Transcript Intro to Heart Failure_HTN_Meds-In Class-2

Introduction to
Heart Failure &
Hypertension &
Associated
Cardiac
Medications
NUR 152
MESA COMMUNITY COLLEGE
CHAPTER 35-IGGY (678-692) &
ASSOCIATED CHARTS IN IGGY
CHAPTER 36-IGGY (PG 709-718) &
ASSOCIATED CHARTS IN IGGY
Learning Objectives
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Describe left, right, and high output heart failure
Describe causes, diagnostics, clinical manifestations, and
compensatory mechanisms of left and right heart failure
Describe common treatments for heart failure
Describe & differentiate the various prototype medications used to
enhance cardiac functioning
Describe essential and secondary hypertension & it’s causes,
diagnostics, clinical manifestations, and treatments
Describe & differentiate the various drug therapies for hypertension
Describe & differentiate the various anticoagulant drug therapies
Heart Failure
Pg. 679
Also called pump failure; inability of heart to work
effectively as a pump
Major types:
Left-sided
Right-sided
High-output
Etiology
Pg. 681
Table 35-1
▪ Systemic hypertension is the cause of heart failure in most cases
▪ About one third of patients experiencing MI also develop heart
failure
▪ Structural heart changes (e.g., valvular dysfunction) cause
pressure or volume overload on heart
Heart failure patients must be unloaded!
Pg 684
Decrease preload &
afterload by decreasing
blood volume and peripheral
vascular resistance thus
Improving cardiac output!
Left Sided Heart Failure
Pg. 682
▪ Formerly known as congestive
heart failure
▪ Typical causes
▪ Hypertension
▪ Coronary artery disease
▪ Valvular disease
▪ Not all cases involve fluid
accumulation
▪ Two types:
▪ Clinical manifestations
▪
▪
▪
▪
Weakness
Fatigue
Dizziness
Acute confusion
▪ (low flow)
▪ Pulmonary congestion
▪ Residual LV volume-backs up
▪ Breathlessness
▪ Oliguria
▪ Systolic
▪ Diastolic
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Right Sided Heart Failure
Pg. 682
▪ Causes
▪ Left ventricular failure
▪ Right ventricular MI
▪ Pulmonary hypertension
▪ Right ventricle cannot empty
completely
▪ Increased volume and pressure in
venous system and peripheral edema
▪ Clinical manifestations
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▪
▪
▪
▪
▪
▪
Jugular vein distention
Increased abdominal girth
Dependent edema
Hepatomegaly
Hepatojugular reflux
Ascites
Weight most reliable indicator of fluid
gain/loss
▪ Assessment:
▪ Laboratory
Electrolytes
Hemoglobin and hematocrit
BNP
Urinalysis (proteinuria/high specific
gravity)
▪ ABGs
▪
▪
▪
▪
▪ Imaging
▪ CXR
▪ Echocardiography (best diagnostic
tool)
▪ ECG
▪ Pulmonary artery catheter
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Pulmonary Artery Catheter (Swan-Ganz)
(Nice to know not need to know for block I - provided as
visual only)
Blood Studies/Other tests Pg. 683-684
▪ Electrolytes
▪ Renal studies
▪ Drug levels
▪ BNP (helps with differential)
▪ CBC
▪ UA
▪ ABG
▪ Echocardiogram
▪ ECG
▪ Chest X-Ray
Chest X-Ray
▪ Gives information on the size of the heart
▪ Position of the heart
▪ Condition of the lungs
▪ Routine screening
▪ Often old films available for comparison
High Output Failure-Not a common type of HF
▪ Cardiac output remains normal or above normal
▪ Caused by increased metabolic needs of hyperkinetic conditions
▪ Septicemia
▪ Anemia
▪ Hyperthyroidism
Compensatory Mechanisms
Pg 679
▪ When cardiac output is insufficient to meet body’s demands, these
mechanisms operate to increase cardiac output:
▪ Sympathetic nervous system stimulation
▪ Other renin-angiotensin system activation
▪ Chemical responses (BNP)
▪ Myocardial hypertrophy
Indications for Worsening or Recurrent Heart Failure
▪ Rapid weight gain
▪ Decrease in exercise tolerance
▪ Cold symptoms
▪ Excessive awakening at night to urinate
▪ Development of dyspnea/angina at rest
▪ Increased edema in feet, ankles hands
The heart is special because...
