Hypertension
Complications of Hypertension
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Hypertensive Cardiovascular Disease
Hypertensive cerebrovascular disease
Hypertensive Renal Disease
Aortic Dissection
Atherosclerosis
Vision Changes
Collaborative Management of
Hypertension
• Pharmacologic
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Diuretics
ACE Inhibitors/Angiotensin Receptor Blockers (ARBs)
Calcium channel blockers
Nitrates
• Non-Pharmacologic
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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)
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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)
Percent of Population
14
11.6
12
12.4
10
7.2
8
5.2
6
4
2
2
0.3
1.5
0.2
0
20-39
40-59
Men
60-79
Women
Prevalence of heart failure by age and sex
(NHANES: 1999-2004). Source: NCHS and NHLBI.
80+
Discharges in Thousands
700
600
Male
500
Female
400
300
200
100
0
79 80
85
90
95
00
Years
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..
04
Per 1,000 Person Years
50
40
43.0
Men
30
30.7
22.3
20
10
Women
14.8
9.2
4.7
0
65-74
75-84
85-94
Age
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.
Natural History of Heart Failure
Diabetes
Obesity
Diabetes
HTN
Diabetic
Cardiomyopathy
LVH
CHF
Smoking
Lipids
Normal LV
structure
and function
Diastolic
dysfunction
MI
LV remodeling
Systolic
dysfunction
Subclinical LV
dysfunction
Overt heart
failure
Vasan RS, Levy D. Arch Intern Med. 1996;156:1789–1796.
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 reninangiotension 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).
Physiologic Actions of
Endogenous BNP
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
Hemodynamic
(balanced vasodilation)
 Veins
 Arteries
 Coronary arteries
Neurohormonal
  aldosterone
  endothelin
  norepinephrine
Renal
  sodium and water excretion
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
ISDN
+Hydralazine
Placebo
-0.1
-0.5
.01
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
Primary composite
Score
p
Components of
Primary Composite
Score
Kaplan-Meier survival analysis showed that the survival benefit with ISDN plus
hydralazine appeared at around 180 days and increased progressively from then on.
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
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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 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
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
A
High risk for
developing heart failure
B
Asymptomatic
heart failure
C
Symptomatic heart
failure
D
Refractory end-stage
heart failure
Hypertension, diabetes
mellitus, CAD, family history
of cardiomyopathy
Previous MI, LV dysfunction,
valvular heart disease
Structural heart disease,
dyspnea and fatigue, impaired
exercise tolerance
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)

B
Asymptomatic HF

C
Symptomatic HF

D
Refractory
end-stage HF

Hypertension
 CAD
 Diabetes mellitus
 Family history of cardiomyopathy
Previous MI
 LV systolic dysfunction
 Asymptomatic valvular disease
Known structural heart disease
 Shortness of breath and fatigue
 Reduced exercise tolerance
Marked symptoms at rest despite maximal
medical therapy
Psychosocial Assessment
• Anxiety
• Depression
• Empower Patient
Labs
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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] Digitalis
Came from?
Digoxin level
S/S
[2] BB
Beta Blockers
Action
Side effect
What to watch for before giving?
Surgical interventions
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LVAD
BI-V
Cardiac transplant
Intra-aortic Balloon Pumping
CRT
Non-pharmacological Interventions
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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, nonsignificant 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
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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
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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] Surgical
a. Valve repair
b. 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