Nursing Care of Patients with Cardiac Problems
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One in five Americans possess some form of
cardiovascular disease
With increase in metabolic syndrome and
aging babyboomers, numbers increasing
Cardiovascular disease is the number one
cause of death in women in US.
Major cause of mortality in 21st century
Number of cardiovascular problems that can
occur
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Pericardium
Epicardium
Myocardium
Endocardium
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Right side of heart—workload is light
compared to left side; pulmonary circulation
Left side of heart—high pressure system,
systemic circulation
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S1 caused by closure of mitral and tricuspid
valves
S2 caused by the closure of aortic and
pulmonic valves
Splitting of S1 and S2 can be accentuated by
inspiration
Gallops=S3 and S4
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S3 is ventricular gallop—normal in children. In
those over 35, indicates early heart failure,
VSD or decreased ventricular compliance
S4 is an atrial gallop—seen in hypertension,
anemia, aortic or pulmonic stenosis and
pulmonary emboli
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Systolic murmurs—aortic stenosis and mitral
regurgitation. Occur between S1 and S2.
Diastolic murmurs—aortic or pulmonic
regurg and mitral stenosis. Occur between S2
and S1.
Grades I-VI; 1 very faint, 2 faint but
recognizable, 3 loud but moderate in
intensity, 4 loud w/thrill, 5 loud, thrill,
stethoscope partially off chest, 6 audible w/o
stethoscope
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Heart perfused by coronaries during diastole
Right coronary
Left coronary
Circumflex
Must be 60-70 to maintain perfusion of vital
organs
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Left coronary perfuses left ventricle, septum,
chordae tendinae, papullary muscle and
portion of right ventricle
Right coronary—supplies right atrium, right
ventricle, inferior portion of left ventricle
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Automaticity—intercalated discs
Conductivity
Contractility
Excitability
Cardiac conduction system
1. SA node
2. Internodal tracts
3. AV node/junction
4. Bundle of His
5. Right and left bundle branches
6. Purkinje fibers
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Stimulation of the cardiac working cells
(myocytes) is reliant on exchange of ions
across particular channels in cell membrane
Channels regulate the movement and speed
of the ions, specif., sodium, potassium, and
calcium
Sodium travels across fast channels, calcium
across slow channels
Potassium is primary intracellular ion, sodium
is the primary extracellular ion
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Phase O—cellular depolarization initiated as
positive ions influx into cell. Sodium moves
rapidly into myocytes; depolarization of SA
and AV nodes via slow calcium channels
Phase 1—Early cellular repolarization occurs
as potassium exits intracellular space
Phase 2—plateau phase, rate of
repolarization slows, calcium ions enter
intracellular space
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Phase 3—Marks completion of repolarization
and return of the cell to resting state
Phase 4-resting phase before next
depolarization
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During this phase, cells are incapable of being
stimulated
Absolute refractory period—unresponsive to
any electrical stimulus, Phase O to middle of
Phase 3
Relative refractory period—brief period at
end of Phase 3. Strong enough impulse can
cause depolarization prematurely. This
increases the risk for serious dysrhythmias.