Uses all oxygen delivered by coronary arteries.
Skeletal muscle uses 25-30%.
Only way to increase oxygen supply is to vasodilate and increase heart
rate.
Strengthen contraction to increase output
Starling’s Law (fiber length and tension)
Nice to know but not need to know: ↓
Atrial and ventricular muscle cells have own intrinsic timer.
SA node paces 60-100 times per minute
AV node paces 40-60 times per minute
Ventricular muscle cells pace 20-40 times per minute
Extrinsic Control of Cardiac Output
Sympathetic nervous system
alpha fibers - increased rate (chronotropic)
beta fibers - increased force of contraction (inotropic)
Parasympathetic nervous system
Vagus nerve - slowing of heart rate, reduces contractility to decrease
stroke volume
Common Cardiac Related Medications Pg. 686
▪ Prototype-
Digoxin (Lanoxin)
Cardiac Glycoside
▪ Actions
▪ Positive inotropic action
▪ Negative chronotropic action
▪ Negative dromotropic action
▪ Increase stroke volume
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For further knowledge:
ATI- Pharmacology Made Easy- Drug Therapy
for Heart Failure- Cardiac Glycosides
Cardiac Glycoside: Pg. 686
Digoxin (Lanoxin)
▪ Therapeutic Effect/Use
▪ Treatment of HF
▪ Treatment of atrial tachycardia, flutter, and fibrillation
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Cardiac Glycoside: Digoxin
▪ Mode of Action/Pharmacodynamics
▪ Inhibits sodium-potassium ATPase =>
▪ Increases intracellular calcium =>
▪ Cardiac muscle fibers contract more efficiently
▪ Heart rate slows
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Cardiac Glycoside: Digoxin
Digitalis Toxicity (drug alert pg 687)
Skyscape
▪ Side Effects
Anorexia
N/V
HA
Blurred vision (halos)
Fatigue
Severe (symptomatic)
bradycardia
▪ CHF therapeutic drug levels:
▪
▪
▪
▪
▪
▪
▪ Adverse Reactions
▪ Bradycardia
▪ AV block
▪ Dysrhythmias
▪ 0.5-0.8 ng/mL
▪ Toxic = >2 ng/mL
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Cardiac Glycoside: Digoxin/Digitalis Toxicity
▪ Treatment for Digitalis Toxicity
▪ Digoxin immune Fab (digibind)
▪ Binds with digoxin and is excreted in the urine
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Cardiac Glycoside: Digoxin
▪ Interactions
▪ Increase risk of digoxin toxicity
▪ Thiazide diuretics
▪ Loop diuretics
▪ Why?
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Cardiac Glycoside: Digoxin
▪ Nursing Implications
▪ Assessment
▪ Apical Pulse: if <60 Hold and notify MD
▪ ECG
▪ Labs: potassium level, Digoxin Level
▪ Evaluation
▪ After dose given watch for SE
▪ Teaching
▪ How to take pulse
▪ S/S of toxicity
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NITRATES (Pg . 686)
(Nice to know, not need to know for block I)
▪ Nitroglycerin
▪ Dilate Veins
▪ Decreased Preload
▪ Dilate Coronary Arteries
▪  O2 supply
▪ Dilate Arterioles
▪ Decreased Afterload
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▪
▪
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Side effects: BP, Headache
Develop resistance
Manufactured in many forms: oral, SL, spray, paste, IV
12 hour nitrate free period
Factors Affecting Myocardial Oxygen Demand and
the Effect of Various Cardiac Medications
Actions of Antianginal Drugs
▪ Improve blood delivery to the heart muscle
by dilating blood vessels
▪ Increase the supply of oxygen
▪ Improve blood delivery to the heart muscle
by decreasing the work of the heart
▪ Decrease the demand for oxygen
Nitroglycerin
(Nice to know, not need to know for block I)
▪ Side effects
▪
▪
▪
▪
▪
N/V
Dizziness
Flush
Pallor
HA
▪ Adverse Reactions
▪ Hypotension
▪ Tachycardia
▪ Circulatory collapse
Nitrate: nitroglycerin (Nitro-Dur, Nitrostat) (Pg
765-766)
(Nice to know not need to know for block I)
▪ Therapeutic Effects/Uses
▪ Control angina pectoris
▪ Acute MI
▪ Management of CHF
Nitrate: Nitroglycerin
(Nice to know not need to know for Block I)
▪ Nursing Implications
▪ Assessment
▪ VS
▪ Pain assessment
▪ Nursing Diagnoses
▪ Decreased cardiac output
▪ Anxiety
▪ Acute Pain
Nitrate: Nitroglycerin
(Nice to know not need to know for block I)
▪ Nursing Interventions
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▪
▪
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Monitor VS: Q5 min
Positioning?
