Explain cardio physiology with images

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Cardiovascular Physiology

Sources: Guyton and Hall Textbook of Medical Physiology | Costanzo Physiology 7th Edition | Ganong's Review of Medical Physiology

1. Heart Structure and Blood Flow

The heart is a four-chambered pump that keeps two circuits running simultaneously: the pulmonary circulation (right heart → lungs → left heart) and the systemic circulation (left heart → body → right heart).

The wall has three layers:

Endocardium - inner lining
Myocardium - muscular middle layer (does the pumping work)
Epicardium - outer layer, covered by the pericardium

Heart structure, chambers, valves, and blood flow direction

Figure 9.1 - Guyton & Hall: Structure of the heart and course of blood flow through chambers and valves.

Blood from the body (deoxygenated) enters the right atrium via the superior and inferior venae cavae → through the tricuspid valve → right ventricle → through the pulmonary valve → pulmonary artery → lungs (gas exchange) → pulmonary veins → left atrium → through the mitral valve → left ventricle → through the aortic valve → aorta → systemic tissues.

2. Cardiac Muscle Microstructure

The heart is composed of three types of cardiac muscle:

Atrial muscle - contracts to push blood into ventricles
Ventricular muscle - contracts powerfully to eject blood into arteries
Specialized excitatory/conductive fibers - generate and propagate the electrical signal (SA node, AV node, His-Purkinje system)

Cardiac muscle is striated (like skeletal muscle) and uses actin-myosin sliding filament mechanism. The key structural feature is the intercalated disc - cell membrane junctions containing gap junctions that allow free ion diffusion, making the heart a functional syncytium: when one cell fires, the action potential spreads to all cells rapidly.

Cardiac muscle syncytium showing intercalated discs between fibers

Figure 9.2 - Guyton & Hall: Syncytial interconnecting nature of cardiac muscle fibers with intercalated discs.

The left ventricle has a unique double-helix fiber arrangement: subepicardial fibers spiral leftward, subendocardial fibers spiral rightward. This creates a twisting/torsion motion during systole that maximizes ejection efficiency, and a recoil (untwisting) during diastole that facilitates rapid filling.

Left ventricular fiber arrangement and rotational motion during contraction

Figure 9.3 - Guyton & Hall: (A) Subendocardial and epicardial fiber orientation. (B) Net counterclockwise rotation of apex and clockwise rotation of base during systole.

3. Cardiac Action Potential

The ventricular muscle action potential has 5 phases and lasts about 300 ms (15x longer than skeletal muscle).

Phases of ventricular action potential with associated Na+, Ca2+, and K+ ionic currents

Figure 9.5 - Guyton & Hall: Action potential phases in cardiac ventricular muscle with corresponding ionic currents.

Phase	Name	Ionic Event	mV Change
0	Rapid depolarization	Fast Na⁺ channels open	-85 → +20 mV
1	Initial repolarization	Fast Na⁺ channels close; K⁺ exits	+20 → ~0 mV
2	Plateau	L-type Ca²⁺ channels open (slow); K⁺ channels close	~0 mV sustained
3	Rapid repolarization	Ca²⁺ channels close; slow K⁺ channels open	0 → -85 mV
4	Resting potential	K⁺ leak	-85 to -90 mV

The plateau phase (Phase 2) is unique to cardiac muscle and is critical because:

It allows prolonged contraction for adequate stroke volume
Ca²⁺ entry during plateau directly triggers myofilament contraction (vs. skeletal muscle which uses only SR calcium)
It prevents tetanic summation (which would be fatal in the heart)

Comparison: Purkinje fiber vs. Ventricular muscle

Rhythmical action potentials in Purkinje fibers vs ventricular muscle showing plateau

Figure 9.4 - Guyton & Hall: Purkinje fibers (top, red) have a longer plateau and higher resting potential (~-100 mV) compared to ventricular muscle (blue, ~-85 mV).

4. Refractory Period

Cardiac muscle has a long refractory period (~0.25-0.30 sec), roughly matching the duration of the plateau. This means the ventricle cannot be re-stimulated while it is contracting - preventing sustained tetanus (summation), which would stop cardiac output entirely.

There is also a shorter relative refractory period (~0.05 sec) after the absolute period, during which the muscle can be excited only by a very strong stimulus (producing a weaker, premature contraction).

$Cardiac refractory period, relative refractory period, and premature contractions$

Figure 9.6 - Guyton & Hall: Force of ventricular contraction showing refractory periods. Note premature contractions cannot summate (unlike skeletal muscle).

