Nursing Care and Interventions
NURS3105
Dr. Jane Tyerman
Copyright © 2014 Elsevier Canada, a division of
Reed Elsevier Canada, Ltd.
• Electrocardiogram (P, QRS, T, U waveforms)
•
P wave - depolarization of the atria.
• QRS complex - depolarization of the ventricles.
• T wave - repolarization of the ventricles.
• U wave, if present - repolarization of the Purkinje fibres or
may be associated with hypokalemia.
• PR, QRS, and QT intervals reflect the length of time it takes
for the impulse to travel from one area of the heart to
another.
Cardiac output (CO) = blood pumped/min
Normal 4-8L/min (Ave 5L/min)
Cardiac index (CI)
Heart rate (HR)
Stimulation from SNS
Stimulation from PNS
Stroke volume (SV) = beat
SV = CO/HR
Average 75 ml
Cardiac reserve
Increase HR or SV
Pulse pressure (40 mmHg)
Differences between SBP and DBP
Normally 1/3 of SBP
Mean Arterial Pressure (MAP)
MAP = SBP + 2(DBP)
3
 Indicator of blood flow (better than SBP)
 MAP >60 needed to maintain adequate tissue perfusion
Commonly used to titrate medication MAP 65
(ie. Norepinephrine/Levophed)
 Volume of blood in ventricles at end of diastole
 Affected by the amount of blood delivered to
the heart
 Starling’s Law: greater stretch = greater
preload
 Conditions that diminish preload:
Decreased blood volume (hemorrhage, dehydration, shock)
AV valve dysfunction (hinder free flow into ventricle)
Vasodilation (increase vascular space, same volume)
 Conditions that increase preload
Increase blood volume (renal failure, fluid resus, increased aldosterone)
Poor EF/CHF-”back up” d/t inability to eject
The heart's ability to function as a pump
Ejection Fraction: index of myocardial function (60%)
Percentage of blood ejected with each stoke volume
SV divided by end diastolic volume
Conditions that affect contractility
↑ contractility (Inotropes) and vasoconstriction
Calcium release
Digoxin, dopamine, dobutamine
↓ contractility:
HYPOXIA (considered negative inotrope)
ischemia
and drugs (narcotics, anesthetics)
 Myocardial Contractility and Calcium
Influx
 Cardiac muscle does not store calcium
like skeletal muscles
 Importance of serum calcium levels
and medications that affect calcium
Calcium 2.25 – 2.75 mmol/L
The peripheral resistance against which the left ventricle
must pump
The relationship among flow, resistance, and pressure
Arterial pressure=flow (CO) x resistance (afterload)
Impact of afterload on CO
If afterload ↑, CO ↓, arterial pressure ↑
If afterload ↓, CO ↑, arterial pressure ↓
Conditions that affect afterload
↑ afterload:
vasoconstriction- SNS, hypertension,
renal failure, increase volume,
medications, stenosis of valve
impeding EF
↓afterload:
• vasodilation- PNS, shock, spinal
cord injury
 Stimulation of SA and AV
nodes
 Conditions that:
 increase heart rate
 SNS stimulation
 Pain, anxiety, fear, perceived threats, medications
 Conditions that cause ↓ SV (to maintain CO)
 Cardiac conduction syndromes (WPW)
Conditions that:
 decrease heart rate
 PNS stimulation (muscarinic
receptors/vagal nerve)
 Valsalva
 Medications, conduction issues
Subjective data
 Past health history
 Past and current medications
 Surgery or other treatments
 Cues to cardiovascular problems
 Fatigue, abdominal obesity, fluid
retention, irregular heart rate,
dyspnea, pain, calf tenderness,
dizziness, altered neurological
function, leg pain




Objective data
Physical examination
Vital signs
Peripheral vascular system
 Inspection: Colour, hair distribution, venous blood flow,
edema, jugular veins
 Palpation: Neck and extremity pulses,
pressure of pulse wave, rigidity of
vessel
 Auscultation: Major arteries,
bruit assessment
Copyright © 2014 Elsevier Canada, a division of
Reed Elsevier Canada, Ltd.
