Overview of Cardiac Physiology and Arrhythmias

Cardiac arrhythmia

Refers to abnormal rhythm due to defects in the heart's conduction system.

Heart sounds

Sounds produced by the heart during the cardiac cycle, often assessed during a physical examination.

Cardiac output

Volume of blood ejected from left (or right) ventricle into aorta (or pulmonary trunk) each minute.

Stroke volume

The amount of blood ejected per beat from each ventricle.

Regulation of heart rate

The mechanisms that control the speed of the heartbeat.

Premature beats

Most common arrhythmia, usually harmless, often caused by exercise, stress, caffeine, nicotine, alcohol or other drugs.

Atrial fibrillation (AF or A fib)

Most common problematic arrhythmia affecting about 1% of Americans, characterized by misfiring of the SA node.

Bradycardia

A slowed heartbeat defined as under 60 bpm, considered normal unless accompanied by fatigue, dizziness, lightheadedness or fainting.

Tachycardia

A rapid heartbeat defined as more than 100 bpm in adults, felt as palpitations or noticeable rapid heart action.

Ventricular arrhythmias

The most severe and life-threatening arrhythmias, including ventricular tachycardia and ventricular fibrillation.

Ventricular tachycardia (V tach)

A rapid heartbeat arising in the ventricles that can lead to ventricular fibrillation.

Ventricular fibrillation

Occurs when the ventricles go out of control, quivering and beating ineffectively, stopping the pumping action.

Defibrillation

The process of delivering an electric shock to restore a normal heart rhythm.

Cardiac output formula

CO = stroke volume (SV) x heart rate (HR).

Resting cardiac output range

Between 4.8 and 6.4 L per min.

Stroke volume formula

Stroke volume = EDV - ESV.

End-diastolic volume (EDV)

The maximal amount of blood that the ventricle can hold just prior to ventricular contraction.

End stroke volume (ESV)

The amount of blood remaining in the ventricle after contraction (systole).

Example of stroke volume calculation

For a 70 kg male: EDV about 120 ml, ESV about 50 ml, Stroke volume = 120 ml - 50 ml = 70 ml.

Heart palpitations

The sensation of feeling the heart skip a beat, have a double beat, or an especially strong beat.

Standard estimate

1 ml/1kg body weight

Average resting HR

About 75 beats per min

Cardiac Output (CO)

CO = 70 ml x 75 bpm = 5250 ml/min or 5.25 L/min

Total blood volume of a 70 kg male

~ 5 L

Regulation of stroke volume

Three factors regulate stroke volume and ensure left and right ventricles pump equal volumes of blood

Factors that alter stroke volume (SV)

1. Preload 2. Contractility 3. Afterload

Preload

Degree of stretch on the heart before it contracts

Frank-Starling law

The more the heart fills with blood during diastole, the greater the force of contraction during systole

End Diastolic Volume (EDV)

Determined by 1. Duration of ventricular diastole 2. Venous return - volume of blood returning to right ventricle

Contractility

Strength of contraction

Positive inotropic agents

Increase contractility, often promote Ca2+ inflow during cardiac action potential

Negative inotropic agents

Decrease contractility, examples include very low blood oxygen levels, high or low pH, some anesthetics, beta blockers

Afterload

Pressure that must be overcome before a semilunar valve can open

Effect of increased afterload

Causes stroke volume to decrease; blood remains in ventricle at the end of systole

Factors increasing afterload

Hypertension, atherosclerosis, aortic narrowing, or physical pressure on the aorta

Regulation of Heart Rate

Cardiac output depends on heart rate and stroke volume

Heart rate adjustments

Largely controlled by direct innervation of the autonomic nervous system (ANS), hormones (especially epinephrine and norepinephrine), and cations

Influence of ANS

The sympathetic and parasympathetic divisions of the ANS can modify timing and/or strength of each heartbeat

Autonomic HR regulation

Originates in cardiovascular center of medulla, receives input from a variety of sensory receptors

Types of receptors influencing HR

Proprioceptors, Baroreceptors, Chemoreceptors

Sympathetic HR regulation

Sympathetic neurons called cardiac accelerator nerves extend to heart, triggering release of norepinephrine (NE)

Effects of norepinephrine (NE)

1. In autorhythmic fibers speeds rate of spontaneous depolarization 2. In contractile fibers enhances Ca2+ entry increasing contractility

Parasympathetic HR regulation

Parasympathetic impulses reach heart via the vagus nerve, triggering release of acetylcholine (ACh)

Effect of acetylcholine (ACh)

Decreases heart rate by slowing rate of spontaneous depolarization

Checkpoint Questions

1. Which type of heart arrhythmia is most life-threatening? 2. Which heart arrhythmia is best treated with an artificial pacemaker? 3. What does it mean if a physician states that a patient is 'tachy'? 4. What is the formula to calculate stroke volume (SV)? 5. What is the relationship between cardiac output (CO) and SV? 6. Given an EDV of 130ml, an ESV of 75ml, and a HR of 72bpm, calculate CO. Is the CO in the average range? 7. Consider preload, contractility, and afterload. An increase in which parameter decreases CO? 8. In general, would you expect the sympathetic division of the ANS to increase or decrease HR?