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NUR_4206--Patients_with_Cardiac_Problems

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					Nursing Care of Patients with Cardiac Problems
   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
   Pericardium
   Epicardium
   Myocardium
   Endocardium
   Right side of heart—workload is light
    compared to left side; pulmonary circulation
   Left side of heart—high pressure system,
    systemic circulation
   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
   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
   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
   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. 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
   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-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
   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 end-
  diastolic volume that is ejected, ~50-70%
   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. Low levels
    predispose to atrial and ventricular
    dysrhythmias. Increased levels depress
    contractility and excitability of heart.
   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.
   Case Studies
   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. 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.
So pacemaker that is VVIOO would indicate?
DDIRD.
   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
   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
   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
   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
   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 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
   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
   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
   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
   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. 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.
   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
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. Decreases preload and afterload.
   Primacor (milrinone )—phosphodiesterase
    inhibitor, delays IC calcium release, acts as
    vasodilator. Decreases preload and afterload.
   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

				
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