Risk factors.(CHF)
i. Primary risk factors/ causes
1. Hypertension*
2. CAD*
3. Rheumatic heart disease
4. Congenital heart defects
5. Pulmonary hypertension
6. Cardiomyopathy
7. Hyperthyroidism
8. Valvular disorders
9. Myocarditis
ii. Comorbidities that contribute to development of HF
1. Diabetes
2. Metabolic syndrome
3. Advanced age
4. Tobacco use
5. Vascular disease
 iii. Genetic mutations related to
1. CAD
2. Hypertension
3. Cardiomyopathy
c. Pathophysiology.(CHF)
i. Decreased ventricular function and subsequent HF caused by changes in
1. Preload
2. Afterload
3. Myocardial contractility
4. Heart rate
ii. Left-sided heart failure
1. More common than right-sided
2. Caused by inability of LV to
a. Empty adequately during systole
b. Or fill adequately during diastole
3. Types
a. Systolic failure aka heart failure with reduced ejection fraction
(HFrEF)
i. Heart is inefficient as a pump - LV can’t generate
enough force to push adequate amounts of blood
towards and through aorta
ii. More common in men
iii. EF < 45%, may be as low as 5-10% (normal value is 55-
60%)
iv. Possible causes of systolic failure
1. Impaired contractile function, such as from MI
2. Increased afterload, such as from hypertension
3. Cardiomyopathy
4. Mechanical abnormalities, such as valvular heart
disease
v. Over time
1. Heart muscle weakens
2. LV dilates and hypertrophies
3. Fluid backs up through left atrium and into lungs,
causing pulmonary congestion and edema
b. Diastolic failure aka heart failure with preserved ejection
fraction (HFpEF)
i. Ventricles are stiff and can’t fill adequately
ii. EF is w/in normal parameters but only because the total
ventricle fill is reduced, so even though it is also ejecting
an inadequate amount of blood, the ratio is “normal”
iii. Hypertension is main cause
iv. Other risk factors
1. Female
2. Old
3. Diabetes
4. Obese
v. End result is same as HFrEF: pulmonary congestion
c. Mixed systolic and diastolic failure - seen in dilated
cardiomyopathy (ventricles dilate and thin and are unable to
relax)
iii. Right-sided heart failure
1. RV fails to pump effectively
2. Fluid backs up into venous system, causing
a. Peripheral edema
b. Hepatomegaly
c. Splenomegaly
d. Ascites
e. Jugular venous distention (JVD)
3. Causes
a. Most common = left-sided HF: fluid backed up into lungs creates
increased pressure for RV to overcome and eventually it fails
b. RV infarction
c. Pulmonary embolism
d. Cor pulmonale - RV dilation and hypertrophy caused by
pulmonary disease
iv. Compensatory mechanisms - mechanisms used by overloaded heart to try to
maintain cardiac output when ventricles are failing
1. Neurohormonal responses
a. Two responses
i. RAAS
1. As blood flow decreases to kidneys,
juxtaglomerular apparatus releases renin in
attempt to bring more blood to the kidneys via
a. SNS activation to increase BP and HR
b. Release of aldosterone from adrenal
cortex to retain sodium and water
c. Increased peripheral vasoconstriction
d. Stimulation of pituitary gland to release
ADH
2. Ends up overloading the heart even more and
further reducing heart’s ability to circulate blood
to the organs
ii. Sympathetic nervous response
1. Catecholamines (epinephrine and
norepinephrine) are released in response to
inadequate cardiac output
2. Effects
a. Increased peripheral vasoconstriction
b. Increased HR
c. Increased contractility
3. Beneficial at first but counterproductive in long
run as they increase workload, preload, and O2
demand on failing heart
b. Cause ventricular remodeling
i. Large, abnormally-shaped contractile cells
ii. Increased ventricular mass impairs contractility and
increases O2 demand
iii. Risk factor for life-threatening dysrhythmias and SCD
2. Dilation
 a. Ventricles stretch to accommodate increased volume
b. Initially increased preload results in stronger contraction (Frank-
Starling law), increasing CO
c. Eventually fibers get overstretched and can’t contract effectively
and CO is reduced
3. Hypertrophy
a. Heart muscle strain and overwork bulks up the muscle of the
heart wall
b. Initially provides more contractile power and increases CO
c. Contractility can’t maintain over time
d. Increased muscle mass requires more O2 and compresses
coronary vessels with its added bulk
e. Prone to dysrhythmias
v. Counterregulatory mechanisms
1. Counteract the compensatory mechanisms
2. ANP/BNP
a. Hormones release from heart in response to increased blood
volume in heart
b. Effects
i. Increased GFR and diuresis
ii. Excretion of sodium (natriuresis)
iii. Inhibits aldosterone and renin secretion
iv. “Interferes” with ADH release
3. Nitric oxide and prostaglandins
a. Released by vascular endothelium
b. Relax arterial smooth muscle, which vasodilates and reduces
afterload
vi. Compensated HF - compensatory mechanisms are able to maintain CO
adequate to perfuse tissues
vii. Decompensated HF - compensatory mechanisms cannot maintain CO adequate
to perfuse tissues
d. Clinical manifestations (CHF)
i. Acute decompensated heart failure (ADHF)
1. Sudden onset of s/s of HF and requires urgent medical care
2. Progression