Ointment: Do not use fingers
Where to place transdermal application?
On 12 hours/Off 12 hours
Teaching
▪ How to self administer SL nitroglycerin?
▪ Storing NTG
▪ Avoid alcohol
▪ Self administration of transdermal patch.
Prototype Potassium-Sparing Diuretic:
Spironolactone (Aldactone) (Pg. 686)
▪ Therapeutic Effects/Uses
▪ Counteract K+ loss with other diuretics
▪ Edema & Hypertension
▪ When combined with other diuretics
Prototype Potassium-Sparing Diuretic:
Spironolactone (Aldactone)
Mode of Action
▪ Promote Na+ and H2O excretion and K+ retention in the collecting duct
renal tubules.
▪ Blocks action of aldosterone
Prototype Potassium-Sparing Diuretic:
Spironolactone (Aldactone)
▪ Side Effects
▪
▪
▪
▪
Dizziness
Clumsiness
HA
Constipation
▪ Adverse Reactions
▪ Hyperkalemia
▪ Arrhythmias
Prototype Potassium-Sparing Diuretic:
Spironolactone (Aldactone)
▪ Nursing Interventions
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Monitor UO
Monitor VS
Monitor for s/s of hyperkalemia
When to administer?
Teaching
▪ When to take at home?
▪ High Potassium Foods
Thiazide diuretics: Prototype hydrochlorothiazide
(HCTZ) – Microzide (Pg. 686)
▪ Mechanism of action:
▪ Inhibits H2O, Na+, Cl- reabsorption
▪ Used in conjunction with other antihypertensives to ↓BP
▪ Diuresis occurs and K+ Mg+ lost
Common Cardiac Related Medications cont.(Pg
685-686)
▪ Prototype: Furosemide (Lasix)
▪ Loop Diuretic
▪ Inhibits Na+ & H20 reabsorption in renal
tubules
▪ Decreased Na+ reabsorption →
▪ Increased Na+ excretion through the kidneys→
▪ Increased H20 excretion through the kidneys
(H20 usually follows Na+)
▪ Decreased reabsorption of other electrolytes
is also common with use of diuretics (K+)
▪ Main Uses:
▪ Decrease edema
▪ Decrease HTN (indirectly)
▪ Potassium “wasting” vs. “sparing”
▪ For further knowledge: Refer to ATIPharmacology Made Easy- Drug Therapy for
Heart Failure- Loop Diuretics
Common Cardiac Related Medications Continued
▪ Potassium Supplements (Potassium acetate)
▪ Treats potassium depletion (in the use of potassium
wasting diuretics, ACE inhibitors, or angiotensin II
antagonists) p.o. route
▪ Tablets are very large: assess swallowing ability
▪ Treats hypokalemia (usually I.V. route: slowly
and carefully!)
Nursing Diagnoses for HF
▪ Activity Intolerance
▪ Excess Fluid Volume
▪ Impaired Gas Exchange
▪ Anxiety
▪ Deficient Knowledge
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DRUGS FOR HYPERTENSION
Pg 715-716 – Chart 36-1
Hypertension (>60 y.o.
BP>150/90
<60 y.o. BP>140/90)
JNC 8 Guidelines for HTN
http://www.aafp.org/afp/2014/1001/p449.html
Essential
Secondary
▪ Results in damage to vital organs
▪ Common causes
▪ Causes medial hyperplasia
(thickening) of arterioles
▪ Common risk factors
▪
▪
▪
▪
Obesity
Smoking
Stress
Family history
▪ Table 36-4/Pg 710
▪ Renal disease
▪ Primary aldosteronism
▪ Pheochromocytoma
▪ Cushing’s syndrome
▪ Medications
▪ Table 36-4/Pg 710
Hypertension Pg 709
Assessment
Life Style Changes
▪ Patient history
▪ Sodium restriction
▪ Physical assessment
▪ Weight reduction
▪ Psychological assessment
▪ Diagnostic assessment
▪ Reduce alcohol intake
▪ Exercise
▪ Decrease stress levels
▪ Avoid smoking
Prototype: metoprolol (Lopressor)
▪ Beta-Adrenergic Blockers
▪ ↓ vascular resistance → ↓ BP
▪ Monitor for orthostatic hypotension
▪ Check pulse daily
▪ Can cause fatigue, depression,
sexual dysfunction
Beta Adrenergic Blockers
▪ Reduce cardiac output (CO) => decreased vascular resistance =>
decreased BP
▪ Decrease renin release
▪ Less effective in African Americans
▪ Non-selective vs cardioselective beta blockers
▪ “OLOL”
Prototype Beta-Adrenergic Blocker:
Metoprolol (Lopressor)
▪ Therapeutic Effect/Uses
▪
▪
▪
▪
▪
HTN
Angina
Prevent MI
Decrease mortality in pts. with recent MI
Ventricular arrhythmias
▪ Mode of Action
▪ Cardioselective blockade of B1 adrenergic receptors.
