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What is the primary mechanism of action of organic nitrates?
What is the primary mechanism of action of organic nitrates?
What is the primary effect of β-blockers on cardiac oxygen demand?
What is the primary effect of β-blockers on cardiac oxygen demand?
What is the primary effect of Ca++ channel blockers on cardiac oxygen demand in classic angina?
What is the primary effect of Ca++ channel blockers on cardiac oxygen demand in classic angina?
What is the side effect of β-blockers that can worsen asthma?
What is the side effect of β-blockers that can worsen asthma?
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What is the primary effect of Ca++ channel blockers on cardiac oxygen supply in variant angina?
What is the primary effect of Ca++ channel blockers on cardiac oxygen supply in variant angina?
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What is the side effect of Ca++ channel blockers that is not responsive to diuretics?
What is the side effect of Ca++ channel blockers that is not responsive to diuretics?
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What is the mechanism of action of organic nitrates that leads to increased oxygen supply?
What is the mechanism of action of organic nitrates that leads to increased oxygen supply?
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What is the primary effect of β-blockers on cardiac output?
What is the primary effect of β-blockers on cardiac output?
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What is the side effect of Ca++ channel blockers that can lead to poor left ventricular filling?
What is the side effect of Ca++ channel blockers that can lead to poor left ventricular filling?
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What is the cardiovascular effect of organic nitrates that leads to decreased cardiac work?
What is the cardiovascular effect of organic nitrates that leads to decreased cardiac work?
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What is the definition of Angina Pectoris?
What is the definition of Angina Pectoris?
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What is the primary cause of anginal pain?
What is the primary cause of anginal pain?
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What is the most common underlying condition leading to anginal pain?
What is the most common underlying condition leading to anginal pain?
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What is the primary action of anti-angina drugs?
What is the primary action of anti-angina drugs?
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What is the role of arteriovenodilators in hypertensive emergencies?
What is the role of arteriovenodilators in hypertensive emergencies?
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What is the effect of insufficient oxygen supply to the heart?
What is the effect of insufficient oxygen supply to the heart?
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What is the underlying pathology of atherosclerosis?
What is the underlying pathology of atherosclerosis?
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What is the primary consequence of atherosclerosis of the coronary arteries?
What is the primary consequence of atherosclerosis of the coronary arteries?
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What is the relationship between anginal pain and oxygen demand?
What is the relationship between anginal pain and oxygen demand?
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Which of the following is NOT a type of direct vasodilator?
Which of the following is NOT a type of direct vasodilator?
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What is the primary mechanism of action of hydralazine?
What is the primary mechanism of action of hydralazine?
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Which of the following is an example of a venodilator?
Which of the following is an example of a venodilator?
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What is the effect of diazoxide on blood vessels?
What is the effect of diazoxide on blood vessels?
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Which of the following is NOT a direct vasodilator?
Which of the following is NOT a direct vasodilator?
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What is the effect of direct vasodilators on blood vessels?
What is the effect of direct vasodilators on blood vessels?
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Which of the following is an example of an arteriodilator?
Which of the following is an example of an arteriodilator?
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What is the main mechanism of action of organic nitrates in the treatment of angina?
What is the main mechanism of action of organic nitrates in the treatment of angina?
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What is the primary cardiovascular effect of β-blockers in angina treatment?
What is the primary cardiovascular effect of β-blockers in angina treatment?
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What is the side effect of β-blockers that can mask a hypoglycemic coma?
What is the side effect of β-blockers that can mask a hypoglycemic coma?
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What is the effect of Ca++ channel blockers on cardiac oxygen supply in variant angina?
What is the effect of Ca++ channel blockers on cardiac oxygen supply in variant angina?
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What is the common side effect of Ca++ channel blockers that is not responsive to diuretics?
What is the common side effect of Ca++ channel blockers that is not responsive to diuretics?
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What is the cardiovascular effect of organic nitrates that leads to decreased cardiac work?
What is the cardiovascular effect of organic nitrates that leads to decreased cardiac work?
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What is the primary effect of β-blockers on cardiac output?
What is the primary effect of β-blockers on cardiac output?
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What is the side effect of Ca++ channel blockers that can lead to poor left ventricular filling?
What is the side effect of Ca++ channel blockers that can lead to poor left ventricular filling?
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What is the primary cardiovascular effect of Ca++ channel blockers in classic angina?
What is the primary cardiovascular effect of Ca++ channel blockers in classic angina?
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What is the common side effect of β-blockers?
What is the common side effect of β-blockers?
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What is the primary goal of treating heart disease with certain classes of drugs?