Auscultation
• S1 = the closure of the tricuspid and mitral valves (AV atrial
ventricular) valves = LUB
• S2 = the closure of the aortic and pulmonic valve (semilunar)
= DUB
-Extra heart sounds (best heard with the bell of a stethoscope
as they are low-pitched)
• S3 = ventricular vibration (mitral valve
regurgitation
• S4 = occurs in patients with CAD,
left ventricular hypertrophy or
aortic stenosis
Noninvasive studies
 Chest radiograph
 Electrocardiogram
Ambulatory electrocardiogram monitoring
Transtelephonic event recorder
 Exercise or stress testing
Echocardiogram EF, valves, chamber size
 Nuclear cardiology
 Magnetic resonance imaging (MRI)
 Computed tomography (CT) – CAD
Blood studies
Cardiac markers (serial CKs)
• CK, CKMB (4-6 h), Troponin I or T (6 h)
Serum lipids
Lipoprotein-associated phospholipase A2
• athrosclerosis
C-reactive protein
Homocysteine
• Risk of CAD, stroke, thromboembolism
Cardiac natriuretic peptide markers (CNPM)
• Distinguish between cardiac and respiratory
cause of dyspnea
Invasive studies
• Cardiac catheterization and
coronary angiography
• Electrophysiology study – node
function
• Intracoronary ultrasound
• Blood flow and pressure
measurements
• Peripheral vessel blood flow
• Hemodynamic monitoring
Nursing Management:
Hypertension
High blood pressure is one of the most
important modifiable risk factors that lead
to cardiovascular disease.
35-23
35-24
Cardiac output (CO) is the total blood flow through the
systemic or pulmonary circulation per minute.
CO can be described as stroke volume (SV, or the amount of
blood pumped out of the left ventricle per beat [~70 mL])
multiplied by the heart rate (HR) for 1 minute.
Systemic vascular resistance
(SVR) is the force opposing
the movement of blood
within the blood vessels.
35-25
• Sustained elevation of systemic arterial
blood pressure (BP)
• High BP is the most significant modifiable
risk factor for cardiovascular disease and
mortality in Canada.
• As BP increases, so does
the risk for myocardial
infarction (MI), heart
failure, stroke, and renal
disease.
35-26
Normal BP: 120 mm hg/80 mm Hg
Persistent elevation of
Systolic blood pressure (SBP) ≥140 mm Hg or
Diastolic blood pressure (DBP) ≥90 mm Hg or
Current use of antihypertensive medication(s)
35-27
• Age
• Women
• Indigenous people
• ‘Silent Killer’
35-28
Isolated systolic hypertension (ISH)
Sustained elevation of SBP ≥140 mm Hg and a
DBP <90 mm Hg
Common in older persons, related to loss of
elasticity in large arteries
35-29
Primary (essential) hypertension
•
•
Majority of adult patients
Focus on primary hypertension related to
prevalence in clinical practice
Secondary hypertension
•
•
•
5 to 10% of adults
Many causes; treatment aimed
at eliminating the underlying
cause
Contributing factors to
hypertensive urgency
35-30
Primary (essential) hypertension
Contributing factors
•
•
•
•
•
•
↑ SNS activity
↑ Sodium-retaining hormones and vasoconstrictors
↑ Sodium intake
Diabetes mellitus
> Ideal body weight
Excessive alcohol intake
35-31
• Advancing age
• Heavy alcohol consumption
• Cigarette smoking
• Diabetes mellitus
• Elevated serum lipids
• High dietary sodium
• Gender
35-32
Clinical findings that suggest secondary
hypertension include
• Unprovoked hypokalemia
• Abdominal bruit
• Variable pressures with a history of
tachycardia, sweating, and tremor
• Family history of renal disease
35-33
Causes
• Coarctation or congenital narrowing of the aorta
• Renal disease such as renal artery stenosis and
parenchymal disease
• Endocrine disorders such as pheochromocytoma,
Cushing’s syndrome, and hyperaldosteronism
• Neurological disorders such as brain tumours,
quadriplegia, and head injury
• Sleep apnea
• Medications
• Pregnancy-induced hypertension
Genes
Sodium and water retention
Altered renin–angiotensin–aldosterone
mechanism
Stress and increased SNS activity
Insulin resistance and hyperinsulinemia
Endothelial cell dysfunction
Obesity
The animation referenced below can be viewed in the PowerPoint Animations asset.
