Module V:

Atherosclerosis, Coronary Artery Disease, Heart

Failure and Atrial Fibrillation
HYPERLIPIDEMIA
Lipoproteins
Lipid molecules are not soluble in plasma,
they must be specifically packaged for
transport through the blood

Lipoproteins-
◦ Consist of various amounts of cholesterol,
triglycerides, and phospholipids along with a
protein carrier
◦ Classified according to their size, weight or
density
 Hyperlipidemia Review
Lipoproteins Main Function
VLDL Transport triglycerides from liver to adipose tissue and
(very low-density lipoproteins) muscle
LDL Transport cholesterol from liver to tissues
(low density lipoproteins)
HDL Transport surplus cholesterol from tissues back to liver
(high density lipoproteins)

 Where does cholesterol come from?

 What role does cholesterol play in the body?
 What are the goals for hyperlipidemia blood values?
◦ Total cholesterol
◦ LDL
◦ HDL
◦ TG
 Why is it so important to control cholesterol?
 Which cholesterol component is most closely related to heart disease?
Purpose of testing cholesterol:
◦ Significant metric for determining risk of atherosclerotic
heart disease
◦ Combine with age and other factors to determine risk of
CV events over 10 years
◦ ASCVD Risk Estimator Calculator
Hyperlipidemia: elevation of one or more lipids
Drugs for Hyperlipidemia
 Lifestyle modifications are always first and then in combination with
medications if initiated

I. HMG-CoA Reductase Inhibitors (“Statins”)

II. Nicotinic Acid
III. Bile Acid Sequestrants/Resins
IV. Ezetimibe
V. Fibric Acid Derivatives

 Selection of drug and dose depends on:

◦ 10 – year cardiovascular risk (risk calculators)
◦ Patient allergies and medication tolerability
◦ LDL and TG levels
◦ Co-morbid conditions
 Figure 23.1
Adams, page 332
Drug Class Antihyperlipidemic
Prototype Atorvastatin (-statin)
Mechanism of Action • Inhibit HMG-CoA reductase (a rate-limiting enzyme in endogenous cholesterol
biosynthesis)
• Increases the LDL receptor sites on liver cells thus increasing the uptake of LDL
from the blood
Adverse Effects • Liver dysfunction
• Myopathy– muscle pain, tenderness, weakness- most common reason for
discontinuation
• Rhabdomyolysis
Contraindications Pregnancy
Drug Interactions • Many CYP 3A4 interactions-Grapefruit juice can increase concentrations of some
statins
• Other medications that cause myopathy
Route Oral
Clinical • Statins have been shown to slow the progression of CAD and to reduce mortality
Considerations from cardiovascular disease
• Check LFTs prior to initiation and clinically thereafter if indicated
• Limit alcohol and acetaminophen use
• Take with evening meal
• Maximize therapeutic effectiveness & minimize GI upset
• Since cholesterol biosynthesis is greatest at night (not required for
atorvastatin or rosuvastatin)
• Use reliable contraception
Rate-Limiting Step in Cholesterol Biosynthesis

Cellular cholesterol= endogenous (liver)

Drug Class Antihyperlipidemic
Prototype Niacin (nicotinic acid)
Mechanism of Action • Partial inhibition of free fatty acid release from adipose tissue
• Increased lipoprotein lipase activity (increases the TG removal from plasma)
• Reduces total cholesterol, TG, VLDL, LDL, and increases HDL (>30%)
Adverse Effects • Intense flushing of the face, head and neck
• 80% of patients at therapeutic doses
• Can be reduced by taking aspirin (30 minutes) or ibuprofen (60
minutes) before each dose because flushing is prostaglandin mediated
• GI tract upset- Nausea, bloating, diarrhea (take with food)
• Hepatotoxic (especially with SR)
• Hyperglycemia- not usually given for patients with diabetes
• Gouty arthritis
Contraindications Active hepatic disease or elevated LFTs; active peptic ulcer; arterial hemorrhage
Drug Interactions • May enhance hepatotoxic and myopathy effects of statins
• May decrease oral diabetes mellitus medication efficacy
• Alcohol increases flushing adverse effects and can increase hepatotoxicity
risk
Route Oral
Clinical Considerations • Nicotinic acid or niacin is a B complex vitamin- Dose for lowering
cholesterol is 2 to 3 g/day; as a vitamin 25 mg/day
• May increase blood glucose levels
• Monitor LFTs
• Not a first line agent
Figure 23.8 Niacin inhibits lipolysis in
adipose tissue, resulting in decreased hepatic
VLDL synthesis and production of LDLs in
the plasma. VLDL= very-low-density
lipoprotein; LDL = low-density lipoprotein.
Drug Class Antihyperlipidemic- Bile Acid Sequestrant
Prototype cholestyramine
Others (colestipol colesevelam)
Mechanism of Action • Form a non-absorbable complex with bile acids in the intestine
• Inhibits reuptake of bile acids containing cholesterol and is
excreted in the feces which reduces LDL levels
Adverse Effects • Constipation, bloating, nausea
• May impair fat soluble vitamin absorption (ADEK)
• May raise triglyceride levels
Contraindications Complete biliary obstruction
Drug Interactions Take other medications 2 hours before or 4 hours after taking bile
sequestrants
• Will block absorption if taken too closely together
Route • Oral, powdered and granular forms
Clinical • Take before meals
Considerations • Increase bulk and fluid in diet for constipation prevention
• Mix with 60-180ml of water, juices, or pulpy fruits (no carbonated
drinks) and drink immediately to avoid irritation or obstruction in
the GI tract
BAS = Bile Acid Sequestrant

