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Congestive Heart Failure & Valvular Disease

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Presentation on theme: "Congestive Heart Failure & Valvular Disease"— Presentation transcript:

1 Congestive Heart Failure & Valvular Disease
Keith Rischer RN, MA, CEN Impaired cardiac pumping CAD and age are primary risk factors…HTN, DM, smoking, obesity, high cholesterol can contribute HTN most significant contributor along w/DM HF caused by any interference in CO…this can involve preload, afterload, contractility, HR Impacts 5 million Americans 550,000 new cases annually Affects 10% of all those over 65 Most common reason for adm to hospital for the elderly Prevelance is increasing probably due to increased treatment Terminal dx-80% will be dead in 8 years if dx after age 65 Most often due to dysfunction of the LV Overall patient’s quality of life is ↓ by HF, even when it is mild to moderate. The pt has less energy, a lower fitness level, engages in fewer social activities and has more physical complaints. The cost of HF mgmt has been est. at 38.1 billion-5.4% of the total. MGMT DEPENDANT ON PT COMPLIANCE-NSG…PT EDUCATION ESP MEDS-YOU CAN MAKE A DIFFERENCE!

2 Todays Objectives… Review essential cardiac patho concepts
Compare and contrast left-sided heart failure to right Describe special considerations for older adults with heart failure Discuss the prevention of complications for patients with heart failure Prioritize nursing care for clients with heart failure Identify common nursing diagnoses and collaborative problems for patients with heart failure Evaluate the effects of interventions for reducing preload and afterload through pharmacological management Compare and contrast common valvular disorders

3 Introduction Definition of CHF Left sided vs. Right sided
Etiology HTN MI Left sided vs. Right sided Rt sided COPD Systolic vs. Diastolic Ejection Fraction 50-70% normal Definition of CHF: physiologic state in which the heart is unable to pump enough blood to meet the metabolic needs of the body. The LV is unable to eject a sufficient quantity of blood Like a car with bad timing, the damaged heart does not function smoothly. HTN causes 75% Left sided vs. Right sided Systolic vs. Diastolic Systolic refers to ventricular dysfunction Diastolic-LV unable to relax adequately during diastole-inadequate relaxation or stiffening prevents ventricle from filling-decr SV though EF may be normal-not as common

4 CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm)
Cardiac Output CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm) Daily pumps 1800 gallons 657,000 gallons every year Over 80 year lifetime: 52,560,000 gallons Every 10 days fills a gallon swimming pool Every year appx 36 pools Over lifetime appx 3000 pools Factors that influence CO are preload, afterload, myocardial contractility, and HR 4

5 Definitions Pre-load Stroke volume Systole
primarily venous blood return to RA Right and left side of heart filling pressure (atria>ventricles) Pressure/Stretch in ventricles end diastole Stroke volume Amount of blood ejected from the ventricle with each contraction Systole Contraction; myocardium are tightening and shortening Preload Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also true What cardiac meds will most strongly influence preload??? How will volume depletion such as by dehydration or blood loss affect preload???

6 Definitions Inotropic state/contractility Afterload: Diastole
Force of resistance that the LV must generate to open aortic valve Correlates w/SBP Diastole Muscle fibers lengthen, the heart dilates, and cavities fill with blood Contractility- Afterload Arterial vasodilation will decrease Important when in AMI we need to decr workload of heart by intentionally lowering afterload NTG indirectly affects afterload through decreasing preload What meds??? B-blockers….ACE inhibitors calcium channel blockers and arterial vasodilators such as hydralazine Epi will do what to afterload???

