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NUR 4206 By Linda Self

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Title: NUR 4206 By Linda Self


1
NUR 4206 By Linda Self
  • Nursing Care of Patients with Cardiac Problems

2
Assessment of the Cardiovascular System
  • 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

3
Review of Heart AP
  • Pericardium
  • Epicardium
  • Myocardium
  • Endocardium

4
Heart Chambers
  • Right side of heartworkload is light compared to
    left side pulmonary circulation
  • Left side of hearthigh pressure system, systemic
    circulation

5
Heart Sounds
  • 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
  • GallopsS3 and S4

6
Gallops
  • S3 is ventricular gallopnormal in children. In
    those over 35, indicates early heart failure, VSD
    or decreased ventricular compliance
  • S4 is an atrial gallopseen in hypertension,
    anemia, aortic or pulmonic stenosis and pulmonary
    emboli

7
Murmurs
  • Systolic murmursaortic stenosis and mitral
    regurgitation. Occur between S1 and S2.
  • Diastolic murmursaortic 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

8
Coronary Arteries
  • Heart perfused by coronaries during diastole
  • Right coronary
  • Left coronary
  • Circumflex
  • Must be 60-70 to maintain perfusion of vital
    organs

9
Coronaries
  • Left coronary perfuses left ventricle, septum,
    chordae tendinae, papullary muscle and portion of
    right ventricle
  • Right coronarysupplies right atrium, right
    ventricle, inferior portion of left ventricle

10
Unique characteristics of the heart
  • Automaticityintercalated discs
  • Conductivity
  • Contractility
  • Excitability

11
Assessment of Cardiovascular Function
  • Cardiac conduction system
  • SA node
  • Internodal tracts
  • AV node/junction
  • Bundle of His
  • Right and left bundle branches
  • Purkinje fibers

12
Cardiac action potential
  • 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

13
Action Potential
  • Phase Ocellular depolarization initiated as
    positive ions influx into cell. Sodium moves
    rapidly into myocytes depolarization of SA and
    AV nodes via slow calcium channels
  • Phase 1Early cellular repolarization occurs as
    potassium exits intracellular space
  • Phase 2plateau phase, rate of repolarization
    slows, calcium ions enter intracellular space

14
Cardiac Action Potential
  • Phase 3Marks completion of repolarization and
    return of the cell to resting state
  • Phase 4-resting phase before next depolarization

15
Refractory Period
  • During this phase, cells are incapable of being
    stimulated
  • Absolute refractory periodunresponsive to any
    electrical stimulus, Phase O to middle of Phase 3
  • Relative refractory periodbrief period at end of
    Phase 3. Strong enough impulse can cause
    depolarization prematurely. This increases the
    risk for serious dysrhythmias.

16
Refractory Period
  • Factors increasing likelihood of premature
    depolarization
  • Hypokalemia
  • Hypomagnesemia
  • Hypothermia
  • Myocardial injury
  • Acidosis
  • hypercarbia

17
Quick look analysis of cardiac dysrhythmias
  • 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

18
Systematic analysis
  • Calculate heart rate
  • Heart rhythm
  • Analyze P waves
  • Measure P-R interval
  • Measure QRS duration
  • Interpretation

19
Analysis dependent on specific criteria
  • PR interval lt.20 second
  • QRS interval lt or equal to .12 second
  • QT interval variable, generally less than .42
    second
  • P for every QRS

20
Normal rhythms
  • Normal sinus rhythm60 to 100
  • Sinus dysrhythmia
  • l

21
Dysrhythmias
  • Tachydysrhythmias--gt120
  • Bradydysrhythmias--lt60
  • Premature complexes
  • Repetitive rhythmsatrial flutter
  • Escape complexesidioventricular rhythm

22
Common dysrhythmias
  • Sinus tachycardia
  • Sinus bradycardia
  • Supraventricular rhythms
  • Atrial fibrillation or flutter
  • 1st, 2nd, 3rd degree heart blocks
  • Vtach, Vfib, asystole

23
Cardiac Hemodynamics
  • 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
  • Diastoleventricles are relaxed, AV valves open,
    atria fill first, ventricles fill, electrical
    impulse, atria contract, impulse is propagated to
    ventricles, ventricles fill then will contract

24
Cardiac Output
  • 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

25
Control of Stroke Volume
  • Affected by
  • preloaddegree 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
  • contractilityforce generated by the contracting
    myocardium
  • Ejection Fraction--Percentage of end-diastolic
    volume that is ejected, 50-70

