ACS Time Is Muscle

MCC NURSINGDiana Blum MSNACS Time Is MuscleMore than 71 million Americans have cardiovascular disease

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4Cardiac output is the amt of blood leaving the left ventricle per minute. SV x HR. Normal is 4-8 liters per minute.Normal HR is 60-100 bpm.Stroke volume is the amt of blood leaving the left ventricle with each contraction. Normal is 60-100ml per contraction. These are important because of perfusion to tissues and organs are compromised when these are compromised.

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5Built in control center of the bodyRegulates functions not under conscious controlBlood vessels innervated by sympathetic systemFight or flight Nerve endings are adrenergic and nuerotransmitter is norepinephrineIncreases HR and BPParasympathetic is responsible for rest and digestCholinergics are the nerve endings and acetylcholine is the neurotransmitterDecreases HR and BPParasympathetic and sympathetic innervates heartGeneral appearance looks at pt physical appearance. Lethargy, exhaustion, breathless,. Also facial expressions play a key role. They can show apprehension pain fear or that impending doom type expression. Mentation is key in that confusion could indicate hypotension or low cardiac output.Color could mean a number of things. For example cyanosis could be from septal defect HF poor circulation, etc. pallor could be from anemia. Clubbing nails could be from o2 deficiency. Neck veins could indicate JVD because of excess fluid on board. We palpate for edema. Skin turgor indicates dehydration or ageCap refill should be 2-3 seconds if more then it couldbe perfusion issue.Lack of pulse could be from perfusion or clot.And we auscultate for heart lung and bowel tones.

Abnormal Heart tonesS3= sounds like kentucky (ventricular)S4= sounds like tennesee (atrial)Gallop=when s3 and 4 heardRub= related to inflammation high pitched sweaky yet muffled like sandpaperMurmur=vibrations from turbulent flow aka bruit6If you remember from 2520 these were discussed.6CADArteries have 3 layers: tunica intima, tunica media, and tunica adventitia (figure 32-1)Disease process that occurs over time Starts in infancyRisk factors: age gender diet sedentary life smokingAtherosclerosis affects medium arteries that feed heart brain and kidneys as well as aorta7Responsible for approx 50% of cardiac events in both genders under 75.Arteriosclerosis: thickening and calcification of arteryAtherosclerosis: component of arteriosclerosis that causes reduced myocardial blood flowPlaque (cholesterol, lipid, cellular debris)3 stages of plaque growth:1:yellow lesion (fatty streak)in intimal layer2:plaque matures creating a lipid core with fibrous cap (white in appearance) and are mostly in bifurcated arteries3:well established fibrous cap/lipid core possible ruptureAngina which results from a lack of 0xygen to the heart muscle4Es that increase o2 demand=exercise, eating, emotion, exposure to coldWeakness, diaphoresis, SOBN/V

Pg. 9207Coronary Arteries 2 branches off Aorta: Supplies posterior & inferior myocardium: 1. Right (Longest) coronary artery *occlusion results in inferior MI (30% of inferior MIs include right ventricle) *lower mortality than anterior MI *more mild AV node dysrhymias (first & second degree blocks) SYMPTOMS OF INFERIOR MI: - hypotension from a decrease in preload available to the LV due to d RV emptying

882 branches off the right coronary artery: a. Right marginal artery: b. Posterior descending artery:

supplies blood to right atrium, right ventricle, bottom portion of both ventricles and back of septum

2. Left coronary artery begins out of Left side of ascending aorta and divides into the: left anterior descending artery(LAD) = supplies anterior and bottom of Left vent and front of the septum most involved with occlusions Blockage here results in anterior MI which has higher mortality rate AND more serious dysrhythmias !!!!!may include 2nd & 3rd degree blocks diminished ejection fraction & symptoms of heart failure !!!!!When > 40% of left vent. Is damagedmortality is extremely high

circumflex= supplies the left atrium & back of left vent

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1111Types of Chest Pain:

1. Stable Angina: - no or minimal myocardial injury - collateral circulation develops - pain begins with exertion or stress - pain relieved with rest - pain lasts less than 20 minutes - relieved by NTG (may take SL up to 3 times every 5 minutes) If not relieved after these 3 doses, pt may be infarcting -ST segment depression with pain then returns to normal with pain subsides 1212the myocardial demand for oxygen exceeds the ability of the coronary vasculature to supply it.reduced blood flow = reduced Hgb, or smoking-low oxygen content- excessive O2 demand relative to perfusion =hypertension, exercise, metabolic rate-atherosclerosis-valvular dysfunction-hypotension-coronary vasospasmburning, squeezing tight band- heaviness, pressure in lower sternum- may radiate to neck, jaws, shoulders, arms, stomachOTHER symptoms specific to African-American & women: -fatigue, SOB,indigestion, shoulder/ back discomfort