7 Patho: Starling’s Law of the Heart
Maximum efficency of CO achieved when myocardium stretched appx 2 ½ times length Think rubber band CO decreased with lower preload/filling pressures or too high HF occurs when it takes higher filling pressures to accomplish normal contractile force Incr in preload cause a decrease in SV and higher LVEDP This causes back pressure into lungs causing leakage of fluid into alveoli causing PE 7

8 Compensatory Mechanisms in CHF
Increased Sympathetic Nervous System Stimulation Renin-angiotensin system activation Natriuretic peptides BNP Ventricular hypertrophy compensatory mechanisms- When the heart begins to fail, the body activates several defense mechanisms in an attempt to maintain CO and O2 to vital organs. sympathetic nervous system stimulation is the least effective comp. mechanism triggered by ↓ CO. Produces venous & arteriole vasoconstriction-↑resistance (afterload) and ↑myocardial workload. In addition, Symp. Stim. Reduces renal blood flow, and the kidneys respond by activating the renin-angiotensin system causing Na & H2O retention. The ↑ blood vol. ↑ the myocardial O2 demand on an already compromised heart. Renin-angiotensin-reduced flow to kidneys…RAS…vasoconstriction pronounced…incr …aldosterone secretion causes sodium and water retention…angiotensin II contributes to ventricular remodeling causing myocardial cell contractile dysfunction over time BNP Hormone that promote vasodilation and diuresis through sodium loss to counterbalance the RAS Ventricular hypertrophy Represents and ↑ in myocardial muscle mass and cardiac thickness in an attempt to ↑ CO. The heart works harder hence ↑ myocardial O2 demand. Cardiac decompensation occurs when the heart, despite these mechanisms are unable to meet the metabolic demands→CHF develops

9 Acute Pulmonary Edema:
Elevated capillary pressure within the lungs  fluid pushed from circulating blood to interstitial tissues  then to the alveoli, bronchioles, and bronchi *Results from LV failure in clients with severe decompensation *A medical emergency – can cause death from suffocation if untreated

10 Nursing Assessment:Left Failure
Dyspnea Cough Bilateral crackles Orthopnea PND Pulmonary Edema S3 (ken-tuck-ee) confusion fatigue and muscular weakness nocturia increase retention of sodium and water due to lowered glomerular filtration  edema S3 occurs at the end of the rapid filling period of the ventricle during the beginning of (ventricular) diastole.  An S3, if heard should occur msec after S2. A patient could have a left sided S3 (best heard with the bell of the stethoscope at the apex of heart while the patient is in the left lateral decubitus position), a right sided S3 (best heard with the bell of the stethoscope in the tricuspid region with the patient in the supine position during inspiration) or both. An S3 can either be physiological or pathological. A normal S3 is common in: children young adults (sometimes up to age 35-40) third trimester of pregnancy An abnormal S3 (an S3 heard in anyone above 40) (also known as a ventricular gallop) is associated with: decreased myocardial contraction myocardial failure volume overload of a ventricle (such as from mitral or tricuspid regurgitation)

11 Nursing Assessment: Right Failure
Dependent edema – early sign symmetric pitting edema Bedrest-sacral edema anasarca- late sign of CHF Ascites Anorexia, nausea and bloating Cyanosis of nail beds Anxious, frightened, depressed Weight gain >2# daily

12 Diagnostic Assessment
Chest x-ray Cardiac Enlargement 12 lead EKG Echocardiogram assess ejection fraction Labs BNP Liver enzymes…AST, ALT Creatinine/GFR 12 lead EKG cardiac dysrhythmia, PACs or atrial fib Increased BUN and creatinine levels – sign of decreased renal perfusion BNP ( Brain Natriuretic Peptide): A simple test that could diagnose pts. w/CHF. BNP a hormonal ↑ levels by heart tissue when organ is overloaded w/ pressure & vol. is expanded. ↑ BNP is highly sensitive and specific for the Dx. Of HF-it is also useful for differentiating pulmonary and cardiac causes of dyspnea.