26
Control of Stroke Volume
  • 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
  • Contractilityforce of generated by the
    contracting myocardium

27
Gerontologic Considerations
  • 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

28
Heart disease risk factors
  • Cigarette smoking
  • Genetics
  • Physical inactivity
  • Obesity
  • Hyperlipidemia
  • Diabetes mellitus
  • Hypertension

29
Health History and Clinical Manifestations
  • History
  • Chest pain or discomfort
  • SOB
  • Peripheral edema and weight gain
  • Palpitations
  • Fatigue
  • Dizziness, syncope, changes in level of
    consciousness

30
Differing kinds of chest pain
  • Angina pectoris
  • Pericarditis
  • Pulmonary disorderspneumonia, PE
  • Esophageal disorders
  • Anxiety and panic disorders
  • Musculoskeletal disorders--costochondritis

31
Women and symptoms of MI
  • Atypical presentation
  • Fatigue, sleep disturbances, shortness of breath
  • Historically undertreated due to ambiguous
    presentation

32
Physical Assessment
  • General appearance and cognition
  • Inspection of the skin
  • Blood pressuredifference 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

33
Physical Assessment
  • JVD when head of bed is elevated 45 to 90 degrees
  • Heart soundsS1, 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

34
Physical Assessment
  • Assess clubbing by the Schamroth method
  • Blood pressurehypertension
  • Prehypertension120-130/80-89
  • Postural hypotensionBP decrease by 20 torr
    systolic or 10 torr diastolic plus 10-20
    increase in heart rate. Supine,sitting, standing.
  • Ankle-brachial indexassess vascular status of
    LE. LE SBP divided by brachial BP. Should be 1,
    .8 moderate disease, .5 severe

35
Gerontologic Considerations
  • Changes in AP diameter
  • Isolated systolic hypertensionincreases 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

36
Diagnostic Evaluation
  • Cardiac biomarkers
  • Creatine kinase and CK-MBmost specific in MI
  • Myoglobinheme 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 Iproteins found only in cardiac
    muscle, detected within 3-4 hours, peak in 4-24
    and remain elevated for 1-3 weeks

37
Blood chemistry, hematology and coagulation
studies
  • Lipid profileobtain after a 12 hour fast
  • Brain (B type) Natriuretic Peptideneurohormone
    that regulates BP and fluid volume. Level
    increases as increased ventricular pressure as
    seen in heart failure. gt51.2 is considered
    abnormal.
  • C Reactive Proteinprotein released by liver and
    reflects systemic inflammation. Normal is less
    than 1.0

38
Diagnostic Studies
  • ECGgraphic recording of the electrical activity
    of the heart. Up to 18 leads.
  • Telemetryradiowaves
  • Holter monitoring
  • Wireless mobile cardiac monitoring
  • Exercise stress test
  • Pharmacologic stress testPersantine and
    adenocard are given, simulate effects of
    exercise dobutamine also, helpful on those with
    bronchospasm

39
Lipids
  • Total cholesterol 122-200
  • Triglycerides122-200
  • HDL55-60
  • LDL60-180
  • HDL LDL ratio31

40
Blood chemistries cont.
  • Homocysteineindicates risk for CVD. Linked to
    development of atherosclerosis. 12- hour fast
    needed for reliable monitoring of level. Normal
    5-15 micromol/L
  • Magnesiumnecessary 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.

41
Diagnostic Testing cont.
  • Echocardiographynoninvasive 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

42
Diagnostic Testing
  • PET scan can be used to measure cardiac
    dysfunction
  • MRI
  • Cardiac catheterization with angiographycontrast,
    know BUN/creatinine, INR, PT, PTT
  • Must be fasting. Have IV access.
  • Following cath, observe catheter access site for
    bleeding
  • Monitor extremityCSM

43
Cardiac Catheterization cont.
  • Bedrest for 2-6 hours
  • Monitor for dysrhythmias
  • Monitor for contrast agent induced renal failure,
    IO, hydration
  • Ensure patient safetyinstruct no lifting for
    24h, no straining, avoid tub baths, s/s of
    bleeding, swelling, bruising, pain or fever

44
Drug Therapy for dysrhythmias
  • Class IA Na channels.Depress depolarization,
    prolong repolarization. For atrial and
    ventricular dysrhythmias. Pronestyl
    (procainamide). Proarrhythmic. Lupus-like
    syndrome.
  • Class IBminimal depression of depolarization,
    shortened repolarization. Treats ventricular
    dysrhythmias. Xylocaine (lidocaine) and Mexitil
    (mexilitene). CNS changes.

