Cardiac - Lecture notes 1 PDF

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Adult Health Cardiac Module completed...

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Care of Persons with Cardiac Issues NURS 3102 NURS 3102 Adult Health: Care of Persons with Cardiac Issues Spring 2015 Readings: NURS 2112/2113 Alterations in Health: Modules Adams, M.P., Josephson, D.L., Holland, L.N., & King, S. (2010). Pharmacology for nurses: A pathophysiological approach. Canadian Ed. Toronto: Pearson Prentice Hall.   

Chapter 23 Drugs for Angina Pectoris, Myocardial Infarction, and Cerebrovascular Accidents Chapter 24 Drugs for Heart Failure Chapter 43 Drugs for Renal Disorders and Diuretic therapy (focus on Diuretics)

Copstead, L., & Banasik, J. (2013). Pathophysiology (5th ed). St. Louis, MO: Elsevier.  

Chapter 18 Alterations in Cardiac Function Chapter 19 Heart Failure and Dysrhythmias: Common Sequleae of Cardiac Disorders

Day, R., Paul, P., Williams, B., Smeltzer, S. & Bare, B. (2010). Brunner and Suddarth’s textbook of Canadian medical-surgical nursing (2nd Ed). Philadelphia: Lippincott Williams and Wilkins.   

Chapter 26 Assessment of Cardiovascular Function (732-765). Chapter 27 Management of Patients with Dysrhythmias and Conduction Problems (772784) Chapter 30 Management of Patients with Complications from Heart Disease (p. 883-910)

Paul, S. & Hice, A. (2014). Role of the acute care nurse in managing patients with heart failure using evidence-based care. Critical Care Nursing Quarterly, 37(4), 357-376. Overbaugh, K.J. (2009). Acute coronary syndrome: Even nurses outside the ED should recognize its signs and symptoms. American Journal of Nursing, 109(5), 42-52. Alberta Health Services (AHS) Cardiac Discharge Checklist and Heart Failure posted on Blackboard for case study work Suggested Websites:  Canadian Cardiovascular Society http://ccs.ca/index.php/en/

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Canadian Hypertension Education Program (CHEP) https://www.hypertension.ca/en/chep Heart and Stroke Foundation of Canada: http://www.heartandstroke.com/ ; also this patient resource: http://www.heartandstroke.com/atf/cf/%7B99452D8B-E7F1-4BD6A57D-B136CE6C95BF%7D/manage-heart-failure-en.pdf St Michael’s Hospital, Toronto – some good patient and health care provider information: http://www.stmichaelshospital.com/programs/heartvascular/heartfailure/resources.php

Additional Suggested Resources: Gulanick, M. & Myers, J.L. (2014). Nursing care plans: Diagnoses, interventions, and outcomes (8th ed.). Philadelphia, PA: Elsevier/Mosby. Vallerand, A.H., Sanoski, C.A., & Deglin, J.H. (2015). Davis's drug guide for nurses (14th ed.). Philadelphia, PA: FA Davis Company. Van Leeuwen, A.M., Poelhuis-Leth, D.J., & Bladh, M.L. (2013). Davis's comprehensive handbook of laboratory and diagnostic tests with nursing implications (5th ed.). Philadelphia, PA: FA Davis Company. Learning Objectives At the end of this module, the student should be able to: 1. Integrate and analyze knowledge required to care for patients with alterations in cardiac status – specifically those presenting with Acute Coronary Syndrome (ACS) and Heart Failure (HF). 2. Examine and analyze patterns of the determinants of health and health promotion that impact persons (individual, family, community) affected by the alteration in cardiac function. 3. Review and apply knowledge related to the pathophysiology and pharmacology of ACS and heart failure. 4. Describe nursing assessments, interventions, and evaluations of care related to patients with ACS and heart failure.

Guided Questions Heart Failure

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Insufficient cardiac output (CO) due to cardiac dysfunction o Symptoms: fatigue, shortness of breath and congestion related to inadequate perfusion of tissue and retention of fluid

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Two Types (assessment of ejection fraction (EF) determines type of HF): o Diastolic Heart Failure 

An alteration in ventricular filling

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EF normal

o Systolic Heart Failure 

An alteration in ventricular contraction

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EF is less than 40%

Etiology: o HF results from a variety of CV diseases 

Coronary Artery Disease (CAD) -

Primary cause of HF (more than 60%)

-

Narrowing of blood vessels that supply oxygen and blood to heart (due to atherosclerosis)