Pg 933

2. Unstable Angina: - pain resolves with NTG - similar to stable angina BUT angina occurs more freq with less exertion - often begins at rest with increasing severity - normal cardiac enzymes - ST depression with prolonged CP

1313Pg 9333. variant (Prinzmetal) angina: - rare & associated with angina at rest - tend to be younger women (smokers) & pain occurs in early am & with menstrual - ST elevation (reversible) but cardiac enzymes norm - CAUSE: coronary artery spasm occurs at stenosed area Treat: responds to NTG long-term: calcium channel blockers1414Pg. 933Other causes of CP:A. reflux or peptic ulcer diseaseB. chest wall pain (pain reproduced on palpation and localized) - occurs from bruised/ fx ribsC. esophageal problems - achalasia, esophageal spasmD. pericarditis (will be sed rate, low-grade fever, viral cause (coxsackievirus)E. pneumoniaF. Aortic dissection (CV EMERGENCY) watch for severe pain radiating to back1515

p.923 When it comes to injury of myocardial cells if blood flow is not restored in 20 minutes irreversible damage ensues.

There are 3 areas the area of infarction, zone of injury, and zone of ischemia.

If reperfusion occurs within the 20 minutes then apoptysis or cell death will abort.

Fibrinolytics aka clot busters have a 12 window from symptom onsetTo salvage the myocardial cells. 16Goal in treatment of Angina:dilate vessels, O2 availability, O2 demand

HOW?NitroglycerinChange lifestyleIF INCREASING in freq & intensity may need stress testing, cardiac cath beta blockers angioplasty or CABG to risk of MI

17Angina or MIAngina without MI} often relieved with rest and NTGAngina with MI } may be relieved with rest, NTG, 02, MS, rescue angioplasty, etc.Think MONAMorphine OxygenNitroglycerinAspirinhttp://www.youtube.com/watch?v=4GlQmTlP2jE&feature=related

18http://www.doctorsecrets.com/your-medicine/heart-attack-cause-symptoms-treatment.html Pg 945-957Pain doesnt resolve with NTGs/s: crushing, poorly localized substernal pain, radiates to shoulder, arm, jaw, diaphoretic, sense of impending doom, N/V, tachycardia or bradycardia, dyspnea, ST elevation, Q waves (occurs after 12 hoursDuration: > 30 minutes with no reliefNot relieved by rest & can even occur @ rest

18MI subdivided into STEMI or NSTEMI - actual necrosis of myocardial tissue - most cases, atherosclerotic heart disease present other cases is from artery spasm - IDENTIFICATION OF MI IS MOST IMPORTANT AS WITHIN 6 hours there is irreversible damage!!!!1919NSTEMINo st segment elevation presentIf enzymes are increased it means severe injury Higher probability of deathSTEMIST segment elevation on EKG Severe anoxiaCellular damage present (ex. Complete blockage)If blood flow not re-established in 20 min. cell death occursPG.948

2020MI patterns (as more areas of heart becomes damaged, the more dangerous the MI becomes)Common patterns: Ant/lat inf/post ant/septal

25% of MI are silent : presents without chest pain (esp in diabetics with neuropathy) Patient presents with heart failure, shock, confusion, delirium (esp in elderly)2121PG 949

Anterior STEMI

2222INFERIOR MI M LEADS 2 3 AND AVFLEAD 1 AND AVLANTERIOR MI LEADS V1-V4 2 3 AVFANTEROLATERALV1-V4 1 AVL V5 V62 3 AVFLATERAL 1 AVL V5 V6 V1-V42 3 AVFPOSTERIOR RECIP CHANGES IN V1 AND V2 ONLY

CHART 32-12

Anterior STEMI

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2424Complications of MIDepends on which vessel involved & region of the heart muscleIschemia of condux system, causes arrythmiasIf lg enough area, CHF developsOcclusion of Left descending artery: left heart failureOcclusion of Right descending artery: Rt heart failureInfarct of vent wall can result in rupture, heart hemorrhage into pericardial sac leads to tamponade can be quickly fatal2525Treat STEMI Goal: reperfuse the heartSymptoms ECG within 10 minutes ST elevated ASA, Troponin, CPK-MB, Morphine, Heparin Thrombolytic with 30 minutes if PCI not avail PCI in24 hours if avail, within 90 min. stent angioplasty

2626ENGRAIN THIS IN YOUR MEMORY

Angioplasty with StentProcedure done at the time of cardiac cath.Balloon angioplasty is accomplished to widen or open specific coronary vessel-stent is inserted to maintain patency of the vessel. pre-procedure Plavix given with follow up Plavix

