Cardio

1. Your Heart & Blood Vessels = Pump & Water Park

Think of your body as a water park:

  • Heart = Pump → pushes water (blood) everywhere.

  • Blood vessels = Slides and hoses → carry water to all areas.

    • Arteries = fast slides sending water away from the pump under high pressure.

    • Veins = slower slides returning water to the pump; sometimes hold extra water (blood reservoir).

  • Blood Pressure (BP) = how hard the pump pushes water through the slides.

Quick note: Harder push or tighter slides = higher pressure; looser slides = lower pressure.

2. Pump Mechanics: Stroke Volume & Heart Rate

  • Stroke Volume (SV) = water per push (blood per heartbeat).

  • Heart Rate (HR) = pushes per minute (beats/min).

  • Cardiac Output (CO) = total water delivered per minute:

CO=SV×HRCO = SV \times HRCO=SV×HR

If either SV or HR goes up, CO usually goes up.

Mini quiz: If HR ↑ but SV ↓ proportionally, what happens to CO? → Roughly the same.

3. Pipes & Resistance: Blood Pressure Basics

  • Mean Arterial Pressure (MAP) = average pressure in the slides.

MAP≈CO×SVRMAP ≈ CO × SVRMAP≈CO×SVR

  • SVR (Systemic Vascular Resistance) = how tight the small pipes are.

    • Tiny pipes (arterioles) matter most because resistance skyrockets if diameter shrinks:

Resistance∝1/r4Resistance ∝ 1/r^4Resistance∝1/r4

  • Tighter pipes → higher BP

  • Looser pipes → lower BP

Analogy: Even a tiny kink in a small hose makes it much harder to push water through.

4. Body’s Quick Fix: Baroreceptor Reflex

Baroreceptors = little alarm sensors in your pipes.

  • BP drops suddenly (like standing up fast):

    • Alarm triggers → heart beats faster (HR ↑)

    • Pipes squeeze (vasoconstriction ↑)

  • This quickly raises BP back toward normal.

Kidneys = slow helpers

  • Adjust water volume over hours/days (RAAS system) for long-term BP control.

5. Preload, Afterload & Wall Tension

  • Preload = how full the heart is before squeezing (like filling a water balloon).

  • Afterload = how hard the heart must push against resistance (like squirting water through a narrow straw).

  • Wall tension = how much the heart muscle stretches/works.

More preload or afterload → heart works harder → uses more oxygen.

Mini quiz: If veins dilate → less blood returns → wall tension ↓ → oxygen demand ↓.

6. Types of Heart Drugs

Type

Goal

Example

Prophylactic

Stop problems before they happen

Aspirin to prevent clots, beta-blockers post-MI

Symptomatic

Relieve symptoms only

Nitroglycerin for chest pain, loop diuretics for pulmonary edema

Causal / Etiologic

Fix the actual problem

Thrombolytics after a heart attack

Most drugs you’ll study are prophylactic or symptomatic, not causal.

7. Opposites You Need to Know

Action

Heart

Vessels

BP

Drug example

Contract

Systolic

Vasoconstriction

Hypertension

Vasopressor

Relax

Diastolic

Vasodilation

Hypotension

Vasodilator

Fast/strong

Positive chronotropy/inotropy

—

—

—

Slow/weak

Negative chronotropy

—

—

—

Autonomic tone

Sympathetic

Parasympathetic (vagal)

—

—

Tip: “Contracts = push, relax = let go.”

8. Blood Vessel Control

Diameter changes of vessels are controlled by:

  • Nerves: sympathetic = squeeze, parasympathetic = relax

  • Endothelium: signals like NO (relax), endothelin (squeeze)

  • Hormones: angiotensin II (squeeze), epinephrine (squeeze)

  • Autoregulation: metabolic byproducts, oxygen levels

Small arteries (arterioles) dominate resistance and BP.