a. LV fails causing increased pulmonary pressure
b. If lymphatic vessels fail to accommodate, interstitial edema
occurs in lungs
c. Pt becomes tachypneic
d. Alveoli lining cells are disrupted, and RBCs move into alveoli
causing alveolar edema
e. Alveoli become flooded with fluid, reducing PaO2 and increasing
PaCO2
f. Pulmonary edema
i. Life-threatening
ii. Lungs fill with serosanguinous fluid
iii. Usually caused by left-sided HF secondary to CAD
iv. Signs/ symptoms
 1. Dyspnea and orthopnea (can’t breathe laying
down)
2. JVD
3. Anxious, pale, cyanotic
4. Cold clammy skin (due to vasoconstriction from
SNS)
5. RR >30
6. Wheezing and coughing, possibly with light-pink
sputum
7. Rales/ crackles breath sounds
8. S3 and S4 heart sounds
9. Rapid HR
3. 4 categories based on whether or not the pt has volume overload (wet)
and/or adequate perfusion (warm)
a. Dry-warm - no congestion, adequate perfusion
b. Wet-warm - congestion, adequate perfusion
c. Dry-cold - no congestion, inadequate perfusion
d. Wet-cold - congestion, inadequate perfusion
ii. Chronic heart failure
1. Definition
a. Progressive worsening of ventricular function
b. Ventricular remodeling that arises from chronic neurohormonal
activation
c. Signs and symptoms depend on pt age and type and extent of
HF
i. Right-sided heart failure
1. Signs
a. RV heaves
b. Murmurs
c. JVD
d. Peripheral edema
e. Weight gain
f. Increased HR
g. Hepatomegaly
2. Symptoms
a. Fatigue
b. Anxiety and depression
c. Right upper quadrant pain
d. Anorexia and GI bloating
e. Nausea
ii. Left-sided heart failure
1. Signs
a. LV heaves
b. Pulsus alternans (alternating strong and
weak pulses)
c. Increased HR
d. PMI displaced inferiorly and laterally
e. Decreased O2 and increased CO2
f. Crackles
 g. S3 and S4
h. Pleural effusion
i. Mental status changes
j. Restlessness, confusion
2. Symptoms
a. Weakness/ fatigue
b. Anxiety/ depression
c. Dyspnea
d. Paroxysmal nocturnal dyspnea -
waking in a panic struggling to breathe
e. Orthopnea
f. Dry, hacking cough
g. Nocturia
h. Pink frothy sputum
e. Collaborative (interprofessional) care (CHF)
i. Diagnostics
1. Can be difficult to diagnose - tests are aimed at determining underlying
cause
2. Diagnostics differ slight for ADHF and chronic HF
a. Both
i. History and physical examination
ii. Determination of underlying cause
iii. Serum chemistries, cardiac biomarkers, BNP, liver
function, thryoid function, CBC, lipid profile, kidney
function, urinalysis
iv. Chest x-ray
v. 12-lead ECG
vi. Echo helps determine EF
vii. Nuclear imaging
viii. Cardiac cath
b. ADHF
i. Measurement of LV function
ii. Hemodynamic monitoring
iii. Endomyocardial biopsy in some patients
c. Chronic HF
i. Exercise stress test
ii. 6-min walk test
iii. Sleep studies for some patients
ii. Treatment of Acute Decompensated Heart Failure (ADHF)
1. Unstable patients go to ICU
a. Heart rhythm and O2 sat monitored continuously
b. Vitals and urine output checked hourly
c. May have hemodynamic monitoring
d. Supplemental O2 administered
e. May need BiPAP
2. Stable pt
a. Telemetry or step-down unit
b. Assess vitals, pulse ox, etc., every 4 hours
c. Record I&O and daily weights to evaluate fluid status
 3. Ultrafiltration (UF) aka aquaphoresis
a. For pt with volume overload
b. Removes excess salt and water to reduce fluid volume without
changing the tonicity of the blood
4. Circulatory assist devices
a. Intraaortic balloon pump therapy (IABP) - uses counterpulsation
to increase coronary blood flow to heart muscle and decrease
workload
b. Ventricular assist devices (VAD) - mechanical pump surgically
implanted that pumps blood from LV to aorta
5. Drug therapy
a. Diuretics - to reduce fluid volume and therefore preload
b. Vasodilators - reduce afterload and preload
c. Morphine - dilates pulmonary and systemic vessels and reduces
dyspnea and anxiety
d. Positive inotropes - increase strength of contraction, but also
increase O2 demand and so are only for short-term use in pt
who haven’t responded to the above drugs
iii. Chronic Heart Failure
1. Main goals of treatment
a. Reduce symptoms
i. Supplemental O2
ii. Rest and reduced activity
b. Improve ventricular function
i. Implantable cardioverter defibrillator (ICD):
 Indicated for persistent life-threatening
arrhythmias
 Reduces incidence of cardiac arrest and sudden
death
 Detects dangerous rhythms and automatically
delivers low energy shock
ii. Cardiac resynchronization therapy (CRT) - leads placed
into heart to ensure ventricles pump at the same time
c. Improve quality of life - cardiac rehab programs
d. Preserve target organ function
e. Reduce mortality and morbidity
2. Drug therapy
a. Diuretics
b. RAAS inhibitors
i. ACE inhibitors
ii. ARBs
iii. Combo therapy
iv. Aldosterone antagonists (e.g. aldactone)
c. Beta-blockers
d. Vasodilators
e. Positive inotropes (e.g. digitalis)
i. Increases strength of contraction, reduces HR
ii. Watch out for hypokalemia as it can hasten dig toxicity;
hyperkalemia inhibits its action
 f. Cardiac sinus node inhibitor - ivabradine (Corlanor) reduces HR
3. Nutritional therapy
a. Salt intake must be reduced to 2g/ day.