Factors increasing likelihood of premature
depolarization
 Hypokalemia
 Hypomagnesemia
 Hypothermia
 Myocardial injury
 Acidosis
 hypercarbia
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P wave-atrial depolarization
PR-duration of time from SA to AV nodes
QRS-ventricular depolarization
QT-total time needed for depolarization and
repolarization
T wave-represents ventricular repolarization
U wave if prominent represents electrolyte
abnormality
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Calculate heart rate
Heart rhythm
Analyze P waves
Measure P-R interval
Measure QRS duration
Interpretation
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PR interval <.20 second
QRS interval < or equal to .12 second
QT interval variable, generally less than .42
second
P for every QRS
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Normal sinus rhythm—60 to 100
Sinus dysrhythmia
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Tachydysrhythmias-->120
Bradydysrhythmias--<60
Premature complexes
Repetitive rhythms—atrial flutter
Escape complexes—idioventricular rhythm
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Sinus tachycardia
Sinus bradycardia
Supraventricular rhythms
Atrial fibrillation or flutter
1st, 2nd, 3rd degree heart blocks
Vtach, Vfib, asystole
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Based on principle that fluid flows from region of
higher pressure to one of lower pressure
Right side of heart has lower pressure than does
left
Systole-pressure in ventricles increases, forces
AV valves to close, forces semilunar valves to
open, and blood is ejected
Diastole—ventricles are relaxed, AV valves open,
atria fill first, ventricles fill, electrical impulse,
atria contract, impulse is propagated to
ventricles, ventricles fill then will contract
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HR x SV= CO
Ranges between 4-7 L/min in adults
CI = CO divided by BSA
Amount of blood pumped by each ventricle
during given period
Stroke volume is amount of blood ejected per
heartbeat, ~70ml
Affected by
 preload—degree of stretch of cardiac muscle
fibers at the end of diastole, amount of blood
returning to right side of heart
 afterload –amount of resistance to ejection
 contractility—force generated by the
contracting myocardium
 Ejection Fraction--Percentage of enddiastolic volume that is ejected, ~50-70%
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Pulmonary vascular resistance (PVR)—
resistance of the pulmonary BP to right
ventricular ejection
Systemic vascular resistance (SVR)—
resistance of the systemic BP to left
ventricular ejection
Contractility=force of generated by the
contracting myocardium
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Increased size of left atrium
Thickening of endocardium
Myocardial thickening
Thickening and rigidity of AV valves
Calcification of aortic valve
Decreased number of SA, AV, Bundle of His,
right and left bundle branch cells
Stiffening vasculature
Decreased sensitivity to baroreceptors
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Cigarette smoking
Genetics
Physical inactivity
Obesity
Hyperlipidemia
Diabetes mellitus
Hypertension
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History
Chest pain or discomfort
SOB
Peripheral edema and weight gain
Palpitations
Fatigue
Dizziness, syncope, changes in level of
consciousness
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Angina pectoris
Pericarditis
Pulmonary disorders—pneumonia, PE
Esophageal disorders
Anxiety and panic disorders
Musculoskeletal disorders--costochondritis
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Atypical presentation
Fatigue, sleep disturbances, shortness of
breath
Historically undertreated due to ambiguous
presentation
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General appearance and cognition
Inspection of the skin
Blood pressure—difference between the
systolic and diastolic blood pressure is called
the pulse pressure. Pulse pressure less than
30 torr signifies a serious reduction in cardiac
output and requires evaluation
Postural BP changes
Arterial pulses, pulse quality-check side to
side
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JVD when head of bed is elevated 45 to 90
degrees
Heart sounds—S1, S2 ; gallops (vibration),
snaps and clicks (stenosis of mitral valve),
murmurs (turbulent flow) and friction rubs
(harsh grating sound)
Inspection of extremities
Lungs
Abdomen
Skin temperature
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Assess clubbing by the Schamroth method
Blood pressure—hypertension
Prehypertension—120-130/80-89
Postural hypotension—BP decrease by 20 torr
systolic or 10 torr diastolic plus 10-20%
increase in heart rate. Supine,sitting,
standing.
Ankle-brachial index=assess vascular status
of LE. LE SBP divided by brachial BP. Should
be 1, .8 moderate disease, .5 severe
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Changes in AP diameter
Isolated systolic hypertension—increases risk
for morbidity and mortality
S4 will be present in ~90% of elderly patients
due to decreased ventricular compliance
S2 may be split
60% of elderly have murmurs, reflective of
sclerotic changes of aortic leaflets
Cardiac biomarkers
 Creatine kinase and CK-MB—most specific in
MI
 Myoglobin—heme protein. Released from
myocardial tissue within 1-3 hours after
injury. Less specific as may be elevated in
renal and musculoskeletal disease
 Troponin T and I—proteins found only in
cardiac muscle, detected within 3-4 hours,
peak in 4-24 and remain elevated for 1-3
weeks
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Lipid profile—obtain after a 12 hour fast
Brain (B type) Natriuretic Peptide—
neurohormone that regulates BP and fluid
volume. Level increases as increased
ventricular pressure as seen in heart failure.
>51.2 is considered abnormal.
C Reactive Protein—protein released by liver
and reflects systemic inflammation. Normal
is less than 1.0
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ECG—graphic recording of the electrical
activity of the heart. Up to `18 leads.
