Hypertension

Complications of Hypertension

• Hypertensive Cardiovascular Disease• Hypertensive cerebrovascular disease• Hypertensive Renal Disease• Aortic Dissection• Atherosclerosis• Vision Changes

Collaborative Management of Hypertension

• Pharmacologic– Diuretics– ACE Inhibitors/Angiotensin Receptor Blockers (ARBs)– Calcium channel blockers– Nitrates

• Non-Pharmacologic– Stress reduction– Weight control– Decrease alcohol intake– Beware of OTC drugs– Stop Smoking

DASH Diet

Hypertensive Emergencies

• High B/P• Urgencies• Emergencies

Nursing Diagnoses

• Knowledge Deficit• Impaired Health Maintenance

Nursing Interventions: (NIC)

• Anticipatory guidance• Behavior Modification• Calming Techniques• Coping Enhancement• Electrolyte Management and Monitoring• Exercise Promotion• Nutrition Counseling• Teaching: Disease Process• Teaching: Medications

Nursing Outcomes (NOC

• Health seeking behavior• Knowledge of diet, disease process,

medications…. etc.• Adherence (compliance) behavior

Heart Failure

Review• The basic function of the renin-angiotensin-aldosterone

system• Use of the following in HTN/HF:

– ACE/ARB– CCB– Beta Blockers

• Diagnostic criteria for Hypertension (JNCC 7) http://hin.nhlbi.nih.gov/nhbpep_slds/jnc/jncp2_1.htm

• Incidence, prevalence, epidemiology of hypertension, heart failure

• Clinical presentation of right and left sided heart failure.• Function of ANP/BNP• Vascular assessment findings r/t arterial and venous

insufficiency.

Learn:• Definition and defining characteristics of

– Ineffective Health Maintenance r/t deficient knowledge regarding treatment and control of disease process

– Decreased cardiac output r/t impaired cardiac function– Ineffective Tissue Perfusion

• Definition and indicators for these NOCs: – Health Promoting Behavior – Tissue integrity: Skin and Mucous Membranes– Hemodynamic regulation

• Review these NICs:– Circulatory Care: Arterial Insufficiency– Circulatory Care: Venous Insufficiency

• Cardiac resynchronization therapy

Objectives:

• Plan, implement and evaluate care for patients with acute and chronic heart failure.

• Plan, implement and evaluate care for patients with hypertension, and patients experiencing hypertensive emergencies.

• Describe nursing strategies for promoting adherence with medication therapy for HTN, HF

• Describe health promotion strategies for patients at risk for HTN.

Fact: CHF Incidence=550,000 cases/year (AHA,2005)

Prevalence= 5 million living with HF (AHA, 2005).

CHF office/hospital visits = 12 -15 million office visits per year. -6.5 million hospital days/year (AHA, 2005).

Hospital discharges= $5,471 per discharge -377,000 (1999) /yr - 970,000 (2002) /yr, a 157% increase (AHA,2005).

Cost/year/Hospital admissions = 27.8 billion in 2000 (CMS 2003, AHA 2005)

Cost/year/managing CHF= $56 billion,70% due to hospitalization (Bhalla, 2004)

Summary: (AHA,2005)

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2

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11.6

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4

6

8

10

12

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Prevalence of heart failure by age and sex (NHANES: 1999-2004). Source: NCHS and NHLBI.

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100

200

300

400

500

600

700

79 80 85 90 95 00 04

Years

Dis

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Hospital discharges for heart failure by sex(United States: 1979-2004). Source: NHDS, NCHS and NHLBI.

Note: Hospital discharges include people discharged alive, dead and status unknown..

9.2

22.3

4.7

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20

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50

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Incidence of Heart Failure* by age and sex. (FHS: 1980-2003).Source: NHLBI.* HF based on physicians review of medical records and strict diagnostic criteria.

Review Blood Circulation

What is heart failure?

• The American College of Cardiology/American Heart Association (ACC/AHA) (2005) provides a scientific statement defining heart failure as “A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema (p. e160).”

• Heart failure usually occurs when another problem makes the heart weak or stiff so it doesn’t pump or fill normally.

Vasan RS, Levy D. Arch Intern Med. 1996;156:1789–1796.