b. Fluid restrictions implemented for pt with moderate to severe HF
and renal insufficiency - 2L/day
f. Nursing care.(CHF)
i. Based on these principles
1. HF is progressive disease and treatment plans are established along
with quality-of-life goals
2. Symptom management is controlled by patient with self-management
tools (daily weights, adhering to drug regimens, diet, and exercise)
3. Salt, and at times, water must be restricted
4. Energy must be conserved
5. Support systems are essential to the success of the entire treatment plan
ii. Nursing diagnoses.(CHF)
1. Impaired gas exchange r/t increased preload and alveolar-capillary
membrane changes
2. Decreased cardiac output r/t altered contractility, altered preload, and/or
altered stroke volume
3. Excess fluid volume r/t increased venous pressure and decreased renal
perfusion secondary to heart failure
4. Activity intolerance r/t imbalance between O2 supply and demand
secondary to cardiac insufficiency and pulmonary congestion
iii. Nursing interventions.(CHF)
1. See above section on treatment of ADHF
2. For pt with dyspnea
a. Bed in high Fowler’s to increase thoracic capacity
b. Legs horizontal on bed or dangling to reduce venous return to
heart
3. Provide supplemental O2
4. Anxiety reduction
5. Teaching
a. Dietary therapy
b. Activity program
c. Ongoing monitoring - know signs and symptoms of worsening
condition
d. Health promotion such as recommended vaccines
e. Rest
f. Drug therapy
g. Complications (CHF)
i. Pleural effusion - fluid builds up in pleural cavity, making it painful and difficult to
breathe
ii. Dysrhythmias - esp at risk for atrial dysrhythmias, but both atrial and ventricular
dysrhythmia risk is increased, along with thrombi formation and risk of emboli
iii. Left-ventricular thrombus - forms from reduced CO and enlarged LV
iv. Hepatomegaly which can lead to cell death, fibrosis, and cirrhosis
v. Renal failure from decreased perfusion

Vascular Disorders
12. Peripheral arterial disease (PAD)
a. Definition
i. Thickening of artery walls in upper and lower extremities
ii. Results in progressive narrowing of arteries
b. Risk factors.(PAD)
i. Major risk factors
1. Tobacco use*
2. Chronic kidney disease
3. Diabetes
4. Hypertension
5. Hypercholesterolemia
ii. Risk factors compounded when pt is
1. African-American
2. Female
iii. Other risk factors
1. Elevated CRP
2. Family history
3. Hypertriglyceridemia
4. Increasing age
5. Sedentary lifestyle
6. Stress
c. Pathophysiology.(PAD)
i. Cholesterol and lipids deposit within arterial wall
ii. Intima and media (innermost and middle layer) of arterial walls become thicker
iii. Artery narrows and there is less space for blood to flow through
iv. Likely caused by inflammation and endothelial injury
v. Typically affects
1. Coronary arteries
2. Carotid arteries
3. Arteries in lower extremities
d. Clinical manifestations(PAD)
i. Symptoms appear when arteries are 60-75% blocked
1. Intermittent claudication - ischemic muscle pain in legs experienced
during exercise and relieved by rest
2. Paresthesia - numbness/ tingling in toes or feet
3. Peripheral neuropathy - shooting or burning pain in extremity esp
common in diabetics
4. Rest pain
a. Occurs commonly in toes and feet
b. Blood flow is insufficient to meet metabolic demands of the
tissues
c. Made worse by elevation, and better by lowering limb
5. Critical limb ischemia (CLI)
a. Characterized by one of the following
i. Chronic ischemic rest pain for more than 2 weeks
ii. Arterial leg ulcers
iii. Gangrene of the leg
b. Pt with certain comorbidities are at particular risk
i. Diabetes
ii. Heart failure
iii. History of stroke
ii. Appearance of affected extremity
1. Skin
a. Thin
b. Shiny
c. Taut
d. Hair loss
2. Pulses diminished or absent
3. Elevation pallor - extremity becomes pale when elevated
4. Dependent rubor - extremity becomes red when lower than heart
e. Collaborative (interprofessional) care (PAD)
i. Diagnostics
1. Doppler ultrasound to map blood flow
2. Segmental blood pressures taken at different points in the leg
3. Ankle-brachial index (ABI)
a. Divide ankle systolic BP by highest brachial systolic BP
b. Normal range: 0.9-1.4
c. <0.9 indicates PAD
 ii. Risk factor modification = first treatment goal
1. Tobacco cessation
2. Diabetes management
3. Lipid and hypertension management via diet and drugs
iii. Antiplatelet agents to reduce risk of CVD events (aspirin, Plavix)