27http://preop.medselfed.com/asp/center.asp?centerId=heart&partnerId=preop&id=&cachedate=&emailId=&affId=&campId=&hideNav= Holds open the coronary artery where narrowedDrug eluding stent (DES) decreases /prevents endothelial overgrowthAntiplatelet therapy needed (Plavix)

PREPROCEDURE PLAVIX IS A LOADING DOSE OF 300MGFOLLOWED BY 75 MG QDAY27

2828NSTEMI and Unstable AnginaAssessment & TreatmentNo ST elevation Draw Troponin I If elevated Cardiac cath vs Medical Management Echo, Stress test2929Monitoring/interventions MI (continued)Continuous cardiac monitoringOxygen IV lineHemodynamic monitoring (discuss in a bit)Bed restEmotional supportNeed passive & active ROM to reduce risk of thromboembolism (immobility)

3030Medical treatment in MI treatmentFor low cardiac output: - dobutamine +inotropic -milrinone +inotropicFor hypotension: - dopamine ( or at low doses used to improve renal perfusion) May need Intraaortic balloon pump3131BALLOON PUMP PG 954-960

reduces afterload of left ventricle AND increases blood flow to coronary arteries - used for cardiogenic shock or as cardiac augmentation until surgery - usually inserted into femoral artery - placed in descending thoracic aorta - is synchronized with pts own heart rate - timed to inflate IMMEDIATELY after aortic closure (or left ventricle would pump against great resistance) this is during ventricular diastoleforces blood back into coronary arteries

Complications of IABP: - circulation to leg to insertion site is compromised - EXTREMELY IMPORTANT TO MONITOR AND DOCUMENT PULSES, TEMP, APPEARANCE OF LEG BELOW INSERITON SITE. Must be WEANED off pump; - the ratio of heart contraction to inflation of balloon is 1:1 so, then go to 2:1 , then 4:1 (one inflation for every 4 contractions of hrt)Some of the pumps, able to wean by decreasing balloon volumeIf balloon ruptures: reason for rapid dissolving helium

http://people.brunel.ac.uk/~emstawk/IABP.htm

3232Contraindications for Balloon Pump:Aortic or ventricular aneurysmsVentricular septal defectsAortic regurgitation3333Recovery MIBegins as soon as MI stopScar tissue dev. at necrotic area (takes 6-8 wksMay see stages of grief in pt with MI - - we need to identify depression as mortality at 1 to 5 years with associated depression !!!!MUCH TEACHING NEEDED; - MODIFY RISK FACTORS, LIFESTYLE CHANGES, WORK WITH BOTH FAMILY/PT3434Lethal complications of MI that can occur 5 to 10 days post MI:Papillary muscle ruptureVentricular aneurysmVentricular rupture3535MedsPrecautions with Nitrates and Viagra use: - reports of sudden death, dramatic drop in blood pressure, and further compromising restricted coronary arterial perfusion3636Medical support (MI continued)Vasodilators to reduce preload/afterload - nitroglycern or nitroprussideACE inhibitors: - reduce afterloadBeta blockers: - reduce myocardial oxygen consumption - decrease heart rate and BPStatins: - restrict development of artherosclerosis& also have anti-inflammatory effectsPlatelet inhibitors: - ASA 3737PG 953-957

38Platelet activation = treat with GP IIb/IIIa inhibitors examples: Abciximab (ReoPro): 0.25mg/kg IV bolus followed by 0.125ug/kg/min for 12 hours (others: Integrilin, Aggrastat)39What precaution should we take with beta blockers ???Heart has Beta 1: so Beta Blockers lower BP slowing heart rate Lung has Beta 2: so Beta blockers constrict bronchioles, making it harder to breathePropranolol blocks both types of beta receptors so SHOULD NOT BE USED IN ASTHMATICS Metopolol CAN be used since it is specific for Beta 1 and DOES NOT CONSTRICT BRONIOLES SO SAFE WITH ASTHMATICS. 4040PG. 953Specifics on Fibrinolytic agents:must be within 12 hour of symptomsStreptokinase: depletes fibrinogen to predisposed to systemic bleeding & allergic reaction possible with second time useAlteplase (tPA, Activase): used most oftenReteplase (rPA, Retavase) a synthetic, 2nd generation that works more quickly & lower bleeding 4141Nursing Interventions if fibrinolytic used:Minimal arterial or venous sticksUse finger oximetryAvoid automated blood pressure cuffs (bruisingAssess for signs of bleeding(hypotension, tachycardia, reduced level of consciousness)Reperfusion arrhythmias common - bradycardia and V-tach most commonIF BLEEDING COMPLICATIONS: -stop fibrinolytic agent, FFP &/or cryoprecipitate to replenish fibrin & clotting factors, Aminocaproic acid (Amicar)4242Absolute Contraindications to Thrombolytic Therapy:Hx of intracranial hemorrhageKnown structural cerebrovascular lesionKnown intracranial tumorIschemic stroke 92%Holter monitoring: 24+ hr of EKG + eventsStress test: treadmill or pharmacologicalCardiac Catheterization: invasive, NPO 6-8h, consent. Visualizes chambers, valves, arteries, pressures, COHeart-CT scan: assesses CADNuclear scans: assess heart muscle viabilityEPS: NPO, consent, IV, assess electrical activity4848Education of MI Pt49Low fat low cholesterol dietPrescribed exercise program 5-7 days a weekKnows correct use of NTG for anginaManagement of DM, HTNStop smokingMedications to reduce work load or dilate

