Uh, see, I have my university exams, like, uh, you know, just a few days, and I haven't studied physiology at all the whole first year. So now I have to study. So I'm going to give you some topics, like, accordingly, and you explain it to me very, very nicely, okay? So that I can understand also, and I can write it in such length that, uh, I get rewarded good marks for them. Okay. So for LAQ, like LAQ, accordingly, you should know the length. So for LAQ, we have to write a lot. So, uh, for LAQ topics, we have cardiac cycle, coronary circulation, blood pressure, circulatory shock, ECG, and, um, mean arterial pressure, like define, enumerate mechanisms regulating, especially the baroreceptor mechanism. Uh, yeah, that's-- And cardiac output. Cardiac output also. Like, everything. Explain everything.

Reading File

I get it - first year physiology, exam in a few days, and you've got a stack of Long Answer Questions to prep. Let's be smart about this rather than trying to cram everything at once, because each of these LAQs deserves proper depth if you want full marks (and cramming all of them shallowly in one go won't help you write a good 8-10 mark answer).

Here's the map of what you've listed:

Cardiac Cycle - phases (systole/diastole), pressure-volume changes, heart sounds, Wiggers diagram
Coronary Circulation - anatomy, phasic flow changes, regulation, coronary reserve
Cardiac Output - definition, normal value, Fick principle, factors regulating (preload, afterload, contractility, heart rate), measurement methods
Mean Arterial Pressure (MAP) - definition, determinants, and full regulation: baroreceptor reflex (short-term), plus chemoreceptors, CNS ischemic response, renal/hormonal (long-term - RAAS, ANP)
Blood Pressure - definition, normal values, short-term vs long-term regulation mechanisms
ECG - genesis, waves (P-QRS-T), intervals, leads, normal values, clinical correlation
Circulatory Shock - definition, types (hypovolemic, cardiogenic, septic, anaphylactic, neurogenic), stages, compensatory mechanisms, decompensation

Quick overview: these topics are all interlinked - they're basically the entire cardiovascular physiology "core." Cardiac cycle explains the mechanical events, ECG explains the electrical events behind it, cardiac output and coronary circulation deal with pump function and its own blood supply, and BP/MAP/baroreceptors/shock deal with how the body regulates and can fail to regulate perfusion pressure. Many university exams (especially MAP + baroreceptor, and shock) reuse content, so once we do 2-3 of these deeply, the rest go faster.

Asking for Preferences

Which LAQ topic should we do first, in full exam-writing depth?

Here's the map of what you've listed:

Cardiac Cycle - phases (systole/diastole), pressure-volume changes, heart sounds, Wiggers diagram
Coronary Circulation - anatomy, phasic flow changes, regulation, coronary reserve
Cardiac Output - definition, normal value, Fick principle, factors regulating (preload, afterload, contractility, heart rate), measurement methods
Mean Arterial Pressure (MAP) - definition, determinants, and full regulation: baroreceptor reflex (short-term), plus chemoreceptors, CNS ischemic response, renal/hormonal (long-term - RAAS, ANP)
Blood Pressure - definition, normal values, short-term vs long-term regulation mechanisms
ECG - genesis, waves (P-QRS-T), intervals, leads, normal values, clinical correlation
Circulatory Shock - definition, types (hypovolemic, cardiogenic, septic, anaphylactic, neurogenic), stages, compensatory mechanisms, decompensation

Since you want each one explained "very nicely" and at LAQ-length, let's tackle them one at a time so each answer is genuinely exam-ready (diagrams described, mnemonics, structured with definition-classification-mechanism-clinical correlation) rather than rushed.It looks like my question got interrupted. No worries - since you specifically called out "especially the baroreceptor mechanism" under MAP, let's start there since it's clearly a priority for you. I'll go deep on Mean Arterial Pressure and its regulation (with full baroreceptor mechanism) now, and we can move to Cardiac Output, Cardiac Cycle, Coronary Circulation, ECG, and Shock one by one after.

