Cardiovascular

Electrical Events of the Cardiac Cycle

Atrial and ventricular depolarization and repolarization.

Mechanical Events of the Cardiac Cycle

Atrial and ventricular diastole and systole.

Propagation of Electrical Signals in the Heart

SA node → Internodal pathways → AV node → AV bundle → Bundle branches → Purkinje fibers

P-wave

Atrial depolarization.

QRS complex

Ventricular depolarization.

T-wave

Ventricular repolarization.

PR interval

Start of atrial depolarization to start of ventricular depolarization.

QT interval

Start of ventricular depolarization to end of ventricular repolarization.

PR segment

End of atrial depolarization to start of ventricular depolarization.

ST segment

End of ventricular depolarization to start of ventricular repolarization.

Bradycardia

Delay in SA node depolarization.

Tachycardia

Rapid firing of SA node.

Atrial fibrillation

• Abnormal impulses from SA node.

• Disorganized conduction through inter-nodal pathways.

Ventricular fibrillation

Disorganized electrical impulses through ventricles.

ST elevation and depression

Abnormal ventricular depolarization and repolarization.

AV blocks

Delay in AV node depolarization.

Risk Factors of Heart Disease

• Modifiable (smoking, weight, activity levels, alcohol consumption, diet)

• Non-modifiable (age, genetics, ethnicity, gender, diseases)

Blood Pressure Measurement

Systolic over diastolic pressure as an indicator of CVD and arteriosclerosis.

Arteriosclerosis Development

Formation of stable or vulnerable plaques from cholesterol in arteries.

Baroreceptors Function

Afferent and efferent responses to changes in mean arterial pressure (MAP).

Baroreceptor response to increased blood pressure

• Increased firing rate of baroreceptors.

• Decreased release of norepinephrine.

• Alpha receptors vasodilate blood vessels.

• Peripheral resistance decreased.

• Beta cells decrease force of contraction and heart rate.

• Cardiac output decreases.

Baroreceptor response to decreased blood pressure

• Decreased firing rate of baroreceptors.

• Increased release of norepinephrine.

• Alpha receptors vasoconstrict blood vessels.

• Peripheral resistance increases.

• Beta receptors increase force of contraction and heart rate.

• Cardiac output increases.

Impact of Elevated BP on Baroreceptors

• Desensitization.

• Set point resetting.

• Damage to blood vessels.

Electrical signaling

• SA node depolarizes.

• Electrical impulse travels rapidly through inter-nodal pathways.

• AV node depolarizes.

• Depolarization moves through ventricles to apex.

• Depolarization spreads upwards from apex.

Cardiovascular response to exercise

• Cardiac output - Increases

• Blood pressure - Increases

• Heart rate - Increases

• Stroke volume - Increases then plateaus

• Total peripheral resistance - Decreases

Preload

• Initial stretching of cardiac muscle prior to contraction.

• Increases with exercise - Greater filling, higher end diastolic volume.

• “Stretch to empty”

Afterload

• Amount of pressure the heart needs to exert to eject blood during ventricular contraction.

• Decreases during exercise - More emptying, lower end systolic volume.

• “Back pressure”

Contractility

• Ability of the heart to eject a stroke volume at a given preload and afterload.

• Increases with exercise - Higher pressure, more emptying.

• “Systolic punch”

Volume load

The volume of blood that the heart has to pump.

Pressor load and reflex

• Factors influencing resistance and blood pressure.

• Raises baseline blood pressure during exercise. Up and to the right on graph.

Concentric hypertrophy

• Wall thickness increases because of increased afterload.

• Anaerobic.

Eccentric hypertrophy

• Cavity size increases because of increased preload.

• Aerobic.

Physiological hypertrophy

• Reversible.

• Increased pressure with exercise.

• Adaptive remodelling.

• Thickening of the myocardium in proportion to expansion of cavity.

Pathological hypertrophy

• Non reversible.

• Impaired contractile function.

• Maladaptive remodelling.

• Lengthening of individual cardiomyocytes.

• Longer and weaker cells.