Cardiology

Pharmacotherapy III

Auscultation

Listening to heart sounds through a stethoscope, valvular abnormalities and cardiac shunts. (Abnormal blood flow) can be detected as murmurs.

Electrocardiography (ECG)

Uses temporary electrodes on the chest and limbs to monitor and document the electrical activity of the heart • Used in the diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, and pericarditis

Holter monitors

Portable ECG used to measure heart activity over 24-hours or longer

Cardiac Imaging

Chest X-ray films used to show shape and size of the heart

Cardiac Computer Tomography scan (CAT)

Many x-rays combined into a 3d model, Iodine based constrast dye highlights blood vessels and creates clearer pictures

Nuclear Imaging

Shows blood flow and used to detect dead or damaged areas of myocardial tissue, with radioactive tracers such as thallium.

Echocardiography

Uses high frequency sound waves (ultrasound), used to record heart valve movements, and image of the heart. Can detect valve abnormalities, congenital defects, changes in heart structure and function.

Cardiac Catheterization

Thin flexible tube (catheter) is inserted into a large artery and is guided to the heart.

Angiography

Done via cardiac catheterization, a contrast dye is injected into the catheter and a series of X-rays show the flow through the coronary arteries. Used to assess valve and heart function, and helps detect clogs in coronary arteries.

Therapeutic interventions for cardiac catheter obstructions

Injection of thrombolytic agent or laser therapy to break down clots

Percutaneous coronary intervention (PCI) formerly known as angioplasty

Uses a balloon to stretch open a narrowed or blocked artery

These procedures are followed by a stent into the coronary artery

Systolic pressure = Systole

Exerted when blood is ejected into the ventricles

CO = HR x SV

Diastolic pressure = Diastole

Relaxation of myocardium required for filling chambers

BP = CO x PR

Regulation of BP - sympathetic nervous system

Increased sympathetic stimulation = vasoconstriction = PR up and BP up

Increased venous return = blood volume up and BP up

Regulation of BP - Hormones

Antidiuretic hormone = BV and BP up

Aldosterone = bv and bp up

Renin and angiotensin = vasoconstriction = pr and BP up also BV up

Etiology of hypertension

Unhealthy diets, excessive salt consumption, no physical activity, tobacco and obesity

Family history of hypertension, age over 65, co-existing diseases, generic ancestry and hormonal factors affecting blood pressure regulation.

Classifications of hypertension

1. primary also called essential _________

2. secondary has identifiable cause from renal or endocrine disorders

3. malignant also called resistant or stage 3 and may result in organ damage

Primary / essential hypertension

1. ≥ 180/110 Hg office BP

2. ≥ 130/80 Hg (diabetes)

3. ≥ 135/85 Hg automated BP

4. ≥ 140/90 Hg OBPM

Signs and symptoms are frequently asymptomatic, initial signs vague and non-specific. Also include fatigue and occasional morning occipital headache

Complications of hypertension

Brain - hemorrhagic stroke, cerebral aneurysms

Eyes - loss of vision (sclerotic changes and rupture of arterioles in retina)

Heart - atherosclerosis, angina, myocardial infarction, congestive heart failure

Kidneys - chronic renal failure

Development of hypertension

Deviation in various physiological processes some of which include functional and structural changes in the autonomic nervous system, renal function notable the renin-angiotensin axis, vascular function, electrolyte balance

Development of hypertension - systemic vasoconstriction

Decreased blood flow to the kidney (RAAS system), meaning BV and PR up

Increased blood pressure can damage the renal blood vessels, increase work for the heart, damage to arteries causing stroke, damage to arterial walls leading to atherosclerosis

Renin-Angiotensin-Aldosterone System (RAAS)

A hormone system that regulates blood pressure and fluid balance by controlling the constriction of blood vessels and the retention of sodium and water in the kidneys.