9. Cardiac Drug Chapters

Chapter

Drug type

Goal

1

Cardiotonic (positive inotropic)

Make heart pump stronger → Heart failure

2

Ischemic heart drugs

Reduce chest pain → Angina

3

Antiarrhythmic drugs

Fix abnormal heartbeat → Arrhythmias

Quiz: Do cardiotonic and antiarrhythmic drugs treat the same problem?

  • Answer: No → one fixes pumping, the other fixes rhythm.

10. Quick “If This Happens” Scenarios

  1. Sudden arterial contraction (vasoconstriction):

    • Pipes tighten → BP ↑, afterload ↑

  2. Standing up fast (blood pools in legs):

    • Preload ↓ → SV ↓ → CO ↓ → BP ↓ → baroreceptors kick in → HR ↑, vessels squeeze

  3. Venous dilation:

    • Less blood returns → wall tension ↓ → myocardial oxygen demand ↓

  4. Heart rate ↑ while SV ↓ proportionally:

    • CO ≈ same → MAP roughly unchanged

  5. Small arteriole vs large artery constriction:

    • Small arteriole radius has HUGE effect on resistance (remember 1/r⁴)

11. Formulas You Need (Middle School Style)

  1. CO = SV × HR → pump × pushes/min

  2. MAP ≈ CO × SVR → pump × pipe tightness

  3. Wall tension ∝ Pressure × Radius / (2 × Wall thickness) → bigger balloon or more pressure → more tension

  4. Resistance ∝ 1 / radius⁴ → tiny pipe changes = huge effect

12. How the Body Maintains Balance

  • Immediate: baroreceptor reflex → adjust HR & vessel tone

  • Long-term: kidney RAAS → regulate blood volume and pressure

1. Excitation, Membrane Potential & Action Potential

Think of a cardiac cell like a tiny battery:

  • Excitation: The spark that makes the heart cell contract (like flipping a switch).

  • Transmembrane potential: The voltage across the cell’s wall.

    • At rest (RMP), heart cells are like a charged battery: ~ –90 mV.

  • Action potential (AP): The rapid change in voltage when the cell is excited.

    • Phases 0–4: Sodium comes in → depolarization, Calcium comes in → contraction, Potassium leaves → repolarization.

Analogy: AP = electrical spark that tells the heart to squeeze.

2. Excitation-Contraction (E-C) Coupling & Calcium’s Role

  1. AP travels along the cell surface (sarcolemma) and into the T-tubules.

  2. L-type Ca²⁺ channels open → small Ca²⁺ enters.

  3. This triggers a bigger release of Ca²⁺ from the sarcoplasmic reticulum (SR) via Ryanodine receptors (RyR2).

  4. Ca²⁺ binds troponin C → tropomyosin moves → actin + myosin interact → contraction.

  5. Relaxation: Ca²⁺ is pumped back into SR (SERCA) and out via NCX.

Analogy: Small Ca²⁺ is a key that opens the main Ca²⁺ vault → makes the heart squeeze. SERCA = heart’s cleanup crew putting Ca²⁺ back.

3. Calcium-Handling Proteins

Protein

Location

Job

L-type Ca²⁺ channels

T-tubule membrane

Let initial Ca²⁺ in from outside

Ryanodine receptor (RyR2)

SR membrane

Release lots of Ca²⁺ → contraction

SERCA pump

SR membrane

Pump Ca²⁺ back in → relaxation

Phospholamban (PLB)

SR membrane

Controls SERCA (phosphorylation ↑ activity)

Na⁺/Ca²⁺ exchanger (NCX)

Sarcolemma

Pump Ca²⁺ out of cell

4. cAMP Regulation

  • cAMP = second messenger → like the car accelerator for the heart.

  • Made after β-adrenergic stimulation (adrenaline/norepinephrine).

  • Activates PKA → phosphorylates:

    • L-type Ca²⁺ channels → more Ca²⁺ in

    • RyR2 → more Ca²⁺ released from SR

    • Phospholamban → SERCA works faster

  • Net effect: Stronger, faster heartbeats + faster relaxation

Memory: cAMP = heart accelerator → stronger + faster + quicker reset.