What is the primary goal of treating heart disease with certain classes of drugs?
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Which of the following classes of drugs is effective in treating heart disease?
Which of the following classes of drugs is effective in treating heart disease?
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What is the benefit of using ACE inhibitors in heart disease treatment?
What is the benefit of using ACE inhibitors in heart disease treatment?
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Which of the following is NOT a benefit of using beta blockers in heart disease treatment?
Which of the following is NOT a benefit of using beta blockers in heart disease treatment?
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What is the role of diuretics in heart disease treatment?
What is the role of diuretics in heart disease treatment?
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Study Notes
ACE Inhibitors
- Decrease blood pressure by decreasing peripheral resistance without affecting cardiac output or heart rate
- Do not cause reflex tachycardia, making them safe for patients with ischemic heart disease
Diuretics
- Thiazide diuretics: Hydrochlorothiazide
- Loop diuretics: Frusemide
- Potassium-sparing diuretics: Spironolactone, Triamterene
Calcium Channel Blockers
- Mechanism of action: block calcium channels
- In the heart: decrease heart rate and contractility, thus decreasing cardiac output
- In blood vessels: vasodilation, decreasing peripheral resistance
- Examples: Non-Dihydropyridine (Diltiazem, Verapamil), selective to the heart
Beta Blockers
- Mechanism of action: act mainly by blocking β1 receptors, decreasing heart rate
- Examples: Non-selective β-blockers (Propranolol, Carvedilol), selective β1-blockers (Atenolol, Bisoprolol)
- Adverse effects: bradycardia, fatigue, cold extremities, erectile dysfunction, bronchospasm (especially non-selective)
- Interactions: increased toxicity with other negative inotropic drugs (e.g., verapamil, lidocaine)
Organic Nitrates
- Mechanism of action: generation of NO leading to vasorelaxation
- Cardiovascular effects: increase O2 supply, decrease cardiac work (decrease O2 demand) by vasodilation
- Side effects: venodilation (postural hypotension, reflex tachycardia, dizziness, syncope), arteriodilation (throbbing headache, flushing), tolerance
Beta Blockers (Cardiovascular Effects)
- Reduce anginal pain by decreasing cardiac O2 demand through blockade of β1 receptors
- Side effects: dizziness, weakness, headache, impotence, β2 blocking (bronchospasm, disturbance of blood glucose and lipid levels, masking hypoglycemic coma, bradycardia)
Ca++ Channel Blockers (Angina)
- In classic angina: reduce anginal pain by decreasing cardiac oxygen demand
- Decrease heart rate and contractility
- Decrease arterial pressure (afterload)
- In variant angina: promote relaxation of coronary artery spasm, increasing cardiac O2 supply
Ca++ Channel Blockers (Side Effects)
- Arterial dilation: headache, flushing, dizziness, ankle edema (not responding to diuretics, especially nifedipine)
- Decrease contractility: poor left ventricular filling
- Heart block (especially with β-blockers and digoxin)
Heart Failure
- Definition: congestive heart failure
Adverse Effects of ACE Inhibitors
- Dry cough (5-30%)
- Angioedema
- Hyperkalemia
- Teratogenic (not used in pregnancy)
Diuretics
- Mechanism of action: decrease blood volume, cardiac output, and blood pressure
- Decrease blood pressure due to decreased cardiac output
Beta Blockers
- Mechanism of action: block β1 receptors, decreasing heart rate
- Examples: non-selective β-blockers (Propranolol, Carvedilol), selective β1-blockers (Atenolol, Bisoprolol)
- Adverse effects:
- Bradycardia
- Fatigue
- Cold extremities
- Erectile dysfunction
- Bronchospasm (especially non-selective)
Interactions of Beta Blockers
- Increased toxicity with other -ve inotropic drugs (e.g., verapamil, lidocaine)
Centrally Acting Adrenergic Drugs
- α2-agonist (e.g., Clonidine) diminishes central adrenergic outflow
- α-Methyldopa: another α2-agonist, valuable in treating pregnant hypertensive patients
- Used in infusion in hypertensive emergencies
Arteriovenodilators
- Example: Sodium Nitroprusside
Angina Pectoris
- Definition: sudden pain beneath the sternum, often radiating to the left shoulder and arm
- Causes: insufficient oxygen supply to meet oxygen demand, often due to atherosclerosis of coronary arteries
Anti-Anginal Drugs
- No specific examples provided
Non-Pharmacological Management of Hypertension
- Weight reduction is recommended to manage hypertension
- A diet rich in fruits, vegetables, and low-fat dairy products with reduced saturated and total fat content is beneficial
- Restricting daily dietary sodium intake is essential
- Regular aerobic physical activity is recommended
- Stopping alcohol consumption and quitting smoking are advised
- Managing stress and controlling diabetes mellitus and atherosclerosis are important
ACE Inhibitors and Angiotensin Receptor Blockers (ARBs)
- ACE inhibitors: Enalapril, Ramipril, and Captopril
- Angiotensin receptor blockers (ARBs): Losartan and Valsartan
- These medications are eliminated primarily by the kidneys, so dosage adjustments are necessary in renal insufficiency cases
Calcium Channel Blockers
- Mechanism of action: blocking calcium channels
- Effects on the heart: decreased heart rate and contractility, leading to decreased cardiac output
- Effects on blood vessels: vasodilation, leading to decreased peripheral resistance
- Examples: Diltiazem and Verapamil (non-dihydropyridine, more selective to the heart)
Direct Vasodilators
- Arteriodilators: Hydralazine, Minoxidil, and Diazoxide
- Venodilators: Nitroglycerine (I.V.)