5050Exercise5-7 X week is goal to include stretches with warm-up, progressive walking program, light weights, stretches with cool down.Strengthens heart muscle, reduces BP, BS, weight, stress, tension, appetite, LDLs.Increases HDLs, energy and self esteem and improves immune system

51PG 952Principles of exercisePractice on regular basisKnow how to do own pulseStrive for target heart rateStop if chest pain occursComplications: CHF & Dysrhythmias

51Nursing DiagnosisDecreased cardiac output r/t DysrhythmiasPain r/t lack of 02 to myocardiumAnxiety r/t to feeling of doom, lack of understanding of medical diagnosis

52962-96452You are asked to evaluate a 55-year old Caucasian woman who presents to the Emergency Department with the chief complaint of chest pain for several hours.She awoke with the discomfort at 4:00AM today, and it has been a "ten out of ten" since then. The pain is substernal, radiates to her back, and is associated with moderate-to-severe shortness of breath and nausea. No previous such episodes are reported, but the patient states there is a strong family history of cardiac disease, and that she has smoked one-half pack of cigarettes daily for the past thirty-five years.Other than that, she denies past medical or surgical conditions, takes only hormone replacement therapy, and has no known drug allergies.Social history reveals that the patient is married, has three children, and works as an accountant.On physical exam, the patient appears to be in mild discomfort due to chest pain, but otherwise appears normal.Temperature is 97.7F, pulse is 110, blood pressure is 150/100, and respirations are 20.Head and neck, lung, heart, and abdominal exams are normal.An EKG is performed, which shows nonspecific T-wave changes in the lateral leads.Other tests, including troponin-I, cardiac enzymes, and chest x-ray have been performed, but results are still pending.

53What are risk factors?What are you concerned with?What to do?

5454Cardiac SurgeryCoronary artery bypass graft- done after confirmation with cardiac catheterization.Re-route blood vessels using mammary or saphenous v from aorta around block in coronary artery. Valve replacement or repairSeptal repair and other congenital repairsCCU post op, chest tubesPre-op teaching with post op expectations

55PG 964-67

Pt cooled to reduce O2 demandPlaced on cardiopulmonary bypass which diverts blood from heart but oxgenates & removes CO2New procedures include working on a beating heart or the MIDCAB

55Physiological consequences of CABG:1. damage to blood (platelets, RBCs WBCs & plasma proteins)2. Incorporation of abnormal substances into blood (bubbles, fibrin, platelet aggregates)3. a systemic inflammatory response4. increase in systemic vascular resistance5. increase catecholamines

5656Nursing interventions for CABG1. fluid status (fluid leaks from vessels)2. O2 sats (indicates excess capillary leaking)3. postop bleeding from anticoagulation for procedure4. hemodynamic monitoring5. pain relief6. dysrhythmia control7. warming pt may need vasopressors to maintain BP initially (undesirable to let pt shiver as oxygen demands) (use warmed blankets, warmed blood to infuse, warmed inspired gases)5757Nursing interventions CABG (continued)8. bleeding not to exceed 300 mL/hour in first couple hours then 150-200 ml/hour but average blood loss is 1 L.Notify physician if excessive.Autotransfusion of medialstinal blood is filtered & infused9. aggressive suctioning then enc coughing10. monitor electrolytes to prevent dysrhthmias585811. dysrhythmias treated pharmacologically12. pacing wires placed on right atrium and ventricle before surgical closure. Postop BRADYCARDIA most common indication for need of pacer.5959Complications of CABGHemorrhage, cardiac tamponade, MI, ventricular dysfunction, dysrhythmias, deathCardiac tamponade: - watch for pts that have bleeding in chest tube (significant) then suddenly STOPS bleeding & becomes hypotensive - reopen & immed return to OR6060Congestive Heart Failure