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Characterized by insufficient delivery of oxygenated blood to the myocardium due to arterosclerotic arteries. Demand exceed supply myocardium becomes ischemic

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Hypertension -

Systemic or pulmonary HTN increases afterload (resistance to ejection)  increased workload  hypertrophy

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Valve dysfunction

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Cardiomyopathy -

Detioration of the function of the myocardium

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Dilated most common  decreased contractility (systolic failure) o Can be idiopathic or can result from myocarditis, pregnancy or cytotoxic process (such as alcohol)

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Hypertrophic and restrictive cardiomyopathy lead to decreased ventricular filling (diastolic failure)

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Dysrhythmias

Pathophysiology o Systolic Heart Failure 

Decreases amount of blood ejected from the ventricle 

 stimulates sympathetic nervous system to release epinephrine and norepinephrine (to support failing myocardium, but continued response causes loss of beta-adrenergic receptor sites and for damage to heart muscle cells)  increases HR, BP and heart contractility

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 decrease in renal perfusion  activation of rennin-angiotensin mechanism (vasoconstrictor)  release of aldosterone (promotes sodium and fluid retention)

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increase in ANP and BNP (atrial and beta natriuretic peptide)  vasodilation (increases diuresis)

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increase in endothelin (vasoconstrictor) and vasopressin (promotes sodium and fluid retention)

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 increases preload and afterload  increases work load of heart  contractility decreases  ventricular dilation (enlarging of the ventricle)  increased workload  ventricular hypertrophy (increase thickness of heart muscle) NOT accompanied by adequate increase in blood supply  myocardial ischemia

o Diastolic Heart Failure 

Increased workload on heart  ventricular hypertrophy and altered myocellular functioning  resistance to ventricular filling  decreased ventricular filling  decreased CO (low CO and high ventricular filling pressures cause same neurohormonal responses as in systolic heart failure)

Clinical Manisfestations o GENERAL: 

Pale, cyanotic skin, dependant edema (edema of lower extremities), decreased activity tolerance

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Apical impulse, 3rd heart sounds, murmurs, tachycardia, increased jugular venous distention

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Lightheadness, dizziness, confusion

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Nausea, anorexia, enlarged liver, ascites

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Decreased urinary frequency during day, nocturia

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Dyspnea on exertion, orthopnea, (difficult breathing when lying flat) paroxysmal nocturnal dyspnea (sudden attacks of orthopnea at night), bilateral crackles

o Left sided Heart Failure (pulmonary congestion – occurs when left ventricle cannot pump blood out of ventricle to the body) 

Dyspnea, cough, pulmonary crackles, low O2 saturation, 3rd heart sound may be detected

o Right sided Heart Failure (congestion of viscera and peripheral tissues – cannot accommodate all the blood that normally returns from venous circulation) 

Dependant edema, hepatomegaly (enlargement of liver), distented jugular veins, ascites (accumulation of fluid in peritoneal cavity, weakness, anorexia, nausea and weight gain due to fluid retention

Diagnostics o Echocardiogram o Determine Ejection Fraction (EF) o Chest x-ray and electrocardiogram (ECG) o Exercise testing o Lab 

BUN, creatinine, BNP, thyroid stimulating hormone, CBC, routine urinalysis

Management o Objectives 

Eliminate or reduce etiologic contributory factors (atrial fibrillation and excession ETOH consumption)

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Reduce workload on the heart by reducing afterload and preload

o Medications 

Angiotensin-Converting Enzyme Inhibitors

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Angiotensin II Receptor Blockers

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Hydralazine and Isosorbide Dinitrate

