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Questions and Answers
Which equation represents the calculation for Cardiac Output (CO)?
Which equation represents the calculation for Cardiac Output (CO)?
What does Vascular Tone refer to?
What does Vascular Tone refer to?
What determines the systolic ventricular wall stress?
What determines the systolic ventricular wall stress?
What is the effect of increased capacitance of the venous system on preload?
What is the effect of increased capacitance of the venous system on preload?
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What is the effect of increased resistance of the arterial system on afterload?
What is the effect of increased resistance of the arterial system on afterload?
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What do endothelial cells produce to locally regulate VSMC tone?
What do endothelial cells produce to locally regulate VSMC tone?
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What does myocardial O2 supply rely on?
What does myocardial O2 supply rely on?
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What does myocardial O2 demand rely on?
What does myocardial O2 demand rely on?
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What is the therapeutic strategy for treating angina?
What is the therapeutic strategy for treating angina?
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Which of the following is a clinical use of nitrates?
Which of the following is a clinical use of nitrates?
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What type of angina can nitrates be used to treat?
What type of angina can nitrates be used to treat?
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How do nitrates reduce preload?
How do nitrates reduce preload?
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What adverse effect is commonly associated with moderate doses of nitrates?
What adverse effect is commonly associated with moderate doses of nitrates?
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What adverse effect is commonly associated with larger doses of nitrates?
What adverse effect is commonly associated with larger doses of nitrates?
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What is contraindicated in patients using nitrates?
What is contraindicated in patients using nitrates?
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What happens in unstable angina?
What happens in unstable angina?
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What effect do nitrates have on platelet aggregation?
What effect do nitrates have on platelet aggregation?
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What is the main symptom of myocardial ischemia?
What is the main symptom of myocardial ischemia?
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Which type of vasculature do PDE5 inhibitors selectively target?
Which type of vasculature do PDE5 inhibitors selectively target?
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Which medication should not be used in conjunction with PDE5 inhibitors?
Which medication should not be used in conjunction with PDE5 inhibitors?
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What is the primary route of administration to bypass the first-pass metabolism of nitrates?
What is the primary route of administration to bypass the first-pass metabolism of nitrates?
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What is the half-life of ISDN (Isosorbide dinitrate)?
What is the half-life of ISDN (Isosorbide dinitrate)?
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What is the primary mechanism of nitrate tolerance?
What is the primary mechanism of nitrate tolerance?
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How can tolerance to nitrates be prevented?
How can tolerance to nitrates be prevented?
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What is the main symptom of Angina?
What is the main symptom of Angina?
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What is the primary factor that determines end-diastolic volume the heart pumps?
What is the primary factor that determines end-diastolic volume the heart pumps?
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Which type of calcium channel blockers primarily cause vasodilation of resistance arteries, has substantial 1st pass metabolism, rapid onset of action and short half life?
Which type of calcium channel blockers primarily cause vasodilation of resistance arteries, has substantial 1st pass metabolism, rapid onset of action and short half life?
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Which calcium channel blocker is known for its slower metabolism and longer half-life and has positive change at physiologic pH tat allow it to bind to the negatively charged cell membrane?
Which calcium channel blocker is known for its slower metabolism and longer half-life and has positive change at physiologic pH tat allow it to bind to the negatively charged cell membrane?
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Which calcium channel blocker is associated with flushing as an adverse effect and can cause aggravation of MI (relex tachycardia)?
Which calcium channel blocker is associated with flushing as an adverse effect and can cause aggravation of MI (relex tachycardia)?
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Which calcium channel blocker should not be used in excess or in combination with beta-blockers due to increased risk of mortality in heart failure?
Which calcium channel blocker should not be used in excess or in combination with beta-blockers due to increased risk of mortality in heart failure?
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Which calcium channel blocker has the potential to induce a precipitous drop in blood pressure when used in conjunction with nitrates?
Which calcium channel blocker has the potential to induce a precipitous drop in blood pressure when used in conjunction with nitrates?
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What is primarily used for the treatment of hypertension, arrhythmias, and angina?
What is primarily used for the treatment of hypertension, arrhythmias, and angina?
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Which calcium channel blocker is known for its significant less reflex tachycardia compared to other calcium channel blockers?
Which calcium channel blocker is known for its significant less reflex tachycardia compared to other calcium channel blockers?
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Which calcium channel blocker is primarily selective for vascular smooth muscle cells?
Which calcium channel blocker is primarily selective for vascular smooth muscle cells?
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Which calcium channel blocker is primarily selective for cardiac tissue?
Which calcium channel blocker is primarily selective for cardiac tissue?
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Which receptor is blocked by beta-blockers to decrease inotropy and chronotropy and therefore decrease cardiac output?
Which receptor is blocked by beta-blockers to decrease inotropy and chronotropy and therefore decrease cardiac output?
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What is the primary mechanism of action of beta-blockers?
