Cardiac Wellness
Institute of Calgary
Updated May 2010

Material to be Covered
 ACSM’s Resource Manual for Guidelines for
Exercise Testing and Prescription ( 6 th edition)
− Chapter 6 (pg. 115-116)
− Chapter 8 (pg. 145-147)
− Chapter 38 (pg. 622-624)
 ACSM’s Guidelines for Exercise Testing and
Prescription (8 th edition)
− Appendix A (pg. 274-291)
 Pharmacology for Nursing Care 5 th ed
.

Beta Blockers
 Prescribed for: Angina, Myocardial Infarction
(MI), arrhythmia, essential tremors (shaking), migraines
 Mechanism of Action :
– Competitively block ß-adrenergic receptors
–
–
ß
1 receptors - cardiac stimulation
ß
2 receptors - vascular and bronchial smooth muscle dilation
– Cardioselective ß-blockers (blocks ß
1 not ß
2
)

Beta-Blockers
 Hemodynamic Effects:
–  myocardial O
2 time) demand (  HR,  diastolic filling
–  HR, BP, myocardial contractility (rest & ex)
–  ischemia
 Exercise Capacity:
–
–
 patients with angina
 or
 patients without angina
– GXT for ischemia - false negative

Beta-Blockers
 Adverse Effects:
–  BP - lightheaded or dizzy
– Coronary artery vasoconstriction/worsening spasm
– Exacerbate acute Congestive Heart Failure (CHF)
–  claudication pain in people with Peripheral Arterial
Disease (PAD); cold hands & feet
– Precipitation/worsening of bronchospasm
– Bradycardia or AV block
– Mask S/S of hypoglycemia in diabetes
– Fatigue, depression, insomnia, vivid dreams
–  triglycerides,  HDL-C

Beta-Blockers
 Common ß-blockers
– Metoprolol/Lopressor
– Atenolol/Tenormin
– Bisoprolol/Monocor

Nitrates
 Prescribed for: Angina & CHF
 Mechanism of Action:
– Direct relaxation of vascular smooth muscle
–  myocardial O
2 supply by dilating collateral arteries
(not atherosclerotic arteries)
–  preload & afterload, therefore
 end diastolic volume

Nitrates
 Hemodynamic Effects:
–
–
–
 Rest HR (Baroreceptor-mediated tachycardia)
 or

Ex HR
 Rest BP &  or

Ex BP
–  time to ischemia
–
–
 myocardial O
2 consumption
May  coronary blood flow d/t  collateral flow or
 ventricular diastolic pressure
– Prevention of spasm

Nitrates
 Routes of Administration:
– Sublingual
– Oral
– IV
– Transdermal
 Use:
– PRN or prophylactically
 Nitrate Tolerance
– 10 - 12 hour NTG-free interval

Nitrates
 Adverse Effects:
– Headache
– Dizziness or lightheaded
– Weakness
–  HR
– Flushed face
– Skin irritation
 Not for use with drugs such as Viagra, Cialis,
Levitra etc. (Hypotension!)

Nitrates
 Common Nitrates
–
–
–
Nitroglycerin spray
Isosorbide mononitrate/Imdur
Nitro-Dur (patch)

Calcium Channel Blockers
 Prescribed for: Angina, MI, spasm, hypertension
 Mechanism of Action:
– Selective blockade of transmembrane calcium flow
 Limits calcium entry into cardiac & smooth muscle cells
OR
 Relaxation of vascular smooth muscle

CCBs
 No direct effect on myocardial contractility or
SA/AV node conduction
– Most CCBs work only on arterioles
 Exception : Diltiazem & Verapamil
–  HR
–  AV node conduction

CCBs
 Hemodynamic Effects:
–
–
–
 or

Rest HR & Ex HR
 BP
 ischemia
 Exercise Capacity:
–
–
 in patients with angina
 in patients without angina

CCBs
 Adverse Effects: (vary with each medication)
–
–
–
–
–
–
–
–
–
–
CHF
Hypotension
Bradycardia
Dizzy/syncopal
Flushing
Swelling
Headaches
Constipation
Dry mouth
Nausea

CCBs
 Common Calcium Channel Blockers
– Amlodipine/Norvasc
– Diltiazem/Cardizem/Tiazac
– Verapamil/Isoptin
– Nifedepine/Adalat

Angiotensin Converting
Enzyme (ACE) Inhibitors
 Prescribed for: HTN, CHF, MI and Diabetic nephropathy
 Mechanism of Action:
– ACE Inhibitors block the reaction of angiotensin I to angiotensin II, which is a potent vasoconstrictor.