iv. Exercise therapy
1. 30 mins/ day, 3x/week for 3 months
2. Especially important in women who have greater functional decline with
PAD than men
3. Patients that are more active tend to have better survival rates
v. Nutritional therapy to maintain or lower BMI to 25
vi. Caring for leg with critical limb ischemia
1. Bypass surgery is optimal to restore blood flow.
2. Percutaneous transluminal angioplasty is an option when bypass is not.
3. Patients who are not candidate for either above procedure are treated
with prostanoids (ex. iloprost)
4. Conservative management
a. Protect from trauma
b. Decrease pain
c. Prevent/ control infection
d. Improve perfusion
5. Interventional radiology catheter-based procedures
a. Alternative to surgery
b. Performed in cath lab with catheter inserted into femoral artery
c. Types of procedures
i. Percutaneous transluminal angioplasty (PTA) - squish
plaque to sides of arteries with inflated balloon
ii. Stents - holds squished plaque in place
iii. Atherectomy - removing plaque with drill or laser
iv. Cryoplasty - cold therapy to reduce smooth muscle cell
activity in vessel wall, limiting restenosis
6. Surgery
a. Bypass - with vein from own body or synthetic graft
b. Endarterectomy - opening artery and removing plaque
c. Patch graft angioplasty - opening artery, removing plaque, and
sewing patch to widen the lumen
d. Amputation
f. Nursing care.
i. Possible nursing diagnoses.(PAD)
1. Ineffective peripheral tissue perfusion r/t deficient knowledge of
contributing factors (? this one seems weird)
2. Activity intolerance r/t imbalance between O2 supply and demand
3. Chronic pain r/t ischemia, inflammation, and swelling
4. Ineffective health management r/t lack of knowledge of disease and self-
care measures
 ii.Nursing interventions.(PAD)
1. Teaching
a. Controlling risk factors
b. Diet modification to reduce cholesterol, saturated fat, refined
sugar
c. Foot care
d. Injury avoidance
2. After surgery or radiologic intervention
a. Every 15 mins and eventually every 1 hr, check extremity
i. Color
ii. Temperature
iii. Capillary refill
iv. Peripheral pulses
v. Sensation
vi. Movement
b. Pt may need aggressive pain mgmt due to increased opioid
tolerance
c. Report certain findings immediately to HCP
i. Dramatic increase in pain
ii. Loss of previously palpable pulse
iii. Pallor or cyanosis in affected extremity
iv. Numbness or tingling
v. Cold extremity
d. Get pt out of bed - sitting with leg in dependent position
increases risk of DVT
e. Elevate limb if edema develops
g. Complications(PAD)
i. Atrophy of skin and muscles
ii. Minor trauma, such as blisters or toe-stubbing, can result in delayed wound
healing, infection, and tissue necrosis, esp in diabetic patients.
iii. Arterial ischemic ulcers develop over bony prominences.
iv. Gangrene is the most serious complication, which can lead to amputation if blood
flow is not able to be restored.

13. Deep vein thrombosis (DVT)

a. Definition
i. Blood clot (thrombus) forms in association with inflammation in a vein
ii. There is also superficial vein thrombosis which is serious but not as deadly as
DVT.
iii. Venous thromboembolism (VTE) - term encompassing deep vein thrombosis
and pulmonary embolism
b. Risk factors.(VTE)
i. Virchow’s triad - three main factors that cause venous thrombosis
1. Risk factors for venous stasis (slow blood flow in veins, usually legs)
a. Advanced age
b. A fib
c. Bed rest
d. Chronic heart failure
 e. Fractured leg/hip
f. Long trips without exercise
g. Obesity
h. Orthopedic surgery
i. Pregnancy and postpartum period
j. Prolonged immobility
k. Spinal cord injury or limb paralysis
l. Stroke
m. Varicose veins
2. Risk factors for endothelial damage
a. Abdominal and pelvic surgery
b. Caustic hypertonic IV drugs
c. Fractures of pelvis, hip, leg
d. History of previous venous thromboembolism
e. Indwelling, peripherally inserted central vein catheter
f. IV drug abuse
g. Trauma
3. Risk factors for hypercoagulability of blood
a. Antiphospholipid antibody syndrome
b. Antithrombin III deficiency
c. Dehydration or malnutrition
d. Elevated factor VIII or lipoprotein a
e. Erythropoiesis-stimulating drugs (epoetin a)
f. High altitudes
g. Hormone therapy
h. Hyperhomocysteinemia
i. Cancer
j. Nephrotic syndrome
k. Oral contraceptives esp in women >35 who use tobacco
l. Polycythemia vera
m. Pregnancy and postpartum period
n. Protein C deficiency
o. Protein S deficiency
p. Sepsis
q. Severe anemias
r. Tobacco use
c. Pathophysiology.(VTE)
i. Venous stasis around valve cusps of veins results in platelet aggregation.
ii. Platelets and fibrin trap RBCs and WBCs and more platelets and a thrombus
forms.
iii. Thrombus may entirely block lumen of vein.
iv. If thrombus doesn’t entirely block lumen of fein
1. Endothelial cells cover thrombus and it stops getting larger.
2. Thrombus may detach and travel through progressively wider veins until
it gets to the heart and meets the narrowing arteries of the pulmonary
circulation.