5. Beta-Adrenoceptor Pathway

  1. β₁-Adrenoceptor binds adrenaline/norepinephrine.

  2. Activates Gs protein → stimulates adenylyl cyclase (AC).

  3. AC converts ATP → cAMP.

  4. cAMP activates PKA → phosphorylates L-type channels, RyR2, PLB, and troponin I.

  5. Result: ↑ contractility, ↑ heart rate, faster relaxation.

Memory: β → Gs → AC → cAMP → PKA → stronger/faster beats.

6. Drugs That Boost Heart Contraction via Calcium

Drug

How it boosts Ca²⁺

Example

β-adrenergic agonists

↑ cAMP → ↑ Ca²⁺ influx

Dobutamine

PDE inhibitors

Stop cAMP breakdown → sustained Ca²⁺ influx

Milrinone

Digitalis (cardiac glycosides)

↑ Na⁺ inside → ↓ NCX → ↑ cytosolic Ca²⁺

Digoxin

Tip: “Agonists, PDE blockers, and digitalis all raise Ca²⁺ → stronger beats.”

7. Myocardial Ischemia & Angina

  • Definition: Heart muscle isn’t getting enough oxygen.

  • Why it happens:

    • ↑ demand: faster heart rate, stronger contraction, bigger wall stress

    • ↓ supply: blocked coronary arteries, anemia, low oxygen

Types of Angina

Type

Trigger

Treatment Goal

Stable

Exercise/stress

↓ O₂ demand

Unstable / ACS

Minimal exertion

Restore blood supply fast

Variant / Prinzmetal

Coronary spasm

↑ O₂ supply / relieve spasm

Memory: Supply < demand → pain (angina).

8. Drugs for Ischemic Heart Disease (IHD)

A. Nitrates (Nitroglycerin)

  • Release NO → ↑ cGMP → relax veins > arteries

  • ↓ preload → ↓ O₂ demand

  • Use: acute attacks (sublingual), prophylaxis (long-acting)

  • Can combine with beta-blockers or CCBs to avoid reflex tachycardia

  • Memory: Nitrates = relax veins = less work for heart

B. Beta-blockers (Metoprolol, Atenolol)

  • Block β1 → ↓ HR & contraction → ↓ O₂ demand

  • Use: stable angina prevention, post-MI

  • Avoid in variant angina (can worsen spasm)

  • Memory: Slow the beat → lower heart’s “heat”

C. Calcium Channel Blockers (CCBs)

  • Block L-type Ca²⁺ channels → ↓ contraction + vasodilation

  • Types:

    • Dihydropyridines (Amlodipine, Nifedipine): mostly vessels → ↓ afterload

    • Non-DHPs (Verapamil, Diltiazem): ↓ HR & contraction → ↓ O₂ demand

  • Use: variant angina, some stable angina

  • Memory: Chill the heart + widen the pipes

D. Ranolazine

  • Inhibits late Na⁺ → ↓ Ca²⁺ overload → ↓ wall tension → ↓ O₂ demand

  • Use: chronic angina when others fail

  • Doesn’t affect HR/BP much

E. Antiplatelets (Aspirin, P2Y12 inhibitors)

  • Prevent platelet sticking → ↓ clot formation

  • Use: ACS, post-PCI, secondary prevention

  • Memory: Platelets stick? Stop ’em quick

F. Statins

  • Inhibit HMG-CoA reductase → ↓ LDL cholesterol → stabilize plaques

  • Use: long-term IHD prevention

  • Memory: Statins = strong walls for vessels

9. Quick Recall Tips

  • Supply vs Demand: Angina = supply < demand

  • Acute vs Chronic: Nitrates = quick relief; others = prevention

  • Spasm vs Exertional Angina:

    • Beta-blockers → help exertional, may worsen spasm

    • CCBs → help spasm

  • Combo Therapy: Nitrates + beta-blockers/CCBs → balance HR + B