3 Cardiac cycle; arterial pressure regulation

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Cardiac cycle (draw)
1. Aortic pressure
2. Atrial pressure
3. Ventricular pressure
4. Ventricular volume
5. ECG
6. Phonocardiogram

In later FC: Each line separate a new phase. Termed A, B, C, D etc. Use ECG for reference

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. Preceded by the P-wave
2. Contributes to the last 20% of ventricular filling
3. Venous pressure is also increased due to the increase in atrial pressure (damming of small amounts of blood)
4. Filling of the ventricle by atrial systole may cause a heart sound: the fourth heart sound. It is not audible in normal adults

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. Begins after the onset of QRS wave
2. AV valve close due to the build up of pressure → First heart sound
3. Mitral valve closes slightly before tricuspid valve (the first heart sound may be split)
4. No blood leaves the ventricles in this phase because the aortic and pulmonary valve is closed

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. When ventricular pressure exceeds aortic pressure, aortic valve opens
2. Due to the pressure difference, blood flows into the arteries
3. Most of the stroke volume is ejected in the first part of this phase; and just small amounts in the last 1/3
4. Atrial filling begins
5. Ends just before T wave is complete

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. Repolarization is now completed (T-wave)
2. Aortic valve closes, followed by pulmonary valve: second heart sound (inspiration can cause a splitting of this sound)
3. AV valves remains closed during this phase
4. Ventricular pressure decreases

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. AV valves opens when the ventricular pressure have decreased enough
2. Aortic pressure continues to decrease because the blood is flowing away in the systemic circulation
3. Rapid flow of blood from the atria into the ventricles cause the third heart sound (which is normal in childen, but is associated with disease in adults)

Cardiac cycle:
A. Atrial systole
B. Isovolumetric ventricular contraction
C. Ventricular ejection
D. Isovolumetric ventricular relaxation
E. Rapid ventricular filling
F. Reduced ventricular filling

1. Is the longest phase: Diastasis
2. Ventricular filling continues in a slower rate
3. Time required for diastasis and ventricular filling depends on HR. Increase in HR decrease the time available for ventricular filling

Name the most important mechanisms for regulating arterial pressure (according to BRS)

1. Fast neurally mediated baroreceptor mechanism
2. Slower, hormonally regulated renin-angiotensin-aldosterone mechanism

Important mechanisms for regulating arterial pressure:
1. Fast neurally mediated baroreceptor mechanism (the negative feedback loop)
2. Slower, hormonally regulated renin-angiotensin-aldosterone mechanism

↓Pa → ↓Stretch on baroreceptors → ↓Firing rate of carotid sinus nerve (Hering's nerve). This leads to the vasomotor center and gives the following effects:
1. ↓Parasympathetic outflow → ↑HR
2. ↑Sympathetic out flow → ↑HR, ↑Contractility, ↑Constriction of arterioles, ↑Constriction of veins
All this mechanism leads to: ↓Unstressed volume; ↑Venous return; ↑Mean systemic pressure → ↑Pa

How to check the baroreceptor reflex

Valsalva maneuver
1. Expire against closed glottis increases the intrathoracic pressure which decreases venous return → ↓Pa
2. This should lead to an observable ↑HR

Important mechanisms for regulating arterial pressure:
1. Fast neurally mediated baroreceptor mechanism
2. Slower, hormonally regulated renin-angiotensin-aldosterone mechanism (the negative feedback loop)

↓Pa → ↓Renal perfusion pressure → ↑Renin from juxtaglomerular cells (enzyme) → ↑Angiotensinogen to angiotensin I → Angiotensin I by ACE to angioetensin II → ↑Angiotensin II has the following four effects:
1. Vasocontrictions leading to ↑TPR
2. ↑Thirst
3. ↑Na⁺/H⁺-exchange in proximal tubules → ↑Na⁺ reabsorption
4. ↑Aldosterone → ↑Na⁺ reabsorption in distal tubule (this reaction is slow but is the probably the most effective)
All these mechanisms leads to ↑Pa

Other regulation of arterial blood pressure (according to BRS)

1. Cerebral ischemia
2. Chemoreceptors in the carotid and aortic bodies
3. Vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)

Other regulation of arterial blood pressure
1. Cerebral ischemia
2. Chemoreceptors in the carotid and aortic bodies
3. Vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)

1. When the brain is ischemic, the partial pressure of CO₂ increases
2. This can elevate the arterial pressure tremendously
3. Cusing reaction (increased pulse pressure, decreased HR and irregular breathing) is an example of the response where CSF pressure compresses vessels in the brain which further leads to the ischemic response
4. It causes high excitation in the vasomotor center and thus, increased sympathetic outflow

Other regulation of arterial blood pressure
1. Cerebral ischemia
2. Chemoreceptors in the carotid and aortic bodies
3. Vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)

1. Very sensitive to decrease in pressure of pO₂
2. It is only significant when the arterial pressure is very low; but it can activate the vasomotor centers to produce vasoconstriction
3. ↑TPR → ↑Arterial pressure

Other regulation of arterial blood pressure
1. Cerebral ischemia
2. Chemoreceptors in the carotid and aortic bodies
3. Vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)

1. Is mostly involved in e.g. hemorrhage; but not in minute-to-minute regulation
2. Atrial receptors respond to decrease in blood pressure and cause release of vasopressin from posterior pituitary. It causes to effects:
A. Potent vasoconstrictor by activating V₁ receptors on the arterioles
B. Increases water reabsorption by the renal distal tubule and collecting ducts by activating the V₂ receptors

Other regulation of arterial blood pressure
1. Cerebral ischemia
2. Chemoreceptors in the carotid and aortic bodies
3. Vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)

1. Is relased from the atria in response to an increase in blood volume and atrial pressure
2. Causes:
A. relaxation of vascular smooth muscle
B. Increased excretion of Na⁺ and water
C. Inhibits renin secretion

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