3. When the thrombus enters the pulmonary circulation, it is a pulmonary
embolism (PE).
d. Clinical manifestations(VTE)
 i. If thrombus is in one lower extremity
1. Leg edema
2. Pain
3. Tenderness with palpation
4. Dilated superficial veins
5. Sense of fullness in calf or thigh
6. Warm skin
7. Erythema
8. Systemic temperature <100.4 F
ii. Both legs may be edematous and cyanotic if inferior vena cava is involved.
iii. If superior vena cava involved, similar signs will be seen in neck, back, face, and
arms.
e. Collaborative (interprofessional) care (VTE)
i. Diagnostics
1. Blood labs namely clotting studies
2. Ultrasound
3. CT, MRI, and contrast studies
ii. Prevention/ prophylaxis
1. Early/ aggressive mobilization
a. Cheapest way to prevent VTE
b. Bed rest pt change position every two hours
c. Pt who are allowed to must flex and extend knees, hips, feet
every 2-4 hours while awake.
d. Pt should eat meal in chair if they can get out of bed.
e. Pt should walk 4-6 times per day.
2. Graduated compression stockings
3. Intermittent pneumatic compression devices
iii. Goals for confirmed VTE
1. Prevent new clot formation
2. Prevent spread/ growth of clot
3. Prevent embolization
iv. Drug therapy
1. Three major classes of anticoagulants
a. Vitamin K antagonists - warfarin
b. Thrombin inhibitors - heparin
c. Factor Xa inhibitors
2. For prophylaxis
a. Not necessary for pt with low risk
b. LMWH (low-molecular weight heparin: Lovenox) or UH
(unfractionated heparin: regular heparin) for pt with moderate
risk (general, gynecologic, urologic surgery)
c. LMWH or UH until discharge for pt with high risk such as from
trauma
3. To treat VTE
a. Initial treatment involved LMWH, UH, or factor Xa drug
b. INR maintained between 2.0 and 3.0 - lower is associated with
PTS development
c. Active treatment needed for 3 months or longer
4. Thrombolytic therapy - catheter delivers thrombolytic drug (e.g. tPA,
urokinase) directly to site of thrombus to dissolve clot
 v. Surgery
1. Rare but sometimes done on patients who are not responding to medical
therapies and who aren’t candidates for catheter procedures
2. Types
a. Venous thrombectomy - removal of thrombus through incision in
vein
b. Vena cava interruption devices
i. Filter that is inserted into vessel to trap clots before they
travel to lungs
ii. Can become clogged and need replacement
f. Nursing care.
i. Role of nurse:
1. Assess patients for VTE risk and monitor for VTE in at-risk patients.
2. Teach patients who are at risk for VTE about preventive measures.
3. Assess for use of dietary supplements that would interact with
anticoagulants.
4. Monitor lab results and side effects of anticoagulant therapy.
5. Assess for complications of VTE such as PE and chronic venous
insufficiency.
6. Teach patient and caregiver clinical manifestations of PE and to call 911.
7. Discharge teaching about compression stockings, drugs, diet, labs,
giving own shots.
8. Teaching safety precautions to prevent injuries that might result in
bleeding.
9. Instructing how to use pressure to stop bleeding and to contact ERS in
cases of prolonged bleeding.
10. Teaching lifestyle measures to prevent VTE.
ii. Possible nursing diagnoses.(VTE)
1. Acute pain r/t venous congestion, impaired venous return, and
inflammation
2. Ineffective health management r/t altered peripheral tissue perfusion
3. Risk for impaired skin integrity r/t altered peripheral tissue perfusion
4. Potential complication: bleeding r/t anticoagulant therapy
5. Potential complication: PE r/t embolization of thrombus, dehydration, and
immobility
iii. Nursing interventions.(VTE)
1. Acute care
a. Focus is on prevention of emboli and reducing inflammation.
b. Review anticoagulants with pt and remind about possible
interactions with herbs, vitamins, etc.
c. Monitor labs for clotting time and HIT
d. Monitor for increased bleeding.
e. Assist with ambulation.
2. Ambulatory care
a. Focus discharge teaching on
i. Modifying risk factors
ii. Monitoring lab values
iii. Diets and drugs
iv. Smoking cessation
 v. Dangers of oral contraceptives
vi. Importance of movement during long periods of travel
 g. Complications(VTE)
i. Pulmonary embolism
ii. Post-thrombotic syndrome (PTS) - recurring pain, swelling, and other
symptoms that occur in 20-50% of VTE pt within a few months to a few years
after VTE
iii. Phlegmasia cerulea dolens - swollen, blue, painful leg that is rare but sometimes
appears in advanced cancer patients
h. State deep vein thrombosis and pulmonary embolism preventative measures and
hospital protocols.
i. Joint Commission developed 6 core measures to prevent VTE.
ii. VTE prevention should be implemented for all adult patients starting at
admission.
14. Varicose veins aka varicosities
a. Definition - dilated, twisty, superficial veins commonly found in saphenous vein system
(legs) having a diameter of over 3 mm
b. Risk factors.(varicose veins)
i. Family history of chronic venous disease
ii. Weakness in vein structure
iii. Female
iv. Hispanic
v. History of VTE
vi. Venous obstruction from extrinsic pressure from tumors
vii. Thrombophilia
viii. Phlebitis
ix. Previous leg injury
x. Occupations that require prolonged standing or sitting (nursing!)
c. Pathophysiology.(varicose veins)
i. Veins with weak walls bulge and sort of buckle and valves aren’t able to fully
close.
ii. Blood backflows through open valves, particularly when person is standing.
iii. Venous pressure increases and further distention occurs.