BAS

BAS
IV. Ezetimibe
 Mechanism of Action:
◦ Inhibits cholesterol absorption in the small intestine
◦ Blocks absorption of both dietary (exogenous) and bile-secreted
(endogenous) cholesterol, “food and family”
◦ Often given together with statins

Route: oral

 Drug-drug interactions:
◦ Slight increased risk of liver damage, myopathy with statins
Drug Class Fibric Acid Agent
Prototype Gemfibrozil and fenofibrate
Use Hypertriglyercides
Mechanism of Action Activate lipoprotein lipase which increases the breakdown and
elimination of triglyceride rich particles from the plasma
Adverse Effects • Dyspepsia, diarrhea, nausea and cramping
• Predisposition to form gallstones
Contraindications • Do not use in patients with severe hepatic or renal dysfunction
• Patients with pre-existing gallbladder disease
Drug Interactions • Risk of myopathy with statins
• DO NOT give gemfibrozil with statins
• Fenofibrate CAN be given with statins if needed for high
triglycerides
• Increased warfarin effects- monitor INR
• Increased effects of hypoglycemic medications- monitor blood
glucose levels
ATHEROSCLEROSIS
Vascular Injury
Vascular Endothelium
◦ Modified simple squamous (epithelial tissue)
◦ Inner lining of blood vessels
◦ vulnerable to injury

Major injurious agents to endothelium:

◦ Hypertension
◦ Hyperglycemia
◦ Hyperlipidemia
Atherosclerosis Pathogenesis

Figure 15-9
Capriotti, page 323
Arteriosclerosis vs. Atherosclerosis
Arteriosclerosis
◦ Chronic disease of the arterial system; thickening and
hardening of vessel walls- calcification

Atherosclerosis
◦ Form of arteriosclerosis; soft deposits of fat and fibrin
on the vessels harden over time
◦ Narrowing and hardening of arteries
◦ atherosclerosis video
Outcomes of Atherosclerosis
Coronary artery disease
Cerebrovascular disease
Heart Attack
Stroke
Peripheral vascular disease
Aneurysms
Embolism

NOTHING GOOD!
Atherosclerosis Treatment
Stabilize
plaque and prevent thrombus
LIPID LOWERING WITH STATINS!
Other methods:
◦ ASA
◦ ACEI/ARB
◦ Fish oil
◦ Exercise
QUESTION
Vascular endothelium is a very thin tissue and
vulnerable to injury. Which of the following
disease states would not increase the risk of
endothelial injury?
A. HDL 63 mg/dL
B. LDL 167 mg/dL
C. A BP of 160/98
D. An HA1c of 7.7 (average blood glucose of 174)
QUESTION
Which of the following statements indicates that a
patient may need additional counseling for
atherosclerosis management? (select all that apply)
A. “I don’t need to watch my diet because I am taking a
statin medication.”
B. “Atherosclerosis can lead to many bad outcomes such
as stroke, heart attack, and vascular diseases.”
C. “I can discontinue my statin because my LDL is < 100.”
D. “ In addition to taking my medicines I need to monitor
my blood pressure and blood sugar too.”
QUESTION
A patient is taking an HMG-CoA
reductase inhibitor. Which of the
following tests should be performed at the
start of therapy?
A. Electrolyte levels
B. CBC
C. Liver function tests
D. EKG
CORONARY ARTERY DISEASE
(CAD)
Coronary Artery Disease (CAD)
1 in 13 Americans > 18 years have CAD
 Heart Disease accounts for 1 out of 4 deaths
 May be clinically apparent by age 40
 Develops gradually, 85% of deaths are in patients >
65 years
 The frequency of CAD is similar between black and
white populations but African Americans are 30%
more likely to die from heart disease
 CAD is an umbrella term that encompasses many
different syndromes of the heart and coronary
vessels
Pathophysiology of CAD
Inadequate supply of blood to the myocardium
because of an imbalance between oxygen supply
and demand
 Results:
◦ Lack of oxygen anaerobic metabolism  lactic
acid accumulates causing muscle pain (angina)
◦ Left ventricular function is impaired because of the
hypoxia,
 Contractility reduced – less force and velocity
 Wall motion abnormal in ischemic region = less
blood ejected from heart with each contraction =
increase pressures within heart
Decreased O2 supply Increased O2 demand
 Coronary plaque presence  ↑ HR
 ↓ perfusion pressure  ↑ Preload
 ↓ arterial oxygen content  ↑ Afterload
 ↑ Contractility