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DEFINITION:EF < 40% or when the myocardium is no longer able to pump efficiently and fluid accumulates in the lungs and or selected areas of the body as a resultChapter 34. NORMAL EF IS 55-70%61Causes of CHFCAD, advancing ageHTN is a major factor > CHF x 3 DM, Smoking, ObesityValvular incompetency, alcohol or other chemicals, idiopathic,(unknown)

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63Pg 1027-28Right side failure: (blood backing up causing congestion in body) s/s due to blood pooling JVD, dependent edema, hepatic congestion, a-fib, fatigue, wt loss, cyanosis With a-fib be aware of risk for embolization Echocardiogram: reveals CO

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64Pg 1027S/S of Left Sided CHF (blood backing up into pulmonary structures)FatigueAnginaTachycardiaCool extremitiesHacking coughCracklesFrothy sputumGallop

64Biventricular failureInability of either ventricles to pump effectivelyBoth rt and lt failureSymptoms are a combo of both65System CompensationMediated thru Sympathetic Nervous System: as CO drops, baroreceptors alert brain>>>signals adrenal glands to release catecholamines{norepinephrine and epinephrine}This causes stimulation Beta 1=>>HRStimulation Beta 2= bronchodilationActivate Alpha receptors peripherally=constriction=>>bp

66Pg 1028-1029There are stages to heart failure a-d but I will not make you know theseFurther breakdown into classes 1-4 based on symptom presentationCausing S/S of CHF because: Contractility decreasesStroke volume and CO continue to decreaseAfterload (pressure on the other side of the aorta) increasesPreload ( pressure caused by increase volume to heart creating an exaggerated stretch in the muscle) increases

66Renal CompensationCO drops initiating renin-angiotensin mechanismResults in powerful vasoconstrictor angiotensin II,>> aldosterone (hormone) which causes kidneys to retain Na and H20 which increases blood volume

67Pg. 102967Ventricular HypertrophyThe heart enlarges which results in strain

The increase in volume causes the ventricles to dilate

Eventually remodeling will occur

6868Diagnostic TestsH&P Chest x-ray: see size of heart and fluid in lungsEKG: strain, MIEchocardiogram: size of heart and COCBC: anemia CMP: screening Thyroid function ABGsBNP=B type natriuretic peptide= hormone released in response to Ventricular stretch ( CHF peptide) Nuclear studies to determine heart function, EF, tissue viabilityCardiac Cath to determine exact nature of heart function

69Pg 103369CHF ManagementDirected at: Improving LV function (Contractility) by decreasing intravascular volume and decreasing vascular resistanceDecreasing venous return (Preload)Decreasing BP (Afterload)Improving gas exchange and 02Increasing the CO and reducing anxiety

70Pg 1033 Treat underlying causeRest and hi Fowlers to reduce work load and improve ventilation02 at 2-6 L/min with 02 sats >92% to increase available 02 and prevent hypoxemiaFreq VS and cardiac monitoring

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7171Treatment continuedI & O q shift Daily am weights before breakfast and after voiding. 2-3# weight gain in 1-4 days call MD Sodium restricted dietMedications: to decrease intravascular volume thus reducing venous return, dilate and reduce BP and improve contractilitysurgeryhttp://chfsolutions.com/zip_how_aquapheresis_works.html# 72Aquaphoresis can remove fluid from the blood at the same rate that fluid can be naturally recruited from the tissue

72Ultrafiltration Compared to Loop DiureticsSchrier. J Am Coll Cardiol. 2006;47:1-8.Ultrafiltrate is isotonic with plasma, whereas the diuresis of loop diuretics is virtually always hypotonic to plasmaUltrafiltration removes more sodium than diuretic therapy No electrolyte disturbancesUltrafiltration decreases ECF volume more than a comparable volume of diuretic-induced fluid lossSlide 731Point 2: Ultrafiltration removes more sodium than diuretics for a similar given volume. Approximately 3 g of sodium per liter of ultrafiltrate.1

Point 4: Since sodium and its anion are the major determinants of extracelllular fluid (ECF) volume, ultrafiltration decreases ECF volume more than a comparable volume induced by diuretics. Therefore, it follows that ultrafiltration decreases more ECF volume than diuretics.1

Reference: 1. Schrier R. Role of diminished renal function in cardiovascular mortality. J Am Coll Cardiol. 2006;47:1-8.