Antihypertensive Drugs
- ACEIs (Angiotensin-Converting Enzyme Inhibitors) decrease blood pressure by decreasing peripheral resistance without affecting cardiac output or heart rate.
- They do not cause reflex tachycardia, making them safe for patients with ischemic heart disease.
- Examples of ACEIs: Enalapril, Ramipril, and Captopril.
- Examples of Angiotensin Receptor Blockers (ARBs): Losartan and Valsartan.
Pharmacokinetics and Adverse Effects of ACEIs and ARBs
- ACEIs and ARBs are eliminated primarily by the kidneys; therefore, the dose should be adjusted in renal insufficiency.
- Adverse effects of ACEIs and ARBs include:
- Dry cough (5-30%)
- Angioedema
- Hyperkalemia
- Teratogenic effects (not used in pregnancy)
Centrally Acting Adrenergic Drugs
- α2-agonist Clonidine diminishes central adrenergic outflow, reducing blood pressure.
- α-Methyldopa is another α2-agonist, specially valuable in treating pregnant hypertensive patients.
Organic Nitrates
- Organic nitrates, such as glyceryl trinitrate (nitroglycerin), generate NO, leading to vasorelaxation.
- Cardiovascular effects:
- Increase O2 supply and decrease cardiac work (decrease O2 demand) by vasodilation.
- Side effects:
- Venodilation → postural hypotension, reflex tachycardia, dizziness, and syncope.
- Arteriodilation → throbbing headache and flushing.
- Tolerance
β-Blockers
- Cardiovascular effects:
- Reduce anginal pain by decreasing cardiac O2 demand.
- Primarily through blockade of β1 receptors.
- Side effects:
- Most common: dizziness, weakness, headache, and impotence.
- β2 blocking → bronchospasm (asthma), disturbs blood glucose and lipid levels.
- Masks hypoglycemic coma and bradycardia.
Ca++ Channel Blockers
- In classic angina: Ca++ channel blockers reduce anginal pain by decreasing cardiac oxygen demand.
- Decrease heart rate and contractility.
- Decrease arterial pressure (afterload).
- In variant angina: Ca++ channel blockers promote relaxation of coronary artery spasm, increasing cardiac O2 supply.
- Side effects:
- Arterial dilation → headache, flushing, dizziness, and ankle edema (not responsive to diuretics, especially nifedipine).
- ↓ Contractility → poor left ventricular filling.
- Heart block (especially with β-blockers and digoxin).
Congestive Heart Failure
- Definition: Congestive heart failure is a condition where the heart cannot pump enough blood to meet the body's needs.
Hypertensive Crisis
- Sudden and severe increase in blood pressure to 180/120 mm Hg or greater
Diuretics
- Mechanism of action: Diuretic action → decrease blood volume → decrease cardiac output → decrease blood pressure
Classification of Diuretics
- Thiazide diuretics: Hydrochlorothiazide
- Loop diuretics: Frusemide
- Potassium-sparing diuretics: Spironolactone, Triamterene
Side Effects of Loop Diuretics
- Hypocalcemia
- Hyperuricemia
- Hyperglycemia
Effective Classes of Drugs for Hypertension
- ACE inhibitors
- β-adrenergic blocking agents
- Diuretics
- Aldosterone antagonists
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Description
This quiz covers the effects of ACE inhibitors on blood pressure, peripheral resistance, cardiac output, and heart rate, particularly in patients with ischemic heart disease.