45
  • Case Studies

46
Anti-Dysrhythmics
  • Class ICmarked depression of depolarization
    little effect on repolarization. Tx of atrial and
    ventricular dysrhythmias. Tambocor (flecainide)
    and Rythmol (propafenone). Proarrhythmic, HF, AV
    blocks
  • Class IIBeta blockers.Decrease automaticity and
    conduction. Treats atrial and ventrcular
    dysrhythmias. Tenormin (atenolol), Lopressor
    (metoprolol), Inderal (propranolol), bradycardia,
    heart failure, bronchospasm, masks hypoglycemia

47
Anti-Dysrhythmics
  • Class IIIPotassium 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.

48
Anti-Dysrhythmics
  • Class IVblock calcium channels. For atrial
    dysrhythmias. Cardizem (diltiazem), Calan
    (verapamil). Bradycardia, AV blocks, Hypotension,
    peripheral edema

49
Cardioversion and Defibrillation
  • Timed electrical current to terminate a
    tachydysrhythmia
  • Defibrillation-treatment of choice for
    ventricular fibrillation and pulseless VTach

50
Pacemaker Therapy
  • 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

51
Pacemakers
  • Universal code indicates five letters
  • Identifies chamber being paced. V, A, D (dual).
  • Indicates chamber(s) being sensed. A, V, D, O
    (meaning sensing function is off)
  • Indicates type of response to the sensing.
    Inhibition and Triggered responses. I, T, O.

52
Pacemakers
  • 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.

53
Complications of Pacemaker Use
  • 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.

54
Complications of Pacemakers
  • Nonsensing
  • Noncapture
  • Nonpace

55
Implantable Cardioverter/defibrillator
  • 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

56
Electrophysiologic Studies
  • 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

57
Coronary Artery Disease
  • Inflammation affecting arterial walls
  • Results in plaque formation
  • Impedes flow
  • Results in atherosclerosis

58
CAD
  • High lipids
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Family history
  • Metabolic syndrome

59
CAD modifiable risk factors
  • Cholesterol
  • Tobacco use
  • Weight
  • Hypertension
  • Diabetes mellitus

60
Diet for therapeutic lifestyle changes
  • Total fat25-35 of total calories
  • Saturated fatlt7
  • Polyunsaturated fat --up to 10 of total
    calories
  • Monounsaturated fatup to 20 of total
    calories
  • CHO 50-60 of total calories
  • Fiber20-30gm per day
  • Protein 15 of total calories
  • Cholesterol--lt200mg/day

61
Medications affecting lipoprotein metabolism
  • 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

62
Statins
  • 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

63
Others
  • Vytorincontroversial at this time
  • Zetia (ezetimibe)selective cholesterol
    absorption inhibitor
  • Lovaza (omega 3 fish oil)need 3-4 gms per day,
    good in hypertriglyceridemia

64
Modifying risk factors
  • Promote smoking cessation-Nicoderm, Zyban
    (bupropion), Chantix
  • Manage hypertensionprehypertensive if BP gt
    120/80 inflammatory process
  • Control diabeteshyperglycemia promotes
    dyslipidemia, increased platelet aggregation,
    increased thrombus formation impair endothelial
    cell-dependent vasodilation and smooth muscle
    function

65
Gender
  • 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

66
Angina Pectoris
  • Clinical syndrome characterized by episodes or
    paroxysms of pain or pressure secondary to
    insufficient coronary blood flow decreased
    oxygen supply

67
Pathophysiology of Angina
  • Caused by atherosclerosis
  • Obstructions of coronaries

68
Types of Angina
  • Stable anginaoccurs on exertion
  • Unstable anginacrescendo, threshold lower,
    sometimes pain at rest
  • Refractory angina
  • Variant angina-vasospasm, reversible ST elevation
  • Silent ischemiaECG changes but w/o symptoms

69
Manifestations
  • 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

70
Diagnosis
  • ECG
  • Echo
  • Stress test
  • CRP
  • Cardiac cath or angiography

71
Medical Management
  • Decrease oxygen demand and increase oxygen supply
  • Pharmacologic therapy
  • Reperfusion therapies (percutaneous coronary
    interventions such as atherectomy, intracoronary
    stents and PTCA)

72
Pharmacologic Therapy
  • Nitrates mainstay
  • Beta blockersreduce myocardial oxygen
    consumption
  • Calcium channel blockersdecrease SA node
    conduction, decrease workload, decrease BP,
    decrease vasospasm. Norvasc (amlodipine) ,
    Cardizem (diltiazem)