Aldosterone Regulation Mechanism
35-36
Hypertension is a silent disease.
Frequently it is asymptomatic until it
becomes severe and target-organ
disease has occurred.
Secondary symptoms with severe
hypertension include fatigue, reduced
activity tolerance, dizziness, palpitations,
angina, and dyspnea.
Hypertensive heart disease
Coronary artery disease
Left ventricular hypertrophy
Heart failure
Cerebrovascular disease
Peripheral arterial disease
Nephrosclerosis
Retinal damage
• Urinalysis
• Blood chemistry (potassium, sodium, blood urea, and
creatinine)
• Fasting blood glucose
• Fasting total cholesterol and high-density lipoprotein
cholesterol, low-density lipoprotein cholesterol, and
triglycerides
• Standard 12-lead electrocardiography
• Assess urinary albumin excretion in patients with
diabetes
• All patients with treated hypertension need to be
monitored for the appearance of diabetes.
• Ambulatory blood pressure monitoring
• 24-hour readings
• Useful in diagnosis of uncomplicated mild-tomoderate hypertension
• Helpful in patients with suspected white coat
hypertension, masked hypertension, apparent
medication resistance, hypotensive symptoms
with hypertensive medications, episodic
hypertension, or autonomic nervous system
dysfunction
Risk stratification
Lifestyle modifications
Nutritional therapy
Weight reduction
Modification in alcohol consumption
Physical activity
Avoidance of tobacco products
Stress management
FIG. 35.3 Treatment of systolic/diastolic hypertension (HTN) without
other compelling indications.
Nursing assessment
Subjective data
• Important health information
• Symptoms: Dyspnea, fatigue, intermittent claudication,
nocturia, dizziness, erectile dysfunction
Objective data
• Cardiovascular: BP, pulse
• Musculoskeletal: Truncal obesity
• Neurological: Mental status changes
• Possible findings
Medications”
• Diuretics (Furosemide, HCTZ)
• Antihypertensives (ACE Inhibitors, Calcium Chanel
blockers)
Overall goals
Achieve and maintain target BP
Understand and implement therapeutic plan
Minimal or no unpleasant adverse effects
Confident of ability to manage and cope with
condition
Adherence
Nursing implementation
Health promotion
• Individual patient evaluation
• Screening programs
• Cardiovascular risk factor modification
Ambulatory and home care
• Physical activity
• Home blood pressure monitoring
• Patient adherence
Evaluation
35-45
Hypertension is common in individuals age 60+ years.
Age-related changes
• Loss of tissue elasticity
• Increased collagen content and stiffness of the
myocardium
• Increased peripheral vascular resistance
• Decreased β-adrenergic receptor sensitivity
• Blunting of baroreceptor reflexes
• Decreased kidney function
• Decreased renin response to sodium and water depletion
• Severe, abrupt increase in DBP (defined as
>120–130 mm Hg)
• Rate of increase in BP is more important than
the absolute value
• Often occurs in patients with a history of
hypertension who have failed to adhere to their
medication regimen or who have been
undermedicated
Nursing Management:
Coronary Artery Disease and Acute Coronary Syndrome
Heart disease is the second major cause of
death in Canada, with 27.6% of all deaths.
2.4 million Canadians over age 20 will
experience ischemic heart disease.
36-49
36-50
Prevalent Etiologies of CAD
CAD is one of the leading
Atherosclerosis: partially or
causes of morbidity and
completely blocked coronary
mortality in the US and Canada. arteries
Coronary vasospasm
CAD results in ischemia and
infarction of myocardial tissue. Microvascular angina
LAD (left anterior descending
artery) is most commonly
affected.
Highly sensitive CRP (hsCRP)
Reduction of Risk Factors
Smoking cessation
Weight loss–DASH
Lowering cholesterol levels
Glycemic control
Stress reduction
Medication compliance
↑ Activity/exercise
CAD is one of the leading
causes of morbidity and
mortality in Canada.
CAD results in ischemia and
infarction of myocardial tissue.
