Nursing Care of Patients with

Cardiac Problems
 One in five people possess some form of
cardiovascular disease
 With increase in metabolic syndrome and
aging baby boomers, numbers increasing
 Cardiovascular disease is the number one
cause of death in women.
 Major cause of mortality in 21st century
 Number of cardiovascular problems that can
occur
 Pericardium
 Epicardium
 Myocardium
 Endocardium
 Right side of heart
 Left side of heart
 S1
 S2
 Splitting of S1 and S2 can be
accentuated by inspiration
S3 is ventricular
S4 is an atrial
 Systolic murmurs
 Diastolic murmurs
 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
 Heart perfused by coronaries during diastole
 Right coronary
 Left coronary
 Circumflex
 Must be 60-70 to maintain perfusion of vital
organs
 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
 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
 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
 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
 Phase 3—Marks completion of repolarization
and return of the cell to resting state
 Phase 4-resting phase before next
depolarization
 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.
Factors increasing likelihood of premature
depolarization
 Hypokalemia
 Hypomagnesemia
 Hypothermia
 Myocardial injury
 Acidosis
 hypercarbia
 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
 Calculate heart rate
 Heart rhythm
 Analyze P waves
 Measure P-R interval
 Measure QRS duration
 Interpretation
 PR interval <.20 second
 QRS interval < or equal to .12 second
 QT interval variable, generally less than .42
second
 P for every QRS
 Normal sinus rhythm—60 to 100
 Sinus dysrhythmia
l
 Tachydysrhythmias-->120
 Bradydysrhythmias--<60
 Premature complexes
 Repetitive rhythms—atrial flutter
 Escape complexes—idioventricular rhythm
 Sinus tachycardia
 Sinus bradycardia
 Supraventricular rhythms
 Atrial fibrillation or flutter
 1st, 2nd, 3rd degree heart blocks
 Vtach, Vfib, asystole
 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-
 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
 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
 afterload
 contractility
 Ejection Fraction
 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
 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
 Cigarette smoking
 Genetics
 Physical inactivity
 Obesity
 Hyperlipidemia
 Diabetes mellitus
 Hypertension
 History
 Chest pain or discomfort
 SOB
 Peripheral edema and weight gain
 Palpitations
 Fatigue
 Dizziness, syncope, changes in level of
consciousness
 Angina pectoris
 Pericarditis
 Pulmonary disorders—pneumonia, PE
 Esophageal disorders
 Anxiety and panic disorders
 Musculoskeletal disorders--costochondritis
 Atypical presentation
 Fatigue, sleep disturbances, shortness of
breath
 Historically undertreated due to ambiguous
presentation
 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
 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
 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
 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
 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
 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
 Total cholesterol 122-200
 Triglycerides—122-200
 HDL—55-60
 LDL—60-180
 HDL: LDL ratio—3:1
 Homocysteine—indicates risk for CVD.
Linked to development of atherosclerosis. 12-
hour 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.
 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
 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
 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
 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.
 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
 Class III—Potassium channels. Prolong
repolarization, for atrial and ventricular
dysrhythmias especially when ventricular
dysfunction present.
 EX. Cordarone (amiodarone), Corvert
(ibutilide).
 SE: pulmonary toxicity, corneal
microdeposits, bradycardia, AV blocks, heart
failure, hypotension with IV administration,
peripheral edema.
 Class IV—block calcium channels. For atrial
dysrhythmias. Cardizem (diltiazem), Calan
(verapamil). Bradycardia, AV blocks,
Hypotension, peripheral edema
 Timed electrical current to terminate a
tachydysrhythmia
 Defibrillation-treatment of choice for
ventricular fibrillation and pulseless VTach
 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.
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.
 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.