d. Clinical manifestations(varicose veins)
i. Symptoms are usually worse in women and include
1. Heavy, achy feeling or pain after prolonged standing or sitting
2. Pressure
3. Itchy, burny, tingly, throbby, or crampy leg sensation
4. Swelling, restless or tired legs, fatigue, nocturnal leg cramps
e. Collaborative (interprofessional) care (varicose veins)
i. Diagnosed with physical examination.
ii. Ultrasound used to evaluate venous anatomy, valve competence, and venous
obstruction.
iii. Treatment
1. Rest with limb elevation
2. Compression socks
3. Leg strengthening exercises such as walking
4. Weight loss if indicated
 iv. Drugs
1. Natural and synthetic venoactive agents - these have generally not been
approved by the FDA and may have interactions with medications.
a. Coumarins
b. Defibrotide
c. Flavonoids
d. Rutosides
e. Plant extracts
v. Sclerotherapy
1. Injecting a substance into the vein that will destroy it
2. Done in the office and causes minimal discomfort
vi. Transcutaneous laser therapy
vii. Endovenous ablation
viii. Surgery - basically just cutting out the weird parts
f. Nursing interventions.(varicose veins)
i. Teach prevention
1. Avoid sitting or standing for long periods.
2. Maintain ideal body weight
3. Take precautions against injury to the extremities.
4. Avoid constrictive clothing
5. Go for walks every day.
ii. After ligation surgery
1. Encourage deep breathing to promote venous return.
2. Check extremities for
a. Color
b. Movement
c. Sensation
d. Temperature
e. Edema
f. Pedal pulses
3. Elevate legs to limit edema.
4. Apply compression stockings
iii. Long term management of varicose veins
1. Focused on
a. Improving circulation
b. Improving appearance
c. Relieving discomfort
d. Avoiding complications and ulceration
g. Complications(varicose veins)
i. Can lead to chronic venous insufficiency and venous ulcers
 15. Venous ulcers
a. Risk factors.(venous ulcers)
i. Can result from long-standing varicose veins
b. Pathophysiology.(venous ulcers)
i. Usually found in ankle area above medial malleolus
ii. Caused by chronic venous insufficiency (CVI)
iii. Serous fluid and RBCs leak into tissues producing edema and chronic
inflammation
iv. Enzymes break down RBCs, turning area brown
v. Fibrous tissue replaces skin and subcutaneous tissue and skin becomes thick,
hardened, and contracted
c. Clinical manifestations(venous ulcers)
i. Leathery skin on lower leg
ii. Eczema is common
iii. Edema
iv. Pain
d. Collaborative (interprofessional) care
i. Key to healing = compression
ii. Moist dressings to apply to wound.
iii. Diet must have adequate protein, calories, and nutrients.
iv. Antibiotics if wound is infected
v. Skin graft in extreme cases
e. Nursing interventions.(venous ulcers)
i. Teach self-care measures
1. Compression = most important
2. Moisturization
3. Activity vs standing/ sitting for long periods
4. Limb elevation
f. Complications(venous ulcers)
i. Can become infected, which may in turn lead to osteomyelitis
ii. Amputation in severe cases

Hematologic Problems
16. Iron-deficiency anemia
a. Risk factors.(Iron def. anemia)
i. People at particular risk
1. Premenopausal women
2. Pregnant women
3. Low SES
4. Older adults
5. Anyone losing blood
b. Pathophysiology.(Iron def. anemia)
i. Less iron available results in decreased production of hemogobin (Hgb) (the
molecule that carries oxygen)
ii. RBCs become smaller because they aren’t filled with as much hemoglobin.
iii. Not as much oxygen can be carried through blood due to smaller RBCs with less
hemoglobin
iv. Tissues and organs become hypoxic if the anemia becomes severe enough.
 v. Causes
1. Inadequate dietary intake - not eating enough foods rich in iron
a. Liver
b. Muscle meats
c. Dried fruits
d. Legumes
e. Dark leafy veggies
f. Whole-grain and enriched cereals and breads
2. Malabsorption of iron in GI tract
a. Certain GI surgeries such as removal of all or part of duodenum
(where iron is absorbed)
b. Malabsorption syndrome that affects duodenum
3. Blood loss
a. GI bleeding
i. Not always readily apparent as it takes 50-75ml of blood
loss to make stool appear black
ii. Can go undetected for some time resulting in a lot of
total blood loss
iii. Causes
1. Peptic ulcer
2. Gastritis
3. Esophagitis
4. Diverticula
5. Hemorrhoids
6. Neoplasia (cancer)
b. Menstrual bleeding - causes loss of about 22mg of iron
4. Hemolysis
c. Clinical manifestations(Iron def. anemia)
i. Asymptomatic in early stages
ii. General anemia manifestations that present as disease becomes chronic (and
severe: <6g/L Hgb)
1. Skin - pallor, jaundice, pruritis
2. Eyes - yellow, retinal hemorrhage, blurred vision
3. Mouth - glossitis, smooth tongue
4. Cardio - tachycardia, increased pulse pressure, systolic murmurs,
intermittent claudication, angina, heart failure, myocardial infarction
5. Pulmonary - tachypnea, orthopnea, dyspnea at rest
6. Neurologic - headache, vertigo, irritability, depression, impaired thought
processes
7. GI - anorexia, hepatomegaly, splenomegaly, difficulty swallowing, sore
mouth
8. Musculoskeletal - bone pain
9. Also - sensitivity to cold, weight loss, lethargy
 iii. Specifically noted in iron-deficiency anemia
1. Pallor
2. Glossitis - tongue inflammation
3. Cheilitis - lip inflammation
4. Headache
5. Paresthesias
6. Burning sensation in tongue
d. Collaborative (interprofessional) care (Iron def. anemia)
i. Diagnosing
1. Labs
a. Low Hgb
i. Women <12 g/dL
ii. Men <14 g/dL
b. Low hematocrit (Hct)
i. Women <35%
ii. Men <42%
c. Low MCV <80
d. Low serum iron
e. Increased total iron-binding capacity
f. Normal or low transferrin (carries iron in bloodstream)
g. Low ferritin (stores iron in cells)
h. Normal or low bilirubin
i. Normal serum B12
j. Normal folate
2. To determine if there is GI bleeding
a. Stool occult blood test
b. Endoscopy or colonoscopy
ii. Goals of care
1. Treat underlying disease that is causing reduced iron availability
2. Replace iron to correct deficiency
iii.