LAD (left anterior descending
artery) is most commonly
affected.
Highly sensitive CRP (hsCRP)
36-52
36-53
The animation referenced below can be viewed in the PowerPoint Animations asset.
Coronary Artery Disease
36-54
Risk factors for coronary artery disease
Nonmodifiable risk factors
•
•
•
•
Age
Gender
Ethnicity
Family history and genetics
36-55
Modifiable major risk factors
•
•
•
•
•
Elevated serum lipid levels
Elevated blood pressure (BP)
Tobacco use
Physical inactivity
Obesity
36-56
Modifiable contributing risk factors
•
•
•
•
•
Diabetes mellitus
Elevated fasting bold glucose level
Psychosocial risk factors
Homocysteine elevation
Substance use
36-57
Health promotion
• Identification of people at high risk
• Management of people at high risk
• Physical activity
Nutritional therapy
• Reduce serum triglyceride
• Ideal body weight
• Cholesterol <200 mg/day
36-58
36-59
Cholesterol-lowering medication therapy
Antiplatelet therapy
Beta Blockers
Nitrates
Calcium channel blockers
Thrombolytics
36-60
Morphine Sulfate
Analgesic; ↓ anxiety; ↓ tachypnea; relaxes bronchial
smooth muscle; improves gas exchange
β-Blockers
↓heart rate; ↓workload of heart; ↓ oxygen demand of
myocardium
Calcium Channel Blockers
↓conduction through AV node; slow heart rate; ↓
oxygen demand by myocardium
Thrombolytic Therapy
(within protocol guidelines)
Useful when infarction is diagnosed early;
streptokinase and tPA; administered IV
Most effective if given within 6 hours of onset of
chest pain; heparin therapy will usually follow
thrombolytic therapy
Four heart valves:
• Tricuspid and mitral valves
• Pulmonic and aortic valves
• Prevent regurgitation
• Open and close in response
to pressure gradient
changes
• Thickened and stenotic
valve leaflets
• Caused by
 Rheumatic fever
(main)
 Calcification
 Congenital factors
Mitral Valve Stenosis
Early period—may have no
symptoms
Later—excessive fatigue,
dyspnea on exertion,
orthopnea, dry cough,
hemoptysis, or pulmonary
edema
Rumbling apical diastolic
murmur and a-fib are common
Nursing and Collaborative
Management
CHF care
Monitor for a-fib with
thrombus formation
Prophylactic antibiotic therapy
before any invasive procedures
(dental, surgical, childbirth)
May require surgical repair or
valve replacement
Teach about the need for
lifelong anticoagulant therapy
if valve replacement done
Mitral valve regurgitation (MR)
• Insufficient or incompetent mitral valve (prolapse)
• Regurgitation of blood back into LA
• Can lead to left sided heart failure
Aortic valve regurgitation (AR) – aka aortic insufficiency
• Incompetent aortic valve, allows blood from aorta back into LV
during diastole
• LV hypertrophy to maintain SV
• Systolic murmur
• Rheumatic fever
Etiology
CAD, prior MI
Chronic HTN
Cardiomyopathy
Thyroid
Diabetes
Valvular and congenital
heart disease
Pulmonary diseases
Progressive→ cardiac remodeling to
maintain stroke volume and cardiac
output
LV remodeling d/t disease process
CAD, DM, cardiomyopathy, valvular
heart disease
Etoh, drug abuse
Hyperlipidemia, HTN
Risk Factors – Table 13-4
Causes: LV infarct, cardiomyopathy, hypertension
Symptoms: shortness of breath, cough, orthopnea,
pulmonary edema, paroxysmal nocturnal dyspnea
Signs: S3 gallop, tachycardia, inspiratory rales beginning
at lung bases, expiratory wheezes due to bronchospasms
(misdiagnosed with asthma)
Laboratory findings:
• ABGs reveal hypoxemia
• chest x-ray shows pulmonary edema or pleural effusions
• ↑b-type natriuretic peptide (BNP)
BNP levels greater than 500 ng/mL indicate heart failure
is probable.