Finding Sources

Reading File

Good, I've got solid material from Guyton & Hall and Costanzo Physiology. Here's your full LAQ-ready answer.

MEAN ARTERIAL PRESSURE (MAP) - Definition, Regulation, and Baroreceptor Mechanism

1. Definition

Mean Arterial Pressure (MAP) is the average pressure exerted by blood on the walls of arteries throughout the entire cardiac cycle (systole + diastole). It is NOT the simple arithmetic mean of systolic and diastolic pressure, because diastole lasts longer than systole (roughly 2/3 of the cardiac cycle is diastole at resting heart rate).

Formula:

MAP = Diastolic BP + 1/3 (Systolic BP - Diastolic BP)

or equivalently the commonly used clinical formula:

MAP = [SBP + (2 x DBP)] / 3

Worked example (write this in your answer - examiners love a solved example): For BP = 120/80 mmHg, MAP = [120 + (2x80)]/3 = 280/3 = 93.3 mmHg

Normal value: 70-100 mmHg (approximately 93 mmHg at BP 120/80).

MAP is physiologically important because it represents the effective perfusion pressure driving blood to the tissues/organs. A MAP below ~60 mmHg is usually insufficient to perfuse vital organs (brain, kidney, heart) adequately - this is why MAP, not systolic pressure, is monitored in critically ill/shock patients.

Determinants of MAP (write this before regulation, examiners want the physiological basis):

MAP = Cardiac Output (CO) x Total Peripheral Resistance (TPR)

Since CO = Heart Rate x Stroke Volume, ultimately: MAP is determined by Heart Rate, Stroke Volume, and Total Peripheral Resistance - so any mechanism regulating MAP must act by changing one or more of these three variables.

2. Enumeration of Mechanisms Regulating Arterial Pressure

Regulatory mechanisms are classically divided by speed of action:

A. Rapidly acting (seconds) - Nervous mechanisms

Baroreceptor reflex (carotid sinus and aortic arch) - fastest, most important short-term regulator
Chemoreceptor reflex (carotid and aortic bodies) - responds mainly to hypoxia, also to fall in BP below ~80 mmHg
CNS ischemic response - activated only when brain blood flow falls severely (BP < 40-50 mmHg); causes massive sympathetic discharge ("last-ditch stand" mechanism)
Atrial and pulmonary artery reflexes (low pressure receptors/volume receptors) - respond to blood volume changes, trigger reflex tachycardia and affect ADH/renal function

B. Intermediate acting (minutes)

Renin-Angiotensin-Aldosterone System (RAAS) - angiotensin II causes vasoconstriction (minutes) and later aldosterone-mediated Na+/water retention (hours)
Stress-relaxation of vasculature - vessels adjust their tone when overstretched or underfilled
Capillary fluid shift mechanism - fluid moves between plasma and interstitium to correct blood volume

C. Long-term (hours to days) - the most powerful for chronic control

Renal-body fluid (pressure diuresis/natriuresis) mechanism - Guyton's cornerstone concept: rising arterial pressure increases renal excretion of salt and water, reducing blood volume and bringing pressure back down. This is considered the dominant long-term controller of MAP.
Antidiuretic hormone (ADH/vasopressin) - water retention, mild vasoconstriction
Atrial natriuretic peptide (ANP) - released from stretched atria, promotes natriuresis and vasodilation, opposes RAAS

Exam tip: If asked to "enumerate," write all of these as a list first, then go into detail on baroreceptors (since that's explicitly asked).

3. The Baroreceptor Mechanism (Baroreceptor Reflex) - Detailed

This is the most important rapid-acting reflex mechanism for moment-to-moment control of arterial pressure and is a favorite LAQ/SAQ across universities.

Definition

The baroreceptor reflex is a negative feedback neural reflex that buffers acute changes in arterial pressure by reflexively adjusting cardiac output and total peripheral resistance through the autonomic nervous system.