ACE Inhibitors
 Hemodynamic Effects:
–  Rest & Ex HR
–  Rest & Ex BP
–  or prevent ventricular remodeling
 Exercise Capacity:
–
–
 or  in patients with CHF
 in patients without CHF

ACE Inhibitors
 Adverse Effects:
– Dry cough
– Kidney failure
– Swelling of face, tongue or lips (angioedema)
–  BP (dizziness or lightheaded)
 Common ACE Inhibitors
– Ramipril/Altace
– Enalapril/Vasotec
– Fosinopril/Monopril
– Lisinopril/Prinivil/Zestril

Angiotensin II Receptor
Blockers (ARBs)
 Prescribed for: HTN, CHF and Diabetic nephropathy
 Mechanism of Action:
– ARBs block access of angiotensin II to its receptors
 Results in vasodilation and reduced secretion of aldosterone and vasopressin, ultimately reducing
BP and myocardial workload

ARBs
 Hemodynamic Effects:
–  Rest & Ex HR
–  Rest & Ex BP
 Exercise Capacity:
– No effect
 Adverse Effects:
– Headache
– Angioedema
– Low Blood Pressure

 Common ARBs
–
–
–
Irbesartan/Avapro
Losartan/Cozaar
Valsartan/Diovan
ARBs

Diuretics
 Prescribed for: HTN, CHF, Peripheral edema
 Mechanism of Action:
–  renal secretion of salt and water
– Inhibits sodium re-absorption at various sites of the nephron
–  intravascular volume & edema

Diuretics
 Hemodynamic Effects:
–
–
–
 in Rest & Ex HR
 or  in Rest & Ex BP

, PVCs or false positive on ECG
 Exercise Capacity:
– No change

Diuretics
 Adverse Effects:
– Electrolyte abnormalities
–
 Hyper/Hypokalemia
 LDL-C & triglycerides
– Hypovolemia
 Common Diuretics
– Esidrix/Hydrochlorothiazide (HCTZ)
– Furosemide/Lasix
– Spironolactone/Aldactone

Digitalis
 Prescribed for : CHF and Atrial Arrhythmia
 Mechanism of Action:
– Inhibits Na + -K + -ATPase
 Limits ionic movement across myocardial cell membrane
– Positive inotropic effect (  myocardial contractility)

Digitalis
 Hemodynamic Effects:
– Sinus rhythm:  HR
–
–
Afib or CHF:  Rest & Ex HR

Rest & Ex BP
– “Dig effect”
 Non-specific ST-T changes and false positive exercise ECG
 Exercise Capacity:
–
–
 in patients with Afib or CHF
 in others

Digitalis
 Adverse Effects:
– Toxicity
 Visual and neurological symptoms
 Arrhythmias
 Common Digitalis Medications
– Lanoxin/Digoxin

Anti-Arrhythmic Agents
 Classified by electrophysiological effect:
 Class I :
–  conduction velocity, excitabilty & automaticity
–  peripheral vasodilation
– Prolong QRS or Long QT Syndrome
 Common Class I Meds
– Lidocaine/Xylocaine
– Propafenone/Rhythmol

Anti-Arrhythmic Agents
 Class II :
ß-Blockers
 Class III :
– Mechanism of Action:
 Blocks Na + channels
 Negative chronotropic effect
  conduction
  myocardial O
2 demand
 Delays repolarization

Anti-Arrhythmic Agents
 Class III (con’t)
– Hemodynamic Effect:



 Rest & Ex HR

Rest & Ex BP

ECG
 Exercise Capacity:
 No effect
 Adverse Effects:



 arrythmias
Bradycardia/AV block
Hypotension
 Photosensitivity
 Dermatological, GI,
 Hepatic or thyroid
 Electrolyte disturbance abnormalities

Anti-Arrhythmic Agents
 Class III ( con’t)
– Common Class III Meds
 Amiodarone/Cordarone
 Sotalol/Betapace
 Class IV :
– Calcium Channel Blockers

Platelet Aggregation Inhibitors
 Mechanism of Action:
– Different for each med
–
–
ASA:
 production of thromboxane A
2
Plavix:
 binding of ADP to its platelet receptor
 Hemodynamic Effect:
– No effect
 Exercise Capacity:
– No effect

Platelet Aggregation Inhibitors
 Adverse Effects:
– Bruise easily
– Bleeding gums
– Cuts and nicks bleed longer
– GI upset
 Common Platelet Aggregation Inhibitors
– Clopidigrel/Plavix
– Ticlopidine/Ticlid
– Aspirin/Asaphen/ASA

Anticoagulants
 Prescribed for: Venous thrombosis, pulmonary embolism, Afib with embolization, prophylaxis after MI
 Mechanism of Action:
– Coumadin : inhibit synthesis of Vit K dependant clotting factors
– Heparin : prevents progression of existing clot by inhibiting any further clotting processes