Factors that decrease coronary blood supply or increase

myocardial oxygen demand can upset the balance and lead
to ischemia and anginal pain

SUPPLY vs DEMAND
 Unmodifiable Modifiable
 Age  Elevated lipid levels
 Gender  Hypertension
 Race  Smoking
 Family history  Obesity
 Physical inactivity
 Stress in daily living
 Diabetes

Risk Factors for CAD

Most common cause of CAD is ____________
ATHEROSCLEROSIS
Ischemia vs. Infarction
Ischemia –
◦ Local state in which cells are temporarily
deprived of blood;
◦ 75% or more of artery is occluded; cells viable
for a limited time; damage is reversible

Infarction –
◦ Death of tissue; occurs if ischemia prolonged;
irreversible
Precipitating Factors
 Exertion
 Eating
 Emotional Distress
 Extreme Temperatures
 Chronic Ischemic Heart Disease
Type of Angina Etiology/Comments
Stable Angina • Most common form of angina
• Pain caused by an imbalance between oxygen
supply and demand; the coronary arteries cannot
provide sufficient oxygen to meet increased
demand on the heart
• Pain is usually predictable and relieved by rest or
nitroglycerin

Variant Angina • Unpredictable attacks of anginal pain (doesn’t have

“Prinzmetal” to be on exertion)
• Pain caused by vasospasm of one or more of the
major coronary arteries

Silent myocardia • One or more coronary arteries are occluded but

ischemia patient remains asymptomatic
• High risk for acute MI and sudden cardiac death

Angina = chest pain

Drugs for Angina Pectoris
Stable angina
◦ Nitrates
◦ Beta blockers
◦ Calcium Channel Blockers
Variant Angina
◦ Nitrates
◦ Calcium Channel Blockers
Prevention for Acute Coronary Syndrome
◦ Antiplatelet drugs
◦ Cholesterol lowering drugs
(Adams)
Drug Class Anti-anginal
Prototype Nitroglycerin
Mechanism of Action • Relaxes both arterial and venous smooth muscle
• Dilation of veins = reduces the amount of blood returning to heart (preload) –
decreases workload on heart
• Dilation of coronary arteries= dilates occluded artery allows more oxygen to
heart muscle, relaxes vasospasm
Adverse Effects • Headache- May see an analgesic given to treat prophylactically
• Hypotension/ orthostasis
• Reflex tachycardia
• Tolerance can develop
Drug Interactions • Hypotensive drugs
• Beta-Blockers & some Calcium-Channel Blockers (verapamil and diltiazem)
• Help to suppress reflex tachycardia
• Sildenafil
• Can intensify nitroglycerin-induced vasodilation (leads to a drop in
blood pressure)
• Warn patients not to take sildenafil within 24 hours of taking
nitroglycerin
• Many clinicians will not prescribe both (but it doesn’t mean they’re not
taking both!)
Route • Quick acting/Rescue: sublingual, translingual spray, IV
• Maintenance therapy: patch, ointment, SR tablets
• The route that is chosen will be based on the onset of action and duration
that is needed
Clinical • Rapidly metabolized. T ½ = 5-7 minutes
Considerations • Nitroglycerin free period for maintenance treatment
• Monitor blood pressure and heart rate

Sublingual • Place under tongue, allow to dissolve… wait 5 minutes

• Ineffective if swallowed
• If pain persists take a second and call 911 and chew ASA if
available
Quick Relief/ Rescue

• Discard unused portion after 24 months

• May be taken prophylactically for anticipated exertion (30 minutes
prior to activity)
Translingual • Spray against the oral mucosa; do not inhale
Spray • Must be primed

