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Cardiovascular
System:
Hypertension
and Heart
Failure
1
What is Perfusion?
• All cells need oxygen and nutrients to
survive.
• Perfusion is the process of transporting
nutrients to the cells and surrounding
tissues.
• The cardiovascular system is the pump that
does this transportation
2
Physiology
• The heart is composed of four chambers: the left
atrium, the right atrium, the left ventricle, and the
right ventricle.
• Blood is circulated throughout the body by a
coordinated sequence of chamber contractions and
valve openings and closings known as the cardiac
cycle.
• The two phases of the cardiac cycle are systole and
diastole.
• Contractions of the heart propel blood through the
vascular system.
3
Physiology (cont.)
• Blood pressure is measured in millimeters of
mercury (mm Hg) and is calculated by measuring
the:
(Amount of blood leaving the heart)
x
(The amount of resistance in the peripheral vessels)
• The formula for measuring blood pressure is:
blood pressure = cardiac output  peripheral
resistance
BP = CO  PR.
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5
Causes of Decreased Perfusion
• Occlusion or restriction of arteries (lipids or clots)
• Impaired electrical conduction
• Malfunction of heart valves -stenosis or insufficiency
• Shock – rapid vasodilation of the blood vessels
• Cardiogenic
• Hypovolemic
• Anaphylactic
• Neurogenic
• Septic
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Consequences of Decreased Perfusion
• Occlusion or restriction of
arteries……………………..
• Impaired electrical
conduction…………………….
• Malfunction of heart
valves (stenosis or
insufficiency)…………………
• Shock – rapid vasodilation
of the blood
vessels…………………………..
Hypertension, Tissue necrosis,
Myocardial infarcts, Stroke
Cardiac arrhythmias
Pooling of blood in the
atrium/ventricles
Clot formation
Loss of oxygen to the brain and
other tissues
Cell death
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Risk Factors for Coronary Disease
Some of the factors that make a person at high risk
for poor perfusion include:
• Certain ethnic groups
• Genetics
• Age
• Diet
• Smoking history
• Obesity
• Hypertension
• Diabetes
• Elevated lipid levels
• Sedentary Lifestyle
8
Physiology of Cardiac Output
• The volume of blood that leaves the left ventricle
in 1 minute is called the cardiac output.
• Cardiac output consists of two elements:
• Stroke Volume and Heart Rate.
• Normal heart rate is 60-100 bpm in adults
• Stroke volume is the amount of blood that leaves
the left ventricle with each contraction (75 mL)
• Increase either one, and you increase cardiac
output (CO)
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Physiology of Cardiac Output
• Stroke volume is dependent on three factors:
• Preload: how much blood volume there is
• Contractility: flexibility of the heart muscle
• Afterload: peripheral artery resistance
• Contractions of the heart are also partly
dependent on the unique electrical conduction
system of the cardiac muscle.
• Affected by cardiac arrhythmias, or abnormal
electrical conduction
10
Heart Failure
• Heart failure is associated with high morbidity
(disease) and mortality (death)
• Processes that may cause HF occur either in the
heart itself or in the body system.
• Cardiac output decreases when the left ventricle
is unable to eject its normal volume of blood
during systole.
• The heart muscle enlarges (called
cardiomyopathy) to provide more contractile
force to try to improve cardiac output.
11
Drugs to Treat Heart Failure
• When the heart cannot achieve the
normal cardiac output, a backlog of blood,
or congestion, occurs and heart failure
develops.
• This is why we commonly say Congestive
Heart Failure, or CHF
• Several drug classes are used to treat CHF.
Polypharmacy is considered the standard
and most effective treatment.
12
Role of Adrenergic Receptors
(Sympathetic Nervous System)
• Adrenergic receptors in the nervous system have a
role in blood pressure management.
• When alpha-1 adrenergic receptors are stimulated,
they cause peripheral constriction.
• Blood pressure increases as a result.
• This effect, which is similar to stimulation of the
sympathetic nerves, is called a sympathomimetic
effect (one that mimics the effect of the
sympathetic system).
13
Role of Adrenergic Receptors
• Alpha-1 receptor sites are located within the body.
