drugs for CHF, angina, arrhythmias Flashcards
What is the fundamental problem in CHF?
The heart cannot pump enough blood to meet the body’s oxygen needs.
How is cardiac output (CO) calculated?
CO = Heart Rate × Stroke Volume
What characterizes left-sided heart failure?
Weakened contraction, reduced ejection fraction, lung congestion, respiratory issues.
What characterizes right-sided heart failure?
Inability to pump blood to the lungs, severe peripheral edema.
What causes angina?
Insufficient oxygen supply to the heart, leading to ischemia and hypoxia.
Why does angina cause pain?
Anaerobic metabolism increases lactic acid, causing a burning sensation.
What is an arrhythmia?
Disruption in normal heart rhythm.
What is the pathway of blood through the heart?
Veins → Right atrium → Right ventricle → Lungs → Left atrium → Left ventricle → Body
What is the function of the right side of the heart?
Pumps blood to the lungs for oxygenation.
What is the function of the left side of the heart?
Pumps oxygenated blood to the body.
What is preload?
The amount of blood filling the ventricles before contraction.
What is afterload?
The pressure the heart must overcome to eject blood.
What happens in left-sided heart failure?
The left ventricle weakens, leading to pulmonary congestion and fluid buildup in the lungs.
What are symptoms of left-sided heart failure?
Shortness of breath, coughing, wheezing, pulmonary edema.
What happens in right-sided heart failure?
The right ventricle can’t pump blood effectively to the lungs, causing blood to back up in veins.
What are symptoms of right-sided heart failure?
Peripheral edema, swelling in legs and ankles.
How does the body respond to heart failure?
Activates the renin-angiotensin-aldosterone system (RAAS).
Why can RAAS activation worsen heart failure?
Increases blood volume, raises blood pressure, and adds strain on the heart.
What does the renin-angiotensin-aldosterone system (RAAS) do in heart failure?
Increases angiotensin, aldosterone, blood volume, and sympathetic activity.
How does increased blood volume worsen heart failure?
Adds pressure on the heart, increases preload, and causes fluid retention (edema).
How does angiotensin II affect heart failure?
Causes vasoconstriction, making the heart pump against higher resistance (increased afterload).
How does the sympathetic nervous system react to heart failure?
Increases heart rate, contractility, cardiac output, and blood pressure.
Further activates RAAS, increasing fluid retention and stress on the heart.
Why is increased heart rate (HR) bad for heart failure?
Raises oxygen demand while the heart is already weak.
How do ACE inhibitors & ARBs help heart failure?
Reduce vasoconstriction (↓ afterload), blood volume (↓ preload), and sympathetic output, fluid retention.
Why do beta blockers help, despite initially seeming counterintuitive?
Reduce RAAS activation, lower heart rate - sympathetic output, and block harmful catecholamine effects.
How does cardiac glycosides lead to stronger heart contractions?
Blocks sodium pump in heart cells → sodium builds up inside cells → High sodium leads to calcium buildup → makes heart contract stronger
How do cardiac glycosides like digoxin work?
Block Na+/K+ ATPase pump, increasing intracellular sodium.
What are the main benefits of digoxin?
Stronger heart contractions, better blood circulation, and symptom relief.
What are the main risks of digoxin?
small therapeutic index—to little doesn’t help
to much is toxic (cns side effect)
little long term benefits
many drug interactions
What triggers stable angina?
Physical exertion or stress (increased oxygen demand).
When does vasospastic angina occur?
At rest, unpredictably, not triggered by exertion.
What causes stable angina?
Atherosclerotic narrowing of coronary arteries.
How long do symptoms of stable angina last?
A few minutes, relieved by rest.
What causes vasospastic angina?
Coronary artery spasms (not necessarily atherosclerosis).
How is vasospastic angina different from stable angina?
It’s caused by arterial spasms, not physical activity.
What causes unstable angina?
Platelet plugs forming in coronary arteries.
Why is unstable angina more dangerous than stable angina?
It signals worsening coronary artery disease and risk of a heart attack.
How is unstable angina different from a heart attack?
Blood flow is reduced but not completely blocked.
Can unstable angina occur at rest?
Yes, it is unpredictable and occurs without exertion.