Telemetry—radiowaves
Holter monitoring
Wireless mobile cardiac monitoring
Exercise stress test
Pharmacologic stress test—Persantine and
adenocard are given, simulate effects of
exercise; dobutamine also, helpful on those
with bronchospasm
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Total cholesterol 122-200
Triglycerides—122-200
HDL—55-60
LDL—60-180
HDL: LDL ratio—3:1
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Homocysteine—indicates risk for CVD.
Linked to development of atherosclerosis. 12hour fast needed for reliable monitoring of
level. Normal 5-15 micromol/L
Magnesium—necessary for absorption of
calcium, maintenance of potassium stores
and metabolism of ATP. Low levels
predispose to atrial and ventricular
dysrhythmias. Increased levels depress
contractility and excitability of heart.
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Echocardiography—noninvasive ultrasound
that is used to examine the size, shape and
motion of cardiac structures.
Transesophageal echocardiogram (TEE)—
provides clearer images of heart . Fasting for
6 hours. IV line. Sedation. Throat
anesthetized. Frequent monitoring.
Thallium or Cardiolite stress test
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PET scan can be used to measure cardiac
dysfunction
MRI
Cardiac catheterization with angiography—
contrast, know BUN/creatinine, INR, PT, PTT
Must be fasting. Have IV access.
Following cath, observe catheter access site
for bleeding
Monitor extremity—CSM
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Bedrest for 2-6 hours
Monitor for dysrhythmias
Monitor for contrast agent induced renal
failure, I&O, hydration
Ensure patient safety—instruct no lifting for
24h, no straining, avoid tub baths, s/s of
bleeding, swelling, bruising, pain or fever
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Class IA— Na+ channels.Depress
depolarization, prolong repolarization. For
atrial and ventricular dysrhythmias. Pronestyl
(procainamide). Proarrhythmic. Lupus-like
syndrome.
Class IB—minimal depression of
depolarization, shortened repolarization.
Treats ventricular dysrhythmias. Xylocaine
(lidocaine) and Mexitil (mexilitene). CNS
changes.
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Case Studies
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Class IC—marked depression of
depolarization; little effect on repolarization.
Tx of atrial and ventricular dysrhythmias.
Tambocor (flecainide) and Rythmol
(propafenone). Proarrhythmic, HF, AV blocks
Class II—Beta blockers.Decrease automaticity
and conduction. Treats atrial and ventrcular
dysrhythmias. Tenormin (atenolol), Lopressor
(metoprolol), Inderal (propranolol),
bradycardia, heart failure, bronchospasm,
masks hypoglycemia
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Class III—Potassium channels. Prolong
repolarization, for atrial and ventricular
dysrhythmias especially when ventricular
dysfunction present. Cordarone
(amiodarone), Corvert (ibutilide). SE:
pulmonary toxicity, corneal microdeposits,
bradycardia, AV blocks, heart failure,
hypotension with IV administration,
peripheral edema.
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Class IV—block calcium channels. For atrial
dysrhythmias. Cardizem (diltiazem), Calan
(verapamil). Bradycardia, AV blocks,
Hypotension, peripheral edema
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Timed electrical current to terminate a
tachydysrhythmia
Defibrillation-treatment of choice for
ventricular fibrillation and pulseless VTach
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Electronic device that provides electrical
stimuli to heart muscle
Composed of generator and electrodes
Universal code about function
Appropriate sensing of intrinsic rhythm,
appropriate pacing and appropriate capture
Complications include: infection,
bleeding,ectopy, performation of
myocardium
Universal code indicates five letters
1. Identifies chamber being paced. V, A, D
(dual).
2. Indicates chamber(s) being sensed. A, V, D,
O (meaning sensing function is off)
3. Indicates type of response to the sensing.
Inhibition and Triggered responses. I, T, O.
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4. Used only with permanent pacemakers.
Ability to modulate rate and increase CO
during times of increased cardiac workload.
Indicated by letters O(none) or R (rate
modulation)
5. Indicates multisite pacing capability. A, V, D
or O.
So pacemaker that is VVIOO would indicate?
DDIRD.
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Infection at entry site
Bleeding and hematoma
hemothorax
Ventricular ectopy
Diaphragmatic stimulation (hiccuping)
Inhibition of permanent pacemakers when
exposed to strong electromagnetic
interference (keep cell phones at least 6
inches away from pacer, not keep in shirt
pocket.