• Alpha-2 receptor sites are located within the brain.
• Beta-1 receptor sites are located mostly in the heart.
• Beta-2 receptor sites are located primarily in the
bronchial (lungs) and vascular walls.
Actions of drugs will depend on which of these
adrenergic receptors are stimulated.
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Cardiogenic Shock
Shock is the result of inadequate tissue perfusion,
leaving the cells without the oxygen and nutrients
they need to function normally and survive.
One of the most frequent indications for
adrenergic agonist drugs is cardiogenic shock.
Sympathomimetic drugs provide extra-adrenergic
stimulation and block some autonomic nervous
system functioning.
Adrenergic Agonists
• Adrenergic agonists are drugs that mimic the action
of the SNS.
• Adrenergic agonists are also classified according to
their selectivity.
• Nonselective adrenergic agonists stimulate both
alpha and beta receptors.
Prototype non-selective adrenergic agonist:
Epinephrine
Epinephrine: Core Drug Knowledge
• Pharmacotherapeutics
• Wide variety of indications—asthma,
anaphylactic allergy, shock, etc.
• Pharmacodynamics
• It stimulates all adrenergic receptors
• Side effects
• Tachycardia, Hypertension
• Adverse effects
• Hypertensive crisis, angina, cerebral hemorrhage,
and cardiac arrhythmias.
Challenge Question
Which of the following receptors is (are) stimulated
by epinephrine?
A. Alpha 1
B. Alpha 2
C. Beta 1
D. Beta 2
E. All of the above
All of the above – it is a potent
sympathomimetic!
Alpha-Adrenergic Antagonists
• Alpha-adrenergic antagonists block the stimulation of alpha
receptors.
Prototype Drug: Prazosin (Minipress)*
• Pharmacodynamics
• Blocks postsynaptic alpha-1 adrenergic receptors to lower
blood pressure.
• Pharmacotherapeutics
• Used to treat congestive heart failure, Raynaud vasospasm,
and prostatic outflow obstruction.
• Off-label use to treat nightmares associated with posttraumatic stress disorder.
Challenge Question:
Why might this drug be useful in treating PTSD related
nightmares?
*Not on drug list
Alpha-2 Adrenergic Agonists
• Alpha-2 adrenergic agonists
• Stimulation of alpha-2 receptors in the CNS
decreases sympathetic outflow by inhibiting the
release of norepinephrine.
Prototype: clonidine (Catapres, Kapvay)
• Catapres is approved to treat hypertension
• Kapvay is approved to treat the symptoms of attentiondeficit, hyperactivity disorder in children.
Side effects
Dizziness, Drowsiness, Orthostatic hypotension
Beta-1 Adrenergic Agonists
• Beta-adrenergic agonists mimic the action of the
SNS and are widely used for cardiovascular problems.
Prototype: Dopamine (Intropin)
• Pharmacotherapeutics
• Used to correct the hemodynamic imbalances
present in shock.
• Pharmacodynamics
• Stimulates alpha-1 and beta-1 receptors. Increases
cardiac output
Dopamine: Core Drug Knowledge
• Side effects
• Nausea and vomiting
• Tachycardia, Palpitation, Hypotension
• Headache
• Adverse effects
• Ectopic (extra) heart beats, Angina
• Maximizing therapeutic effects
• Administer IV using an infusion pump to regulate flow.
• Titrate dose to desired effect.
• Ongoing assessment and evaluation
• Treatment is effective if blood pressure stabilizes, urinary
output returns to normal, and cardiac output returns to
normal.
Beta-Adrenergic Antagonists aka
“Beta Blockers”
• Antagonize both beta-1 and beta-2 receptors to
cause:
• Vasodilation
• Decreased peripheral resistance (lower BP)
• Bronchodilation
Prototypes: atenolol (Tenormin),
propanolol (Inderal),
metoprolol (Lopressor, Toprol XL)
Metoprolol: Core Drug Knowledge
• Pharmacotherapeutics
• Treatment of hypertension, angina, and
controlled congestive heart failure.