Which drugs increase coronary blood flow?
Organic nitrates (nitroglycerin) & DHP calcium channel blockers (amlodipine).
How do organic nitrates help with angina?
Dilate coronary arteries, improving oxygen supply.
What is the role of DHP calcium channel blockers (e.g., amlodipine)?
Dilate coronary arteries and increase blood flow for chronic angina prevention.
When are organic nitrates most useful?
For acute angina attacks (rapid relief, especially sublingual nitroglycerin).
Which drug classes reduce heart workload?
Beta blockers, non-DHP calcium channel blockers, and nitrates.
How do beta blockers help with angina?
Slow heart rate and reduce contractility, lowering oxygen demand.
Why aren’t beta blockers useful for acute attacks?
They act too slowly to provide immediate relief.
Which calcium channel blockers work like beta blockers?
Non-DHP calcium channel blockers (verapamil, diltiazem).
How do nitrates help reduce cardiac workload?
Dilate veins (reducing preload) and lower blood pressure (reducing afterload).
Why is sublingual nitroglycerin preferred for acute angina?
Works within minutes, provides fast relief, and has a short duration (15–30 min).
How does nitroglycerin work?
Releases nitric oxide (NO), causing vasodilation, increase blood flow, reducing heart workload.
Which drugs interact dangerously with nitrates?
PDE5 inhibitors (Viagra, Cialis, Levitra). erticle dysfunction medicatoins
Why should patients sit when taking nitroglycerin?
Prevents fainting due to sudden blood pressure drop.
Why is the combination of nitrates and ED meds dangerous?
Causes excessive vasodilation, leading to severe hypotension and fainting.
What is the mechanism behind this dangerous interaction?
Nitrates increase NO, while PDE5 inhibitors prevent cGMP breakdown—together, they cause extreme blood vessel dilation.
Where does the electrical signal originate in the heart?
SA (Sinoatrial) Node, the natural pacemaker (60–100 bpm).
What does the P wave on an ECG represent?
- Small upward bump
- Represents atria depolarizing
- First electrical activity in cycle
- Shows SA node started the beat
correctly
What is the role of the AV (Atrioventricular) Node?
Delays the signal, allowing the atria to fully contract before ventricles.
Which part of the ECG represents ventricular depolarization?
The QRS complex.
How does the signal spread through the ventricles?
Via Purkinje fibers, causing ventricular contraction.
What does the T wave represent on an ECG?
Ventricular repolarization (resetting for the next beat).
What are the characteristics of a normal sinus rhythm (NSR)?
Rate: 60–100 bpm
Each P wave followed by a QRS complex
Regular, evenly spaced beats
Clear return to baseline between cycles
Sodium Channel Blockers Example drug?
Lidocaine
Sodium Channel Blockers Acts on atrial or ventricular arrhythmias?
Ventricular
Beta Blockers Example drug?
Propranolol
Sodium Channel Blockers Main use?
Ventricular fibrillation
Sodium Channel Blockers Effect on cardiac action potential?
Slows rate of depolarization (Phase 0)
Beta Blockers Effect on heart function?
Slows heart rate & AV conduction
Beta Blockers Acts on atrial or ventricular arrhythmias?
Atrial (supraventricular)
Beta Blockers Main use?
Supraventricular tachycardia (SVT)
Potassium Channel Blockers Acts on atrial or ventricular arrhythmias?
Ventricular
Potassium Channel Blockers Example drug?
Amiodarone
Potassium Channel Blockers Main use?
Ventricular fibrillation
Potassium Channel Blockers Effect on cardiac action potential?
Prolongs repolarization (Phase 3)
Calcium Channel Blockers (CCBs) Main use?
Supraventricular tachycardia (SVT)
Calcium Channel Blockers (CCBs) Acts on atrial or ventricular arrhythmias?
Atrial (supraventricular)
Calcium Channel Blockers (CCBs) Example drugs?
Verapamil, Diltiazem
Calcium Channel Blockers (CCBs) Effect on heart function?
Slows heart rate & AV conduction
Atrial problems are more likely to use which classes?
Class 2 & 4
Ventricular problems are more likely to use which classes?
Class 1 & 3
