Cardiovascular System

CV System

• Definition: Composed of heart and blood vessels

• Function: to supply oxygen through blood

Mechanism of CV = CV Disease

• As demands for oxygen increase → the heart & blood vessels compensate

  • Cardiac force/rate of contraction increases to pump larger volumes under higher pressure

  • Fails when the heart and/or blood vessels fail to meet sufficient oxygen

Cardiovascular Disease

• disease of the heart and blood vessels that results in failure

  • hypertension

  • coronary artery disease

  • cardiac arrhythmia

  • congestive heart failure

CV Disease-Induced Dental Clinical Conundrums

• 1. Weigh benefits of therapy against risks of complications (CV disease higher risks)

• 2. Weigh potential stress against patient’s ability to withstand it (reduced functional reserve)

• 3. With local, benefits of using epinephrine weighed against CV risks (epinephrine)

• 4. With anti-thromboembolic agents, benefits of therapy must be weighed against risks of bleeding

Hypertension

Definition:

• Volume of blood being pumped through CV system exceeds capacity

  • due to failure in fluid volume homeostasis in the RAAS system OR SANS stimulation

Classification:

• normal: <120/<80

• elevated: 120-129/<80

• hypertension stage I: 130-139/80-89

• hypertension stage II: 140+/90+

• Hypertensive crisis: 180+/120+

Hypertension

Treatment of Hypertension

• Non-Drug Treatment: reduce weight, limit alcohol, increase physical activity, restrict sodium intake, and smoking

A. Diuretics:

• Mechanism: reduce plasma volume and systemic blood pressure

• 4 Drug Types:

  • Thiazide → HCTZ

  • Loop → Furosemide

  • K-sparing → Triamterene (Dyrenium)

  • Combination → Triamterene/HCTZ (Dyazide)

• Clinical Uses: hypertension and congestive heart failure

• Adverse Side effects: xerostomia (fungal infection), orthostatic hypotension, and hypokalemia (except K-sparing and combo)

• Dental considerations: NSAIDs decrease effectiveness

B. Calcium Channel Blockers (A-D-N)

• Main Action: vasodilation, reduce heart rate, and cardiac activity

• 3 Drug Types:

  • amlodipine (Norvasc)

  • diltiazem (Cardizem)

  • nifedipine (Procardia)

• Adverse side effects: orthostatic hypotension and constipation

• Dental considerations: no interaction with NSAIA’s, gingival enlargement, and dysgeusia

Ba. Alpha-1 Blockers (-zostin)

• Mechanism: produce peripheral vasodilation

• 2 Drug types:

  • doxazosin (Cardura)

  • terazosin (hytrin)

• Adverse side effects: orthostatic hypotension (possibly severe with epinephrine) and xerostomia

• Dental considerations: interfere with epinephrine in LAs, and NSAIDs decrease effectiveness

RAAS Antihypertensive System:

• 1. Body detects reduced blood flow to kidneys (indicates low blood pressure)

• 2. Renin is released

• 3. Renin converts angiotensinogen into angiotensin I

• 4. ACE (angiotensin-converting enzyme) converts angiotensin I into angiotensin II

2 Pathways:

• A: angiotensin II → vasoconstriction → increase BP → increase blood flow

• B: angiotensin II converts to angiotensin III → aldosterone release → retains salt and water → increase BP → increase blood flow

C. RAAS Antihypertensive Agents: ACEI and ARBS

• 2 Categories:

  • ACE inhibitors (-pril)

  • Angiotensin II Receptor Blockers (-sartan)

Ca. RAAS Antihypertensive Agents: ACE Inhibitors (-pril)

• Mechanism: inhibits ACE (angiotensin-converting enzyme) from converting angiotensin I to angiotensin II

• Drug examples: lisinopril (Prinivil) and ramipril (Altace)

• Clinical Uses: produce systemic vasodilation to treat hypertension and congestive heart failure

• Adverse Side effects: include orthostatic hypotension and dry cough

• Dental Drug Interactions: NSAIDs decrease effectiveness

Cb. RAAS Antihypertensive Agents: Angiotensin II Receptor Blockers (-sartan)

• Mechanism: block angiotensin II from binding to receptors → blocking vasoconstriction

• Drug examples: irbesartan (Avapro) and valsartan (Diovan)

• Clinical Uses: same as ACEI

• Adverse Side Effects: orthostatic hypotension and headache

• Dental Drug Interaction: NSAIDs decrease effectiveness and are NOT used during pregnancy