e. Nursing care.
i. Nursing diagnoses.(Iron def. anemia)
1. Possible ones (taken from general anemia category)
a. Fatigue r/t inadequate oxygenation of blood
b. Imbalanced nutrition: less than body requirements r/t inadequate
nutritional intake and anorexia
c. Ineffective health management r/t lack of knowledge about
appropriate nutrition and medication regimen
ii. Nursing interventions.(Iron def. anemia)
1. Teach which foods are good sources of iron (see above section on risk
factors)
2. Supplemental iron may be required if dietary intake cannot meet needs.
a. Oral iron is cheapest and easiest.
b. Take with orange juice to increase absorption.
c. If it doesn’t cause GI upset, take 1 hr before meals to maximize
absorption.
3. Pt with excessive blood loss may need blood products.
17. Aplastic anemia
a. Definition: Pancytopenia - pt doesn’t have enough of any type of blood cell (WBC, RBC,
platelets)
b. Risk factors.(aplastic anemia)
i. Causes of
1. Can be idiopathic (unsure of the cause)
2. Autoimmune
3. Chemical agents and toxins (ex. Benzene, insecticides, arsenic, alcohol)
4. Drugs (ex. Alkylating agents, antiseizure drugs, antimetabolites,
antimicrobials, gold, NSAIDs, antithyroid meds, allopurinol)
5. Radiation
6. Viral and bacterial infections
c. Pathophysiology.(aplastic anemia)
i. Can arise abruptly (in a few days) or slowly over weeks to months and vary in
severity
ii. The stem cells that give rise to all three blood cell types (WBCs, RBCs, platelets)
are wiped out by some cause (see above), resulting in deficient numbers of all
three types of cells.
d. Clinical manifestations(aplastic anemia)
i. Each type of cell deficiency has its own signs/symptoms.
1. Reduced white blood cells (neutropenia) makes pt susceptible to
infection and septic shock/ death. Consider even a low-grade fever
(100.4) a medical emergency.
2. Low platelets (thrombocytopenia) results in predisposition to bleeding
(petechia, ecchymosis, epistaxis)
3. Low RBCs = typical anemia symptoms (fatigue, dyspnea, etc.)
e. Collaborative (interprofessional) care (aplastic anemia)
i. Care is focused on identifying and removing causative agent, when possible.
ii. Provide supportive care until pancytopenia reverses (aka until normal cell levels
are restored).
iii. Treatment
1. Immunosuppressive therapy
2. Stem cell transplant
f. Nursing care.
i. Nursing diagnoses.(aplastic anemia) [I copied these from the e-care plans found
on the evolve resource for our textbook]
1. Fatigue related to inadequate oxygenation of the blood as evidenced by
increased pulse and blood pressure in response to activity, anorexia,
impaired concentration, and/or patient verbalization of an overwhelming
lack of energy
2. Risk for bleeding related to decreased platelets, treatment-related side
effects, and/or inherent coagulopathies
3. Risk for infection related to inadequate secondary defenses
(immunosuppression), altered response to microbial invasion, and
environmental exposure to pathogens
ii. Nursing interventions.(aplastic anemia)
1. Addressing anemia - interventions focus on providing adequate rest for
fatigued patient and monitoring cardiopulmonary responses to activity
 2. Addressing neutropenia - interventions focus on infection prevention
3. Addressing thrombocytopenia - interventions focus on bleeding risk
g. Complications (aplastic anemia)
i. Infection due to reduced number of WBCs and as effect of immunosuppressant
therapies that aim to treat the condition
ii. Hemorrhage from reduced platelets.

18. Polycythemia
a. Definition:
i. Too many RBCs
ii. Can result in hyperviscosity (thick blood) and hypervolemia, which may impair
circulation
b. Risk factors.(polycythemia)
i. Mutations in JAK-2 gene
ii. Situations that place pt at risk for hypoxia
1. High altitude
2. Pulmonary disease
3. Alveolar hypoventilation
4. Defective O2 transport
5. Tissue hypoxia
iii. Kidney tumors
c. Pathophysiology.(polycythemia)
i. Types
1. Primary polycythemia aka polycythemia vera
a. Proliferative disorder that makes too many RBCs, WBCs, and
platelets
b. Enhanced blood viscosity and volume
c. Organs and tissues become congested with blood -
splenomegaly and hepatomegaly are common
d. Hypercoagulopathies predispose pt to clotting
e. Caused by genetic mutation that is not inherited but acquired
during person’s lifetime (as opposed to was born with it)
2. Secondary polycythemia
a. Only RBCs are increased in number
b. Two subcategories
i. Hypoxia-driven
1. Physiologic response to compensate for low O2,
not a pathologic response (aka not its own
disease)
2. Erythropoietin (EPO) from kidneys is released
when blood O2 levels are too low.