What is the primary mechanism of action of beta-blockers?
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What is the therapeutic use of beta-blockers?
What is the therapeutic use of beta-blockers?
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What is the outcome of beta-blocker therapy?
What is the outcome of beta-blocker therapy?
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Which of the following is regulated by Beta-1AR-mediated phosphorylation?
Which of the following is regulated by Beta-1AR-mediated phosphorylation?
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What effect does PKA phosphorylation have on inotropy?
What effect does PKA phosphorylation have on inotropy?
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What effect does PKA phosphorylation have on chronotropy?
What effect does PKA phosphorylation have on chronotropy?
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Study Notes
Cardiac Output and Vascular Concepts
- Cardiac Output (CO) is calculated using the equation: CO = Stroke Volume x Heart Rate.
- Vascular Tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state.
Ventricular Stress and Hemodynamics
- Systolic ventricular wall stress is determined by factors such as pressure within the ventricle, ventricular radius, and wall thickness.
- Increased capacitance of the venous system leads to decreased preload, as more blood is accommodated in the veins.
- Increased resistance in the arterial system results in elevated afterload, making it harder for the heart to eject blood.
Endothelium and Oxygen Supply
- Endothelial cells produce vasodilators like nitric oxide (NO) to locally regulate vascular smooth muscle cell (VSMC) tone.
- Myocardial O2 supply is reliant on coronary blood flow and oxygen content of the blood.
- Myocardial O2 demand is determined by factors such as heart rate, contractility, and wall stress.
Angina and Nitrate Therapy
- The therapeutic strategy for treating angina includes the use of nitrates to relieve symptoms.
- Nitrates are effective in treating stable and variant angina.
- Nitrates reduce preload by causing venodilation, which decreases the volume returning to the heart.
Side Effects and Contraindications
- Common adverse effects of moderate doses of nitrates include headache and flushing.
- Larger doses of nitrates may lead to more severe hypotension.
- Nitrates are contraindicated in patients taking phosphodiesterase-5 (PDE5) inhibitors due to the risk of severe hypotension.
Angina and Ischemia
- In unstable angina, there is an increased frequency of angina attacks, often without physical exertion.
- Nitrates decrease platelet aggregation, which can help in managing ischemic conditions.
- The main symptom of myocardial ischemia is chest pain or discomfort.
Pharmacology of Calcium Channel Blockers
- PDE5 inhibitors selectively target vascular smooth muscle cells.
- Concurrent use of nitrates with PDE5 inhibitors is not advised due to risk of hypotension.
- The primary route to administer nitrates to avoid first-pass metabolism is sublingually.
- Isosorbide dinitrate (ISDN) has a half-life of about 4-6 hours.
Tolerance and Nitrate Usage
- Nitrate tolerance develops primarily due to compensatory mechanisms and can be mitigated by intermittent dosing regimens.
- The principal symptom of angina is chest pain or pressure during physical exertion or stress.
Calcium Channel Blocker Profiles
- Dihydropyridine calcium channel blockers primarily cause vasodilation of resistance arteries and are subject to significant first-pass metabolism with rapid action and short half-life.
- Amlodipine is known for its slower metabolism and longer half-life, binding effectively to negatively charged cell membranes at physiologic pH.
- Nifedipine is associated with flushing and reflex tachycardia, potentially aggravating myocardial infarction.
- Verapamil should not be used in excess or with beta-blockers due to mortality risk in heart failure.
- Combining nitrates with certain calcium channel blockers can lead to drastic drops in blood pressure.
Therapeutic Roles
- Calcium channel blockers are primarily used to treat hypertension, arrhythmias, and angina.
- Diltiazem is favored for having less reflex tachycardia compared to other calcium channel blockers.
- Amlodipine selectively targets vascular smooth muscle cells, while verapamil is more selective for cardiac tissues.
Beta-Blockers Mechanism and Effects
- Beta-blockers decrease inotropy (contractility) and chronotropy (heart rate) by blocking beta-1 adrenergic receptors, thereby lowering cardiac output.
- The primary mechanism of action of beta-blockers involves competitive inhibition of adrenergic receptor stimulation.
- Therapeutic uses of beta-blockers include managing hypertension, arrhythmias, angina, and heart failure.
- Outcomes of beta-blocker therapy may include reduced heart rate and myocardial oxygen demand.
Cellular Mechanisms and Effects
- Beta-1 adrenergic receptor-mediated phosphorylation affects phosphorylation levels regulated by cyclic AMP-dependent protein kinase (PKA).
- PKA phosphorylation enhances inotropy and chronotropy, leading to increased cardiac output during demand situations.
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Description
Test your knowledge on cardiovascular physiology with this quiz! Learn about the formulas for calculating cardiac output and blood pressure, as well as the importance of vascular tone. Challenge yourself to understand concepts like preload, afterload, and venous return.
