Cardiovascular
Part 1
What are the electrical and mechanical events of the cardiac cycle?
Electrical
Atrial depolarization
Atrial repolarization
Ventricular depolarization
Ventricular repolarization
Mechanical
Atrial diastole
Atrial systole
Ventricular diastole
Ventricular systole
How does the electrical depolarization and repolarization propagate through the heart muscle?
SA node
Internodal pathways
AV node
AV bundle
Bundle branches
Purkinje fibers
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.
What is a normal ECG from lead I? Label it including all waves, segments and intervals.
Lead 1
Downwards deflection = Flow towards negative electrode (right arm)
Upwards deflection = Flow towards positive electrode (left arm)
Waves
P-wave = Atrial depolarization
QRS complex = Ventricular depolarization
T-wave = Ventricular repolarization
Segments
PR segment = End of atrial depolarization to start of ventricular depolarization
ST segment = End of ventricular depolarization to start of ventricular repolarization
Intervals
PR interval = Start of atrial depolarization to start of ventricular depolarization
QT interval = Start of ventricular depolarization to end of ventricular repolarization
Use the four steps from figure 14.15 to identify arrhythmias. Bradycardia, tachycardia, Atrial and ventricular Fibrillations, ST segment Elevations and depressions, AV blocks
Bradycardia - Slow heart rate
Delay in SA node depolarization.
Tachycardia - Fast heart rate
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.
Part 2
What are the risk factors and health implications of heart disease.
Modifiable
Smoking, alcohol consumption, diet, weight, activity levels
Non-modifiable
Age, sex, gender, ethnicity/heritage, genetics, diabetes
How do we measure and monitor blood pressure as an indication of CVD and arteriosclerosis?
Systolic pressure over diastolic pressure.
How does arteriosclerosis develop?
The formation of plaques from cholesterol in the arteries. Can be stable plaques or vulnerable plaques.
What are Baroreceptors and how do they maintain blood pressure at rest? Specifically, what are the afferent and efferent responses to changes in MAP?
Stretch receptors in the aorta and carotid artery.
Increased pressure = Increased firing rate of baroreceptors
Decreased pressure = Decreased firing rate of baroreceptors
Afferent = Vasoconstriction and vasodilation of blood vessels to change resistance?
Efferent = Increase or decrease in stroke volume and heart rate to change cardiac output?
What impact does chronically elevated BP have on baroreceptors?
Desensitizes them.
Resets their set point.
Damaged blood vessels.
Part 3
What are the primary cardiovascular responses to the onset and increased intensity of exercise Q, BP, HR, SV, TPR
Cardiac output - Increases
Blood pressure - Increases
Heart rate - Increases
Stroke volume - Increases then plateaus
Total peripheral resistance - Decreases
What variables consistent increase or decrease from rest to maximal aerobic intensity of exercise? What is the SV response?
Cardiac output - Increases.
Blood pressure - Increases.
Heart rate - Increases.
Stroke volume - Increases then plateaus.
Total peripheral resistance - Decreases.
How are preload, afterload and contractility enhanced during exercise?
Preload
Initial stretching of cardiac muscle prior to contraction.
Increases with exercise - Greater filling, higher end diastolic volume.
Afterload
Amount of pressure the heart needs to exert to eject blood during ventricular contraction.
Decreases during exercise - More emptying, lower end systolic volume.
Contractility
Ability of the heart to eject a stroke volume at a given preload and afterload.
Increases with exercise - Higher pressure, more emptying.
How can BP rise above the resting range during exercise?
Cardiac output increases which directly affects mean arterial pressure raising blood pressure along with the decrease in resistance from the vasodilation of blood vessels.
What are volume and pressor loads?
Volume load
The volume of blood that the heart has to pump.
Pressor load
Factors influencing resistance and blood pressure.
Pressor reflex - Raises baseline blood pressure during exercise. Up and to the right.
Differentiate between concentric and eccentric hypertrophy?
Eccentric
Cavity size increases because of increased preload
Concentric
Wall thickness increases because of increased afterload.
What is physiological hypertrophy and how do different modes of exercise impact its effect?
Reversible.
Increased pressure with exercise.
Adaptive remodelling.
Thickening of the myocardium in proportion to expansion of cavity.
What is pathological hypertrophy?
Non reversible.
Impaired contractile function.
Maladaptive remodelling.
Lengthening of individual cardiomyocytes.
Longer and weaker cells.
How are athletes screened for cardiac abnormalities?
Using an ECG increases the ability to detect underlying cardiovascular conditions, but it has its limitations.