Natural History of Heart Failure

HTN

Smoking

Lipids

Obesity Diabetes

MI

LVH

CHF

Normal LV structure

and function

LV remodeling

Subclinical LV

dysfunction

Overt heart failure

Diastolicdysfuncti

on

Systolicdysfuncti

on

DiabetesDiabetic

Cardiomyopathy

HF……

……..complex progression of domino effects involving cardiac and neurohormonal systems……..

Compensatory Mechanisms

• Sympathetic Nervous System Stimulation

• RAAS

• Neurohormonal responses TNF / Interlukins 1 and 6 BNP Endothelin

[1] Sympathetic Nervous System Stimulation

• Normal adaptive mechanism:– As a response to decreased CO, the body attempts to

compensate:– increased release of catecholamines

• Undersirable effects of catecholamine release:– Afterload is increased, increasing cardiac work load– SV Inc----Starling’s Law----– Arterial vasoconstriction----leading to---Inc afterload—LV

requiring more energy to eject----SV declines

[2] Neurohormonal Responses

[1] After MI release of proinflammatory cytokines (TNF) and interleukins (IL 1 & IL 6) , leading to ventricular remodeling.

[2] BNP release promote diuresis, (vasodilates) counteract RAAS decrease preload decrease CO Decreased cerebral perfusion release of vasopressin/ ADH (fluid retention) from the PPG causes vasoconstriction

worsening HF

[3] RAAS

– Blood flow to kidneys reduced, which activates the renin-angiotension system (RAS)

– Activation of RAAS, leads to production of renin, ACE 1, ACE 2, Aldosterone, leading to NA and water retention……..

– Preload and afterload increase– Leading to ventricular remodeling , consisting of left

ventricular dilatation, myocyte hypertrophy and elongation.– Enhanced neurohormonal stimulation can lead to apoptosis,

aggravation of ventricular contractility and death (ACC/AHA, 2005).

[3] Release of endothelins (potent vasoconstrictor) increased peripheral resistance, increase B/P ( worsening of HF).

[4] Myocardial Hypertrophy

• Final compensatory mechanism• Heart wall thickens increased

contractions increase CO leading to hypertrophied cardiac muscle increase O2 consumption

myocardial reserve exhausted HF!!!

• HF is a common outcome for many cardiovascular diseases that results in symptomatic or asymptomatic left ventricular dysfunction (LVD).

• HF is a vicious cycle if left untreated.

• Dysfunction begets additional dysfunction that culminates in the demise of the patient (Ramakrishnan, et al., 2005).

Summary:

Role of B-type natriuretic peptide (BNP) in HF

• BNP is a group of natriuretic peptides that are involved in the regulation of diuresis.

• Antagonizes and counteract the vasoconstricting effects of the renin angiotensin-aldosterone system (RAAS), thereby regulating blood pressure and fluid balance (Chiong & Miller, 2002).

• Is a neurohormone released from the cardiac ventricles in response to increased volume and cardiac overload (Mark & Felker, 2004).

Hemodynamic(balanced vasodilation) Veins Arteries Coronary arteries

Neurohormonal aldosterone endothelin norepinephrine

Renal sodium and water excretion

Cardiac Antifibrotic Antiremodeling

Abraham WT et al. J Card Fail. 1998;4:37Clemens LE et al. J Pharmacol Exp Ther. 1998;287:67Marcus LS et al. Circulation. 1996;94:3184Tamura N et al. Proc Natl Acad Sci U S A. 2000;97:4239 Zellner C et al. Am J Physiol. 1999;276(3 pt 2):H1049

Physiologic Actions of Endogenous BNP

BNP/RAAS : Blood Pressure and Fluid Balance

RAAS (constriction)BNP(dilation)

A-HEFT Study

Combination Drugs:[a] Isosorbide dinitrate is an NO donor and [b] hydralazine an antioxidant that inhibits

destruction of NO.[3,4]

Aheft Trial Results

Kaplan-Meier survival analysis showed that the survival benefit with ISDN plus hydralazine appeared at around 180 days and increased progressively from then on.

ISDN +Hydralazine

Placebo p

Primary composite Score

-0.1 -0.5 .01

Components of Primary Composite Score

All Cause Mortality

6.2 10.2 .02

First hospitalization for HF

16.4 24.4 .001

Change in QOL scores 6 months

-5.6 -2.7 .02

Conclusion:

• A-HeFT data "support, but do not prove the existence of a protective role of NO even in the presence of neurohormonal blockade." They call for "a strategy to identify genotypic and phenotypic characteristics that would transcend racial or ethnic categories to identify a population with heart failure in which there is an increased likelihood of favorable response to such therapy."

