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Nursing Care of Patients with Cardiac Problems

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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

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