Drugs that act on the (RAAS) system (A)

• Angiotensin Converting Enzyme (ACE) Inhibitors • Angiotensin Receptor Blockers (ARBs) • Direct Renin Inhibitors

B1-Adrenergic Antagonists (Beta Blockers) (B) Hypertension

• B1-selective, non-selective, with or without ISA

Other Antihypertensive drugs

3. Calcium Channel Blockers (CCBs)

4. Thiazide/like Diuretics 5.

5. Alpha1-adrenergic Antagonists (Alpha Blockers) • Centrally Acting Antihypertensive Agents

Compelling indications - Hypertension diabetes mellitus

• With albuminuria, renal disease, CVD, or additional cardiovascular risk factors • ACE inhibitor or ARB • Without complications • ACE inhibitor, ARB, long-acting dihydropyridine CCB, or thiazide diuretic

Compelling indications - Cardiovascular and cerebrovascular disease

• Coronary artery disease

ACE inhibitor or ARB; beta-blocker for patients with stable angina

• Recent MI

Beta-blocker and ACE inhibitor

• Heart failure

ACE inhibitor and beta-blocker

Angiotensin Converting Enzyme Inhibitors ACE Inhibitors

Drugs ending in “pril”

First line for patients with uncomplicated hypertension and aren’t black. Patients with diabetes, ischemic heart disease, recent MI, heart failure, or chronic kidney disease. ACE converts Angio I and II. Drug interactions include K+ supplements, NSAIDS, lithium. Contraindicated in pregnancy, dry cough, hyperkalemia, angioedema.

Angiotensin II receptor blockers ARBs

Drugs ending in “sartan”

First-line for uncomplicated hypertension, diabetes, or ischemic heart disease, good alternatives when ACE inhibitors are indicated but not tolerated. ARBS displace angiotensin II from the receptor, thus antagonizing angiotensin II-induced vasoconstriction and aldosterone. Interactions include K+ supplements and NSAIDS. Contraindicated in pregnancy, hyperkalemia.

Direct Renin Inhibitors

Aliskiren (Rasilez)

Add-on agent after all the first line therapies have been tried, not combined with ACE inhibitors or ARBS. Binds directly to the ____ enzyme to suppress the RAAS system, results in a reduction of renin activity, angio I and II and aldosterone. AVOID GRAPEFRUIT JUICE and contraindicated in pregnancy. Can cause diarrhea and rare dry cough.

Chronotrope

Influences rate, positive = speed up the heart, negative vice versa.

Inotrope

Influences force or strength, positive = heart beats with stronger contractions, negative vice versa.

Beta-Blockers (BB)

Beta-blockers competitively inhibit endogenous catecholamines (dopamine, epinephrine and norepinephrine) from binding to beta receptors. Clinical effects depend on receptor selectivity and additional properties.

Nonselective (BB)

Act at both B1 (In the heart, gastrointestinal tract and kidney) and B2 (in the heart, vascular and bronchial smooth muscle, gastrointestinal

B1-Selective (cardioselective) (BB)

Act more on B1 receptors than others

Intrinsic sympathomimetic activity (ISA) (BB)

Partially agonize beta receptors (smaller reduction in resting heart rate and cardiac output)

Beta blockers Drugs

“lol” ending drugs

Blocks beta receptors from endogenous catecholamines = vasodilation, negative chronotrope and negative inotrope

First line for patients younger then 60, stable angina, heart failure, myocardial infarction, arrhythmias, heart failure, and migraine prophylaxis

Bradycardia with digoxin or nondihydropyridine CCB’s (verapamil, diltiazem)

Cardiodepressant effects with nondihydropyridine CCBs and amiodarone

Beta blocker drug precautions and adverse effects

• Fatigue and decreased exercise tolerance • Bradycardia • Vivid dreams, insomnia, and possible depression

CONTRAINDICATED

• Heart block • Severe peripheral artery disease

CAUTION • > 60 years old • Diabetics • Hyperglycemia, loss of blood glucose control, failure to recognize hypoglycemia • Reactive airway disease (can cause bronchospasm)- avoid non-selective agents