13 Acute Left Failure/Pulmonary Edema: Collaborative Management:
O2 treatment Drug Treatment Diuretics Vasodilators-NTG MS Digitalis Semi- Fowler’s position Frequent Heart and Lung Assessment Dietary Restrictions Planned rest periods Weigh daily Report to MD immediately: persisting productive cough; dyspnea; pedal edema; restlessness

14 Drug therapy: Diuretics ACE Inhibitors Beta Blockers
Calcium Channel Blockers Nitroglycerine Positive Inotropic agents Digitalis Beta Adrenergic Stimulator Dopamine,Dobutamine . Digitalis: has inotropic effect, increased C.O. different preparations are available contra-indicated: cardiac tamponade and constrictive pericarditis use with caution in acute MI, can cause increase myocardial O2 demand watch for s/s of toxicity; G.I.; CNS; CV; visual, slow HR Dopamine – has dose related effect A naturally occurring catecholamine with alpha-adrenergic, beta adrenergic, and dopaminergic activity check apical pulse Dobutamine – a synthetic derivative of Dopamine and has strong beta stimulatory effects; increases the heart rate Capable of increasing CO without increasing the myocardial O2 demand or reducing coronary blood flow NTG-Venous dilating, ↓ afterload primarily through decr preload, properties that ↓ LV congestion Isosorbide dinitrate reduces angina by dilating both the veins and the arteries. Isosorbide dinitrate is in the class of drugs called anti-anginal medications Nitroprusside releases a chemical call nitric oxide (NO). Nitric oxide enters the muscle cells in the walls of the blood vessels and causes them to relax. When the muscles relax, the blood vessels become wider and the blood pressure decreases.

15 Pharmacologic: Diuretics
Mechanism of Action: Thiazides, Loop, Potassium Sparing S/E: fluid and electrolyte imbalances CNS effects GI effects Nursing Considerations: Monitor for orthostatic hypotension Hypokalemia Thiazides, Loop, Potassium Sparing Patho-block Na+ reabsorption in nephron-Na+ follows water and increases water/urine excretion Loop of henle has highest concentration of Na+ in filtrate from glomerulus therefore they are the most potent Recommended for initial drug therapy of uncomplicated HTN (along with beta-blocker Newly diagnosed HTN preferred durg combo for initial treatment = diuretics and beta blockers Thiazides first and most commonly used due to more gentle diuresis

16 Angiotensin Converting Enzyme (ACE) Inhibitors
Mechanism of Action S/E: Hypotension cough Hyperkalemia…esp w/CHF, CKD, DM Angioedema Facial/laryngeal swelling Nursing considerations: Do not use with potassium sparing diuretic Metabolized by liver-excreted by kidneys CO falls blood flow decreases-kidneys secrete enzyme renin>angiotensin 1> converted to Angiotensin 2 most potent vasoconstrictors kown by converting enzyme in lungs Angiotensin 2 causes adrenal cortex to release hormone Aldosterone incr Na+ reabsorption which causes water retention>salt and water retention…incr blood volume and elevates BP/vasoconstriction By blocking angiotensin II decreases BP through lowering peripheral resistence-AFTERLOAD….and decreasing blood volume-PRELOAD

17 Adrenergic Inhibitors: Beta Blockers
Mechanism of Action Recommended for initial drug therapy of uncomplicated HTN (along with diuretic) S/E: Orthostatic hypotension bradycardia bronchospasm Nursing considerations: monitor pulse regularly By decr HR and contractility reduce CO and lower SBP…also block/inhibit renin secretion and resultant formation of Angiotensin II For example a patient receiving Rx for minipress (Prazosin HCL) make sure you tell them to take it at bedtime.

18 Calcium Channel Blockers
Amlodipine, Diltiazem, Nifedipine Mechanism of Action: S/E: Nausea H/A Peripheral edema Nursing considerations: use with caution in patients with heart failure Orthostatic changes contraindicated in patients with 2nd or 3rd degree heart block Concurrent use w/b-blockers incr risk of CHF By blocking channels of Ca++-decr contractility and relax smooth muscle lowering peripheral resistence-AFTERLOAD Reduces the force of contraction Slows AV node-decreases HR Vasodilation of smooth muscle in the blood vessels decreased peripheral resistance  reduces BP and dec afterload  reduced O2 needs. Dilates coronary arteries  provide more O2 to myocardium ACTIONS: Decrease BP Decrease Angina Decrease Heart Rate/ Dysrhythmias

