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

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 A&P
Pericardium
Epicardium
Myocardium
Endocardium

4. Heart Chambers
Right side of heart—workload is light compared to left side; pulmonary circulation
Left side of heart—high 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
Gallops=S3 and S4

6. Gallops
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

7. Murmurs
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

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

9. Coronaries
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

10. Unique characteristics of the heart
Automaticity—intercalated 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 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

14. Cardiac Action Potential
Phase 3—Marks 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 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.

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 <.20 second
QRS interval < or equal to .12 second
QT interval variable, generally less than .42 second
P for every QRS

20. Normal rhythms
Normal sinus rhythm—60 to 100
Sinus dysrhythmia l

21. Dysrhythmias Tachydysrhythmias-->120 Bradydysrhythmias--<60
Premature complexes
Repetitive rhythms—atrial flutter
Escape complexes—idioventricular 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
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

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
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%

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
Contractility=force 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
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 disorders—pneumonia, 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 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

33. Physical Assessment 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

34. Physical Assessment Assess clubbing by the Schamroth method
Blood pressure—hypertension
Prehypertension— /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

35. Gerontologic Considerations
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

36. Diagnostic Evaluation
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

37. Blood chemistry, hematology and coagulation studies
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

38. Diagnostic Studies
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

39. Lipids Total cholesterol 122-200 Triglycerides—122-200 HDL—55-60
LDL—60-180
HDL: LDL ratio—3:1

40. Blood chemistries cont.
Homocysteine—indicates risk for CVD. Linked to development of atherosclerosis. 12- hour fast needed for reliable monitoring of level. Normal 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.

41. Diagnostic Testing cont.
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

42. Diagnostic Testing 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

43. Cardiac Catheterization cont.
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

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 IB—minimal depression of depolarization, shortened repolarization. Treats ventricular dysrhythmias. Xylocaine (lidocaine) and Mexitil (mexilitene). CNS changes.

45. Case Studies

46. Anti-Dysrhythmics
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

47. Anti-Dysrhythmics
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.

48. Anti-Dysrhythmics
Class IV—block 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 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

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 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

64. Modifying risk factors
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

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 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

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 blockers—reduce myocardial oxygen consumption
Calcium channel blockers—decrease 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 Assessment—presentation, description of pain
Treat anginal symptoms—ntg, 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
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)

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 Tx—PCI, thrombolysis
Continue therapy—Plavix, IV heparin, Glycoprotein IIb/IIIA inhibitors
Bedrest 12-24h
Rehab—gradual physical conditioning

79. Invasive Coronary Artery Procedures
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

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 >70% 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 catheter—hemodynamic 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 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

89. Hypertension <120/80 mm Hg normal 120/129/80-89 prehypertension
/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 changes—hemorrhages, cotton wool spots (small infarctions), papilledema (swelling of disc)
Left ventricular hypertrophy
Renal dysfunction
CVA

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

95. Medical Management 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)

96. Pharmacologic Therapy
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

97. Medication therapy for hypertension
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

98. Medication Tx for hypertension
Vasodilators: Corlopam (fenoldopam), Apresoline (hydralazine), Nipride (nitroprusside)
ACEIs: Vasotec (enalapril), Accupril (quinapril)
ARBs: Diovan (valsartan), Micardis (telmisartan)
Renin inhibitors—Tekturna (aliskiren)

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

100. Hypertensive Crises
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.

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
Systolic—weakened heart muscle
Diastolic—stiff 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 Myocardial dysfunction Activation of RAAS
Activation of baroreceptors
Stimulation of vasomotor regulatory centers in medulla
Activation of sympathetic nervous system
Ventricular remodeling

105. Heart Failure 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 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 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

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 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

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.
Dobutamine—beta 1 stimulation.

118. Nursing Management of the Patient with Heart Failure
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

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 therapy—diuretics, vasodilators, inotropes, vasopressors
IABP

127. Nursing Management Constant monitoring—BP, HR Cardiac rhythm
Hemodynamics
Fluid status
Adjust meds based on assessment
Watching for s/s of complications