A. Receptors (Baroreceptors)

Type: Spray-type / stretch receptors (mechanoreceptors) - NOT stimulated by pressure itself, but by the stretch/distension of the vessel wall that pressure produces.
Location:
1. Carotid sinus - slight dilatation of the internal carotid artery just above the bifurcation of the common carotid artery
2. Aortic arch
Carotid sinus baroreceptors respond to both rise AND fall in pressure; aortic arch baroreceptors are more sensitive to rises in pressure.

B. Afferent Pathway

From carotid sinus -> Hering's nerve -> glossopharyngeal nerve (CN IX) -> Nucleus Tractus Solitarius (NTS) in the medulla
From aortic arch -> vagus nerve (CN X) -> same NTS in medulla

C. Center

Nucleus Tractus Solitarius (NTS) in the medulla receives and integrates the afferent signal, then connects to:
- Vasomotor/vasoconstrictor center (excitatory, in rostral ventrolateral medulla)
- Cardioinhibitory (vagal) center (nucleus ambiguus/dorsal motor nucleus of vagus)

D. Efferent Pathway

Sympathetic fibers -> heart (SA node, myocardium) and blood vessels (arterioles, veins)
Parasympathetic (vagal) fibers -> SA node of the heart

E. Mechanism of Action - Response to a RISE in Arterial Pressure

Increased arterial pressure -> increased stretch of carotid sinus/aortic arch walls
Increased firing rate of baroreceptor afferents -> NTS
NTS response: increases parasympathetic (vagal) outflow to heart AND inhibits sympathetic outflow to heart and vessels
Effects (all act to bring pressure back DOWN toward normal):
- Decreased heart rate (negative chronotropic, vagal)
- Decreased contractility -> decreased stroke volume -> decreased CO
- Vasodilation of arterioles -> decreased TPR
- Venodilation -> decreased venous return

F. Response to a FALL in Arterial Pressure (e.g., hemorrhage) - reverse pattern

Decreased stretch -> decreased baroreceptor firing -> decreased vagal outflow + increased sympathetic outflow, producing 4 compensatory changes (this table is high-yield, write it in exam):

Parameter	Response to fall in MAP
Heart rate	Increased
Contractility	Increased
Total Peripheral Resistance	Increased (arteriolar constriction, sparing brain & heart)
Venous tone (unstressed volume)	Decreased -> increased venous return, increased stressed volume
Net effect	Cardiac output and TPR both rise -> MAP restored toward normal

G. Response Characteristics (important for LAQ marks)

Operating range: Carotid sinus baroreceptors are silent below ~50-60 mmHg, respond progressively up to about 180 mmHg
Maximal sensitivity is at the normal operating point around 100 mmHg - i.e., the reflex is most sensitive exactly where it is needed most (a small change in pressure around normal produces a large change in reflex signal)
Rate sensitivity: Baroreceptors respond more strongly to a rapidly changing pressure than to a sustained/stationary pressure at the same value
Adaptation/Resetting: Baroreceptors adapt within 1-2 days to a sustained change in pressure (e.g., in chronic hypertension, the set-point resets to the new higher pressure). This is why the baroreceptor reflex is considered important only for short-term, not long-term, BP control - a key point examiners specifically test.

H. Physiological Significance

Buffers transient changes in BP during postural change (e.g., standing up), exercise, and Valsalva maneuver
Central compensatory mechanism in hemorrhage and shock (this links directly to your Circulatory Shock topic - same reflex, different context)
Clinically relevant in carotid sinus massage/hypersensitivity, carotid sinus syncope, and baroreceptor stimulation devices used in resistant hypertension

Here is the classic diagram to draw in your answer (draw this - examiners give marks for correctly labeled diagrams):

Baroreceptor system for controlling arterial pressure - showing carotid sinus, aortic arch baroreceptors, Hering's nerve, glossopharyngeal and vagus nerves, and medullary centers

