6) Cardiac Physiology

True or False: Arteries and veins are defined based on their oxygenation level.

False - it’s based on where they carry blood (to vs away)

Describe the heart's "two pumps."

Low-pressure pump (right side, pulmonary circulation)

Large, high-pressure pump (left side, systemic circulation)

Describe the circulatory pathway.

1. Deoxygenated blood from the vena cavae enters the right atrium

2. Deoxygenated blood passes through the tricuspid valve into the right ventricle

3. Blood is pumped at relatively low pressure from the right ventricle, through the pulmonary (semilunar) valve to the lungs and back to the left atrium

4. Blood enters the left ventricle through the MITRAL valve

5. Blood is pumped at high pressure via the aortic (semilunar) valve to the entire body

6. Returned to the right atrium, via the vena cavae

What supports and frames the four heart valves?

fibrous, non-contractile tissue of the heart’s skeleton

What are the 2 semilunar valves? How do the semilunar valves close?

1. Pulmonary valve

2. Aortic valve

→ backsurge of blood after each pulse opens the leaflets like umbrellas; as they open, their edges push together to form a seal

What is the function of papillary muscle contraction in AV valves?

isometric + stabilizes valve leaflets via chordae tendineae to prevent back-flow (it doesn’t pull the valves open)

Unlike skeletal muscle, how does cardiac muscle increase its force since it cannot use "recruitment"?

→ EVERY cell contracts with each beat

• if more force is needed, each cell contracts harder via “inotropy”

Since ALL muscles are activated, which mechanism can only alter force generation?

• Changes in fiber length

  • preload; length-dependent activation, or how much the fiber contracts

• changes in inotropy

  • length-independent activation, or how rapidly (how hard) the fiber contracts)

  • ↑ inotropy = ↑ contraction strength for the same stretch or preload (muscle length)

What is the difference between a positive and negative inotrope?

(+) inotropes (e.g., Digoxin) ↑ contraction strength (without increasing its length/pre-load)

(-) inotropes (e.g., Beta blockers) weaken it

What are thin & thick fibers of Sarcomeres composed of?

1. Thick fibers

   • Myosin

2. Thin fibers

   • Actin – globular protein with myosin-binding site

   • Tropomyosin – runs along actin to block myosin binding site

   • Troponin – globular protein which binds Ca²⁺

     • Once bound, a conformational change occurs that removes tropomyosin’s inhibition, allowing contraction

What is the function of T-tubules in cardiac myocytes?

membrane invaginations that carry AP to the SR for Ca²⁺ release

Where are t-tubules of cardiac myocytes located?

Z-lines (intercalated discs)

Describe what occurs when AP travels down the the T-tubules at the dyad.

Ca²⁺ release

1. AP triggers Ca²⁺ release from the SR to the cytoplasm

2. Ca²⁺ binds to troponin, which moves the tropomyosin, exposing myosin binding sites

Sliding filament theory

1. Myosin head attaches to actin myofilament

2. Working stroke - myosin head pivots and bends as it pulls on the actin filament, sliding it towards the M line

3. ATP binds to myosin head, detaching it from cross bridge

4. ATP → ADP + Pi

5. Myosin head cocks up

6. Repeat cross-bridge cycle

Ca²⁺ uptake

1. As [Ca²⁺]_{intracellular} falls, Ca²⁺ dissociates from troponin

2. Tropomyosin goes and blocks myosin binding sites

3. Ca²⁺ leaves cytoplasm to SR, during prolonged relaxation period

Fill this out.

The magnitude of a cardiomyocyte contraction is proportional to what?

[Ca²⁺]_{intracellular}

List 3 junctions of the Intercalated discs. Mention their functions.

Desmosomes– ensure fibers stay attached in a line during contraction

Gap junctions - allow AP to spread along a linear row of cardiomyocytes during contraction

Fascia adherens – anchoring sites for actin

Why can AP readily pass from 1 cardiac muscle cell to the next?

they have very low electrical resistance

What ion movement causes depolarization (muscle contraction) in cardiac cells?

Opening of:

Fast voltage gated Na⁺ channels → Na⁺ enters

Slow voltage gated Ca²⁺ channels → Ca²⁺ enters

What ion movement causes repolarization (muscle relaxation) in cardiac cells?

Opening of:

Voltage gated K⁺ channels → K⁺ exits

Slow voltage gated Ca²⁺ channels → Ca²⁺ enters

Is action potential the signal to contract or is it the contraction itself.

Signal to contract

Describe the 4 phases of the heart’s action potential.

Phase 0: fast Na⁺ channels open → Na⁺ flows into the cell (depolarizes) → rapid upstroke (Q)

Phase 1: Na⁺ channels close (partial repolarization)

Phase 2: K⁺ efflux; Ca²⁺ influx (plateau phase)

Phase 3: K⁺ efflux > Ca²⁺ influx (repolarization) → membrane potential decreases to baseline

Phase 4: Resting phase

Define an ECG in relation to myocardial cells.

summation of the depolarization wave across all the myocardial cells

Define Inotropy.

force of contraction during systole

Define Lusitropy.

amount of relaxation during diastole

Define Chronotropy.

heart rate

True or False - Both Sympathetics and Parasympathetics affect the SA and AV nodes.

True

True or False: Both Sympathetics and Parasympathetics affect the ventricles.

False - ventricles receive only sympathetics

How does sympathetic stimulation affect the ventricles?