Emerging Biomarkers for HF[1] BNP[2] Mid-regional adrenomedullin[3] Gal3= Galactin 3[4] MPO= Myeloperoxidase[5] ST2 = interleukin receptor family member[6] Markers of Renal Function (a) BUN/ Creat (b) EGFR (c) Cystatin C [7] Markers of Renal Injury (a) Albuminuria (b) NGAL =N eutrophil gelatinase associated lipocalin

Summary: BNP

• Regulates B/P and fluid balance.• BNP elevated with ventricular stretch.• BNP increases with volume overload.• BNP = biomarker for CHF.• weaker the heart = HIGHER BNP levels.

Causes of heart failure

• high blood pressure (75%) CAD diabetes problems with the heart valves ETOH abuse chemotherapy or radiation Unknown (Idiopathic dilated

cardiomyopathy)

Types of Heart Failure

• Left-sided HF Systolic Dysfunction = EF<40%

Diastolic dysfunction = EF high • Right sided HF

Left sided HF

[1] Exertional dyspnea (DUE)

[2] Orthopnea (dyspnea at rest (lying flat)

[3] Paroxysmal Nocturnal dyspnea (PND)(sudden awakening with a feeling of

breathlessness 2 -5 hours after falling asleep)

Left Sided HFDecreased CO[1] Fatigue[2]Weakness[3] Oliguria during the day[4] angina[5] Confusion/restlessness[6] Dizziness[7]Tachycardia[8] Pallor[9] Weak peripheral pulses[10] Cool extremities

Pulmonary Congestion[1] hacking cough, worse at

night[2] Dyspnea[3] Crackles/wheezes in lungs[4] Frothy, pink-tinged sputum[5] Tachypnea

[6] S3/S4 Gallop[7] AFIB is common

Right Sided HF

Systemic Congestion[1] JVD[2] Enlarged liver and spleen[3] Anorexia and Nausea (Megase)[4]Dependent edema (legs and sacrum)[5] Swollen hands and fingers[6] Polyuria at night[7] Weight gain (most reliable indicator of fluid

loss/gain)[8]Increased BP (from excess volume) or decreased BP

(from failure)

Signs and Symptoms of Heart Failure

• The staging of HF was devised to establish the evolution and progression of the disease that can worsen over time.

• These levels or stages can only advance forward and not backward. This classification focuses on patients with HF as well as those who are at risk of developing HF (ACC/ AHA, 2005).

ACC/AHA Classification of Chronic Heart Failure

AHigh risk for developing heart failure

Hypertension, diabetes mellitus, CAD, family history of cardiomyopathy

BAsymptomatic heart failure

Previous MI, LV dysfunction, valvular heart disease

CSymptomatic heart failure

Structural heart disease, dyspnea and fatigue, impaired exercise tolerance

DRefractory end-stage heart failure

Marked symptoms at rest despite maximal medical therapy

NYHA Functional Classification• NYHA I = No limitation of physical activity. Ordinary

physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath)

• NYHA II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

• NYHA III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.

• NYHA IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

New Approach to the Classification of Heart Failure

Stage NYHA functional class

A High risk for developing heart failure (HF)

None

B Asymptomatic HF I Asymptomatic

C Symptomatic HF II Symptomatic with moderate exertion

III Symptomatic with minimal exertion

D Refractory end-stage HF

IV Symptomatic at rest

New Approach to the Classification of Heart Failure

Stage Patient Description

A High risk for developing heart failure (HF)

Hypertension CAD Diabetes mellitus Family history of

cardiomyopathy

B Asymptomatic HF Previous MI LV systolic dysfunction Asymptomatic valvular disease

C Symptomatic HF Known structural heart disease Shortness of breath and fatigue Reduced exercise tolerance

D Refractory end-stage HF

Marked symptoms at rest despite maximal medical therapy

Psychosocial Assessment

• Anxiety

• Depression

• Empower Patient

Labs

• Chest –x-ray• BNP levels• Echocardiogram• Cardiac catheterization• MUGA Scan• TSH, T4 levels