(Guyton & Hall, Fig. 18.5 - Baroreceptor system for controlling arterial pressure)

How to structure this for full LAQ marks

Define MAP + formula + normal value (2 marks)
Enumerate all regulatory mechanisms, short vs long term (2-3 marks)
Detailed baroreceptor mechanism: receptors -> afferents -> center -> efferents -> effects, with labeled diagram (6-8 marks - this is where most marks are)
Special properties: operating range, rate sensitivity, resetting (2 marks)
One line on clinical/physiological significance (1 mark)

Source: Guyton and Hall Textbook of Medical Physiology, Ch. 18 (Nervous Regulation of Circulation) and Costanzo Physiology 7th Edition, Ch. 4 (Cardiovascular Physiology).

That's MAP + baroreceptor mechanism done in full LAQ depth. Next, tell me which one you want: Cardiac Output, Cardiac Cycle, Coronary Circulation, ECG, or Circulatory Shock - and we'll do the same treatment.

The next topic that I'd like to do is the cardiac cycle.

Finding Sources

Reading File

Searching Images

Wiggers diagram cardiac cycle pressure volume ECG heart sounds

THE CARDIAC CYCLE

1. Definition

The cardiac cycle refers to the sequence of mechanical and electrical events that occur from the beginning of one heartbeat to the beginning of the next. Each cycle consists of a period of contraction (systole) and a period of relaxation (diastole) of the atria and ventricles, during which pressure and volume changes cause the cardiac valves to open and close in an orderly sequence, producing unidirectional blood flow.

Duration: The total duration of one cardiac cycle = 60/heart rate (seconds). At a normal heart rate of 72 beats/min: cycle duration = 60/72 = 0.8 second. Of this, roughly systole = 0.3 sec and diastole = 0.5 sec at rest - diastole is longer, which is why increases in heart rate shorten diastole (filling time) proportionally more than systole. This is an important point to mention: at 3x normal heart rate, systole occupies 65% of the cycle instead of 40%, so tachycardia compromises ventricular filling.

Initiation: Each cycle begins with spontaneous depolarization at the SA node, spreading through the atria, then delayed at the AV node (~0.1 sec), allowing atria to contract and act as "primer pumps" before the ventricles (the main pumping chambers) contract.

2. The Seven Phases of the Cardiac Cycle (correlate with Wiggers diagram)

Draw a Wiggers diagram in your answer with 5 stacked tracings: ECG, aortic pressure, left ventricular pressure, left atrial pressure, LV volume, and heart sounds - all plotted against time on the same x-axis. This single diagram, correctly labeled, usually carries the bulk of the marks.

Phase A: Atrial Systole

Triggered by the P wave (atrial depolarization) + PR interval
Left atrium contracts, atrial pressure rises slightly, pushes final ~20-30% of blood into the already-filling ventricle (atrial kick)
Mitral valve is open; aortic valve closed
Produces the a wave of the venous/atrial pressure pulse
S4 (fourth heart sound) may coincide here - not normally audible in healthy adults, heard in reduced ventricular compliance (e.g., ventricular hypertrophy)

Phase B: Isovolumetric Ventricular Contraction

Begins with the QRS complex (ventricular depolarization)
Ventricular pressure rises steeply, exceeds atrial pressure -> mitral valve closes
Ventricular pressure is still less than aortic pressure, so the aortic valve remains closed too
All 4 valves closed -> volume is constant while pressure rises rapidly (hence "isovolumetric" / isovolumic)
Mitral valve closure produces the first heart sound (S1) - "lub"

Phase C: Rapid Ventricular Ejection

ST segment on ECG
Ventricular pressure exceeds aortic pressure -> aortic valve opens
Blood ejected rapidly into the aorta; ventricular volume falls sharply
Both ventricular and aortic pressures rise together and reach their peak/maximum in this phase
No heart sound normally audible here (silent phase)

