The heart functions as a dual pump, circulating blood through two circuits:
Pulmonary circuit: oxygenates blood in the lungs and removes carbon dioxide.
Systemic circuit: delivers oxygen and nutrients to tissues and removes carbon dioxide.
Three types of cells are required for the heart to beat:
Rhythm generators: produce an electrical signal (SA node, the normal pacemaker).
Conductors: spread the pacemaker signal.
Contractile cells (myocardium): mechanically pump blood.
Cardiac tissue possesses inherent rhythmicity or automaticity due to specialized pacemaker cells.
The sinoatrial node (SA node) generates an electrical signal that spreads through specific conducting pathways:
Internodal pathways and atrial fibers
Atrioventricular node (AV node)
Bundle of His
Right and left bundle branches
Purkinje fibers (Fig. 5.1)
Systole: the mechanical event of contraction of contractile cells upon the arrival of a depolarization signal.
Diastole: the mechanical event of relaxation of myocardial cells upon the arrival of a repolarization signal.
Electrical signals precede and cause the mechanical pumping action of the heart (Fig. 5.2).
The SA node initiates each electrical and mechanical cycle as the normal pacemaker.
SA node depolarization leads to atrial muscle contraction.
The AV node delays the electrical signal for approximately 0.20 seconds, allowing atrial contraction before relaying the signal to the ventricles.
The signal is then relayed to ventricles via the bundle of His, right and left bundle branches, and Purkinje fibers.
Purkinje fibers stimulate ventricular muscle contraction (ventricular systole).
Ventricles repolarize and enter diastole during ventricular systole (Fig. 5.2).
The autonomic nervous system modifies heart rate (beats per minute or BPM) and contraction strength through its sympathetic and parasympathetic divisions.
Sympathetic division:
Increases automaticity and excitability of the SA node, increasing heart rate.
Increases conductivity of electrical impulses through the atrioventricular conduction system.
Increases the force of atrioventricular contraction.
Sympathetic influence increases during inhalation.
Parasympathetic division:
Decreases automaticity and excitability of the SA node, decreasing heart rate.
Decreases conductivity of electrical impulses through the atrioventricular conduction system.
Decreases the force of atrioventricular contraction.
Parasympathetic influence increases during exhalation.
Echoes of depolarization and repolarization are detectable via electrodes placed on the body, producing an electrocardiogram (ECG).
The ECG allows inference of the heart’s mechanical activity.
Electrical activity varies through the ECG cycle (Fig. 5.2).
The ECG represents electrical events (depolarization and repolarization), while ventricular systole and diastole represent mechanical events (contraction and relaxation).
Electrical events happen quickly; mechanical events occur slowly.
Mechanical events follow the electrical events that initiate them.
Ventricular repolarization typically begins before the completion of ventricular systole in a resting Lead II ECG.
ECG changes can diagnose interruptions in electrical signal generation or transmission.
During exercise, heart position changes, complicating voltage standardization or quantification.
The ECG pattern includes an isoelectric line (baseline), a P wave, a QRS complex, and a T wave.
Intervals and segments are also components of the ECG (Fig. 5.2).
Isoelectric Line:
It's the baseline, indicating periods when no electrical activity is detected by the ECG electrodes.
Interval:
Time measurement including waves and/or complexes.
Segment:
Time measurement not including waves and/or complexes.
Table 5.1 lists components, what they represent, typical durations, and amplitudes.
P wave:
Represents depolarization of the right and left atria.
Duration: 0.07 – 0.18 seconds.
Amplitude: < 0.25 millivolts.
QRS complex:
Represents depolarization of the right and left ventricles.
Atrial repolarization is masked by the larger QRS complex.
Duration: 0.06 – 0.12 seconds.
Amplitude: 0.10 – 1.50 millivolts.
T wave:
Represents repolarization of the right and left ventricles.
Duration: 0.10 – 0.25 seconds.
Amplitude: < 0.5 millivolts.
P-R interval:
Time from onset of atrial depolarization to onset of ventricular depolarization.
0.12-0.20 seconds.
Q-T interval:
Time from the onset of ventricular depolarization to the end of ventricular repolarization, representing the refractory period of the ventricles.
0.32-0.36 seconds.
R-R interval:
Time between two successive ventricular depolarizations.
0.80 seconds.
P-R segment:
Time of impulse conduction from the AV node to the ventricular myocardium.
0.02 – 0.10 seconds.
S-T segment:
Period representing the early part of ventricular repolarization.
< 0.20 seconds.
T-P segment:
Time from the end of ventricular repolarization to the onset of atrial depolarization.
0.0 – 0.40 seconds.
Tabled values are from a typical Lead II setup (wrist and ankle electrode placement) with a subject heart rate of ~75 BPM and are influenced by heart rate and placement.
A lead is an arrangement of two electrodes (one positive, one negative) with respect to a third (ground) electrode.
Electrode positions are standardized for different leads.
This lesson records from Lead II: positive electrode on the left ankle, negative electrode on the right wrist, and ground electrode on the right ankle.
The QRS complex is the dominant ECG component in a normal standard lead record.
In Lead II, Q and S waves are typically small and negative, while the R wave is large and positive (Fig. 5.2).
Normal and abnormal factors influence QRS complex duration, form, rate, and rhythm.
Normal factors: body size (BSA), body fat distribution, heart size (ventricular mass), heart position, metabolic rate, etc.
In a person with a high diaphragm, the heart's apex shifts upward and to the left, altering the "electrical picture" and decreasing R wave positivity with increased S wave negativity.
Athletes with larger left ventricular mass may show similar Lead II QRS complex changes without cardiac disease.
An abnormal inverted QRS complex results when Lead II Q, R, and S wave amplitudes are all negative.
Abnormal factors include hyper- and hypothyroidism, ventricular hypertrophy, morbid obesity, essential hypertension, and other pathologic states.
Minor heart rate increases/decreases during the resting respiratory cycle reflect adjustments by baroreceptor reflexes to intrathoracic pressure changes (Fig. 5.4).
Inspiration:
Inspiratory muscles contract, reducing intrathoracic pressure, causing thoracic veins to expand slightly.
Venous pressure, venous return, cardiac output, and systemic arterial blood pressure drop.
The carotid sinus reflex causes a momentary increase in heart rate due to reduced baroreceptor firing.
Expiration:
Inspiratory muscles relax, and early resting expiration increases intrathoracic pressure, compressing thoracic veins.
Venous pressure and venous return increase momentarily, reflexively increasing heart rate.
Increased cardiac output and systemic arterial blood pressure increase carotid baroreceptor firing, causing heart rate to decrease.
Average resting heart rate for adults: 60-80 beats/min (70 bpm for males, 75 bpm for females).
Athletes may have slower heart rates (as low as 50 beats/min) due to larger, more efficient hearts (“left ventricular hypertrophy”).
Low heart rate and hypertrophy in sedentary individuals may indicate failing hearts.
ECGs use standardized grids (Fig. 5.4):
Smaller squares: 0.04 seconds on the x-axis.
Darker vertical lines: 0.2 seconds apart.
Lighter horizontal lines: 0.1 mV apart (amplitude).
Darker grid lines: 0.5 mV.