Section 4: Ultrafiltration History and PhysiologyFirst line treatment for right side failure:ACE inhibitors ( proven to mortality in CHFBeta blockers (proved to mortality) - begin once pt diuresis occurs)Diuretics (loop and K+ sparing) Spironolactone (proven to mortality in class IV CHF)Digoxin may be used (doesnt improve mortality in CHF BUT improves symptoms, hosptialization74741033-1039

7575When giving ACE inhibitors to your patient, what should you remember???Food decreases absorptionGive on an empty stomachPostural hypotension (monitor)Watch for hyperkalemia, angioedema, PERSISTENT DRY COUGHNOT TO BE USED WITH PREGNANT WOMEN AS IT IS FETOTOXIC !!!!7676When should Angiotensin-receptor blockers be used:Prototype: LOSARTANSimilar actions to ACE inhibitor These meds are a substitute for pts who cannot tolerate ACE inhibitors (those with severe cough or angioedema) - lowers BP - reduces morbidity & mortality assoc. with hypertensionOnly need once a day dosingAdverse effects similar to ACE inhibitors but without the coughContraindicated with pregnancy 7777

7878Treatment with BETA BLOCKERS with heart failure:ABSOLUTE improved systolic functioning & reverses cardiac remodelingInitially may have exacerbation of symptomsDecreases heart rate & inhibits release of reninTwo drugs approved for heart failure: 1. Carvedilol (nonselective B-adrenoreceptor antagonist that also blocks adrenoreceptors 2. Metoprolol (selective B1 selective antagonist)7979

8080Treatment with direct vasodilators for heart failure:By dilating venous blood vessels, leads to decrease in cardiac preloadBy dilating arterial vessels, leads to reduction of systemic arteriolar resistance & decrease afterloadNITRATES8181DiureticsThe use of loop diuretics in ADHF patients with dyspnea and shortness of breath is standard therapy In patients with ADHF, diuretics May induce a natriuresis Decrease extracellular fluid (ECF) volume Provide symptomatic reliefSchrier. J Am Coll Cardiol. 2006;47:1-8. Slide 821Loop diuretics induce a natriuresis/diuresis by blocking the sodium-potassium-chloride transporter in the ascending portion of the loop of Henle.1

Diuretic therapy with loop diuretics have been shown by some investigators to provide reduction in wedge pressure and increased venous capacitance even before any appreciable urine output is observed.2,3 However in other studies, this effect has not been observed.4 Clearly the paucity of studies in this patient population, as well as conflicting clinical results, makes this drugs true effect somewhat uncertain. Despite this, diuretics remain an important and necessary part of ADHF therapy.

References: 1. Odlind B et al. Renal tubular secretion and effects of furosemide. Clin Pharmacol Ther. 1980;27:784-790.2. Dikshit et al. N Engl J Med. 1973;228:1087-1090.3. Silke et al. Cardiology. 1994;84(suppl 2):115-123.4. Hasenful et al. Clin Card. 1987;10:83-89.Section 3: Diuretic Therapy in Acute Decompensated Heart Failure

Krmer et al. Am J Med. 1999;106:90.Elevated Neurohormones Cause Diuretic ResistanceProximal TubuleAng II increases sodium reabsorptionGlomerulusNorepinephrine (and endothelin) decreases renal blood flow and GFRCollecting DuctAldosterone increases sodium reabsorptionSlide 83There are 2 types of diuretic resistanceshort-term tolerance (braking), which may be mediated by activation of angiotensin II (Ang II) or the sympathetic nervous system (SNS), or long-term tolerance, in which sodium that escapes the loop of Henle is reabsorbed at more distal sites, decreasing overall diuresis; this may be overcome with sequential diuretic blockade.1

Diuretic insensitivity and resistance are conferred largely by activation of various neurohormonal systems. Ang II and renal nerve stimulation activate receptors on the proximal tubule epithelium,2,3 causing proximal tubular reabsorption of water and sodium, which decreases availability of substrates for loop and thiazide diuretics.

Catecholamines (eg, norepinephrine) and endothelin, which mediate some of the renal actions of Ang II, also may decrease renal blood flow and consequently can decrease delivery of diuretics to tubules. Nearly all diuretics must be filtered by the glomeruli to reach their (intraluminal) transport mechanism.4