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Beta-Blockers

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Diuretics

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Digitalis

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Calcium Channel Blockers

1. Describe the statement from 2113 “Heart failure begets heart failure”. What compensatory mechanisms are at work in the body when you have HF? (Copstead & Banasik, p. 464) Heart failure (HF) is “Insufficient cardiac output due to cardiac dysfunction”. HF begets (or gives rise to) HF because in an attempt to compensate for this inadequate blood perfusion to the rest of the body, mechanisms are activated that temporarily restore cardiac output (CO), but are detrimental to the heart in the long term. Enhanced preload and cardiac hypertrophy may allow the heart to compensate for an extended period of time, but these compensatory mechanisms, result in an increase in myocardial work and oxygen requirements and appear to cause detrimental remodeling of the heart. 3 main compensatory mechanisms activated during HF include: 1. Sympathetic Nervous System (SNS) activation: is mainly due to barorecptor (pressure sensors) reflex stimulation in the aorta and carotid arteries due to decrease in BP. The CNS activates this fight or flight response, which leads to increased HR and contractility. The SNS is also activated when the juxtaglomerular cells of kidneys sense a fall in BP. These cells release renin which initiates the renin angiotensin aldosterone system, which ultimately results in water and salt retention by the kidneys, thus increasing Blood volume and BP. SNS activation is a immediate compensatory response to insufficient CO. Because of increased BP associated with SNS activation, long term the heart is has even greater stress. Increased BP results in increased afterload cardiac workload on the left ventricle. Thus treatment of high BP is key in treating HF. Longterm SNS stimulation may also result in heart remodeling, a process resulting in myocyte loss, hypertrophy or remaining cells and interstitial fibrosis. This remodeled tissue is less functional and may worsen HF and cardiac arrhythmias 2. Increased Preload – enhances the ability of the myocardium to contract forcefully with a larger volume ejected. Thus, up to point, an increase in the volume or

preload of the heart will result in a greater force of contraction. Patients with systolic failure require a higher preload to achieve a given stroke volume. 3. Myocardial Hypertrophy and Remodeling- occurs over a longer time period than the previous 2 compensatory mechanisms. Hypertrophy results from chronic elevation of myocardial wall tension. Excessive preload results in eccentric hypertrophy in which muscle fibers elongate. High afterload results in concentric hypertrophy in which the muscle fibers grow in diameter and thicken the ventricular wall. Norepinephrine and angiotensin II also have a hypertrophic/remodeling affect on the heart (Pharm p. 304) HF can be caused by any disorder that decreases the ability of the heart to receive or eject blood including: Mitral stenosis, MI, chronic HTN, CAD, and diabetes mellitus

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The compensatory mechanisms that are at work in the body when you have HF: 

Increased stimulation of sympathetic nervous system

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Renin-Angiotensin Mechanism

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Increased Atrial and Beta Natriuretic Peptide

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Increased release of Endothelin & Vassopressin

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Ventricular Remodeling o Frank Startling Law o Myocardial Hypertrophy

2. What medications do you anticipate to be used in the heart failure population? Why are these so important? ACE Inhibitors- inhibits angiotensin converting enzyme from properly working. Without this

enzyme, the RAAS is not completed and water and salt retention is

not achieved, resulting in normal urination and decreased afterload and BP. They also cause dilation of veins returing blood to the heart, which decreased preload and peripheral edema. They are often drug of

choice of HF. SE: Neutorpenia, increase serum creatinine, severe

hypotension with initial dose,

Angiotensin-receptor blockers (ARBs)- are prescribed for HF if BB or ACE inhibitors are ineffective. ARBs have the same effect as ACE inhibitors but are reserved for patients unable to tolerate SE of ACE inhibitors. Both ARBs and ACE inhibitors are contraindicated in pregnancy and lactation. SE: increase in serum creatinine. Diuretics- are used to decrease systemic and pulmonary congestive symptoms, which result is decreased preload and cardiac workload. Once congestion has cleared, the lowest dose possible should be use to maintain a decreased blood volume/BP. Monitor potassium levels with all non-potassium sparing diuretics. They are used commonly used with ACE inhibitors. Contraindicated in pregnancy/lactation. -blocking agents- block the cardiac effects of SNS activation, thus reducing HR and contractility, which decreases BP and afterload, which slows progression of the disease. The dose is taken carefully, ensuring that too high of a dose is avoided, which could worsen HF. (ex carvedilol, metoprolol). Contraindicated in pregnant/lactation, decompensated HF, COPD, bradycarida and heart block. Vasodilators (Nitroprusside, nitroglycerin, and Natrecor)- are very effective in reducing afterload, and put less stress on the heart when trying to pump. (ex. Hydralazine (acts on arterioles) and isosorbide dinitriate (acts on veins)). These drugs have many SE and are reserved for patients who cannot tolerate ACE inhibitors. Digoxin and Digitoxin- may also be used for HF. Pretty much the same drug but digitoxin has a longer half-life. It slows electrical conduction but increases the force of heart contractions, thus improving cardiac output (CO). Therapeutic Index is narrow, with severe adverse affects, making these drugs, and are reserved for patients unresponsive to other drugs. Hypokalemia increases the risk of digoxin toxicity, so eat lost of potassium rich foods if on this drug. Phosphodiesterase Inhibitors- block the enzyme phophodiesterase in cardiac and smooth muscle , which increases the amount of calcium available for myocardial contraction. Thus it causes positive inotropic (increased force of contraction) of the heart and vasodilation. Are only used as a very last resort if ACE inhibitors and digoxin don’t work.