Interventions

• Medical treatments• Surgical treatments• Non-pharmacologic interventions

Medical Management• Vasodilators

– ACE Inhibitors– Specific beta blockers (not all)– Nitrates

• Aldosterone blockade– Inspra (eplerenone)

• Inotropic Agents– Phosphodiesterase Inhibitors (Milrinone)– Cardiac Glycosides

• Diuretics

• Intravenous Natrecor (nesiritide)

Pharmacologic Interventions

HFSA Guidelines (2006)• Beta –blockers• ACE Inhibitors /ARB• Diuretics / Digoxin• Inotropic drugs Dobutamine

Drugs that reduce afterload

[1] ACEI

[2] Natrecor

Drugs that reduce preload

[1] Diuretics

[2] Venous vasodilators

Drugs that enhance contractility

[1] DigitalisCame from?Digoxin levelS/S[2] BB

Beta Blockers

Action

Side effect

What to watch for before giving?

Surgical interventions

• LVAD• BI-V• Cardiac transplant• Intra-aortic Balloon Pumping• CRT

Non-pharmacological Interventions

• Diet = Low Na • Daily weights• Disease State Management• Assess Sleep Disordered Breathing• Cardiac Rehabilitation

HF-ACTION enrolled 2331 patients at 82 study sites throughout the U.S., Canada and France. Patients were randomized into a group that received usual care or to a group that received usual care plus an exercise training program that began under supervision but then transitioned to home-based, self-monitored workouts.

Conclusion:

Based on the protocol-specified initial analysis, exercise training produced only a modest, non-significant reduction in the primary endpoint of all-cause hospitalization or all-cause death.

QOL:Researchers also found that a higher percentage of those in the exercise group experienced more robust gains. At three months, 54 percent of those in the exercise group saw a five-point gain in overall KCCQ score, while only 28 percent of those in the usual care group met that goal. (p = .0001).

Assessment

• Lung Sounds• Jugular Venous Distention• + Hepatojugular Reflex• Peripheral Edema• EKG findings

Heart Failure: Pearls to Remember

[1] Do not miss correctable causes[2] Common condition with high mortality[3] Get echocardiogram. Get clinical picture

low EF= systolic Hf, normal EF= Diastolic HF[4]Check BNP levels (helpful dyspnea or SOB)[5] ACEI, ARB = decrease mortality[6] BB=increase longevity, reduce morbidity and

mortality

• [7] Digoxin helpful in AFIB.• [8] Spironolactone= reduce mortality in class IV

HF. Watch for hyperkalemia.• [9] AICD for patients with EF<35% (sudden

death)• [10] BI-V for resistant Hf if QRS duration is

>120ms• [11] transplant for resistant HF, if no serious co-

morbidities.

Holistic Nursing Interventions

• Physiological = Physical signs and symptoms• Psychological = depression, anxiety• Emotional = sense of isolation, feeling a

burden• Spiritual = faith, hope

Nursing Diagnoses

• Decreased Cardiac Output• Fluid Volume Excess **• Impaired Gas Exchange **• Activity Intolerance• Knowledge Deficit

Nursing Interventions (NIC)

• Calming Techniques• Cardiac Care

– Rehabilitative• Electrolyte Management and Monitoring• Energy Management

Nursing Outcomes (NOC)

• Tissue perfusion• Cardiac pump effectiveness• Circulatory status

Valvular Disease[1] Mitral stenosis (mostly women)

[2] Mitral Regurgitation (Insufficiency)

[3] Mitral Valve Prolapse (Marfan’s Syndrome)

[4] Aortic Stenosis (Congenital valvular disease or malformation)

[5] Aortic Regurgitation (Insufficiency) (75% men)

Interventions

[1] Non-surgical management:a. Drugs = BB, diuretic, O2 (HF meds) = Prophylactic antibiotics prior to any invasive

surgery = amiodarone (afib, dec.CO 25% -30%)/

cardioversion

b. Rest

Interventions[2] Surgicala. Valve repairb. Balloon valvuloplasty (< 6 months, poor

surgical candidate)c. Direct commissurotomy (heart surgery,

clean, debrides calcium)d. Mitral annuloplasty (reconstruction)e. Valve Replacement Biologic = porcine, bovine Prosthetic = St. Jude’s (coumadin for life!)

Websites:

• www.hfsa.org• www.aha.org