Prototype Beta-Adrenergic Blocker:
Metoprolol (Lopressor)
▪ Contraindications
▪
▪
▪
▪
Uncompensated CHF
Bradycardia or heart block
Pulmonary edema
Cardiogenic shock
Prototype Beta-Adrenergic Blocker:
Metoprolol (Lopressor)
▪ Side Effects
▪
▪
▪
▪
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N/V/D
Dizziness
Fatigue
Weakness
Impotence
▪ Adverse Reaction
▪ Bradycardia
▪ Complete heart block
▪ Bronchospasm
Prototype Beta-Adrenergic Blocker:
Metoprolol (Lopressor)
▪ Nursing Interventions
▪ Monitor VS
▪ Monitor BUN
▪ Teaching
▪
▪
▪
▪
Do not abruptly stop taking medication
OTC: check with MD first
How to take pulse and BP
Orthostatic hypotension teaching
Vasodilator – Prototype: hydralazine (Apresoline)
Skyscape /ATI
▪ Hydralazine (Apresoline)
▪ Hypertensive emergency/urgency
▪ Peripheral vasodilator: ↓ BP and ↑HR, stroke volume, cardiac
output
Prototype-Lisinopril (Zestril)
▪ Angiotensin-Converting
Enzyme Inhibitors (ACE
Inhibitors)
▪ Inhibits formation of angiotensin
II (vasoconstrictor) → ↓BP
▪ Lose Na+ and H2O → ↓BP
▪ Monitor BP carefully: √ for
orthostatic hypotension
Antihypertensives: ACE Inhibitors
▪“PRIL”
▪ These drugs inhibit ACE
▪ ACE converts Angiotension I to Angiotension II
▪ They also block the release of Aldosterone
Prototype ACE Inhibitor: lisinopril (Zestril)
▪ Therapeutic Effect/Use
▪
▪
▪
▪
HTN
CHF
Reduction of risk of death or development of CHF post-MI
Decreases progression of diabetic nephropathy
Prototype ACE Inhibitor: lisinopril (Zestril)
Mode of Action
▪ Block ACE from converting angiotensin I to angiotensin II, leading to a
decrease in blood pressure, a decrease in aldosterone production, and
a small increase in serum potassium levels along with sodium and
fluid loss
Prototype ACE Inhibitor: lisinopril (Zestril)
▪ Side Effects
▪ N/V/D
▪ HA
▪ Dizziness
▪ Adverse Reactions
▪
▪
▪
▪
COUGH
Hyperkalemia
Hypotension
Angioedema
Report nagging cough to prescriber
Prototype ACE Inhibitor: lisinopril (Zestril)
▪ Nursing Interventions
▪ VS
▪ UO
▪ Teaching
▪
▪
▪
▪
Do not abruptly stop taking the medication
Teach how to take own BP
Dizziness may be present during 1st week
Take 20 min to 1 hour before meals
Antihypertensives: ARBs (Angiotension II Receptor Blockers)
▪ “Sartan”
▪ Block Angiotension II from receptors in the tissue.