↑ NE

1. Amount of depolarization/↑ force of contraction = ↑ inotropy

2. Opens an ATP channel that allows SR to soak up Ca²⁺ = ↑ lusitropy → shortens recovery time

3. ↑ Chronotropy

How does Verapamil specifically affect the heart?

• blocks Ca²⁺ entry needed to sustain the plataeu phase→ ↓ contractility → ↓ HR & ↓ blood volume pumped

• Treatment: tachycardia & A-fib

Which parts of the heart's conduction system have intrinsic autorhythmicity?

1. SA node

2. AV node

3. Purkinje fibers

What is the discharge rate of the SA node in a denervated heart?

~100x/min

Why is there an insulating ring (non-conductive tissue) between the atria and ventricles?

ensure they contract in sequence, not together, to move blood effectively

What structures depolarize the ventricles?

Purkinje fibers (modified cardiac muscle cells) within the bundle branches

What is the normal HR range?

60-100bpm

How long does 1 beat last?

0.6-1 sec

How does depolarization appear in the ECG waveform?

(+) upward deflection

What does the P-wave represent?

atrial depolarization and contraction via SA node

What does the PR interval represent? What is its duration?

→ AV conduction time (delay b/w atrial contraction & ventricular contraction)

• Duration time is 0.12 to 0.20 seconds (1 large box)

What does the QRS complex represent? What is its duration?

→ ventricle depolarization via AV nodes

• not longer than 0.10 seconds (less than 3 small boxes)

What is the maximum normal duration for a QRS complex?

0.10 seconds (less than 3 small boxes)

What does the T wave represent?

ventricle repolarization

What is an ST segment?

early ventricular repolarization

What is a QT interval?

→ measured from the Q (initiation of ventricular contraction to the end of the T (repolarization)

• represents ventricular depolarization and repolarization (Na⁺ influx and K⁺ efflux)

What is total time of a normal ECG?

0.6-1.0 sec (5 large boxes=1 sec)

A regular heartbeat is said to have a _________.

A regular heartbeat is said to have a Sinus (node) Rhythm

Define Pre-load. What determines pre-load?

→ magnitude of “pre-stretching” of the cardiac muscle fibers

• Left ventricular end-diastolic volume (LVEDV) determines preload

How does ventricular filling affect preload?

More blood in the ventricle at the end of diastole → greater ventricular wall stretch → increased preload

What is the relationship between preload and cardiac contraction?

↑ preload = stronger & faster contraction

Define After-load.

pressure the ventricle must overcome to eject blood during systole (resistance)

When is afterload measured?

During ventricular ejection = when the aortic valve is open and the left ventricle and aorta share the same pressure

What factors increase afterload?

1. ↑ PVR (e.g., hypertension)

2. ↑ pulmonary blood flow resistance (e.g., lung disease)

What is the core concept of the Frank-Starling Mechanism?

↑ venous return (pre-stretch/preload) → ↑ force of contraction & ↑ SV

Define Stroke volume. What is its average value?

→ volume of blood leaving the ventricle with each beat

• 70 mL

Define Ejection Fraction. What is its average value?

→ fraction of the EDV ejected in each stroke

• 50-55%

Ejection Fraction = SV / EDV

Define Cardiac output. What is its average value?

→ total volume ejected from the left ventricle per unit time

• CO = SV x HR

Factors affecting CO. List 3

• HR

• SV

• Contractility

Remember: CO = SV x HR

Where does fluid back up in right-sided vs. left-sided heart failure?

Right-sided failure → backs up in the body (gravity dependent)

Left-sided failure → backs up in the lungs

• can also lead to right sided failure (cor pulmonare)

Several types of cardiac enzyme tests done when a heart attack is suspected. What enzymes are they detecting? Why?

• creatine phosphokinase (CPK) or creatine kinase (CK)

  • CK-MB (specific form of CPK/CK)

• Myoglobin & Troponins I and T levels

Reason: these substances are released from the heart muscle cells into the bloodstream, when the heart muscle is damaged

Of the different enzymes detected, which ones are cardiac specific?

• Troponins (cardiac specific)

• CPK/CK (works for all damaged tissues)

Describe the main events of the Wigger’s Graph.

1) Atrial Systole (Ventricular Filling Completed)

1. Atrial depolarization (P wave) precedes atrial systole

2. Atrial systole increases atrial pressure enough to open the AV (mitral/tricuspid) valves and push the final amount of blood into the ventricles

3. Ventricles reach their maximum volume (EDV)

4. Atrial pressure then falls as the ventricle fills

→ Ventricle is now fully loaded with blood and ready to contract

2) Isovolumic Contraction

1. Ventricular depolarization (QRS complex) initiates ventricular contraction

2. Ventricular pressure rises rapidly (volume stays the same)

3. When ventricular pressure exceeds atrial pressure: AV valves close → producing the First Heart Sound (S1)

4. Both AV and semilunar valves are closed

3) Ventricular ejection

1. Ventricular pressure continues rising.

2. When ventricular pressure exceeds aortic pressure: Aortic valve opens

3. Blood is ejected from the ventricle into the aorta

4. ↓ Ventricular volume from EDV toward ESV

5. ↑ Pressure in ventricle & aorta rises to a “systolic peak”

4) End of Ventricular Ejection

1. ↓ Ventricular pressure

2. Aortic pressure becomes greater than ventricular pressure

3. Aortic valve closes

What are Asteroid Hyalosis?

→ development of yellow/white glistening “asteroid bodies” in the vitreous

• made of lipid and Ca²⁺

• move with vitreous gel and return to their original position when eye stop moving

• usually over age 50

• unilateral

• asymptomatic with no vision change