19 Vasodilators Mechanism of Action-NTG
Vasodilater-predominant on venous system by relaxing smooth muscles of vessels Dilates coronary arteries/improves collateral flow Up to 20% normal coronaries…30-40% pre/post stenosis Decreases LVEDP…why? Decreases O2 needs myocardium Side effects HA, hypotension, tachycardia Hydralazine arterial vasodilator Vasodilator-which aspect of CO are we manipulating??? Can be given IV, transdermal or sublingual/spray and po as Isordil/isosorbide If subl need to keep pills cool-dry place and replace every 6 months-should gently tingle tongue HYDRALAZINE-direct arterial vasodolator-AFTERLOAD Produce reflex tachycardia-compensatory response to sudden decr in BP---increases workload of heart-negating effect-bblockers can negate this effect 19

20 Priority Nursing Diagnosis
Impaired Gas exchange r/t ventilation perfusion imbalance Decreased Cardiac Output r/t altered contractility, preload and afterload Activity Intolerance r/t imbalance between O2 supply and demand Knowledge Deficit Activity schedule Recognizing worsening heart failure Medications Diet therapy

21 Valvular Heart Disease:Mitral Valve
Mitral Stenosis Patho Mitral Regurgitation Mitral Valve Prolapse Why is the tricuspid and pulmonic valve rarely involved in valvular disease and dysfunction??? Mitral Stenosis Patho- rheumatic fever…valve thickening-stiffening of valve…valve becomes narrow impacting SV to LV LA enlarges-PA pressures rise RV enlarges and can go into RV failure Systolic murmur Mitral Regurgitation or insufficiency Fibrotic and calcification on valve prevent complete closure of valve…blood backflows into LA causign enlargement as well as blood leaking through to LV during diastole incr. SV and then LV enlargement… Rheumatic fever-heart disease most common Begins slowly-heart compensates will see both RV and LV failure Sys. murmur Mitral Valve Prolapse valvular leaflets enlarge and prolapse into LA during systole-usually benign but can progress to mitral regurg

22 Valvular Heart Disease:Aortic Valve
Aortic Stenosis Patho Causes Congenital Atheroclerosis Calcification Aortic Regurgitation (Insufficiency) Aortic Stenosis Patho AV narrows/stiffens and obstructs LV outflow during systole. Increased resistence to ejection or afterload causes LV hypertrophy…due to congenital changes Eventually causes LV failure and resultant CHF sx SOB, angina, fatigue Systolic murmur Aortic Regurgitation (Insufficiency) Patho leaflets do not close during diastole allowing regurgitant blood flow back into LV causing incr SV and LV hypertrophy DIASTOLIC MURMUR…WHY???

23 Treatment Valvular Disease
Non-surgical Management Diuretics Beta blockers Digoxin Antibiotics Before any invasives Coumadin-if artificial valve Surgical Management Balloon Valvuloplasty Open heart Why is AFIB bad with valvular disease….difficult to maintain adequate CO

24 Pericarditis Patho Assessment findings Complications Open heart AMI
Friction rub CP w/insp CP relieves sitting up Global ST elevation Complications Pericardial effusion Cardiac tamponade pericardiocentesis Patho-inflammation of pericardium Most often seen w/cancer…MI, CABG (10-40% develop) Pericardial effusion-excess can cause tamponade which will decr. Diastolic filling…does what to SV??? Does what to BP???

25 Endocarditis Patho Etiology Clinical Manifestations Diagnosis
Valve replacement Structural cardiac defects Invasive procedures Clinical Manifestations New murmur Heart failure Embolic Diagnosis Transesophageal Echo + blood cultures Interventions IV abx Surgical Patho Viral-bacterial infection involving endocardium Healthy-defective or prosthetic valve Etiology Clinical Manifestations Diagnosis Interventions

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