73
Pharmacologic Therapy
  • Antiplatelet and anticoagulant medications
  • ASA
  • Plavix (clopidogrel) and Ticlid (ticlopidine)
  • Heparin (HIT), Fragmin or Lovenox
  • Glycoprotein IIb/IIIa agents (ReoPro (abciximab)
    and Integrilin (eptifibatide))prevent adhesion
    of platelets with fibrinogen
  • oxygen

74
Role of nurse
  • Assessmentpresentation, description of pain
  • Treat anginal symptomsntg, O2, vitals
  • Reduce anxiety
  • Prevent pain
  • Teaching
  • F/U

75
Myocardial Infarction
  • 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

76
MI
  • Clinical manifestations
  • chest pain, discomfort, pressure
  • SOB
  • Indigestion, nausea
  • Anxiety
  • Diaphoresis

77
Assessment and Diagnostic Findings
  • Like patient with angina
  • ECGdamaged 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
  • LabsCK, MB (cardiac specific) peaks in 24h
    troponin (critical marker, may remain elevated
    for weeks), myoglobin (earliest but less specific)

78
Medical Management of MI
  • 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 TxPCI,
    thrombolysis
  • Continue therapyPlavix, IV heparin, Glycoprotein
    IIb/IIIA inhibitors
  • Bedrest 12-24h
  • Rehabgradual physical conditioning

79
Invasive Coronary Artery Procedures
  • PTCAangina, intervention to open blocked
    coronaries
  • Coronary stentsmetal mesh that provides
    structural support to vessel
  • Atherectomy
  • Brachytherapyradioisotope may be delivered by
    catheter or implanted with stent

80
Complications of Invasive Procedures
  • Dissection
  • Perforation
  • Vasospasm
  • MI
  • Dysrhythmias
  • Cardiac arrest
  • Bleeding from insertion site
  • Hematoma

81
Postprocedure
  • 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

82
Coronary Artery Revascularization
  • 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 gt70 occlusion
    (60 in left main coronary)
  • Saphenous or internal mammary arteries used for
    grafts

83
Post-CABG
  • Assess
  • Respiratory status
  • Cardiac status
  • Neurologic status
  • Peripheral vascular status
  • Renal function
  • Fluid and lytes
  • Pain
  • Family needs

84
Post CABG
  • Ett and vent
  • ECG
  • Swan-Ganz catheterhemodynamic monitoring
  • Pacemaker
  • Aline
  • Chest tubes
  • Neuro status
  • NG tube
  • Foley
  • Surgical sites

85
Nursing Interventions
  • 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

86
Pericarditis
  • 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

87
Pericarditis
  • 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

88
Medical Management
  • Determine cause
  • Symptomatic relief (rest, analgesics)
  • Watch for s/s of tamponade
  • Tx with NSAIDshasten 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

89
Hypertension
  • lt120/80 mm Hg normal
  • 120/129/80-89 prehypertension
  • 140-159/90-99 Stage 1 hypertension
  • to 160 or to 100 Stage 2 hypertension

90
Pathophysiology of 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

91
Measuring blood pressure
  • Avoid smoking for 30 before BP check
  • Sit for 5 minutes
  • Appropriate size of cuff
  • Both arms, take the higher BP

92
Gerontologic Considerations
  • Accumulation of atherosclerotic plaques
  • Decreased elasticity of the major blood vessels
  • Decreased stretch so increased pressure
  • Isolated systolic hypertension

93
Clinical Manifestations
  • Overtly may be no s/s
  • Retinal changeshemorrhages, cotton wool spots
    (small infarctions), papilledema (swelling of
    disc)
  • Left ventricular hypertrophy
  • Renal dysfunction
  • CVA

94
Assessment and Diagnostic Evaluation
  • HP
  • Retinal exam
  • UA, chemistry, lytes, creatinine, BS, lipid
    profile, 12 lead ECG
  • 24 hour urine for creatinine clearance
  • microalbuminuria

95
Medical Management
  • BP lt130/80 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)

96
Pharmacologic Therapy
  • Stage 1 hypertensionthiazides, ACEIs, ARBs, CCB,
    renin inhibitor or combination
  • Stage 2 hypertension2 drug combination
  • With compelling indications include heart
    failure, post MI, high CV risk, diabetes, chronic
    kidney disease

97
Medication therapy for hypertension
  • Thiazide diureticsHCTZ
  • Aldosterone receptor blockersAldactone
    (spironolactone)
  • Alpha 2 agonistsAldomet (methyldopa), Catapres
    (clonidine)
  • Beta blockersNo longer first line. Lopressor
    (metoprolol), Tenormin (atenolol)
  • Alpha1 blockersMinipress (prazosin)
  • Combined alpha/beta blockers--Coreg