 Nonsensing
 Noncapture
 Nonpace
 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
 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
 Inflammation affecting arterial walls
 Results in plaque formation
 Impedes flow
 Results in atherosclerosis
 High lipids
 Smoking
 Hypertension
 Diabetes mellitus
 Family history
 Metabolic syndrome
 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
 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
 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
 Promote smoking cessation
 Manage hypertension—prehypertensive if BP
> 120/80; inflammatory process
 Control diabetes
 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
 Clinical syndrome
 characterized by episodes or paroxysms of
pain or pressure secondary to insufficient
coronary blood flow; decreased oxygen
supply
 Caused by atherosclerosis
 Obstructions of coronaries
 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
 Variant angina (Prinzmetal’s angina
 Norturnal angina
 Angina decubitus
 Intractable angina
 Postinfarction angina
 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
 ECG
 Echo
 Stress test
 CRP
 Cardiac cath or angiography
 Decrease oxygen demand and increase
oxygen supply
 Pharmacologic therapy
 Reperfusion therapies (percutaneous
coronary interventions such as atherectomy,
intracoronary stents and PTCA)
 Nitrates
 Beta blockers
 Calcium channel blockers
 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
 Assessment—presentation, description of
pain
 Treat anginal symptoms—ntg, O2, vitals
 Reduce anxiety
 Prevent pain
 Teaching
 F/U
 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
 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)
 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
 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
 Dissection
 Perforation
 Vasospasm
 MI
 Dysrhythmias
 Cardiac arrest
 Bleeding from insertion site
 Hematoma
 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
 Ett and vent
 ECG
 Swan-Ganz catheter—hemodynamic
monitoring
 Pacemaker
 Aline
 Chest tubes
 Neuro status
 NG tube
 Foley
 Surgical sites
 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
 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
 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
 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
 <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
 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
 Avoid smoking for 30’ before BP check
 Sit for 5 minutes
 Appropriate size of cuff
 Both arms, take the higher BP
 Accumulation of atherosclerotic plaques
 Decreased elasticity of the major blood
vessels
 Decreased stretch so increased pressure
 Isolated systolic hypertension
 Overtly may be no s/s
 Retinal changes—hemorrhages, cotton wool
spots (small infarctions), papilledema
(swelling of disc)
 Left ventricular hypertrophy
 Renal dysfunction
 CVA
 H&P
 Retinal exam
 UA, chemistry, lytes, creatinine, BS, lipid
profile, 12 lead ECG
 24 hour urine for creatinine clearance
 microalbuminuria
 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)
 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
 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
 Vasodilators: Corlopam (fenoldopam),
Apresoline (hydralazine), Nipride
(nitroprusside)
 ACEIs: Vasotec (enalapril), Accupril (quinapril)
 ARBs: Diovan (valsartan), Micardis
(telmisartan)
 Renin inhibitors—Tekturna (aliskiren)
 Nondihydropyridines: Cardizem (diltiazem),
Calan (verapamil)
 Dihydropyridines: Norvasc (amlodipine),
Plendil (felodipine)
 Hypertensive emergency:acute, life-
threatening. Greater than 180/120, do not
lower to <140/90.
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.
 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%
 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. Myocardial dysfunction—hypertension, MI
2. cardiac output, systemic blood pressure and
kidney perfusion
3. Activation of renin-angiotensin-aldosterone
system
4. Activation of baroreceptors
5. Stimulation of vasomotor regulatory centers
6. Activation of sympathetic nervous system-
7. catecholamines with resultant
vasoconstriction, afterload, BP, HR
8. Ventricular hypertrophy, impaired contractility
 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
 Left-sided heart failure
 Right-sided heart failure
 High output heart failure
 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
 May be acute or chronic
 May be systolic or diastolic
 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
 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
 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
 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
 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
 Echocardiogram
 ECG
 Cxray
 Labs: CBC, CMP, lipid panel, BUN/creatinine,
TSH, BNP, UA
 O2
 Low sodium (2 gm) diet and fluid restriction
 ACEIs
 ARBs
 Nitrates
 Beta blockers
 Diuretics
 Digitalis
 Calcium channel blockers
 Natrecor (nesiritide)—recombinant BNP,
causes vasodilation, suppresses
neurohormones that cause retention of
sodium.
 Primacor (milrinone )—phosphodiesterase
inhibitor, delays IC calcium release, acts as
vasodilator.
 Dobutamine—beta 1 stimulation.
 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
 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
 Restlessness
 Breathlessness
 Nail bed cyanosis
 Weak pulses
 O2 sat decreased
 Reduce volume overload
 improve ventricular function
 increase/improve respiratory exchange
 Oxygen
 Morphine
 Diuretics
 IV Primacor, dobutamine or Natrecor
 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
 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
 Cerebral hypoxia
 Low blood pressure
 Rapid and weak pulse
 Cold and clammy skin
 Tachypnea
 Decreased urinary output
 Correct underlying problem, e.g.
dysrhythmias
 Improve oxygenation, intubation, positive
pressure ventilation
 Pharmacologic therapy—diuretics,
vasodilators, inotropes, vasopressors
 IABP
 Constant monitoring—BP, HR
 Cardiac rhythm
 Hemodynamics
 Fluid status
 Adjust meds based on assessment
 Watching for s/s of complications