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Nonsensing
Noncapture
Nonpace
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Detects and terminates life-threatening
episodes of tachycardia or fibrillation
Used in those who have survived sudden
cardiac death syndrome
Also useful in those with CM and with
prolonged QT syndrome
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Invasive procedure used to evaluate and treat
various dysrhythmias that have caused
serious symptoms
Identifies impulse formation
Assesses dysfunction of SA and AV nodes
Maps location of dysrhythmogenic foci
Assesses effectiveness of antiarrhythmias
Allows for ablation
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Inflammation affecting arterial walls
Results in plaque formation
Impedes flow
Results in atherosclerosis
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High lipids
Smoking
Hypertension
Diabetes mellitus
Family history
Metabolic syndrome
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Cholesterol
Tobacco use
Weight
Hypertension
Diabetes mellitus
Total fat—25-35% of total calories
Saturated fat<7%
Polyunsaturated fat --up to 10% of total
calories
Monounsaturated fat—up to 20% of total
calories
CHO 50-60% of total calories
Fiber—20-30gm per day
Protein 15% of total calories
Cholesterol--<200mg/day
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HMG-CoA Reductase Inhibitors (statins):
Mevacor (lovastatin), Pravachol (pravastatin),
Zocor (simvastatin), Lescol (fluvastatin),
Lipitor (atorvastatin), Crestor (rosuvastatin);
decreases LDL* and TG, increases HDL
Nicotinic Acid: Niacin; decreases LDL and
TG*, increases HDL*
Fibric Acids: Tricor (fenofibrate); decreases
LDL
Bile Acid Sequestrants: Welchol
(colesevelam), decreases LDL
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Increase endothelial cell function
Reduce degradation of plaque matrix
Anti-inflammatory
Reduce oxidation of LDL and uptake of
macrophages
Reduce platelet aggregation/alter fibrinogen
levels
Reduce smooth muscle proliferation
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Vytorin—controversial at this time
Zetia (ezetimibe)—selective cholesterol
absorption inhibitor
Lovaza (omega 3 fish oil)—need 3-4 gms per
day, good in hypertriglyceridemia
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Promote smoking cessation-Nicoderm,
Zyban (bupropion), Chantix
Manage hypertension—prehypertensive if BP
> 120/80; inflammatory process
Control diabetes—hyperglycemia promotes
dyslipidemia, increased platelet aggregation,
increased thrombus formation; impair
endothelial cell-dependent vasodilation and
smooth muscle function
CV catch up to men 10 years after menopause
 Twice as much CAD in African-American
women than in Caucasian women
 Historically, gender related differences in Tx
 With menopause, risk factors
escalate
 Debate re HT (hormone
Therapy)
 Stress--catecholamines
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Clinical syndrome characterized by episodes
or paroxysms of pain or pressure secondary
to insufficient coronary blood flow; decreased
oxygen supply
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Caused by atherosclerosis
Obstructions of coronaries
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Stable angina—occurs on exertion
Unstable angina—crescendo, threshold
lower, sometimes pain at rest
Refractory angina
Variant angina-vasospasm, reversible ST
elevation
Silent ischemia—ECG changes but w/o
symptoms
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Pain poorly localized
Viselike, substernal
More diffuse in women as affects long
segments of artery rather than discrete
segments
Diabetic may have blunted response due to
damaged nociceptors
Feeling of weaknes, SOB, diaphoresis
May subside with nitro
Presentation in elderly may be less specific
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ECG
Echo
Stress test
CRP
Cardiac cath or angiography
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Decrease oxygen demand and increase
oxygen supply
Pharmacologic therapy
Reperfusion therapies (percutaneous
coronary interventions such as atherectomy,
intracoronary stents and PTCA)
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Nitrates mainstay
Beta blockers—reduce myocardial oxygen
