Hypertension

1. Hypertension

2. Complications of Hypertension • Hypertensive Cardiovascular Disease • Hypertensive cerebrovascular disease • Hypertensive Renal Disease • Aortic Dissection • Atherosclerosis • Vision Changes

3. 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

4. DASH Diet

5. Hypertensive Emergencies • High B/P • Urgencies • Emergencies

6. Nursing Diagnoses • Knowledge Deficit • Impaired Health Maintenance

7. Nursing Interventions: (NIC) • Anticipatory guidance • Behavior Modification • Calming Techniques • Coping Enhancement • Electrolyte Management and Monitoring • Exercise Promotion • Nutrition Counseling • Teaching: Disease Process • Teaching: Medications

8. Nursing Outcomes (NOC • Health seeking behavior • Knowledge of diet, disease process, medications…. etc. • Adherence (compliance) behavior

9. Heart Failure

10. 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.

11. 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

12. 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.

13. 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)

14. Summary: (AHA,2005)

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

16. 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..

17. 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.

18. Review Blood Circulation

19. 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).”

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

21. Natural History of Heart Failure Diabetic Cardiomyopathy Diabetes LVH Diastolic dysfunction Obesity Diabetes CHF HTN Smoking Lipids Systolic dysfunction MI Normal LV structureand function LV remodeling Subclinical LV dysfunction Overt heart failure Vasan RS, Levy D. Arch Intern Med. 1996;156:1789–1796.

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

23. Compensatory Mechanisms • Sympathetic Nervous System Stimulation • RAAS • Neurohormonal responses TNF / Interlukins 1 and 6 BNP Endothelin

24. [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

25. [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

27. [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).

28. [3] Release of endothelins (potent vasoconstrictor) increased peripheral resistance, increase B/P ( worsening of HF).

29. [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!!!

30. 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).

31. Summary:

34. 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).

35. Physiologic Actions of Endogenous BNP • 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;4:37 Clemens LE et al. J Pharmacol Exp Ther. 1998;287:67 Marcus LS et al. Circulation. 1996;94:3184 Tamura 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

36. BNP/RAAS : Blood Pressure and Fluid Balance RAAS (constriction) BNP (dilation)

37. A-HEFT Study Combination Drugs: [a] Isosorbide dinitrate is an NO donor and [b] hydralazine an antioxidant that inhibits destruction of NO.[3,4]

38. 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.

39. 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."

44. 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

45. 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.

46. Causes of heart failure • high blood pressure (75%) • CAD • diabetes • problems with the heart valves • ETOH abuse • chemotherapy or radiation • Unknown (Idiopathic dilated cardiomyopathy)

47. Types of Heart Failure • Left-sided HF Systolic Dysfunction = EF<40% Diastolic dysfunction = EF high • Right sided HF

48. 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)

49. Left Sided HF Decreased 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

50. 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)