BB nonselective

Nadolol

Propranolol

BB Nonselective with ISA

Pindolol

BB B1-Selective

Atenolol

Bisoprolol

Metoprolol

Nebivolol

BB B-1 selective with ISA

Acebutolol

BB B-1 selective with A1 blocking

labetalol

Calcium Channel Blockers Dihydropyridines (CCBs) drugs

“dipine” ending drugs

• amlodipine (Norvasc® ) • felodipine (Plendil® ) • nifedipine (Adalat® XL)

• Long-acting dihydropyridine - first-line for essential hypertension

• Particularly effective in patients who are black and who are elderly

Calcium Channel Blockers Dihydropyridines (CCBs) First line dynamics

• Inhibit the influx of calcium ions into smooth muscle (vascular and cardiac)

• Dihydropyridines - greater effects on vascular smooth muscle = vasodilation

Many potential drug interactions: are metabolized by CYP enzymes

AVOID GRAPEFRUIT JUICE

Pre and ADV • Ankle edema, flushing, headache, palpitations

Calcium Channel Blockers Nondihydropyridines CCBs 2nd line drugs

• diltiazem (Tiazac® - various long-acting oral dosage forms)

• verapamil (Isoptin® SR)

Nondihydropyridine CCBs are second-line for essential hypertension and used more for stable angina and various arrhythmias

CCBs Nondihydropyridines 2nd line drug dynamics

Inhibit the influx of calcium ions into smooth muscle (vascular and cardiac) • Nondihydropyridines have greater effects on cardiac smooth muscle = negative inotropic effects (reduction in force of the heart)

Are metabolized by AND inhibit CYP enzymes

AVOID GRAPEFRUIT JUICE

Headache, dizziness, bradycardia, heart block, new onset or worsening of heart failure (caution in patients with heart failure)

Diuretics

Drugs that increase urine output referred to as “water pills”, may cause dizziness and orthostatic hypotension when first initiated (Though diuretics may cause dizziness, it typically subsides so auxiliary labels are NOT affixed for this potential adverse effect.)

Thiazide and Thiazide-Like Diuretics

•hydrochlorothiazide

•chlorthalidone, indapamide are first-line therapy for uncomplicated hypertension

Thiazides produce diuresis by inhibiting sodium and potassium reabsorption in the distal convoluted tubule of the nephron • The reduction in extracellular fluid volume reduces cardiac output

Increased urination so they are dosed in the MORNING to prevent nocturia

Thiazide and Thiazide-Like Diuretics dynamics

• Hypotension, weakness, muscle cramps, impotence • Hypokalemia, hyponatremia • EAT FOODS RICH IN POTASSIUM • Hyperuricemia (may aggravate gout) • Hyperglycemia • Hyperlipidemia • Photosensitivity and rash • AVOID PROLONGED SUN EXPOSURE

Potential cross allergy with other sulfonamide derivatives!

Potassium-Sparing Diuretics

• amiloride (Midamor®)

• spironolactone (Aldactone®)

• hydrochlorothiazide/triamterene (Apo-Triazide®)

Adjuncts to thiazides (or other drugs that cause hypokalemia), Amiloride inhibits sodium reabsorption and potassium secretion in the renal tubules

Caution with NSAIDs, ACE inhibitors, aliskiren, angiotensin II receptor blockers, K+ supplements: may cause severe hyperkalemia and acute kidney injury

• Hyperkalemia, muscle cramps, headaches, GI symptoms (gastritis, and peptic ulcers), impotence • Spironolactone may also cause gynecomastia, menstrual irregularities

Alpha1-blockers

“sin” ending drugs • doxazosin • prazosin • terazosin

Only used when contraindications or intolerance to first line therapy, or combined with first-line drugs

• Antagonism of the alpha1 receptors in arteries / veins = reduces peripheral vascular resistance, lowers bp

• Caution when adding other hypotensive drugs

Orthostatic hypotension • MAY CAUSE DROWSINESS

Syncope usually occurs at the start of therapy, with rapid dose titration, or when combining other agents • Titrate slowly! • Headache, drowsiness