5. Cardiac Conduction System

The conduction system allows orderly, sequential contraction of atria then ventricles.

Sequence of activation:

SA Node (sinoatrial node) - right atrial wall, near SVC opening. The pacemaker - fastest spontaneous depolarization rate (~60-100 bpm). Sets the rhythm for the whole heart.
Internodal pathways - conduct impulse from SA node across the atria
AV Node (atrioventricular node) - at junction of atria and ventricles. Introduces a 0.1-second delay allowing atria to finish emptying before ventricles contract
Bundle of His - common pathway through the fibrous AV septum
Left and Right Bundle Branches - travel down the interventricular septum
Purkinje Fibers - spread impulse rapidly (4 m/sec) to all ventricular myocardium from apex upward

Key rule: Under normal conditions, the SA node dominates because it depolarizes fastest. If it fails, the AV node takes over (~40-60 bpm), then Purkinje fibers (~20-40 bpm) - these are called escape rhythms.

Ganong's Review of Medical Physiology, p. 520

6. The Cardiac Cycle

Each complete heartbeat consists of 7 phases (Costanzo Physiology):

Phase	Event	ECG Correlation	Valves
A - Atrial Systole	Atria contract; final filling of ventricle	P wave	Mitral/tricuspid open
B - Isovolumetric Ventricular Contraction	Ventricular pressure rises; no ejection yet (all valves closed)	QRS complex	Mitral closes → S1
C - Rapid Ventricular Ejection	Ventricle ejects blood into aorta/pulmonary artery	ST segment	Aortic/pulmonic opens
D - Reduced Ventricular Ejection	Ejection slows; ventricular volume at minimum	T wave	-
E - Isovolumetric Ventricular Relaxation	Pressure falls; no filling yet	After T wave	Aortic closes → S2
F - Rapid Ventricular Filling	Passive filling from atria	-	Mitral opens
G - Reduced Ventricular Filling (Diastasis)	Slow filling; little pressure change	-	Mitral open

Heart Sounds:

S1 ("lub") - closure of mitral and tricuspid valves at start of ventricular systole
S2 ("dub") - closure of aortic and pulmonic valves at end of systole
S3 - pathological (ventricular gallop in heart failure) - rapid filling phase
S4 - atrial contraction against stiff ventricle (hypertrophy)

7. Frank-Starling Law

The Frank-Starling law states: the more the heart is filled during diastole, the stronger the subsequent contraction. Greater stretch of myocytes increases the sensitivity of troponin C to Ca²⁺ and optimizes actin-myosin overlap, producing more force.

Physiologically, this means cardiac output is largely self-regulating: if venous return increases (e.g., during exercise), the heart automatically pumps more without needing neural input. Venous return is the primary determinant of cardiac output under normal conditions.

"When increased quantities of blood flow into the heart, the increased volume of blood stretches the walls of the heart chambers and causes the cardiac muscle to contract with increased force, ejecting the extra blood." - Guyton & Hall, p. 251

8. Cardiac Output and Distribution

Cardiac output (CO) = Heart Rate × Stroke Volume

At rest: CO ≈ 5 L/min (70 bpm × ~70 mL)

The cardiac output equals the sum of all regional blood flows in the body. At rest, the distribution is:

Cardiac output distribution showing right heart, lungs, left heart, and percentage distribution to organs

Figure 20.2 - Guyton & Hall: Cardiac output equals total tissue blood flow. Note splanchnic (27%) and renal (22%) circulations receive the largest shares at rest.

Organ	% of Cardiac Output
Splanchnic (gut/liver)	27%
Kidneys	22%
Skeletal muscle (inactive)	15%
Brain	14%
Skin + other	18%
Heart	4%

During maximal exercise, cardiac output can increase to 20-25 L/min (trained athletes: up to 35-40 L/min), primarily due to increased stroke volume and heart rate, plus massive redistribution of blood to active muscles.

Summary - Key Concepts

Concept	Key Point
Cardiac muscle structure	Syncytium via gap junctions; striated; intercalated discs
Action potential	5 phases; plateau (Phase 2) due to Ca²⁺; ~300 ms duration
Pacemaker	SA node: 60-100 bpm → AV node: 40-60 bpm → Purkinje: 20-40 bpm
Cardiac cycle	7 phases; systole (B-D) + diastole (E-G+A)
Frank-Starling	Stretch → stronger contraction; auto-regulates output
Cardiac output	5 L/min at rest; governed mainly by venous return
Refractory period	~0.25-0.30 sec; prevents tetanus; essential for survival

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