6 - Cardiovascular system (Part 2 - Cardiac cycle) Flashcards
What are the main mechanical events of the cardiac cycle?
Cardiac cycle: Alternative periods of systole (contraction, emptying) and diastole (relaxation, filling) in ventricles
(atria goes through separate systole and diastole cycle)
- Contraction is caused by spread of excitation across the heart
- Relaxation follows the repolarization of the cardiac muscles
Does excitation and contraction happen in the atrium or ventricles first?
Atrial contraction must be completed first
Atrial contraction completes 20% of ventricular filling
What are the stages of the cardiac cycle?
A. Passive filling during ventricular and atrial diastole
B. Late-End of ventricular diastole, Atrial Contraction
C. Ventricular Excitation and Systole, Isovolumetric ventricular contraction
D. Vesicular Ejection
E. Isovolumetric ventricular relaxation
(Look at notes for more details)
What is the equation for the volume of blood pumped by one ventricle in a given period of time (cardiac output)?
CO = HR x SV
HR: heart rate (beat/min)
SV: stroke volume (ml/beat)
CO: Cardiac output (ml/min)
CO is same for both ventricles and same in pulmonary and systemic circulation
An imprtant factor in finding CO is left ventricular end diastolic volume (EDV)
Why is the SA node the pacemaker of the heart?
Because it has the fastest spontaneous rate of depolarization to threshold
When SA reaches a threshold, action potential is initiated and causes heart to contract
How do the sympathetic NS and parasympathetic NS affect HR?
Sympathetic stimulation speeds up HR (epinephrine)
Parasympathetic NS slows down HR (vagus nerve)
What are the three effects of parasympathetic stimulation on the heart?
- Decreases the heart rate
- Acetylcholine (Ach) release increases the permeability of the SA node to K by slowing the closure of K channels
- Action potentials rate are reduced by:
- More K permeability hyperpolarizes the SA node membrane and the inside becomes negative. THis makes it take longer to reach threshold
- Decreases the exitability of the AV node
- Weakens atrial contraction
What are the four effects of the sympathetic stimulation on the heart?
- Increases the heart rate
- stimulates SA node to speed up depolarization so threshold reached faster
- norepinephrine is released, decreasing K+ permeability, so fewer K+ leaving, inside of cell becomes less negative, creates polarizing effect
- Increases conduction velocity
- stimulates the AV node and reduces the AV node delay by speeding up conduction velocity, thru enhancement of the slow inward Ca2+
- Speeds up the spread of the action potential
- (within conduction pathway, bundle of His and Purkinje cells)
- Increases contractile strength
- increased Ca2+ permerability
What types of controls influence stroke volume?
- Intrinsic control: extent of venous return
2. Extrinsic control: extent of sympathetic stimulation
What does the intrinsic control of stroke volume depend on?
Depends on:
- the direct correlation between end-diastolic volume and stroke volume - length-tension relationship of cardiac muscle
- Follows the “Frank-Starling Law of the Heart”
What is the Frank-Starling Law?
- Describes the relationship intrinsic relationship between end diastolic blood volume (EDV) and stroke volume.
- The muscle fibre length is mainly determined by the degree of diastolic filling
higher stroke volume == higher force
higher ventricular end-diastolic volume == Higher stretch
-> SV is proportional to EDV
What are the advantages of the cardiac length-tension relationship?
- Equalizes output between the right and left sides of the heart (blood pumped out by the heart is equally distributed between the pulmonary and systemic circulation)
- If large cardiac output is needed, venous return can be increased through action of the sympathetic nervous system (ex: during exercise, increase in EDV increases SV)
Use this image to help explain the control of cardiac output
How do the extrinsic controls control SV?
- Most important extrinsic controls are the cardiac sympathetic nerves and epinephrine
- Sympathetic stimulation and epinephrine enhance the heart’s contractility and ejection fraction
- Sympathetic stimulation of the heart increases the force of contraction, leading to more complete ejection of the EDV
Describe relationship between sympathetic stimulation and SV
Sympathetic stimulation:
- increases contractibility due to increased CA2+ influx triggered by norepinephrine and epinephrine
- extra cytosolic Ca2+ lets the myocardial fibres generate more force through greater cross-bridge cycling
- Shifts the Frank-starling curve to the left.
(more force for less stretch)
How does sympathetic stimulation increase SV?
- Strengthening cardiac contractility
- Enhancing venous return
- Caused vasoconsrtiction of the veins, which squeezes more blood forward from the veins to the heart, increasing the EDV and therefore SV (according to Frank Starling law)
What three aspects are affected by venous return?
- Contraction or compression of veins returning blood to the heart
- Pressure changes in the abdomen and thorax during breathing
- Sympathetic innervation of veins
-> EDV is determined venous return
What causes heart failure?
- Inability of the cardiac output to keep pace with the body’s demands for supplies and removal of wastes
- Main defect: weakened cardiac muscle
- Decompensated heart failure: point at which heart can no longer pump out a normal stroke volume despite compensatory measures
- Congested heart failure: blood cannot enter and be pumped out and venous system dams up
What is Atherosclerotic Coronary Artery Disease (CAD)?
- Pathological changes within coronary artery walls that diminish blood flow through the vessels (blood supply to the heart)
- Leading cause of death in Canada
- Can cause myocardial ischemia and possibly lead to acute myocardial infarction
- Happens through 3 mechanisms:
1. Profound vascular spasm of coronary arteries
2. Formation of atherosclerotic plaques
3. Thromboembolism
