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Nursing Care of Patients with Cardiac Problems.  One in five Americans possess some form of cardiovascular disease  With increase in metabolic syndrome.

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Presentation on theme: "Nursing Care of Patients with Cardiac Problems.  One in five Americans possess some form of cardiovascular disease  With increase in metabolic syndrome."— Presentation transcript:

1 Nursing Care of Patients with Cardiac Problems

2  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 21 st century  Number of cardiovascular problems that can occur

3  Pericardium  Epicardium  Myocardium  Endocardium

4  Right side of heart—workload is light compared to left side; pulmonary circulation  Left side of heart—high pressure system, systemic circulation

5  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  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  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  Heart perfused by coronaries during diastole  Right coronary  Left coronary  Circumflex  Must be to maintain perfusion of vital organs

9  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  Automaticity—intercalated discs  Conductivity  Contractility  Excitability

11  Cardiac conduction system 1. SA node 2. Internodal tracts 3. AV node/junction 4. Bundle of His 5. Right and left bundle branches 6. Purkinje fibers

12  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  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  Phase 3—Marks completion of repolarization and return of the cell to resting state  Phase 4-resting phase before next depolarization

15  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 Factors increasing likelihood of premature depolarization  Hypokalemia  Hypomagnesemia  Hypothermia  Myocardial injury  Acidosis  hypercarbia

17  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  Calculate heart rate  Heart rhythm  Analyze P waves  Measure P-R interval  Measure QRS duration  Interpretation

19  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 sinus rhythm—60 to 100  Sinus dysrhythmia l

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

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

23  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  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 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  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  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  Cigarette smoking  Genetics  Physical inactivity  Obesity  Hyperlipidemia  Diabetes mellitus  Hypertension

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

30  Angina pectoris  Pericarditis  Pulmonary disorders—pneumonia, PE  Esophageal disorders  Anxiety and panic disorders  Musculoskeletal disorders--costochondritis

31  Atypical presentation  Fatigue, sleep disturbances, shortness of breath  Historically undertreated due to ambiguous presentation

32  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  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  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  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 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  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  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  Total cholesterol  Triglycerides—  HDL—55-60  LDL—  HDL: LDL ratio—3:1

40  Homocysteine—indicates risk for CVD. Linked to development of atherosclerosis. 12- hour fast needed for reliable monitoring of level. Normal 5-15 micromol/L  Magnesium—necessary for absorption of calcium, maintenance of potassium stores and metabolism of ATP. Low levels predispose to atrial and ventricular dysrhythmias. Increased levels depress contractility and excitability of heart.

41  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  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  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  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  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  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  Class IV—block calcium channels. For atrial dysrhythmias. Cardizem (diltiazem), Calan (verapamil). Bradycardia, AV blocks, Hypotension, peripheral edema

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

50  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  Universal code indicates five letters 1. Identifies chamber being paced. V, A, D (dual). 2. Indicates chamber(s) being sensed. A, V, D, O (meaning sensing function is off) 3. Indicates type of response to the sensing. Inhibition and Triggered responses. I, T, O.

52 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  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  Nonsensing  Noncapture  Nonpace

55  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  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  Inflammation affecting arterial walls  Results in plaque formation  Impedes flow  Results in atherosclerosis

58  High lipids  Smoking  Hypertension  Diabetes mellitus  Family history  Metabolic syndrome

59  Cholesterol  Tobacco use  Weight  Hypertension  Diabetes mellitus

60  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  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  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  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  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  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  Clinical syndrome characterized by episodes or paroxysms of pain or pressure secondary to insufficient coronary blood flow; decreased oxygen supply

67  Caused by atherosclerosis  Obstructions of coronaries

68  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  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  ECG  Echo  Stress test  CRP  Cardiac cath or angiography

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

72  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  Antiplatelet and anticoagulant medications 1. ASA 2. Plavix (clopidogrel) and Ticlid (ticlopidine) 3. Heparin (HIT), Fragmin or Lovenox 4. Glycoprotein IIb/IIIa agents (ReoPro (abciximab) and Integrilin (eptifibatide))— prevent adhesion of platelets with fibrinogen 5. oxygen

74  Assessment—presentation, description of pain  Treat anginal symptoms—ntg, O2, vitals  Reduce anxiety  Prevent pain  Teaching  F/U

75  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 Clinical manifestations  chest pain, discomfort, pressure  SOB  Indigestion, nausea  Anxiety  Diaphoresis

77  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  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  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  Dissection  Perforation  Vasospasm  MI  Dysrhythmias  Cardiac arrest  Bleeding from insertion site  Hematoma

81  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  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  Assess: 1. Respiratory status 2. Cardiac status 3. Neurologic status 4. Peripheral vascular status 5. Renal function 6. Fluid and lytes 7. Pain 8. Family needs

84  Ett and vent  ECG  Swan-Ganz catheter—hemodynamic monitoring  Pacemaker  Aline  Chest tubes  Neuro status  NG tube  Foley  Surgical sites

85  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  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  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  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  <120/80 mm Hg normal  120/129/80-89 prehypertension  /90-99 Stage 1 hypertension  ≥ to 160 or ≥ to 100 Stage 2 hypertension

90  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  Avoid smoking for 30’ before BP check  Sit for 5 minutes  Appropriate size of cuff  Both arms, take the higher BP

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

93  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  H&P  Retinal exam  UA, chemistry, lytes, creatinine, BS, lipid profile, 12 lead ECG  24 hour urine for creatinine clearance  microalbuminuria

95  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  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  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  Vasodilators: Corlopam (fenoldopam), Apresoline (hydralazine), Nipride (nitroprusside)  ACEIs: Vasotec (enalapril), Accupril (quinapril)  ARBs: Diovan (valsartan), Micardis (telmisartan)  Renin inhibitors—Tekturna (aliskiren)

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

100  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  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  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  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 Myocardial dysfunction Activation of RAASActivation of baroreceptors Stimulation of vasomotor regulatory centers in medulla Activation of sympathetic nervous system Ventricular remodeling

105 1. Myocardial dysfunction—hypertension, MI 2. cardiac output, systemic blood pressure and kidney perfusion 3. Activation of renin-angiotensin-aldosterone system 4. Activation of baroreceptors 5. Stimulation of vasomotor regulatory centers 6. Activation of sympathetic nervous system- 7. catecholamines with resultant vasoconstriction, afterload, BP, HR 8. Ventricular hypertrophy, impaired contractility

106  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  Left-sided heart failure  Right-sided heart failure  High output heart failure

108  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  May be acute or chronic  May be systolic or diastolic

110  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  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  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  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  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  Echocardiogram  ECG  Cxray  Labs: CBC, CMP, lipid panel, BUN/creatinine, TSH, BNP, UA

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

117  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  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 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  Restlessness  Breathlessness  Nail bed cyanosis  Weak pulses  O2 sat decreased

121  Reduce volume overload  improve ventricular function  increase/improve respiratory exchange

122  Oxygen  Morphine  Diuretics  IV Primacor, dobutamine or Natrecor

123  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  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  Cerebral hypoxia  Low blood pressure  Rapid and weak pulse  Cold and clammy skin  Tachypnea  Decreased urinary output

126  Correct underlying problem, e.g. dysrhythmias  Improve oxygenation, intubation, positive pressure ventilation  Pharmacologic therapy—diuretics, vasodilators, inotropes, vasopressors  IABP

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


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