consumption
Calcium channel blockers—decrease SA node
conduction, decrease workload, decrease BP,
decrease vasospasm. Norvasc (amlodipine) ,
Cardizem (diltiazem)
Antiplatelet and anticoagulant medications
1. ASA
2. Plavix (clopidogrel) and Ticlid (ticlopidine)
3. Heparin (HIT), Fragmin or Lovenox
4. Glycoprotein IIb/IIIa agents (ReoPro
(abciximab) and Integrilin (eptifibatide))—
prevent adhesion of platelets with
fibrinogen
5. oxygen
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Assessment—presentation, description of
pain
Treat anginal symptoms—ntg, O2, vitals
Reduce anxiety
Prevent pain
Teaching
F/U
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Permanent injury
Reduced blood flow in coronary artery due to
rupture of plaque
Synonymous =coronary occlusion, heart
attack, MI
“time is muscle”
ST elevation, non-ST segment elevation,
location of injury (anterior, inferior, posterior,
lateral wall)
Q wave
Clinical manifestations
 chest pain, discomfort, pressure
 SOB
 Indigestion, nausea
 Anxiety
 Diaphoresis
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Like patient with angina
ECG—damaged cells will have changes in
repolarization and depolarization; T wave
inversion, ST segment changes, Q wave (no
depolarization through this tissue)
Echo to evaluate ventricular function
Labs—CK, MB (cardiac specific) peaks in 24h;
troponin (critical marker, may remain
elevated for weeks), myoglobin (earliest but
less specific)
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Rapid transit to hospital
12 lead within 10 minutes, serial ECGs
Labs, biomarkers
Cxray (establish baseline)
O2, Ntg, MS, ASA, beta-blocker, ACEI in 24h
Evaluate for indications for reperfusion Tx—
PCI, thrombolysis
Continue therapy—Plavix, IV heparin,
Glycoprotein IIb/IIIA inhibitors
Bedrest 12-24h
Rehab—gradual physical conditioning
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PTCA—angina, intervention to open blocked
coronaries
Coronary stents—metal mesh that provides
structural support to vessel
Atherectomy
Brachytherapy—radioisotope may be
delivered by catheter or implanted with stent
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Dissection
Perforation
Vasospasm
MI
Dysrhythmias
Cardiac arrest
Bleeding from insertion site
Hematoma
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GIIa/IIIb agents
Pressure over femoral sheath insertion site
Leg straight for several hours (varies accord.
to size of sheath used, amount of
anticoagulant and physician preference)
Watch site for hematoma
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Indicated when unable to control angina
w/meds and PCI
Treatment of left main coronary stenosis or
multivessel CAD
Treatment for complications from an
unsuccessful PCI
Indicated when coronaries with >70%
occlusion (60% in left main coronary)
Saphenous or internal mammary arteries
used for grafts
Assess:
1. Respiratory status
2. Cardiac status
3. Neurologic status
4. Peripheral vascular status
5. Renal function
6. Fluid and lytes
7. Pain
8. Family needs
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Ett and vent
ECG
Swan-Ganz catheter—hemodynamic
monitoring
Pacemaker
Aline
Chest tubes
Neuro status
NG tube
Foley
Surgical sites
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Restore cardiac output
Promote gas exchange
Maintain fluid and electrolyte balance
Minimize sensory-perception imbalance
Relieving pain
Maintaining adequate tissue perfusion
Maintaining normal body temperature
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Inflammation of the pericardium
Caused by: idiopathic, infection (usually
viral), CT disorders (SLE), MI, neoplasia,
radiation therapy, trauma, renal failure, TB
Manifestations: constant chest pain, scratchy
friction rub, increased WBC, increased CRP or
ESR, pain worsens with deep breath and
relieved by leaning forward
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Dx based on history, signs, and symptoms
Echo may show effusion
May need pericardiocentesis
CT helpful in quantifying effusion
12 lead ECG will show concave ST elevations
in many leads
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Determine cause
Symptomatic relief (rest, analgesics)
Watch for s/s of tamponade
Tx with NSAIDs—hasten reabsorption of