• Off-label treatment of migraine headaches
• Off-label treatment of performance
anxiety/panic
• Pharmacodynamics
• Mechanical: Decreased cardiac output and
blood pressure.
• Electrical: Slowing of atrial-ventricular
conduction and suppression of automaticity
Metoprolol: Core Drug Knowledge
• Contraindications and precautions
• Severe bradycardia, cardiogenic shock, airway
diseases
• Side effects
• Diarrhea, dizziness, drowsiness
• Adverse effects
• Cognitive dysfunction, Depression, Hypoglycemia
• Drug interactions
• Several drug interactions
Regulation of Blood Pressure
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Pathophysiology: Hypertension
• Hypertension (HTN) is a chronic disorder that affects
all age groups.
• HTN is common in all racial groups, although some
groups are more prone to hypertension than others.
• The American Heart Association defines adult
hypertension as persistent elevation of systolic
pressure ≥ 140 mm Hg or diastolic pressure ≥ 90 mm
Hg.
• A diagnosis of HTN is not made until the average of
two or more readings, each recorded at two or more
visits.
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Classification of Hypertension
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Lifestyle Modification & Hypertension
• Non-medication therapy consists of lifestyle changes
including reducing weight and adopting the Dietary
Approaches to Stop Hypertension (DASH).
• DASH recommends a diet rich in fruits, vegetables,
and nonfat dairy, along with reduced intake of
saturated and total fat but higher potassium and
calcium intake.
• Lifestyle modifications also include
• Limit alcohol intake
• Regular exercise
• Stop smoking.
29
Drug Therapy and Hypertension
• Drug therapy is now recommended to be started
with every patient who has been diagnosed as
having HTN
• Drug therapy is also recommended in
prehypertension if the patient has compelling
indications.
30
Drug Classifications for
Hypertension
• Diuretics
• Beta blockers
• Calcium channel blockers
• ACE inhibitors
• Angiotensin II receptor blockers (ARBs).
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Second Line of Drugs Used to Treat
Antihypertension
• Selective aldosterone blockers
• Direct acting vasodilators
• Centrally acting alpha-2 agonists
• Peripherally acting alpha-1 blockers
• Peripherally acting anti-adrenergics
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Drug Therapy for Hypertension
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Role of Renin-AngiotensinAldosterone
• Another mechanism involved in blood pressure
regulation is the renin-angiotensin-aldosterone
system.
Normal Physiology
• Renin, which is produced by the kidneys, produces
angiotensin I.
• Angiotensin I is an inactive substance until it is
converted to the active angiotensin II.
• Angiotensin II is a potent vasoconstrictor.
• It also stimulates secretion of aldosterone from the
adrenal glands, which retain sodium to increase BP.
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Angiotensin-Converting Enzyme
(ACE) Inhibitors
• In the renin-angiotensin-aldosterone sequence, an
enzyme is needed to convert angiotensin I to the
active angiotensin II.
• Angiotensin II is a potent vasoconstrictor. Together
with aldosterone, it increases blood pressure.
• ACE inhibitors prevent the conversion of angiotensin
I to angiotensin II thus reducing vasoconstriction
Prototype drug: lisinopril (Zestril)
35
Lisinopril : Core Drug Knowledge
• Pharmacotherapeutics
• HTN, CHF, diabetic nephropathy, and left
ventricular dysfunction
• Pharmacokinetics
• Administered: Oral. Metabolism: liver. Excreted:
kidneys. T½: 2 hours
• Pharmacodynamics
• Inhibits the ACE needed to change the inactive
angiotensin I to the active form angiotensin II
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Lisinopril : Core Drug Knowledge
• Contraindications and precautions
• Second and third trimester of pregnancy
• Side effects
• Hypotension
• Adverse effects
• Persistent nonproductive cough, angioedema,
neutropenia (low neutrocytes – a white blood
cell)
A special problem with all ACE inhibitors is that they
also affect bradykinin. This effect can cause a
persistent, constant, irritating cough.
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ACE Inhibitors – Adverse Event
Case Example
50 yof started lisinopril 5 mg/day for HTN. After 3months, this was increased to 10 mg/day. She started
to have a non-productive cough that worsened when
lying down. Went to an urgent care clinic who said she
had a respiratory infection and gave her an antibiotic.