Transdermal • Apply patch of a hairless area of skin, rotate sites

Patch • Remove patch after 12 to 14 hours allowing 10 to 12 “patch-free”
ance Treatment

hours to prevent tolerance

Ointment • Always remove previous dose before applying new
• Rotate sites
• Apply a ribbon of ointment to applicator paper and apply to skin (arm,
leg, chest, back, abdomen)
(Adams)
IV Nitroglycerin Administration
IV route
◦ Limited to those who have failed other therapies
◦ Titrate slowly
◦ Monitor vitals and EKG continuously
Beta Blockers
 Action: ↓the oxygen demand on the heart by…
◦ Decreasing heart rate and contractility by Beta-1
blockade
◦ Causing a modest reduction in arterial pressure
(afterload)
 Can provide sustained protection against effort-induced
anginal pain
 Decrease the risk of death, especially if previous MI
 Start low, go slow. Goal is to reduce resting HR
 Use: to treat stable angina, NOT effective against
variant angina, why?
(Adams)
Calcium Channel Blockers
Action:
◦ Stable angina – promote relaxation of
peripheral arterioles causing a decrease in
afterload which reduces cardiac oxygen
demand
◦ Variant angina – promote relaxation of
coronary artery vasospasm thus increasing
cardiac oxygen supply
Calcium Channel Blockers
Three drugs used most often:
◦ Verapamil, diltiazem and nifedipine
◦ Verapamil and diltiazem have direct effects on
the heart causing decreased contractility and
decreased heart rate
◦ Use cautiously with beta-blockers and digoxin
(Adams)
 Mechanisms of Antianginal Action Review
Drug Class Stable Angina Variant Angina
Nitroglycerin Decreases oxygen Increases oxygen supply
demand by dilating veins by relaxing coronary
which decreases preload vasospasm
Dilate coronary arteries
with increase
blood/oxygen to heart
Beta Blockers Decrease oxygen demand
by decreasing HR and *NOT USED*
contractility
Calcium Channel Decreases oxygen Increases oxygen supply
Blockers demand by dilating by relaxing coronary
arterioles, which vasospasm
decreases afterload (all
CCB) and by decreasing
HR and contractility
(verapamil and diltiazem)
Invasive Treatments for CAD
PTCA or PCI
◦ Percutaneous transluminal coronary angioplasty, ‘cath’ or
‘cathing’
◦ Good alternative to grafting in elderly patients
◦ Stenting can be done during the procedure
◦ Stent is placed in the occlusion to keep artery open
CABG
◦ Coronary artery bypass graft
◦ Vein from leg or chest is grafted between aorta and artery
that is occluded
Laser angioplasty
◦ Burns plaque
Capriotti, page 351
FIGURE 16-15. CABG is a surgical treatment for ischemic heart disease. During CABG, a healthy artery or
vein from the body is connected, or grafted, to a blocked coronary artery. The grafted artery or vein goes
around the blocked portion of the coronary artery. This creates a new path for oxygen-rich blood to flow to
the heart muscle. Surgeons can bypass multiple coronary arteries during one surgery.
Capriotti, page 352
Myocardial Infarction
 Myocardial cell death is irreversible / cells do not
regenerate

 Leads to abnormal muscle movement, decreased

cardiac output, increased heart rate, dysrhythmias,
heart failure, shock

 Takesup to 6 weeks for scar tissue to form – cannot

contract and relax like healthy myocardial tissue
FIGURE 16-16. Prolonged ischemia leads to MI.
Capriotti, page 351
https://en.wikipedia.org/wiki/Myocardial_infarction#/media/File:Myocardial_infarction_2015.jpg
Angina vs. Myocardial Infarction
Angina Myocardial Infarction
 Substernal  Substernal
 Duration  Duration = >30 min to 2
= <15 min
hr.
(no longer than 30mins)  NO RELIEF from NTG or
 Relief from NTG/rest
rest
 Gradual or sudden onset  SUDDEN onset
 Deep sensation of  SEVERE pressure,
tightness or squeezing squeezing, heaviness
 Precipitating factors  Occurs on exertion or rest
involved  Associated with N/V, SOB,
 Associated with SOB, fatigue, feelings of
nausea, belching impending doom, dizziness
Diagnostic Workup
12 Lead EKG / ECG
Troponin, CK-MB + basic labs (BMP,
etc.)
Past medical history
Coronary angiography
CAD Disorders-ACS
Acute Coronary Syndromes
Unstable angina: myocardial ischemia
caused by plaque disruption and repair

Non-ST segment elevation MI: positive

serum markers without associated ST
elevation

ST segment elevation MI: acute

myocardial injury
 Signs and Symptoms of Cardiac Ischemia

Acute Coronary Syndrome (ACS)

ST Elevation No ST Elevation

+ Biomarkers - Biomarkers + Biomarkers

STEMI Unstable Angina NSTEMI

 ST segment depression: early ischemia
 ST segment elevation: cell injury
 Q waves: may indicate infarcted muscle
SERUM PROTEIN MARKERS
Creatine Kinase- CK
 Intracellular enzyme found in muscle cells.
 CK is a marker for any muscle breakdown
 CK-MB is specific to heart muscle, also called CK-MB index.
 The test for CK-MB is sometimes called the ‘CPK-MB test’