Centrally acting agent (add on therapy)

Clonidine

For hypertension (0.1 mg tablets)

• For the relief of menopausal hot flushing (0.025 mg tablets)

• Off-label include ADHD, treatment of opioid withdrawal, smoking cessation, hyperhidrosis
• Reduces vasoconstriction in peripheral vessels

Centrally Acting Agents

• methyldopa

When first-line antihypertensive agents are ineffective or unsuitable

• Drug of choice for treating hypertension in pregnant people

Reduces sympathetic tone and total peripheral resistance

Vasodilators

• hydralazine

When first-line antihypertensive agents are ineffective or unsuitable; also used in hypertensive emergencies
Choice for treating hypertension in pregnant people

Causes direct vasodilation of the arteriole smooth muscle

Vasodilators severe and last resort

• minoxidil

ONLY in severe, symptomatic hypertension with organ damage

• Direct acting peripheral vasodilator

Causes hirsutism Marketed topically as Rogaine® for alopecia!

Cholesterol

An essential molecule for life • Required for cell membrane function • Precursor for bile acids, steroid hormones, and vitamin D

Sources: • 25% from dietary sources (saturated fats in particular) • 75% is synthesized, primarily in the liver

Insoluble in water (waxy substance) - transported in the blood by lipoproteins

HDL: High-density lipoprotein (the GOOD cholesterol)

• Transports cholesterol away from the peripheral cells to liver • Cholesterol is catabolized (recycled) in liver • Protective against atherosclerosis

• LDL: Low-density lipoprotein (the BAD cholesterol)

• Transports cholesterol from liver to cells • Major factor contributing to atheroma formation

Other cholesterol

• VLDL: Very-low-density lipoproteins transport cholesterol and triglycerides

• Lipoprotein A: LDL particles associated with increased risk of coronary artery diseases

Dyslipidemia

• Disruption in the amount of lipids in the blood

• Lipids being cholesterol and triglycerides

• Caused by a disruption in how lipids are formed, transported, and utilized in the body

Primary Dyslipidemias

• Elevation in lipid levels due to genetic disorders and includes familial hypercholesterolemia and familial combined hyperlipidemia

Secondary Dyslipidemias

Hypothyroidism, obstructive liver disease, chronic renal failure, diabetes mellitus, excessive weight

• Sedentary lifestyle, alcohol excess, diets high in saturated fats, trans fats, and cholesterol

• Drugs! Thiazide diuretics, beta blockers, oral contraceptives, corticosteroids, hormone replacement therapy, retinoic acid

Treatment of Dyslipidemia - Diet

• Reduce dietary cholesterol intake to <300 mg/day • Restrict fat intake to 30% of calories • Increase fruit and vegetable intake • Increase high-fibre intake • Limit simple sugars and alcohol

Treatment of Dyslipidemia

HMG-CoA Reductase Inhibitors “Statin” ending drugs

• First-line for lowering cholesterol; they have the best cardiovascular outcomes

Statins are competitive inhibitors of the enzyme HMG-CoA reductase (prevents cholesterol biosynthesis)

End effect - reduction in LDL, triglycerides, increase in HDL

Dosed in the evening, efficient when the liver synthesizes cholesterol overnight

• Drug interactions • CYP inhibitors (macrolide antibiotics, cyclosporine, azole antifungals), • Other lipid-lowering agents and contraindicated in pregnancy, high alcohol consumption and active liver disease

Cholesterol Absorption Inhibitor

• ezetimibe (Ezetrol®)

• Indicated in combination with statins, or when statins are not tolerated to lower LDL

• Dosed po once daily at any time of the day • Low potential for drug interactions

• Well tolerated • Common: back pain, arthralgia, diarrhea, abdominal pain, fatigue, dizziness, and headache