D. Beta-1 Blockers (-olol)

• Mechanism: reduce heart rate and force of contraction and cardiac activity

• 2 Types:

  • cardioselective: atenolol (Tenormin) and metoprolol (Toprol XL)

  • non-cardioselective: nadolol (Corgard) and propranolol (Inderal)

• Adverse side effects: depression, fatigue, sensitivity to cold, erectile dysfunction

• Dental considerations: epinephrine may have hypertensive side effects with non-cardio-selective beta blockers AND mask symptoms of hypoglycemia in diabetic patients

Da. Alpha-2 Agonists

• Mechanism: reduce SANS output to treat hypertension, manage withdrawal symptoms, migraine prophylaxis, and ADHD

• Drug: clonidine (Catapres)

• Adverse side effects: xerostomia, orthostatic hypotension, bronchoconstriction

• Dental Considerations: bradycardia, CNS depression, fatigue, respiratory depression, xerostomia, and rebound hypertension upon cessation

Db. Alpha/Beta Blockers

• Mechanism: vasodilation and increased BP (alpha-1 blocker) and blocks reflex increase in HR (beta-1 blocker)

• Drug: carvedilol (Coreg)

• Clinical uses: hypertension without reflex bradycardia

• Adverse side effects: orthostatic hypotension, CNS depression, and fatigue

• Dental Considerations: additive hypotensive effect and CNS depression with other meds and may mask signs of hypoglycemia

Coronary Artery Disease

Coronary Artery Disease

• Definition: results from the combination of hypertension and hyperlipidemia in which plaque builds inside coronary arteries → oxygen demand increases, and blood flow is reduced

SYMPTOM RESULTING FROM CAD:

• Angina pectoris: demand for oxygen exceeds the ability of coronary arteries to supply it

  • Symptoms: pain in chest to left arm, neck, back, and lower jaw

  • Precipitated by: physical exertion, emotional stress

IF CHRONIC:

• Myocardial infarction: myocardial tissue is permanently deprived of oxygen, becoming necrotic

  • results in death that is replaced by scar tissue or arrhythmias

Treatment of CAD

A. Nitrates

• Mechanism: increasing coronary artery flow

• 2 categories: NTG (short-acting) and Oral Nitrates (long-acting)

  • NTG → sublingual tablets (Nitrostat) and translingual spray (Nitrolingual)

  • Oral nitrates → isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur)

• Adverse side effects: headache and orthostatic hypotension

• Dental considerations: keep readily available during appointments (acute angina attacks induced by stress) and check expiration date to ensure potency

Action of Antihyperlipidemic Agents

• Mechanism of antihyperlipidemics and CAD:

  • low-density lipoproteins (LDLs): function to transport cholesterol to peripheral cells; when LDLs are elevated, excess cholesterol is discarded in blood

    • LEADS to excess cholesterol and plaque formation

• high-density lipoprotein (HDLs): transfer cholesterol from peripheral cells to liver, in which cholesterol is metabolized and excreted

• CONNECTION:

  • antihyperlipidemic agents inhibit progression of disease by either reducing total cholesterol/LDL or increasing HDL and decreasing LDL

5 Classes of Antihyperlipidemic Agents

• HMG-CoA reductase inhibitors (statins)

• bile Acid sequestrants

• fibrates

• nicotinic acid derivatives

• cholesterol absorption blockers

A. HMG-CoA reductase inhibitors (-statins)

• Mechanism: inhibit enzyme necessary in formation of cholesterol → decreases LDLs

• Drugs: atorvastatin (Lipitor), simvastatin (Zocor), pitavastatin (Livalo), and rosuvastatin (Crestor)

• Adverse side effects: myopathy, possible liver damage, gastrointestinal upset, and anterograde amnesia

• Dental considerations: liver enzyme inhibitors increase statin blood levels; avoid using with azole antifungals (Diflucan), grapefruit, and pomegranate juice

B. Bile Acid Sequestrants

• Mechanism: Bind bile acids in the intestines to lower LDL levels

• Drug: Cholestyramine (Questran)

• Adverse Effects: Constipation and flatulence

• Patient Care Considerations: Interferes with gastrointestinal absorption of other drugs and vitamins for up to 6 hours

C. Fibrates

• Mechanism: Decrease the production of LDLs and increase HDLs

• Example: Fenofibrate (Tricor, Antara).

• Adverse Effects: Gastrointestinal upset, abdominal pain, and diarrhea.

• Patient Care Considerations: Possible myopathy; increases the blood levels of plasma protein-bound drugs

D. Nicotinic Acid Derivatives

• Mechanism: Decrease triglycerides and increase HDLs

• Example: Niacin (Niaspan).