Troponin Levels
 Three subunits that regulate calcium mediated contractile
process in striated muscle
 Cardiac-specific
 Also called CTn and Troponin-I
A graph of cardiac biomarkers that indicate MI
• The most sensitive indicator of MI is Troponin / CTn
• The cardiac enzyme CK-MB (measured by CPK mb test) is also normally
elevated

Capriotti, page 355

Time is Muscle

https://www.heart.org/idc/groups/heart-public/@wcm/@mwa/documents/downloadable/ucm_467056.pdf
Options for transportation of STEMI patients

Writing Committee Members et al. Circulation. 2004;110:588-636

Copyright © American Heart Association, Inc. All rights reserved.
Options for Initial Reperfusion Treatment

Writing Committee Members et al. Circulation. 2004;110:588-636

Copyright © American Heart Association, Inc. All rights reserved.
ACS and MI
American Heart Association Treatment of MI
First Intervention:
◦ Morphine: pain
◦ Oxygen: some patients
◦ Nitroglycerin
◦ Aspirin
◦ Beta Blocker
Goes Home:
◦ Statin
◦ ACEI
◦ Aspirin
◦ Beta Blocker

ACS and MI Video

QUESTION
 A patient comes to the emergency department
complaining of chest pains which started 1 hour ago
while he was mowing the lawn. Nitroglycerin was given
sublingually as prescribed. Which of the following AEs
are likely to occur?
A. Hypotension
B. Dizziness
C. GI distress
D. Headache
QUESTION
A patientarrives to the ED complaining of
angina and shortness of breath. A complete
workup is done. You see this result for troponin:

What does this lab tell you?

What other labs/testing should be performed?
QUESTION
Make your diagnosis for the following:
◦ EKG shows ST depression and + biomarkers labs
◦ EKG shows ST elevation and + biomarkers labs
◦ EKG shows no ST elevation and – biomarkers labs
Time is _____. Most important to address
within _____________.
If the patient will receive fibrinolysis the time
from when the patient is through ED door until
needle is inserted should be ________.
QUESTION
An ED physician tells you to give the patient
“nitroglycerin” for acute chest pain. When you
go to the pyxis you realize that there is
nitroglycerin in a patch, ointment, SL tablet, and
IV formulations. You clarify with physician and
she states that you need the _____ formulation.
Why?
After a heart attack a patient is discharged on
what medications? What patient education
should you deliver regarding SL nitroglycerin?
Heart Failure
Heart Failure
AHA definition
◦ “A complex clinical syndrome that results from any
structural or functional impairment of ventricular
filling (diastole) or ejection of blood (systole).
◦ The heart is unable to pump blood at a rate necessary
to meet the metabolic needs of the body
HF is the potential end point for all serious
forms of heart disease
◦ CAD, mitral stenosis, myocardial infarction, chronic
hypertension, diabetes, hyperthyroidism, dysrhythmias
Mortality: 50% die within 5 years of diagnosis
Heart Failure
HeartFailure is classified by many different
parameters:
◦ Ejection fraction:
 Systolic HF or HFrEF- Heart Failure with reduced ejection
fraction (EF < 40%)
 Diastolic HF or HFpEF- Heart Failure with preserved ejection
fraction (EF > 50%)
◦ Right, left, congested heart failure
Ejection Fraction
◦ A measurement of the percentage of blood leaving
your heart each time it contracts
HF Disease Process
Initialphase of HF: remodeling
◦ Ventricles dilate (become larger)
◦ Hypertrophy (increased wall thickness)
◦ Become more spherical (less cylindrical)
All of the above increase heart wall stress and
reduce ejection fraction
Neurohormonal systems RAAS and sympathetic
nervous system (NS)
◦ Drives the remodeling process
◦ Promote cardiac fibrosis and myocyte death
Compensatory mechanisms:

• Increased sympathetic
nervous system activity

• RAAS activation

Adams, page 397

Labs and Tests for HF
Blood tests
◦ CBC, BMP, TSH, etc. – rule out anemia

NT- ProBNP (N-terminal pro b-type natriuretic peptide)

◦ ‘BNP’ is the common name
◦ A substance secreted from the heart in response to
changes in pressure that occur when heart failure
develops and worsens
◦ Taken when stable and acutely ill (BNP ↑ when HR
worsens)
BNP
Labs and Tests for HF
Chest X-ray
◦ Shows the size of the heart and if there is fluid buildup
around the heart and lungs

Echocardiogram (Echo)
◦ Identifies the underlying cause as well as the type of
severity of HF
◦ Determines ejection fraction (EF)

EKG / ECG
◦ Reveal ischemia, tachycardia and extrasystole
FIGURE 17-24. Chest x-ray showing heart failure. The heart is enlarged (cardiomegaly), and blood
vessels are prominent in the hilar lung fields, which represents pulmonary venous congestion. Kerley lines
are horizontal lines in the base of the lungs close to the chest wall. They are the result of interstitial edema
in the lungs. (From Southern Illinois University/Science Source.)
 • Reduced ejection fraction (< 40%) • Ejection fraction (> 50%)
• Impaired contractility • Impaired filling/
• Thin/weak heart muscle relaxation
• Stiff/ thick heart muscle