References: 1. Brater DC. N Engl J Med. 1998:339:387. 2. Riggleman A et al. Hypertension. 2001;38:105. 3. Bell-Reuss E et al. Effect of renal sympathetic nerve stimulation on proximal water and sodium reabsorption. J Clin Invest. 1976;57:1104-1107.4. Myers BD et al. Effects of norepinephrine and angiotensin II on the determinants of glomerular ultrafiltration and proximal tubule fluid reabsorption in the rat. Circ Res. 1983;37:101-110.Section 3: Diuretic Therapy in Acute Decompensated Heart FailureSo what will diuretics really do for CHF?Decrease plasma vol. which will decrease venous return (preload) which decreases cardiac workload & Oxygen demand Which decreases afterload by reducing plasma volume thus decreasing blood pressure8484DigoxinSince metabolized by the liver before excreted in feces, the pt with hepatic disease may require decreased dosing.HYPOKALEMIA PREDISPOSES THIS PATIENT TO DIGOXIN TOXICITY.What can be used to detoxify the body from dig? DIGOXIN IMMUNE FAB (THIS BINDS AND INACTIVATES THE DRUG)8585Digoxin (continued)ADVERSE EFFECTS: Cardiac: progressively more severe dysrhythmias, eventually to complete heart blockThat is why is is so important to make sure K+ is normal !! GI: anorexia, n/vCNS: headache, fatigue, confusion, blurred vision, alterations of color perception, HALOS

8686Dig Toxicity:Hypokalemia leads to serious arrhythmias - will see this most in pts on thiazide or loop diuretics (prevented by using a potassium-sparing diuretic OR supplement with potassium chloride )ALSO note that: Hypercalcemia AND hypomagnesemia ALSO predispose to dig toxicity !!!!

8787Educating the CHF ClientEducation re: heart failureExplanation of heart failureExpected S/S and when to call MDSelf monitoring of daily weightsKnow medications and need to take them2000mg sodium restricted diet Importance of low level daily exercise program (energy conservation)Prognosis / advanced directives

8888Inflammatory Heart Diseases

89Chapter 3389Rheumatic Heart DiseaseDiagnosis: CBC, Chest X-ray, C reactive protein, EKG, Heart Cath, blood cultures

Interventions: PREVENTION is key, PCN like antibx, NSAIDS for joint pain, Cardiac meds, Bedrest Educate pt and family about prophylactic Antibx treatment90Complication of rheumatic feverLong term damage and scarring of valvesLeading cause of death 100years agoOccurs mostly in kids 5-15 yrs oldDevelops from pharyngitisGroup A beta hemolytic streptococcusIncubation period= 2-4 daysValves swell and vegetation occurs on valvesS/S: 1-6wks after strep (murmur, fever, malaise, HA, swollen tender joints, SOB, increased WBC, CP, tachycardia, HF signsPg 973-97990 Pericarditis

Inflammation of pericardial sac3 causes:InfectiousCoxsackie Virus BRespiratory diseasesNoninfectiousUremiaAMISurgeryAutoimmuneRhuematoidDrug ReactionsConnective Tissue Disorders

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Pg 979

Chest pain is hallmarkFriction rubEffusionTamponade (see slides)Most severe on inspiration, sharp, stabbing, or dull and burning.Pain is relieved by sitting up or leaning forwardDyspnea, chills and fever

Nursing Interventions: ECG monitoring for dysryhthmiasSupplies ready for emergency pericardioicentesisAuscultate cardiac soundsMeds for painArterial blood gases or pulse oxEmotional support and explanations

91Tamponade

92Pg 983-86Medical emergencyAcummulation of pus or blood in pericardial sacPressure increases causing back up of blood into the venous systemDecreases cardiac output**key to finding** Becks TriadDecreased bp, muffled heart tones, JVDWeak pulses also occurMay lose Consciousness

92MyocarditisUncommonFrequently associated with pericarditisUsually viral in natureS/S: fatigue, malaise, achy joints, GI upset, flu like symptomsDx: WBC, chest x-ray, heart cath, echo, cardio enzymes, etcTx: immune therapy, antimicrobials, ACE, Antidysrhythmics, anticoagulants, antianxiety

Scarring causes permanent damage93986-8793EndocarditisInfective endocarditis caused by gram+cocciA deformed or damaged valve is usual focus of infectionDental procedures can cause bacteremiaDiagnosis: cultures, transesophageal echocardiography9494Inner layer: tends to affect the valves (Mitral). Organisms (Bacterial or fungal) present in blood stream and collect (colonize) on the valvesStrepRheumatic heart diseaseMay be from IV drug use or invasive procedures

987-991

S/S of EndocarditisFever- (99-105)Chills and night sweats may accompanyMalaise, fatigue and weight lossAppearance of petechiae in the mouth, conjunctiva and legsChest and abdominal pain indicating embolization9595Treatment and DiagnosticsH&P and Lab testsCBC with diff with leukocytosis, > sed rate, blood culturesMay have heart murmur Echocardiogram to visualize valves and vegetationChest x-ray: CHFLong term antibiotics, rest, limited activity, prophylactic anticoagulants, valve replacement after inflammation treated

96High doses antimicrobials for extended periodsS. aureus & gram- bacilli most likely pathogensVancomycin IV PLUS gentamicin or tobramycin IVFor MRSA : VancomycinUsually improvement in 3 to 10 days