Fibrates

Used if statins aren’t tolerated “fibr” drugs

Lower triglyceride levels and raise HDL; effects on LDL are variable

Drug Interactions • Statins: potential additive hepatotoxicity and myotoxicity • Warfarin: monitor INR • Ezetimibe: increased ezetimibe levels

Upper GI disturbances (nausea, abdominal pain, flatulence) and myalgias

• Possibility of cholelithiasis

“ate” ending drugs aux label DO NOT CRUSH OR CHEW

Bile Acid Sequestrants Resins - Dyslipidemia

• cholestyramine (Olestyr®) • colesevelam (Lodalis®) • colestipol (Colestid®)

Appropriate for children, in pregnant or breastfeeding
+ statin therapy (with or without ezetimibe) to achieve LDL targets

Interfere with the enterohepatic recirculation by binding bile salts, liver diverts cholesterol into formation of bile salts which reduces blood cholesterol levels

Start with once-daily dosing to improve tolerability • Powders/granules are mixed with juice, soup or applesauce (> 90 mL of fluid)

• Long-term and high-dose use can prevent the absorption of fat-soluble vitamins (A, D, E, and K) and folic acid • Common: constipation (>10%), bloating, abdominal fullness, and flatulence

Atherosclerosis

Presence of atheromas in large arteries

• Plaques consisting of lipids and calcium

• Form at the site of endothelial injury

• Related to diet, exercise, and stress

• Arteriosclerosis

• General term for all types of arterial changes

• Degenerative changes in small arteries and arterioles

• Loss of elasticity

• Lumen gradually narrows and may become obstructed

Peripheral Vascular Disease

• Disease in blood vessels outside the heart

• Increased incidence with diabetes

• Most common sites • Abdominal aorta • Carotid arteries • Femoral and iliac arteries

Peripheral Vascular Disease • Diagnostic tests and symptoms

• Blood flow assessed by Doppler studies and arteriography (aka angiography) • Plethysmography measures the size of limbs and blood volume in organs or tissues

• Increasing fatigue and weakness in the legs

• Sensory impairment • Tingling, burning, numbness

• Appearance of the skin • Marked pallor or cyanosis • Skin dry and hairless

Peripheral Vascular Disease • Treatment

• Health behaviours • Cessation of smoking • Weight loss • Increase exercise • Dietary modification • Reduction of sodium intake

• Pharmacotherapy • Antilipidemic drugs

• Surgical intervention • Coronary artery bypass grafting (CABG)

Acute Coronary Syndrome

Clinical symptoms causing acute myocardial ischemia.

• These are: • Unstable angina • Non-ST segment elevation myocardial infarction (NSTEMI) • ST segment elevation myocardial infarction (STEMI)

Angina Pectoris

Pain in the chest

• Most forms of angina are from coronary artery disease (CAD) = the result of atherosclerosis of the coronary arteries

• Narrowing of the coronary arteries • Ischemia

• The sensation often radiates to the jaw, shoulder, back, or arm and may include shortness of breath and anxiety

Angina Pectoris cause

Occurs when there is a deficit of oxygen to meet myocardial needs • Partial obstruction of a coronary artery • Angina may occur in different patterns

Stable angina

• Also called classic angina or exertional angina • Brought on by physical activity or stress • Relieved by rest and nitroglycerin

• Variant angina

• Vasospasm occurs at rest (coronary spasm)

• Unstable angina

• Prolonged pain at rest

• Occurs when coronary artery is almost completely occluded (may proceed a myocardial infarction)

• Requires immediate medical attention

Which is NOT a symptom of classic angina

Nausea, diarrhea and vomiting

Nitrates

Effective both to prevent anginal episodes and to treat acute attacks

Pro-drugs converted to nitric oxide (NO) • NO causes relaxation of venous and arterial smooth muscle

• Vasodilation reduces blood pressure, preload, afterload, and cardiac oxygen demand

Potent vasodilators. • reduce myocardial oxygen demand by reducing how hard the heart must work by:

Nitrates dynamics and precautions

Use with Riociguat (Adempas®) is contraindicated • concurrent use with phosphodiesterase-5 inhibitors is contraindicated