• Adverse Effects: Orthostatic hypotension, flushing, and gastrointestinal upset.

• Patient Care Considerations: Risk of liver toxicity and used illicitly to "flush" urine drug tests

E. Cholesterol Absorption Blockers

• Mechanism: Decrease absorption of dietary cholesterol from food and LDLs.

• Example: Ezetimibe (Zetia).

• Adverse Effects: Fatigue, headache, and dry cough.

• Patient Care Considerations: Possible myopathy

Thromboembolic Disease

• Related terms: coagulation vs. hypercoagulation:

  • Coagulation: normal clotting mechanism (prevents blood loss) when a blood vessel is disrupted

• Hypercoagulation:

  • overactive clotting mechanism that produces clots (thrombi) within undamaged vessels

Oral Antiplatelet Agents

• Mechanism: Inhibits platelet aggregation and clot formation

• 5 Types:

  • aspirin

  • clopidogrel (Plavix)

  • dipyridamole (Persantine)

  • prasugrel (Effient)

  • ticagrelor (Brilinta)

• Clinical Uses: prevention of cardiovascular events in adults (acute coronary syndrome, MI, TIA, stroke, and post-stenting procedures)

• Drug Interaction Consideration:

  • Clopidogrel (Plavix) and ticagrelor (Brilinta) are notable with liver enzyme inducers and inhibitors

  • Exacerbated bleeding with other drugs (NSAIAs and antibiotics)

Oral Anticoagulant Agents: Coumadin

• Mechanism: Prevention and treatment of venous thrombosis, pulmonary embolism, thromboembolism due to

  • Atrial fibrillation

  • Prosthesis

  • Recent MI

• Drug: Coumadin (warfarin)

  • Inhibits the synthesis of Vitamin K-dependent clotting factors

• Patient Care considerations: Increased risk of bleeding that's assessed by INR (international normalized ratio)

  • Value of 1 is “normal”; <3.5 is needed for dental treatment

  • INR test should be done immediately before oral treatment

  • NO contraindications for dental treatment

• Dental considerations: Anticoagulant effect reversed with administration of Vitamin K or whole blood; increased risk of bleeding may be exacerbated (NSAIA’s and Antibiotics)

Oral Anticoagulant Agent: Pradaxa

• Mechanism: Prevention and treatment of venous thrombosis, pulmonary embolism, and thromboembolism due to atrial fibrillation

• Drug: Pradaxa (dabigatran)

  • Inhibits thrombin (factor IIa)

• Patient care considerations:

  • Antidote for reversal: Praxbind

  • No INR testing

  • Increased risk of bleeding may be exacerbated by NSAIDs and Antibiotics

  • NO contraindications for dental treatment

Oral Anticoagulant Agent: 3 Types

• Mechanism: Prevention and treatment of venous thrombosis, pulmonary embolism, thromboembolism due to atrial fibrillation

• 4 Types: Xarelto (rivaroxaban), Eliquis (apixaban), Savaysa (edoxaban)

  • Inhibit factor Xa

• Patient care considerations:

  • Reversal agent for Xarelto and Eliquis: Andexxa

  • No reversal agent for Savaysa

    • No INR testing for monitoring

  • Increased risk of bleeding may be exacerbated (NSAIA’s and Antibiotics)

  • No contraindication for dental treatment

Cardiac Dysrhythmia

• Definition:

  • Malfunction of cardiac conduction system

  • Disruption of normal cardiac sinus rhythm

  • May cause fast or slow heartbeat

  • Results in poor oxygenation of blood and cardiac insufficiency and inefficiency

  • May lead to death

Treatment of Cardiac Dysrhythmias

• Drug employed:

  • antiarrhythmic agents → restore sinus cardiac rhythm

  • antithromboembolic agents → prevent thromboembolism

Antidysrhythmic agents: Potassium Channel Blockers

• Mechanism: reduce cardiac arrhythmias

• Category: amiodarone (Cordarone) and dronedarone (Multaq)

• Disease treated: cardiac arrhythmia

• Adverse side effects: abnormal salivation and altered taste

• Dental considerations: local anesthetics with epi may have additive cardiac effect

Antidysrhythmic agents: Sodium Channel Blockers

• Mechanism: reduce cardiac arrhythmias

• Category:

  • Type IA → quinidine

  • Type IB → lidocaine

  • Type IC → flecainide

• adverse side effects: xerostomia and oral candidiasis (type IA), altered taste (type IB), and nausea (type IC)