Anticoagulants
 Hemodynamic Effects:
– No effect
 Exercise Capacity:
– No effect
 Adverse Effects:
– Bleeding
– Bruising
– GI bleed

Diabetes Management
 Oral hypoglycemic agents
– Used in Type 2 diabetes only
– Used in conjunction with diet and exercise
 1 & 2) Sulfonylureas & Meglitinides
– Mechanism of Action: stimulates release of insulin from pancreatic islets to lower blood glucose
– Adverse Effects: Hypoglycemia
– Common Medications
 Glyburide/DiaBeta
 Repaglinide/Gluconorm

Diabetes
3) Alpha-glucosidase Inhibitors
 Mechanism of Action:
– Reduce the rate of digestion of CHO, primarily lowering postprandial glucose concentrations
 Adverse Effects:
– Flatulance
– Cramps
– Abdominal distension, diarrhea
– Liver dysfunction
– *** Minimal chance of hypoglycemia

Diabetes
4) Biguanides
 Mechanism of Action:
–  production of glucose in the liver;  glucose utilization at the muscle
 Adverse Effects:
– Lactic acidosis, nausea, diarrhea, loss of appetite
– *** no risk of hypoglycemia
 Metformin/Glucophage

Diabetes
5) Thiazolidinediones (Glitazones)
 Mechanism of Action:
–  insulin resistance;  production of glucose by liver,
 glucose uptake by muscle
 Adverse Effects:
–
–
–
–
–
Expands blood volume; weight gain, edema
Headache
Sinusitis
Myalgia
 LDL-C & HDL-C,  Triglycerides
 Pioglitazone/Actos

COPD Management
1) Glucocorticosteroids
 Prescribed for allergy symptoms and asthma
 Mechanism of Action: suppresses inflammation
 Adverse Effects:
– Hoarseness, difficulty speaking, slow growth in children, increased risk of cataracts, osteoporosis & peptic ulcer disease
 Fluticasone Propionate/Flovent

COPD
2) Leukotriene Receptor Antagonists
 To prevent symptoms caused by asthma, chronic bronchitis, emphysema and other lung diseases.
 Mechanism of Action:
– Block cysteinyl leukotrienes from binding to their receptors, preventing bronchoconstriction and mucous production
 Adverse Effects:
– Generally well tolerated
 Monteluekast Sodium/Singulair

COPD
3) Beta
2
-adrenergic Stimulants
 To prevent symptoms caused by asthma, chronic bronchitis, emphysema and other lung diseases.
 Mechanism of Action:
– Selective activation of Beta
2
-adrenergic receptors to promote bronchodilation and relieve bronchospasm.
 Adverse Effects:
– ß
1
–adrenergic receptors in the heart could be stimulated causing Tachyarrhythmias and Angina
– Musculoskeletal tremors
 Albuterol/Ventolin

COPD
4) Anticholinergics
 To prevent symptoms caused by asthma, chronic bronchitis, emphysema and other lung diseases.
 Mechanism of Action:
– Promotes bronchodilation
 Adverse Effects:
– Dry mouth
– Irritation of pharynx
 Atrovent/Ipratropium Bromide

Lipid Management
1) HMG CoA Reductase Inhibitors (STATINS)
 Mechanism of Action:
–  cholesterol production
– Increase number of LDL receptors on hepatocytes, enhancing the elimination of LDL from the blood
 Beneficial Cardiovascular Actions :
–  LDL,  HDL, Promote plaque stability
– Improve abnormal endothelial function; enhanced vessel dilation & reduce risk of thrombosis

Lipids
 Adverse Effects:
– Generally well tolerated
– Headache; rash; GI disturbance; Myopathy
(Rhabdomyolysis)
 Common Medications:
– Atorvastatin/Lipitor
– Simvastatin/Zocor
– Rosuvastatin/Crestor
– Pravastatin/Pravachol

Lipids
2) Ezetimibe/Ezetrol
  TC, LDL, Trigs & can  HDL
 Mechanism of Action:
– Blocks absorption of dietary and bile-secreted cholesterol
 Adverse Effects:
– Generally well tolerated

Lipids
3) Fibric Acid Derivatives (FIBRATES)
 Most effective for

Trigs &

HDL
 Mechanism of Action:
– Activate receptors to accelerate the clearance of
VLDLs, and thereby reduce levels of TGs
 Adverse Effects:
– Generally well tolerated
– Rashes and GI disturbances
 Gemfibrizol/Lopid

Lipids
4) Nicotinic Acid
 Mechanism of Action:  VLDL production, therefore  LDL levels and  HDL levels
 Adverse Effects: flushing, GI disturbances, gallstones, hepatotoxicity
 Common Medications:
– Niacin/Niaspan