fluid; Indocin is contraindicated as it may
decrease coronary flow
Pericardiocentesis (culture fluid)
Pericardial window to allow continuous
drainage (drains into lymph system)
Pericardiectomy to relieve constriction
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<120/80 mm Hg normal
120/129/80-89 prehypertension
140-159/90-99 Stage 1 hypertension
≥ to 160 or ≥ to 100 Stage 2 hypertension
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Is considered a sign, not a disease per se
90% idiopathic
Increased sympathetic nervous system
activity
Increased renal absorption of sodium,
chloride, and water in kidneys
Increased activation of RAAS
Changes in vascular endothelium, less
vasodilation
Resistance to insulin action
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Avoid smoking for 30’ before BP check
Sit for 5 minutes
Appropriate size of cuff
Both arms, take the higher BP
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Accumulation of atherosclerotic plaques
Decreased elasticity of the major blood
vessels
Decreased stretch so increased pressure
Isolated systolic hypertension
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Overtly may be no s/s
Retinal changes—hemorrhages, cotton wool
spots (small infarctions), papilledema
(swelling of disc)
Left ventricular hypertrophy
Renal dysfunction
CVA
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H&P
Retinal exam
UA, chemistry, lytes, creatinine, BS, lipid
profile, 12 lead ECG
24 hour urine for creatinine clearance
microalbuminuria
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BP <130/80 in diabetics
Weight loss
Reduced alcohol and sodium intake
Exercise
Low fat diet with high intake of fruits and
vegetables (DASH diet, dietary approaches to
stop hypertension)
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Stage 1 hypertension—thiazides, ACEIs,
ARBs, CCB, renin inhibitor or combination
Stage 2 hypertension—2 drug combination
With compelling indications include: heart
failure, post MI, high CV risk, diabetes,
chronic kidney disease
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Thiazide diuretics—HCTZ
Aldosterone receptor blockers—Aldactone
(spironolactone)
Alpha 2 agonists—Aldomet (methyldopa),
Catapres (clonidine)
Beta blockers—No longer first line. Lopressor
(metoprolol), Tenormin (atenolol)
Alpha1 blockers—Minipress (prazosin)
Combined alpha/beta blockers--Coreg
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Vasodilators: Corlopam (fenoldopam),
Apresoline (hydralazine), Nipride
(nitroprusside)
ACEIs: Vasotec (enalapril), Accupril (quinapril)
ARBs: Diovan (valsartan), Micardis
(telmisartan)
Renin inhibitors—Tekturna (aliskiren)
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Nondihydropyridines: Cardizem (diltiazem),
Calan (verapamil)
Dihydropyridines: Norvasc (amlodipine),
Plendil (felodipine)
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Hypertensive emergency:acute, lifethreatening. Greater than 180/120, do not
lower to <140/90. Nipride, Cordopam
(felodapam), Cardene, Nitro-Bid.
Goal is to reduce mean BP by up to 25% in
first hour, further reduction over 6 hours
Hypertensive urgency—very elevated BP but
no evidence of impending organ damage.
Characterized by nosebleeds, HAs, anxiety.
Give clonidine, captopril, labetalol.
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Inability of heart to pump sufficient blood to
meet the needs of tissues for oxygen and
nutrients
Results in fluid overload and decreased tissue
perfusion
Problem lies either with contraction (systolic
dysfunction) or with filling of the heart
(diastolic dysfunction)
Increases with age
Two types
 Systolic—weakened heart muscle
 Diastolic—stiff and noncompliant heart
muscle
 Assess EF to determine type of failure
 Normal EF is 50-70%
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I asymptomatic, no limitations of ADL
II slight alterations in ADL, S/S with activity
III marked limitations of ADL, comfortable at
rest, worsening activity tolerance
IV cardiac insufficiency at rest
Myocardial dysfunction
Activation of RAAS
Activation of baroreceptors
Stimulation of vasomotor regulatory centers in medulla
Activation of sympathetic
nervous system
Ventricular remodeling
1.
2.
3.
4.
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6.
7.
8.