▪ Blocks angiotensin II at the receptors in vascular smooth muscle
→ ↓ BP
▪ Prevent release of Aldosterone
Prototype ARB: Losartan (Cozaar)
(Nice to know, not need to know for Block I)
▪ Therapeutic Effect/Use
▪ HTN
▪ CHF
▪ Type II Diabetic Nephropathy
▪ Less cough than ACEI
Prototype CCB: diltiazem (Cardizem)
ATI
▪ Ca++ = increases contractility,
peripheral resistance, and blood
pressure
▪ Calcium Channel Blockers
▪ Interferes with calcium ions → vasodilation
→ ↓BP
▪ Slows calcium channels found in the
myocardium
▪ Slows heart conduction→ Monitor BP & P
daily
▪ Ca++ = increases contractility, peripheral
resistance, and blood pressure
▪ “dipine” except Verapamil & Diltiazem
Prototype CCB: diltiazem (Cardizem)
▪ Therapeutic Effects/Uses
▪ HTN
▪ Angina (Chest Pain)
▪ Dysrhythmias (irregular rhythms)
▪ SVT (supraventricular tachycardia)
▪ A-fib
▪ A-flutter
▪ Mode of action:
▪ Inhibits transport of Ca++ into myocardial and vascular smooth muscle
cells
Prototype Calcium Channel Blocker: diltiazem
(Cardizem)
▪ Contraindications
▪
▪
▪
▪
Hypersensitivity
SSS-sick sinus syndrome (not a need to know for block I)
2nd or 3rd degree AV block (not a need to know for block I)
BP < 90mmHG
Prototype Calcium Channel Blocker: diltiazem
(Cardizem)
▪ Side Effects
▪ Dizziness
▪ Peripheral edema
▪ Adverse Reactions
▪ CHF
▪ Dysrhythmias/Arrhythmias
Prototype Calcium Channel Blocker: diltiazem
(Cardizem)
▪ Drug-Lab-Food Interactions
▪ Drugs
▪ Increased hypotension with other anti-hypertensives
▪ Increased bradycardia with beta-blockers or digoxin
▪ Food
▪ Increased drugs effects with grapefruit juice
Prototype Calcium Channel Blocker: diltiazem
(Cardizem)
▪ Nursing Interventions
▪ May administer with food if GI upset
▪ DO NOT open or crush SR capsules
▪ Teaching
▪
▪
▪
▪
Take same time each day
How to take and monitor BP & pulse
Chest Pain teaching
Avoid foods high in K+
Anticoagulants
▪ aspirin (ASA) (Chart 38-4)
▪
▪
▪
▪
NSAID
Blocks pain impulses in CNS
Reduces Inflammation
Prophylaxis for MI, stroke, angina
▪ Anti-platelet action
▪ Can cause GI bleeding
▪ Not for use in children (Reye’s syndrome)
(ASA is not on med list
for block one but
important drug to
know)
▪ Subcut heparin/enoxaparin (Lovenox)
(chart 32-4)
▪ Anticoagulant injection
▪ Binds to antithrombin II factors
▪ Prevents DVT, PE post surgery, acute MI, unstable
angina
▪ Bleeding complications
Anticoagulant Prototype: Heparin (Chart 324)
▪ Nursing Interventions
▪
▪
▪
▪
Monitor VS
Monitor PTT
Monitor platelet count
Monitor for bleeding
▪ Mouth, urine, stool…
▪ Antidote?
▪ Teaching
▪
▪
▪
▪
▪
▪
Notify MD or DDS
Soft toothbrush
Electric razor
Lab tests: PTT
Medical ID bracelet
OTC drugs
▪ ASA
▪ External hemorrhage
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Anticoagulants continued
▪ warfarin (Coumadin)
(chart 32-4)
▪ Anticoagulant
▪ Depresses synthesis of vitamin K
(factors II, VVII, IX, X)
▪ DVT, MI, CVA prophylaxis, post MI
▪ A-fib embolism prevention
▪ Lab values PT & INR
▪ Bleeding complications
Oral Anticoagulant Prototype: Warfarin
(Coumadin)
▪ Nursing Interventions
▪ Monitor PT/INR
▪ Depends on your patient
▪ KNOW YOUR patient
▪ Administer at same time each
day.
▪ Initially may be given with
Heparin/enoxaparin (bridge)
▪ Teaching
▪ Take as prescribed, do not
double dose
▪ Food teaching
▪ Bleeding precautions
▪ OTC medications
▪ Medical ID bracelet
▪ How long to be effective?
▪ Antidote?
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Anti-platelet
▪ clopidogrel (Plavix)
Chart 38-4
▪ Platelet aggregation Inhibitor
▪ Reduces risk of stroke, MI, TIA’s
vascular death, PAD
▪ Weekly platelet count labs
▪ Can cause bleeding
The End