Influenza shot- HF pts should be immunized against influenza annually and pneumococcal pneumonia to reduce risk of respiratory infections that may seriously aggravate HF.

3. HF is a chronic disease and has no cure. 65-80% of patients die within 6 years of being diagnosed with chronic heart failure. What patient education can you as a nurse focus on to promote self care and improve quality of life? The focus of therapy for HF is to maintain a state of compensation my minimizing cardiac workload while optimizing cardiac output and preventing or delaying ventricular remodeling. Discuss with the patient the importance of: med management, low-sodium diet (< 2g/d), activity, exercise, S & S of worsening condition, weight monitoring, and when to contact a health care provider. Balance between rest and exercise and avoidance of stress are important. Fluid restriction may also be necessary to help with ascites and edema.

4. The New York Heart Association Functional Classification is based on what limitation in the Heart Failure population? Limitation of exertion or exercise. If symptoms of HF are only elicited during intense levels of exertion (triathlon), then their HF is considered to be minimal (Class 1). However, if one experiences symptoms of HF at rest, then his HF is considered to be in its most severe state (Class 5), and his HF with impair his functional capabilities even at rest.

Class

Criteria

I

Symptoms elicited only at levels of exertion that would limit normal individuals

II

Symptoms elicited on ordinary exertion

III

Symptoms elicited on less than ordinary exertion

IV

Symptoms elicited at rest

(Heart Failure article p. 96)

Classification Symptoms 1 -Ordinary physical activity does not cause undo fatigue,

Prognosis GOOD

dyspnea, palpitations, or chest pain -No pulmonary congestion or peripheral hypotension -Patient considered asymptomatic -Usually no limitations of activities of daily living -Slight limitation on ADLs

2

GOOD

-Patient reports no symptoms at rest but increased physical activity will cause symptoms -Basilar crackles and S3 murmur may be dectected -Marked limitations on ADLS

3

FAIR

-Patient comfortable at rest but less than ordinary activity will cause symptoms -Symptoms of cardiac insufficiency at rest

4

POOR

5. “Heart failure is a complex syndrome in which abnormal heart function results in, or increases the subsequent risk of, clinical symptoms and signs of low cardiac output and/or pulmonary or systemic congestion”. Explain the etiology of HF that explains this statement. You may want to refer to your research article to help answer this question. (C & B p. 469) Clinical manifestations of HF differ depending on which ventricle (left or right) is failing to pump blood adequately. Left ventricular failure is most common, and often leads to right ventricular failure, a condition termed “biventricular failure”.

Left-sided heart failure S &

Right-sided heart failure S

S:

& S:

Backward Effects

Backward Effects

 Dsypnea on exertion

 Hepatomegaly &

 Orthopnea

splenomegaly

 Cough

 Ascites

 Paroxysmal nocturnal

 Anorexia

dyspnea

 Subcutaneous edema

 Cyanosis

 Jugular vein distension

 Basilar crackles

Forward Effects

Forward Effects

Same as Forward effects of L-sided

 Fatigue

HF

 Oliguria  increase HR  faint pulse  confusion  anxiety

Forward effects of R & L sided HF are due to insufficient cardiac output with diminished delivery of oxygen and nutrients to peripheral tissues and organs. Inadequate perfusion of the brain may result in restlessness, mental and/or general fatigue, confusion, anxiety, impaired memory, activity intolerance, and letheragy. Forward effects of both R & L-sided HF also result in decreased urine output (oliguria) increased HR, and faint pulses. The backward effects of L-side HF lead to pulmonary congestion. Ineffective pumping of the left ventricle results in the accumulation of blood in the pulmonary circulation. As blood accumulates here and BP increases, fluid it is forced into the interstitial and alveolar spaces, causing edema and respiratory distress. Sitting or standing can help with dyspnea associate with pulmonary edema because it causes blood to pool in lower extremities instead of the lungs. Clinical signs of pulmonary congestion include cough, respiratory crackles (rales), hypoxemia (cyanosis), high left atrial pressure (LAP), and enlarged heart, engorged pulmonary capillaries and lymphatic vessels see on X-ray. 6. Define the term “Ejection Fraction”. What is the normal range for ejection frac...