3. EPO stimulates production of more RBCs
4. Occurs in response to
a. High altitude
b. Pulmonary disease
c. Alveolar hypoventilation
d. Defective O2 transport
e. Tissue hypoxia
 5. EPO levels return to normal once hemoglobin
levels are adequate.
ii. Hypoxia-independent
1. Pathologic, not in response to reduced O2
2. EPO is produced by a tumor
3. EPO levels remain elevated and RBC
production remains high, even when O2 levels
are fine
d. Clinical manifestations(polycythemia)
i. Hypertension from hypervolemia and hyperviscosity can cause
1. Headache
2. Vertigo
3. Dizziness
4. Tinnitus
5. Visual disturbances
ii. General pruritus (esp exacerbated by hot bath)
iii. Paresthesias and erythromelalgia (painful burning and redness of hands and
feet)
iv. Blood vessel distention, impaired blood flow, circulatory stasis, thrombosis, and
tissue hypoxia can lead to
1. Angina
2. HF
3. Intermittent claudication
4. Thrombophlebitis
v. Vessel rupture from overdistention or inadequate platelet function can cause
1. Petechia
2. Ecchymoses
3. Epistaxis
4. GI bleeding
vi. Feelings of satiety and fullness due to hepatosplenomegaly
vii. Plethora - ruddy complexion
viii. Hyperuricemia - high levels of uric acid in the blood
e. Collaborative (interprofessional) care (polycythemia)
i. Diagnosing
1. Labs - particularly looking at levels of RBCs, WBCs, platelets, and EPO
ii. Treatment aims
1. Reduce blood volume and viscosity
2. Reduce bone marrow activity (producing the blood cells)
iii. Phlebotomy is the common treatment.
f. Nursing care.
i. Nursing diagnoses.(polycythemia)
ii. Nursing interventions.(polycythemia)
1. Assist with or perform phlebotomy.
2. Monitor fluid intake and output.
3. Administer myelosuppressive agents if ordered.
4. Teach about drug side effects.
5. Assess nutritional status as pt might not be eating well due to feelings of
fullness from engorged organs.
6. Activities and/or medication to prevent thrombus formation
g. Complications(polycythemia)
i. Stroke from thrombosis with possible death
19. Blood administration
a. Definition - delivering whole blood or components of blood to a pt to manage hematologic
disorders or replace blood lost from trauma or surgery etc.
b. Risk factors (conditions that require blood products)
i. Severe anemia
ii. Blood loss (such as from trauma or surgery)
iii. Bleeding from thrombocytopenia
iv. Hypovolemic shock
v. Hypoalbuminemia
vi. Hemophilia
c. Collaborative (interprofessional) care
i. SUPER IMPORTANT: blood type needs to be checked by 2 licensed individuals
to avoid complications
ii. Blood bank is responsible for typing and matching donor blood to recipient blood
type.
iii. Nurse and 1 other licensed professional confirms the match before administering.
d. Nursing care.
i. Nursing diagnoses.
ii. Nursing interventions.
1. Check blood type match and confirm with another nurse or approved
person.
2. Take vitals before administering so as to have a baseline.
3. Administer for large bore IV at least 22 gauge; 16-18 can be used for
rapid transfusions.
4. Stay with pt for first 15 mins or 50 mL of administration during which time
pt is constantly evaluated for signs of complications.
5. Check vitals after 15 minutes.
6. Check in on pt every 30 mins until 1 hour after transfusion is complete.
7. Maximum administration time <4 hours due to risk of bacterial growth
within blood product once it is out of the fridge.
8. What to do if transfusion reaction occurs
a. Stop transfusion.
b. Maintain patent IV with saline
c. Notify blood bank and HCP immediately
d. Recheck ID tags and numbers
e. Monitor vitals and urine output
f. Treat symptoms per HCP order
g. Save blood bag and tubing and send to blood bank for
examination
h. Collect required urine and blood samples at intervals determined
by hospital policy
i. Document on appropriate forms and patient’s chart
e. Complications
i. Blood transfusion reactions are considered sentinel events, serious incidents that
severely threaten patients health that are caused by something other than the
natural course of their disease
ii. Acute
1. Acute hemolytic reaction - caused by incompatible blood groups. RBCs
get destroyed by body’s immune system
 2. Febrile, nonhemolytic reaction - most common reaction caused by
sensitization to donor WBCs, platelets, or plasma proteins
3. Mild allergic reaction
4. Anaphylactic and severe allergic reaction
5. Circulatory overload reaction
6. Sepsis
7. Transfusion-related acute lung injury (TRALI)
8. Massive blood transfusion reaction
iii. Delayed
1. Delayed hemolytic reaction
2. Hepatitis B
3. Hepatitis C
4. Iron overload
5. Other infections, such as HIV or cytomegalovirus