• The combination of nitrates and PDE5 inhibitors can cause severe hypotension

• Short-acting (sublingual) nitrates: • Lightheadedness, dizziness, or syncope • Burning or tingling sensations in the mouth

• All nitrates: • Headaches • Flushing edema • Hypotension, dizziness, and tachycardia • MAY CAUSE DIZZINESS

Short-Acting Nitrates

• Alleviate acute anginal pain

• Can be used preventatively for angina e.g prior to activities that cause angina or if ongoing pain despite comprehensive management • Not used in acute management of right ventricular infarcts

• Patients should sit down when taking to minimize falls due to light headedness or dizziness

• The dose may be repeated every 5 minutes until the chest pain is relieved

Short-Acting Nitrate drugs

• Nitroglycerin (NitroStat®) • Sublingual tablets • MUST be dispensed in the original glass container and the lid tightly closed after use • A nitroglycerin tablet left out of the bottle will loss its potency within a few hours!

• nitroglycerin (Nitrolingual® Pumpspray) • Translingual sprays – sprayed onto (or under) the tongue • Spray canisters should NOT be shaken or stored near heat sources • Must be primed prior to first use and re-primed after 14 days of no-use

Long-Acting Nitrate drug

• Products • nitroglycerin (Nitro-Dur® , Trinipatch®) • Transdermal patches: APPLY TO CLEAN, HAIRLESS AREA OF THE SKIN

• isosorbide dinitrate (ISDN®) • Extended release oral tablets: DO NOT CRUSH OR CHEW

• isosorbide-5-mononitrate (Imdur®) • Oral tablets

Reduce the severity and frequency of angina attacks, improve quality of life • Tolerance develops rapidly to the use of long-acting nitrates

Myocardial Infarction

Occurs when a coronary artery is totally obstructed causing prolonged ischemia and infarction (necrosis = cell death)

• STEMIs are medical emergencies and require urgent assessment and treatment

• Most common cause is atherosclerosis • A thrombus (clot) forms over a ruptured atherosclerotic plaque

Size and location of the infarct determine the extent of the damage • Myocardial fibers do not regenerate

Early Signs & Symptoms of STEMI

• Pressure, heaviness, or burning in chest, especially with increased activity • Often radiates to the left arm, jaw, or back • Pain may occur that is substernal or crushing

• Sudden shortness of breath, weakness, and fatigue • Skin becomes pale, cool, and clammy

• Nausea and indigestion

• Anxiety and fear

Treatment of STEMI

Reduce cardiac demand

Oxygen therapy • Percutaneous coronary intervention

– Cardiac Cocktail

• Nitrates • Fibrinolytics • Antiplatelets/Anticoagulants • Medication, as needed, to treat underlying causes: • Dysrhythmias, dyslipidemias, hypertension, congestive heart failure

Fibrinolytic drugs

• alteplase (Activase® rt-PA) • IV bolus, then infusion run over 60 minutes

• tenecteplase (TNKase®) • IV bolus over 5 minutes

• Administered as soon as possible after STEMI if no contraindications

• Bind to fibrin in a thrombus and convert the trapped plasminogen to plasmin

Once reconstituted, fibrinolytics are stored 2-30°C for up to 8 hours, then unused portions are discarded

• Hemorrhage: extensive screening process to ensure minimal risk of bleeding

Anticoagulants for MI

• unfractionated heparin 100 unit/mL (injectable solution)

• unfractionated heparin 1,000 unit/mL

• unfractionated heparin 10,000 unit/mL

• Given to all STEMI patients receiving a fibrinolytic

• Heparin inactivates Factor Xa and inhibits the conversion of prothrombin to thrombin = inhibits thrombus formation

• Administered subcut or iv (im route avoided due to increased risk of bruising/bleeding • Monitored by aPTT blood tests

Antiplatelets

• acetylsalicylic acid (ASA, Aspirin)

• significantly reduces mortality in patients with STEMI • It is started promptly and continued long term