98
Medication Tx for hypertension
  • Vasodilators Corlopam (fenoldopam), Apresoline
    (hydralazine), Nipride (nitroprusside)
  • ACEIs Vasotec (enalapril), Accupril (quinapril)
  • ARBs Diovan (valsartan), Micardis (telmisartan)
  • Renin inhibitorsTekturna (aliskiren)

99
Antihypertensives
  • Nondihydropyridines Cardizem (diltiazem), Calan
    (verapamil)
  • Dihydropyridines Norvasc (amlodipine), Plendil
    (felodipine)

100
Hypertensive Crises
  • Hypertensive emergencyacute, life-threatening.
    Greater than 180/120, do not lower to lt140/90.
    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 urgencyvery elevated BP but no
    evidence of impending organ damage. Characterized
    by nosebleeds, HAs, anxiety. Give clonidine,
    captopril, labetalol.

101
Heart Failure
  • 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)

102
Chronic Heart Failure
  • Increases with age
  • Two types
  • Systolicweakened heart muscle
  • Diastolicstiff and noncompliant heart muscle
  • Assess EF to determine type of failure
  • Normal EF is 50-70

103
New York Heart Association Classification of
Heart Failure
  • 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

104
Pathophysiology
105
Heart Failure
  • Myocardial dysfunctionhypertension, 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 system-
  • catecholamines with resultant vasoconstriction,
    afterload, BP, HR
  • Ventricular hypertrophy, impaired contractility

106
Etiology of Myocardial Dysfunction
  • 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

107
Types of Heart Failure
  • Left-sided heart failure
  • Right-sided heart failure
  • High output heart failure

108
Heart Failure--contributors
  • Three types of cardiomyopathy (Dilated,
    hypertrophic and restrictive)
  • Pulmonary hypertensionincreases afterload, leads
    to ventricular hypertrophy
  • Valvular heart diseasevalvular dysfunction leads
    to increasing heart pressures increasing
    cardiac workload
  • Fever, thyrotoxicosis, iron overload, severe
    anemia, cardiac dysrhythmias

109
Left-sided Heart Failure
  • May be acute or chronic
  • May be systolic or diastolic

110
Systolic Heart Failure
  • 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

111
Diastolic Heart Failure
  • 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

112
Left sided heart failure
  • Pulmonary congestiondyspnea, 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

113
Left-sided Heart Failure cont.
  • 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

114
Right-Sided heart Failure
  • 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

115
Assessment and Diagnostic Findings
  • Echocardiogram
  • ECG
  • Cxray
  • Labs CBC, CMP, lipid panel, BUN/creatinine, TSH,
    BNP, UA

116
Medical Management
  • O2
  • Low sodium (2 gm) diet and fluid restriction
  • ACEIs
  • ARBs
  • Nitrates
  • Beta blockers
  • Diuretics
  • Digitalis
  • Calcium channel blockers

117
Intravenous Infusions
  • 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.
  • Dobutaminebeta 1 stimulation.

118
Nursing Management of the Patient with Heart
Failure
  • Historywt. 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 therapymonitor
    electrolytes, urinary output, BP

119
Acute Heart Failure (pulmonary edema)
  • 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

120
Manifestations
  • Restlessness
  • Breathlessness
  • Nail bed cyanosis
  • Weak pulses
  • O2 sat decreased

121
Medical Management
  • Reduce volume overload
  • improve ventricular function
  • increase/improve respiratory exchange

122
Medical Management
  • Oxygen
  • Morphine
  • Diuretics
  • IV Primacor, dobutamine or Natrecor

123
Cardiogenic Shock
  • 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

124
Pathophysiology of Cardiogenic Shock
  • 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

125
Clinical Manifestations
  • Cerebral hypoxia
  • Low blood pressure
  • Rapid and weak pulse
  • Cold and clammy skin
  • Tachypnea
  • Decreased urinary output

126
Medical Management
  • Correct underlying problem, e.g. dysrhythmias
  • Improve oxygenation, intubation, positive
    pressure ventilation
  • Pharmacologic therapydiuretics, vasodilators,
    inotropes, vasopressors
  • IABP

127
Nursing Management
  • Constant monitoringBP, HR
  • Cardiac rhythm
  • Hemodynamics
  • Fluid status
  • Adjust meds based on assessment
  • Watching for s/s of complications
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