Systemic Congestion
Causes: LHF, RV infarct, pulmonary or tricuspid
valve disease, pulmonary HTN, COPD, PE
Symptoms: dyspnea on exertion, fatigue, weight
gain, fluid retention
Signs: ↑ CVP, JVD >3-4 cm, hepatomegaly, ascites,
peripheral or sacral edema, and pleural and
pericardial effusions
Lab Tests: ↑ LFTs, ↑BUN/Cr, ↑ PT/INR,
hyponatremia
Other symptoms and signs
Fatigue
JVD, Edema, Crackles, S3
http://en.wikipedia.org/wiki/File:Elevated_JVP.JPG
Classic respiratory symptoms
Orthopnea
Dyspnea
Paroxysmal nocturnal dyspnea
Diagnostic
Echo, Doppler,12 lead
Medications
ACE Inhibitors
ARBs
Beta blockers
Loop and Thiazide
diuretics
Daily weights
Fluid restrictions
Oxygen
Reposition and perform coughing, and deep breathing
exercises q2h
Limit sodium intake
Fluid restriction only if Na+ <132 mmol/L (mEq/L)
Avoid excessive fluids
Avoid alcohol
Educate on signs of worsening condition
such as weight gain 1.36 kg (3 lb) or 0.45-0.9 kg (1-2
lb) overnight; increasing DOE, orthopnea or PND.
Regular exercise is strongly encouraged
Supply vs demand
Increased demands
↑ heart rate, ↑ contractility, ↑ preload
Decreased supply
CAD, spasm, anemia, hypoxemia, shock
Age
Gender
Race
Family history
Hyperlipidemia
Dietary
Obesity
Sedentary lifestyle
Hypertension
Smoking
Diabetes
Chronic kidney disease
Metabolic syndrome
Menopause
Hyperhomocysteinemia
Vascular inflammation
Multifactoral
Grade 1
Angina occurs with strenuous exertion
Grade 2
Angina occurs w/walking 2 blocks or 1
flight of stairs
Grade 3
Angina occurs w/walking < 2 blocks
Grade 4
Rest angina
Copyright © 2014 Elsevier Canada, a division of
Reed Elsevier Canada, Ltd.
Copyright © 2014 Elsevier Canada, a division of
Reed Elsevier Canada, Ltd.
Women
Discomfort rather than pain
Shortness of breath
Extreme fatigue
Clients with Diabetes
Asymptomatic
Neuropathy
Dyspnea
Elderly clients
Confusion/delirium
Dizziness
Shortness of breath
Copyright © 2014 Elsevier Canada, a division of
Reed Elsevier Canada, Ltd.
Diagnostic studies
•
•
•
•
•
12 lead ECG
Stress test
Holter
Echocardiogram
Cardiac catheterization
12 Lead ECG
ECG (12 lead)
Confirm By Biomarkers
 Troponin
 Myoglobin
 Cardiac enzymes
Drug therapy
• Short-acting nitrates
• Sublingual nitroglycerin
• Long-acting nitrates
• Nitroglycerin ointment
• Transdermal controlled-release nitrates
• β-Adrenergic blockers
• Calcium channel blockers
• Angiotensin-converting enzyme inhibitors
Silent ischemia
•
Nocturnal angina and angina decubitus
Prinzmetal’s (variant) angina
•
Occurs at rest
Treatment
• To prevent MI and reduce symptoms
• ASA
• ABCDEF

Therapy (MONAM)
Monitor
Oxygen
Nitroglycerin
ASA
Morphine
β-Adrenergic blockers
Angiotensin-converting enzyme inhibitors
Antidysrhythmia drugs
Cholesterol-lowering drugs
Stool softeners
Chest pain that is new in onset, occurs at rest, or has
a worsening pattern.
• Unstable angina is unpredictable and
represents an emergency.
• First manifestation of CAD
• May evolve from chronic unstable angina
• Symptoms more subtle in women
-
Fatigue
SOB
Indigestion
anxiety
Stable Angina
• Predictable
• Exertion induced
• Pain relieved by
Ntg + rest
• Short lived <20
min
Unstable Angina
• New onset c/p that can
occur many times per
day
• Pain is increasing in
severity; unrelieved w/
Ntg
• Rest angina
• Indicative of unstable
plaque
• Preinfarct or crescendo