• Acetylsalicylic acid irreversibly binds to and inhibits the enzyme cyclooxygenase (COX)

• Dose for ongoing prophylaxis in STEMI is 81 mg po EC daily

• Daily low dose ASA • Higher ASA doses are used for anti-inflammatory and analgesia/antipyresis

• Interactions: bleeding risk increased with heparin, warfarin, and other NSAIDs

• Nausea, vomiting, gastric/duodenal ulceration • TAKE WITH FOOD • Hypersensitivity reactions

Platelet Aggregation Inhibitors

• clopidogrel (Plavix®) • ticagrelor (Brilinta®)

Used by patients with STEMI treated with fibrinolysis and ASA to improve outcomes in acute coronary syndromes

• bind to adenosine diphosphate receptors on the surface of platelets = inhibits platelet aggregation

• Given as an oral loading dose before PCI and then as a daily po maintenance long term

• Interaction with omeprazole: switch to another PPI • Rabeprazole, pantoprazole

• Precautions and Adverse Effects • Bleeding, rash, and purpura, hemorrhage • Skin rash

Congestive Heart Failure (CHF)

Heart is unable to pump out sufficient blood to meet the demands of the body

• Usually, a complication of another cardiopulmonary condition that develops over time

When the heart cannot maintain pumping capability

• Cardiac output or stroke volume decreases • Less blood reaches the various organs • Decreased cell function

• Various compensation mechanisms maintain cardiac output • Some of these often aggravate the condition!

• Left-sided failure or forward failure

• It often occurs when the weakened and/or stiff left ventricle loses the ability to efficiently pump blood to the rest of the body.

• Leads to congestion in the lungs. • Decreased blood supply to tissues, general hypoxia • Fatigue • Dyspnea

• Backward failure or right sided failure

excess fluid accumulation in the body

• Also known as cor pulmonale or pulmonary heart disease. • Most right-sided heart failure occurs because of left-sided heart • Other causes for right-sided heart failure include: • High blood pressure in the lungs. • Pulmonary embolism.

• Excess fluid is forced back through the lungs, weakening the heart’s right side,

Left-Sided CHF: Backup Effects

• Pulmonary congestion • Dyspnea and orthopnea

• Develop as fluid accumulates in the lungs • Cough • Associated with fluid irritating the respiratory passages • Paroxysmal nocturnal dyspnea

Right-Sided CHF: Backup Effects

• Systemic backup • Pitting edema in feet, legs, or buttocks • Increased pressure in jugular veins leads to distention

• Hepatomegaly and splenomegaly • Digestive disturbances • Ascites

Signs & Symptoms of CHF

• Compensation mechanisms • Tachycardia • Cutaneous and visceral vasoconstriction • Daytime oliguria

• Various compensation mechanisms maintain CO, but they actually aggravate the condition! • Drugs are used to break the cycle of compensation that is causing more harm than good.

Treatment of CHF

• Manage concomitant disease states • CAD, DM, dyslipidemia, hypertension, obesity, and arrhythmias • Moderate regular physical activity in stable patients • No more than 1 alcoholic drink per day • Restrict sodium intake (<2 g/day) • Restrict fluid intake (<1.5 L/day) • Vaccinations (influenza and pneumococcal)

Loop Diuretics CHF

• furosemide (Lasix®) • ethacrynic acid (Edecrin®)

To control volume overload (edema in heart failure, cirrhosis, renal disease)

• Loop diuretics act in the “loop” of Henle and the convoluted tubules • They decrease reabsorption of sodium, chloride, potassium, and water

• Most potent and effective diuretic

• Given orally or IV • Many drug interactions including thiazide diuretics

• Weakness and fatigue • Hypokalemia, hyponatremia • Hyperuricemia • Hyperglycemia (some) • Hyperlipidemia

ACE Inhibitors

Recommended in all patients post MI • Improve symptoms • Reduce the risk of hospitalization, MI, and death • They provide long term vascular protection