Myocardial dysfunction—hypertension, MI
cardiac output, systemic blood pressure and
kidney perfusion
Activation of renin-angiotensin-aldosterone
system
Activation of baroreceptors
Stimulation of vasomotor regulatory centers
Activation of sympathetic nervous systemcatecholamines with resultant
vasoconstriction, afterload, BP, HR
Ventricular hypertrophy, impaired contractility
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Caused by CAD
Cardiomyopathy
Hypertension
Valvular disorders
Atherosclerosis of the coronaries is the
primary cause of heart failure
Ischemia causes resulting hypoxia, acidosis
MI results in decreased contractility, extent of
damage results in degree of heart failure
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Left-sided heart failure
Right-sided heart failure
High output heart failure
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Three types of cardiomyopathy (Dilated,
hypertrophic and restrictive)
Pulmonary hypertension—increases
afterload, leads to ventricular hypertrophy
Valvular heart disease—valvular dysfunction
leads to increasing heart pressures
increasing cardiac workload
Fever, thyrotoxicosis, iron overload, severe
anemia, cardiac dysrhythmias
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May be acute or chronic
May be systolic or diastolic
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Insufficient force to eject adequate amount
of blood into circulation
Preload increases with decreased
contractility and afterload increases as result
of increased peripheral resistance
Ejection fraction will drop
As ejection fraction decreases, tissue
perfusion diminished, blood accumulates in
pulmonary tissues
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Occurs when left ventricle is unable to relax
adequately during diastole
Stiffening prevents ventricle from adequate
filling to ensure adequate cardiac output
Occurs in 20-40% of those with heart failure
S/S similar to those with systolic failure
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Pulmonary congestion—dyspnea, cough,
crackles, low oxygen saturation
S3 secondary to large volume of fluid
entering left ventricle
Dry cough progressing to “pink, frothy”
cough
Inadequate tissue perfusion leading to
increased sympathetic activity so tachycardia
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Decreased renal perfusion results in oliguria
Increased renin results in aldosterone
secretion and increased intravascular volume
Changes in sensorium
Obvious activity intolerance
Skin is pale and cool
Thready pulses
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Congestion in the peripheral tissues and
viscera predominate
Heart unable to effectively eject blood and
accommodate returning blood
JVD and increased hydrostatic pressure
Dependent edema, hepatomegaly, ascites,
nausea, weakness, weight gain
Anorexia due to venous engorgement
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Echocardiogram
ECG
Cxray
Labs: CBC, CMP, lipid panel, BUN/creatinine,
TSH, BNP, UA
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O2
Low sodium (2 gm) diet and fluid restriction
ACEIs
ARBs
Nitrates
Beta blockers
Diuretics
Digitalis
Calcium channel blockers
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Natrecor (nesiritide)—recombinant BNP,
causes vasodilation, suppresses
neurohormones that cause retention of
sodium. Decreases preload and afterload.
Primacor (milrinone )—phosphodiesterase
inhibitor, delays IC calcium release, acts as
vasodilator. Decreases preload and afterload.
Dobutamine—beta 1 stimulation.
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History—wt. gain, orthopnea, cough, activity
changes, chest discomfort, diuresis at night,
nutritional history
Physical assessment-LOC, vitals, heart
sounds, lung sounds, JVD, dependent edema,
weight , skin turgor
Administer medications
Be alert for complications of therapy—
monitor electrolytes, urinary output, BP
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Acute event that results in heart failure
Can occur from acute MI or from chronic HF
exacerbation
Results from inability of left ventricle to
handle fluid volume, pump effectively
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Restlessness
Breathlessness
Nail bed cyanosis
Weak pulses
O2 sat decreased
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Reduce volume overload
improve ventricular function
increase/improve respiratory exchange
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Oxygen
Morphine
Diuretics
IV Primacor, dobutamine or Natrecor
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Inadequate cardiac output leads to
inadequate tissue perfusion and initiation of
shock
Can result after acute MI or result of end
stage heart failure
Also can occur from cardiac tamponade, PE,
CM and dysrhythmias
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Degree of shock is proportional to extent of
left ventricular dysfunction
Decreased SV and CO
Reduction in perfusion causes decreased
oxygen supply to vital organs and to heart
Inadequate emptying results in pulmonary
congestion
Release of catecholamines increasing HR,
increasing afterload, increasing myocardial
oxygen demands
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Cerebral hypoxia
Low blood pressure
Rapid and weak pulse
Cold and clammy skin
Tachypnea
Decreased urinary output
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Correct underlying problem, e.g.
dysrhythmias
Improve oxygenation, intubation, positive
pressure ventilation
Pharmacologic therapy—diuretics,
vasodilators, inotropes, vasopressors
IABP
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Constant monitoring—BP, HR
Cardiac rhythm
Hemodynamics
Fluid status
Adjust meds based on assessment
Watching for s/s of complications