FIGURE 17-15. Normal heart function versus systolic function versus diastolic function.
Capriotti
Left vs Right HF
Left-sided HF:
◦ The left ventricle doesn’t pump enough
blood blood backs up into the lungs
pulmonary edema (left sided HF usually
leads to right sided HF)
Right-sided HF:
◦ The right ventricle doesn’t pump enough
blood  blood backs up into the body’s veins
systemic edema
 “DO CHAP”
Dyspnea
Orthopnea
Cough
Hemoptysis
Adventitious breath
sounds
https://www.pinterest.com/pin/536983955544245550/ Pulmonary Congestion
FIGURE 17-21. Pulmonary edema. Pulmonary edema is a fluid accumulation in the pulmonary
interstitial spaces that hinders oxygen diffusion from alveoli to capillary. The blood cannot become
sufficiently oxygenated and hypoxemia develops. The patient suffers severe dyspnea, cough, and pink
frothy sputum. Pulmonary edema can occur in left ventricular failure.

Capriotti, page 388

Right sided
Heart Failure
Symptoms

Figure 17-23
Capriotti, page 387
 “AW HEAD”
Anorexia and Nausea
Weight gain
Hepatomegaly
Edema (bipedal)
Ascites
Distended jugular vein

https://quizlet.com/10110294/nur-
120-unit-4-cad-cabg-and-chf-51-
61-flash-cards/
Heart Failure Animation

“AW HEAD” “DO CHAP”

https://classconnection.s3.amazonaws.com/660/flashcards/2365660/png/untitled1363459449160.png
Pharmacologic Management by HF Type
Systolic (HFrEF)
◦ low cardiac output – ejection fraction < 40%
◦ This is the primary focus of our pharmacological
discussions
◦ Standard management (next slide)
◦ Left sided heart failure: systolic dysfunction
Diastolic (HFpEF)
◦ Ejection fraction > 50%
◦ Exhibits clinical manifestations of HF
◦ Treatment varies
◦ Not our focus
Pharmacologic Management of HFrEF
(Systolic HF)
 Drugs can relieve the symptoms of HF by a number of
different mechanisms:
1. Reduce preload
2. Reduce afterload (decrease blood pressure)
3. Decrease the remodeling effect of the RAAS and the
sympathetic nervous system
 #1 and 2 provide symptomatic relief but do not reverse
the progression of the disease
◦ Thiazide and loop diuretics, direct vasodilators
 #3can result in a significant reduction in morbidity and
mortality from HF
◦ ACE Inhibitors/ARBs, beta blockers and spironolactone
 Figure 27.1
Adams, page 399
Pharmacologic Treatment
New Drug:
◦ Cardiac glycoside - digoxin

Drugs You Already Know:

◦ ACE inhibitors
◦ ARBs
◦ Vasodilators
◦ Diuretics
◦ Beta-blockers
◦ We will review their implications in HF here. Know
their MOAs, AEs, and education!
Drug Class Cardiac Glycoside
Prototype Digoxin
Mechanism of Action • Positive inotropic action = increases the force / myocardial
contractility
• Decreases the speed of conduction through the AV node
• Decreases the heart rate

Adverse Effects • Dysrhythmias

• Hypokalemia secondary to diuretic use
• Elevated digoxin levels
• Very narrow therapeutic window, 0.5-2 ng/ml
• Monitor for “dig toxicity”, usually levels > 2 ng/ml
B- bradycardia
A- anorexia
N- nausea/vomiting
D- diarrhea
A- abdominal pain
V- visual disturbances (blurry vision or yellow/green
halos)
Drug Interactions • Thiazide and loop diuretics- can cause hypokalemia
• ACE inhibitors -can elevate potassium levels thus decreasing
therapeutic response to digoxin
• Quinidine & Verapamil - can elevate plasma levels of digoxin
Route Oral, slow IV injection
Clinical • Administration
Considerations • Monitor heart rate and rhythm
• Apical pulse for a full 60 seconds!
• Stop & Think if HR less than 60 beats/minute
• Bradycardia: hold & contact provider if HR less than 50
• Be aware of any new digoxin levels (lab results)
• Be aware of any recent electrolytes (Hypokalemia,
hypomagnesemia, hypercalcemia can ↑ dig toxicity)
• Teach patients:
• Take their pulse daily
• Early signs of digoxin toxicity (abdominal pain)
• Careful compliance with medication administration
• Antidote available: digoxin immune Fab
• Can also be used for dysrhythmias
• Lower doses needed in patients with renal dysfunction
• Patients with hypothyroidism (high TSH) are extremely sensitive
to digoxin and may need lower doses
ACE Inhibitors
Action – slow the progression of heart failure
and reduce mortality
◦ Reduce preload
 Dilate veins which reduces preload and reduces peripheral
edema
◦ Reduce afterload
 Lower peripheral resistance (afterload)
◦ Decrease RAAS effects
 Reduce blood volume by inhibiting aldosterone secretion