96Clients with known valvular disease need to be treated with prophylactic antibiotics prior to any invasive procedure including dental. Immunosuppression and any source of contamination places clients at risk

9797Valvular Disorders98

991-100598Insufficiency(Also referred to as regurgitation)The inability of the valves to close completely. Allows the blood to backflow. i.e., After the L A has contracted some of the blood will flow back into the L AMitral valve is the most commonly affected9999Mitral InsufficiencyOften accompanies mitral stenosis as a result of rheumatic fever.Valve leaflet become rigid and shorten, prevents closure of valve.Hypertrophy of Left Atrium and Ventricle = L sided heart failure occursMurmur heard. F/U with echocardiogramEdema and shock appear quicklyAfib is common

TX: vasodilators, same as for stenosis

100993-994100Mitral StenosisMitral valve leaflets become thickened and fibrotic. Rheumatic heart disease is a common causeAffect women age 20-40S/S: dyspnea, afib, dry cough, palpitations, angina, crackles, fatigue, CHF may developTX if failure develops: Digoxin, Lasix, beta blockers, and anti arrhythmics, lo Na diet, etcWill monitor with yearly echocardiogramSurgery if worsensProphylactic antibiotics prior to invasive procedure or dental work

101993101

102Cardiac insufficiency can be caused by many factors by a swelling of the heart muscle (1), an enlargement of the hollow chambers in the heart (2), a heart attack (3) or a blood clot (4).

102Aortic StenosisOccurs when valve cusps become fibrotic and calcify. Most commonly caused by aging and atherosclerosis. Occurs most predominantly in menUntreated will lead to Left sided CHFS/S: dyspnea is most common, syncope, angina

103994-95103Aortic InsufficiencyCaused primarily by rheumatic feverMay also be caused by chronic HTNPredominantly in menHypertrophy of the Left ventricle and eventually to left sided CHFBlood may eventually back up into the pulmonary system and lead to Right Ventricle failureS/S: palpatations, diastolic murmur is classic sign

104995Aortic murmur, tachycardia, palpitations, CHF with fatigue, SOB, AscitesMonitored with echocardiogram assessing L ventricular dilatationChest X-ray-enlargement of heartMay do cardiac cathMay need valve repair or replacement

104Cardiomyopathies: heart muscle diseasePresents with increased ventricular pressures3 common presentations of: 1. dilated (most common) 2. hypertrophic 3. constrictivePrognosis is POORNO CURATIVE MEASURES AT THIS TIME1051051005-1019

106106Dilated cardiomyopathyDilated cardiomyopathy: dilation of cardiac chambers redux of ventricular contractile funxDiagnosed: echocardiogram

TREATMENT: similar to CHF - inotropic agents -diuretics - vasodilators (ACE inhibitors) -beta blockersTo prevent sudden cardiac death; implant cardioverter-defibrillatorNeed intra-aortic balloon to stabilize pt NEED HEART TRANSPLANT 1071071006Causes:IdiopathicInflammatoryAutoimmuneToxic (drugs, alcohol)HereditaryIschemicMetabolic (uremia, vit defic)Endocrine (thyroid)

Hypertrophic cardiomyopathy:Inability of heart to relax during diastoleGoal: reduce afterload (beta-blockers, diuretics)Causes: idiopathic, systemic hypertension, genetic-atrial & vent arrhythmias seen in of these pts are responsible for sudden deathS/S: - dyspnea, angina, arrhythmias cardiac failure, very forceful apical impulse sudden death (most common in ages 10 to 35 and occurs during strenuous exertion)1081081009-15B-blockersCalcium channel blockersDiuretics

Echocardiogram is key

May need heart transplant

Restrictive cardiomyopathy- very noncompliant ventricular muscle-diminished LV cavity dimensions - ventricular volumes decreasedCAUSES: - idiopathic - interstitial disease - radiation - drug toxicity1091091015-16Tx:Diuretics, afterload reducersGoal: to improve diastolic functionEventually hypotension occurs

HEMODYNAMIC MONITORING

110110Monitoring of the blood flow and opressures within the bodyPurposes:Aid in diagnosisAssist in guiding therapiesEvaluating response to therapiesCan be invasive or non invasiveConsent is needed especially if invasive unless in ICU when crashing111Components:Monitor Flush systemTransducerHigh pressure tubing Catheter

111Setup Obtain IV NS 0.9% and transducer systemAttach the transducer to the IV flush solution and prime the tubing, removing air bubblesReplace all vented caps with non vented sterile dead end capsInflate pressure bag to 300mmHgAssist the patient into supine position with HOB