Sxs did not change. Went back to the clinic who then
said she had “allergies” and put her on 2 medications
to treat allergies. Sxs did not change. Finally went
back to her PCP and the lisinopril was stopped. Cough
went away after 2 weeks.
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Angiotensin II Receptor Blockers
• Angiotensin II receptor blockers (ARBs) directly
block the action of angiotensin II from forming to
lower BP
• The indications for ARBs and their efficacy are
similar to those of ACE inhibitors but without the
cough.
Prototype drug: losartan (Cozaar)
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Losartan: Core Drug Knowledge
• Pharmacotherapeutics
• HTN, left ventricle dysfunction
• Do not take while pregnant
• Pharmacodynamics
• Selectively blocking the binding of angiotensin
II to the angiotensin I receptors in many tissues
• Side effects
• Hypotension, diarrhea, dizziness, and fatigue
• Adverse effects
• Risk for angioedema (swelling) even as sudden
onset
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Calcium Channel Blockers
• Calcium Channel Blockers work by inhibiting
influx of calcium ions across myocardial cell
muscles and directly on vascular smooth muscle
causing a reduction in vascular resistance
(afterload) and blood pressure.
Prototypes: Amlodipine (Norvasc)
Nifedipine (Procardia)
41
Amlodipine: Core Drug Knowledge
• Pharmacotherapeutics
• Angina, Heart Failure, Hypertension
• Pharmacokinetics
• Orally administered. Highly protein bound. Duration of
24 hours Metabolized by liver and excreted by
kidneys.
• Side effects
• Dizziness, flushing, palpitations, fatigue, nausea,
sleepiness
• Adverse effects
• Edema
• Increase risk for Angina or acute myocardial
infarction
42
Drugs Used in Severe
Hypertensive Crisis
Prototype drug: nitroprusside (Nitropress)
• Pharmacotherapeutics
• Indicated in emergency hypertensive crisis
• Pharmacokinetics
• Administered: IV. Onset: 2 minutes. T½: 2 minutes
• Pharmacodynamics
• Directly relaxes vascular smooth muscle, allowing
dilation of peripheral arteries and veins
• Adverse effects - Cyanide toxicity (thiocyanate
toxicity)
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Nitroprusside: Teaching,
Assessment, and Evaluations
• Patient and family education
• Explain to patient and families that the drug is
being given to lower blood pressure quickly and
that blood pressure will be monitored constantly
to prevent it from dropping too low.
• Ongoing assessment and evaluation
• Monitor blood pressure throughout nitroprusside
therapy so that it is reduced without sacrifice to
vital organs.
44
Renal System Physiology
• The renal system consists of the kidneys, ureters,
and bladder.
• Usually, the kidneys produce less than 2 L of urine
daily.
• The kidneys play a major role in the reabsorption
and secretion of electrolytes.
• Vast quantities of sodium and chloride are filtered
through the glomerulus. Most of sodium and chloride
(60%-65%) is reabsorbed.
• Blood pressure is significantly affected by the
kidneys
45
Function of the Renal System
The Renal System Physiology
http://www.youtube.com/watch?v=lfGYd1wrTgE
46
Pathophysiology
• When the body cannot maintain a balance of body
fluid levels, fluid overload or volume depletion
occurs.
• Hypovolemia is a result of dehydration or blood
loss.
• Hypervolemia may result from excessive sodium
and water retention.
• Fluid shifts into the interstitial spaces (edema)
may occur with fluid volume excess.
• Peripheral edema increases the cardiac workload
and decreases tissue perfusion.
47
Peripheral Edema
Decreased
Renal
Clearance
Increased Vascular
Volume
(Hypervolemia)
Increased Blood
Pressure
“Third-spacing”
of Fluid into the
interstitial
spaces (Edema)
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Pathophysiology (cont.)
• Diuretic drugs are used in treating conditions
in which fluid overload and/or edema has
occurred.
• This may result in some Blood Pressure drops
due to a reduction in fluid volume.
• These conditions include:
• Chronic heart failure (CHF), pulmonary
edema, hypertension, cirrhosis, nephrotic
syndrome, and kidney failure.