◦ Examples of ACE-inhibitors?
Beta-Blockers
Two approved drugs for HF:
◦ carvedilol
◦ metoprolol extended release
Action:
◦ Decreases sympathetic stimulation
◦ Protect against dysrhythmias
 Remember to check heart rate
 Must be given in low doses initially . Benefits may not
be seen for 1 to 3 months. Observe carefully for
worsening of heart failure.
Direct Vasodilators
Decreases preload
isosorbide dinitrate and other nitrates: dilate veins

Decreases afterload
◦ Hydralazine: dilates arteries / arterioles

Given together to treat HF

Works better for African-American patients

Diuretics
Action:
◦ Increase cardiac output by reducing fluid
volume and decreasing blood pressure
Types:
◦ Loop, Thiazide, Potassium-Sparing
 Ex: spironolactone prolongs survival in HF by
blocking receptors for aldosterone, not causing
diuresis
 According to Joint Commission and
CMS ALL patients with HF should
leave hospital on an ACEI or ARB
PLUS a beta blocker

http://www.aafp.org/afp/2001/0915/p1045.html#afp20010915p1045-t1
REMEMBER
ACE-I/ARBs, Beta-blockers and
spironolactone should NOT BE STOPPED
if symptoms improve because they SLOW
DISEASE PROGRESSION and
DECREASE MORTALITY
Heart Failure Review. Left vs
Right Sided HF, Medications and Interventi
ons
QUESTION
You read in the chart that your patient
has an ejection fraction of 15%. This
is consistent with a diagnosis of
_____ heart failure.
A. Diastolic
B. Systolic
C. Left sided
D. Right sided
QUESTION
Which of the following is a finding
unique to right sided heart failure?

A. Decreased urine output

B. Increased heart rate
C. Hepatomegaly
D. Shortness of breath
QUESTION
A 65 year old female patient with stable systolic
HF comes through the ED with N/V/D and
complains that her “eyes are playing tricks on
her”. You see that her medication list includes
simvastatin, metoprolol, digoxin, and
metformin.

What labs should be ordered?

What medications are missing from this
patient’s list for treatment of HF?
QUESTION
Which medications for HF have been
shown to decreased the risk of death in
patients with systolic HF?
CASE STUDY
A.O. is an 89-year-old woman with a long history of
systolic heart failure secondary to a large left ventricular
infarct when she was in her 70s. She had poor activity
tolerance and required assistance with activities of daily
living. Even minimal activity was associated with
moderately severe dyspnea and exertional chest pain,
which was relieved by rest. A.O. also exhibited marked
pedal edema bilaterally. She is being treated with digoxin,
furosemide (Lasix), KCl, and sublingual nitroglycerin.

 Which type of heart failure (left or right sided) is usually

associated with dyspnea? What other clinical findings are
likely to be present this type of heart failure?
 What is the most likely cause of A.O.’s pedal edema?
Atrial Fibrillation
Atrial Fibrillation
 Dysrhythmia: a condition in which the heart beats
with an irregular or abnormal rhythm
 Atrial fibrillation (Afib) is the most common
sustained cardiac dysrhythmia
 More common with advanced age; affects ~15% of
patients older than age 85
 EKG reflects “irregularly irregular” rhythm
AFib
Rapid firing of multiple ‘irritable foci’ in the atria
generates ineffective atrial contractions
Loss of atrial kick decreases cardiac output 20–
30%, increasing risk of HF
Increased risk of emboli due to pooled, clotted
blood in the atria  risk of stroke
Etiology
◦ Underlying heart disease
◦ Hypertension
◦ Valvular disease
◦ Heart failure, myocardial infarction
◦ Electrolyte imbalances
FIGURE 16-7. Conduction system through the heart.
Impulses begin in the SA node of the right a trium and
continue down into the AV node. The impulses then run
down the right and left bundle of His to the Purkinje fibers. Capriotti, page 346
AFib Conduction

http://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/dxc-20164936
Clinical Manifestations
AFib may be unnoticed
Or, it can cause severe symptoms
◦ Palpitations
◦ Shortness of breath (SOB)
◦ Fatigue
◦ Dizziness
◦ Chest pain
AFib Pharmacologic Management
• Rate, Rhythm and Anticoagulation
• Cardioversion?
• Anticoagulation
• Patients with afib have a 5-fold increase risk of stroke
• Warfarin vs ASA vs TSOAC
• Rate control
• Verapamil or diltiazem (non-pine CCB)
• Beta blockers
• Digoxin
• Rhythm control
• Antidysrhythmic
• Many to choose from, our focus is amiodarone
Patients with atrial fibrillation have a 5-fold
increase risk of ischemic stroke!
 Anticoagulation in AFib
Anticoagulation is determined based
on:
◦ CHA2DS2-VASc Score
◦ Bleeding Risk
◦ Age
 Which Drug Do We Give?
CHA2DS2-VASc Recommended
Score anticoagulation