• Dental considerations: local anesthetics with epi may have additive cardiac effect

Congestive Heart Failure

• Congestive Heart Failure: systemic demand for blood (and oxygen) exceeds pumping capacity of heart

  • Inadequate cardiac output to supply oxygen (including the heart itself)

  • Leads to decreased perfusion of other organs and decreased function (liver and renal function)

Cardiac glycosides:

• mechanism: decrease rate of contractions

• drug: digoxin (Lanoxin)

• clinical use: CHF and cardiac arrhythmia

• adverse side effects: anorexia, hypersalivation, increased gag reflex, and visual disturbances

• dental considerations: epi with caution (increased risk of cardiac arrhythmia)

Considerations for Conundrum

• Physical evaluation based on ASA

  • ASA I, II, III, IV, V, VI

• patient assessment of functional reserve

  • MET 1: light housework and walk a block on ground level

  • MET 4: climb a flight of stairs and run short distance

  • MET 10: strenuous sport activities

• Epinephrine

  • May or may not exacerbate CV disease

  • AVOID if uncontrolled hypertension, hyperthyroidism, severe controlled cardiac disease

  • MRD 0.2mg per appointment or 11 cartridges (healthy) OR 0.04mg/2 cartridge (CV impairment)

• Antithromboembolics

  • Does NOT support routine discontinuation for dental patients

1. Drug Suffixes & Name Memorization Shortcuts

The sources organize cardiovascular medications by specific suffixes, abbreviations, and counts to simplify memorization:

• 4 Diuretics = Hydrochlorothiazide (HCTZ), Furosemide, Triamterene, and Triamterene/HCTZ (Dyazide).

• A-D-N / -dipine = Calcium Channel Blockers (CCBs): Amlodipine, Diltiazem, Nifedipine.

• -zosin = Alpha-1 Blockers (doxazosin, terazosin).

• -pril = ACE Inhibitors (lisinopril, ramipril).

• -sartan = Angiotensin II Receptor Blockers (ARBs) (irbesartan, valsartan).

• -olol = Beta-1 Blockers (atenolol, metoprolol, nadolol, propranolol).

• -statin = HMG-CoA Reductase Inhibitors / Statins (atorvastatin, simvastatin, pitavastatin, rosuvastatin).

• NTG + 2 Isosorbides = Nitrates: Nitroglycerin (NTG), Isosorbide dinitrate, Isosorbide mononitrate.

• 5 Antiplatelet Agents = Aspirin, Clopidogrel, Dipyridamole, Prasugrel, Ticagrelor.

• 5 Anticoagulants = Warfarin, Dabigatran, Rivaroxaban, Apixaban, Edoxaban.

• Single-Drug Classes:

  • Clonidine = Alpha-2 Agonist

  • Carvedilol = Alpha/Beta Blocker

  • Cholestyramine = Bile Acid Sequestrant

  • Fenofibrate = Fibrate

  • Niacin = Nicotinic Acid Derivative

  • Ezetimibe = Cholesterol Absorption Blocker

2. Primary Drug Mechanism Shortcuts

Group the drugs by their core physiological goals:

• Reduce Blood Volume: Diuretics

• Dilate Blood Vessels: Calcium Channel Blockers, Alpha-1 Blockers, ACE Inhibitors, ARBs, and Nitrates.

• Restore RAAS Fluid Homeostasis: ACE Inhibitors and ARBs

• Reduce Cardiac Output / SANS Drive: Beta-1 Blockers and Alpha-2 Agonists

• Increase Cardiac Contractility: Digoxin (Cardiac Glycoside)

• Lower Lipids / Prevent Plaque: Statins, Bile Acid Sequestrants, Fibrates, Niacin, and Ezetimibe.

• Prevent Thromboembolism: Antiplatelets and Anticoagulants.

3. Universal Dental Rules & Red Flags

• NSAID Interactions: NSAIDs decrease the effectiveness of Diuretics, Alpha-1 Blockers, ACE Inhibitors, and ARBs. NSAIDs (and antibiotics) also increase bleeding risks when combined with antiplatelet agents or anticoagulants.

• Orthostatic Hypotension: Expect orthostatic hypotension as a common side effect across almost all antihypertensive and vasodilator drug categories.

• Epinephrine Limits: Healthy Maximum Recommended Dose (MRD) is 0.2 mg (11 cartridges), but for patients with CV impairment, limit epinephrine to 0.04 mg (2 cartridges). Completely avoid epinephrine in cases of uncontrolled hypertension, hyperthyroidism, or severe controlled cardiac disease.