50
Diuretics
• Purposes of diuretics
• Lower blood pressure
• Decrease Peripheral edema
• Help treat Congestive Heart Failure
• Help treat Pulmonary Edema
• Types of diuretics
• Potassium-wasting diuretics
• Thiazide
• Loop
• Potassium-sparing diuretics
• Combination products
51
Kidney Function
Diuretics Act on
Different Segments of
the Renal Tubes.
52
Thiazide Diuretics
• Thiazide diuretics are related structurally to the
antibacterial sulfonamides.
• Action is to promote vasodilation and water + Na
excretion.
• Not useful for immediate diuresis.
• Adverse effect risk for chemistry abnormalities with
thiazides
• ↓ K, Mg
Prototype Drug:
Hydrochlorothiazide (HCTZ)
53
Hydrochlorothiazide: Core Drug
Knowledge
• Pharmacotherapeutics
• Used in the treatment of hypertension
• Pharmacodynamics
• Acts in the distal tubule to increase excretion of
sodium and chloride by slightly inhibiting the ion
pumps that work in sodium and chloride
reabsorption.
• Side effects
• Dizziness and frequent urination
• Adverse effects
• Hypokalemia, hyponatremia, hypochloremia,
hypomagnesemia and hypercalcemia
54
Hydrochlorothiazide: Planning and
Interventions
• Maximizing therapeutic effects
• Administer dose in the AM.
• Monitor fluid intake, urine output, and body
weight for changes.
• Minimizing adverse effects
• Correct any electrolyte imbalance prior to
starting hydrochlorothiazide therapy .
• Monitor serum electrolyte levels.
55
Loop Diuretics
• The loop diuretics work in the loop of Henle to inhibit
reabsorption of sodium and chloride.
• They exert a powerful effect on fluid and electrolyte
balance.
• Should also take K+ supplements with this drug.
Prototype Drug:
Furosemide (Lasix)
56
Furosemide: Core Drug Knowledge
• Pharmacotherapeutics
• Peripheral and pulmonary edema, HTN
• Pharmacokinetics
• Administered: IV or oral. Highly protein-bound
drug. Excreted: kidneys
• Pharmacodynamics
• Inhibits the reabsorption of sodium, chloride, and
water in the ascending loop of Henle
• Side effects
• Alteration in glucose levels
• Urinary urgency or even accidents
• Adverse effects
• Electrolyte imbalance, ototoxicity
57
Furosemide: Planning and
Interventions
• Maximizing therapeutic effects
• Titrate dose slowly.
• In patients with severe CHF, a continuous
infusion is more effective than an equal dose
given as an IV bolus in decreasing edema.
• Minimizing adverse effects
• Closely monitor potassium levels.
• Administer 20 to 40 mg of IV push furosemide
slowly over at least 1 to 2 minutes.
58
Question
The patient who is malnourished is at greater risk for
toxicity from furosemide than the well-nourished
patient.
A. True
B. False
59
Question
The patient who is malnourished is at greater risk for
toxicity from furosemide than the well-nourished
patient.
A. True
B. False
A. True - This is true because the
malnourished patient has less protein in the
body, which will result in more free drug and
furosemide is a highly protein-bound drug.
60
Question
A client is taking furosemide (Lasix) 40 mg daily for
heart failure and hypertension. The nurse knows
that electrolyte imbalances that commonly
occur and should be monitored include:
Risk for low serum potassium, sodium, magnesium,
and calcium.
61
Question
A patient has orders for furosemide (Lasix) daily. Based on
it’s actions, when should the dose be given?
Early in the morning due to heavy diuretic effects.
If the order is for furosemide BID, when should doses be
given?
Preferably early in the morning then again in the afternoon
(e.g. 8am-4pm). Avoid bedtime due to risk for interrupted
sleep due to diuresis.
62
Homework
1. Log onto Shadow Health Digital Clinical
Experience
2. Complete the Anti-Asthmatics Concept
Lab (Will take you 20-30 minutes)
3. Go to Assignments and answer the
questions posed over the treatment of
Asthma.
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