0 no anticoagulation
preferred

1 Oral anticoagulant
suggested

>2 Oral Anticoagulant

recommended

TSOAC Warfarin
Many Anti-adysrrhythmics! http://www.cardiachealth.org/heart-disease-treatment/heart-disease-medications/
blood-pressure-medications/calcium-channel-blockers
Drug Class Antidysrhythmic
Prototype Amiodarone
Mechanism of Action • Prolongs the time between action potentials by blocking potassium
channels
• Decreases AV conduction and sinus node function
Adverse Effects • Pulmonary toxicity
• Cardiotoxicity: can induce other dysrhythmias, specifically due to
QTc prolongation
• GI reactions (common): nausea, can try giving with food
• Liver toxicity
• Hypothyroidism
• Visual impairment
• “smurf” or “blue man syndrome” (extremely rare)
Contraindications Hypersensitivity to iodine, AV block, cardiogenic shock
Drug Interactions • Increases quinidine, procainamide, and phenytoin levels
• Can increase digoxin levels
• Can have combined bradycardic effect with beta blockers
• If amiodarone is added to warfarin, the dose of warfarin must be
reduced by 30-50% or a supratherapeutic INR with bleeding can
occur
• Avoid grapefruit juice (increases amiodarone concentration)
Route Oral, IV infusion
Clinical • Monitor
Considerations • HR, BP, and EKG- Patient must be hospitalized & monitored
on telemetry during initiation of drug
• Thyroid function tests, LFTs
• Regular ophthalmic exams
• Diluted into special IV bag (non-PVC bag)
• Give IV in central line if possible, if given peripherally use an in-
line filter
QUESTION
A patient is given a new diagnosis of
Afib. His CHA2DS2-VASc score is 4.

What are his anticoagulant options?

What options does he have for rate

control?
QUESTION
Which of the following statements leads the nurse to
believe a 52-year-old woman needs additional counseling
for amiodarone?

A. “I should expect some GI upset when I am starting

amiodarone and I can take it with food to help or ask my
doctor to divide my doses.”
B. “Blue pigmentation of the skin is a rare occurrence with long
term amiodarone therapy and usually goes away if the drug is
stopped.”
C. “Long term amiodarone therapy could affect my lungs and I
need my doctor to know if I notice any changes and get
evaluated frequently.”
D. “Warfarin and amiodarone do not interact, so I don’t need to
change my dose or frequency of monitoring.”
QUESTION
 Which of the following are true? Select all that
apply.
A. All patients with afib need anticoagulation
B. Oral anticoagulants should be considered for all
patients with CHA2DS2-VASc score > 2
C. Amiodarone is the only anti-dysrhythmic drug
available
D. Afib increases the chances of having a stroke by 2-
fold
E. Beta blockers and Calcium channel blockers can be
used for rate control in afib
F. All calcium channel blockers can be used for rate
control in afib
Clinical Pearls
Statinsare usually recommended number one for
hyperlipidemia unless there is a contraindication
Do not give statins with gemfibrozil
Help to prevent CAD: quit smoking, reduce stress
and lower blood pressure… and control cholesterol!
TIME IS MUSCLE. 90 minutes to balloon, 30
minutes to needle if using thrombolytics
Post MI, all patients should be on a Statin, ASA,
ACEI/ARB, and Beta Blocker (SAAB) unless there
are contraindications
Clinical Pearls
 Heart Failure is the potential end point for all types of
heart disease
 Heart failure can be classified in many ways but for
pharmacologic treatment by systolic vs diastolic HF
 Drugs that are proven to reduce mortality in HF patients:
ACEI/ARBs, beta blockers, and spironolactone
 Know the common signs and symptoms of digoxin
toxicity: BANDAV
Clinical Pearls
 NT Pro-BNP is a lab used to diagnose and monitor
patients with Heart Failure
 An EKG for patients in afib will show an “irregularly,
irregular” pattern
 Patients with Afib are at 5 fold increase risk for stroke
 Treatment of afib: rate, rhythm, and anticoagulation
 Anticoagulation in afib can be ASA, warfarin, or
TSOAC. Choice is made depending on CHA2DS2-VASc
score, bleeding risk and age