Phase D: Reduced Ventricular Ejection

Coincides with the T wave (ventricular repolarization)
Ejection continues but at a slower rate
Ventricular volume reaches its minimum (= end-systolic volume, ~50 mL)
Aortic pressure begins to fall as blood runs off into the peripheral arterial tree faster than it's being added
Ventricular pressure actually falls slightly below aortic pressure toward the end, but forward momentum keeps blood flowing briefly

Phase E: Isovolumetric Ventricular Relaxation

Ventricle relaxes, pressure falls rapidly
Once ventricular pressure drops below aortic pressure -> aortic valve closes
This closure produces the second heart sound (S2) - "dub" - and produces the characteristic small notch on the aortic pressure curve called the incisura (dicrotic notch)
Mitral valve still closed (LV pressure still above LA pressure momentarily) -> again all 4 valves closed, volume constant while pressure falls steeply

Phase F: Rapid Ventricular Filling

Ventricular pressure falls below atrial pressure -> mitral valve opens
Blood that has been accumulating in the atria (venous return) rushes rapidly into the relaxed ventricle
Ventricular volume rises quickly; pressure stays low
May produce a third heart sound (S3) in this phase if audible - physiological in children/young adults, pathological (suggests volume overload/heart failure) in older adults

Phase G: Reduced Ventricular Filling (Diastasis)

The longest but "quietest" phase - passive filling slows down as ventricular and atrial pressures equalize
Ventricle continues to fill slowly until the next P wave initiates atrial systole again, closing the loop

(Note: some textbooks combine/number these as 5 phases - isovolumic contraction, ejection, isovolumic relaxation, rapid filling, diastasis, plus atrial systole - the content is identical; use whichever numbering your course follows, but include all the events above.)

3. Summary Table (write this - high yield for marks)

Phase	Ventricular volume	Valves	ECG event	Heart sound
Atrial systole	Slight increase	Mitral open, Aortic closed	P wave	S4 (if present)
Isovolumetric contraction	Constant	All closed	QRS	S1
Rapid ejection	Decreases sharply	Aortic open	ST segment	-
Reduced ejection	Decreases (to minimum)	Aortic open	T wave	-
Isovolumetric relaxation	Constant	All closed	-	S2
Rapid filling	Increases sharply	Mitral open	-	S3 (if present)
Diastasis	Increases slowly	Mitral open	-	-

4. Pressure and Volume Values to Quote

Left ventricular pressure: rises from ~0-8 mmHg (diastole) to ~120 mmHg (peak systole)
Aortic pressure: oscillates between ~80 mmHg (diastolic) and ~120 mmHg (systolic)
Left atrial pressure: low throughout, ~2-10 mmHg, with three small waves: a wave (atrial contraction), c wave (bulging of AV valve into atrium during isovolumic contraction/early ventricular contraction), and v wave (atrial filling against closed mitral valve)
End-diastolic volume (EDV): ~110-120 mL
End-systolic volume (ESV): ~50 mL
Stroke volume (EDV - ESV): ~70 mL
Ejection fraction (SV/EDV): ~60-65% normally - this links directly into your Cardiac Output topic

5. Heart Sounds (mechanism - a common sub-question)

S1 ("lub"): closure of mitral and tricuspid (AV) valves at start of systole; caused by vibration of the tensed valve leaflets and chordae tendineae when back-surging blood abruptly stops them; duration ~0.14 sec, lower pitch (AV valves less taut)
S2 ("dub"): closure of aortic and pulmonary (semilunar) valves at end of systole; vibration of taut semilunar valves and elastic recoil of arterial walls; duration ~0.11 sec, higher pitch (semilunar valves are tauter)
S3: rapid ventricular filling phase - physiological in youth, pathological if loud in adults (volume overload, heart failure, dilated ventricle)
S4: atrial contraction against a stiff, non-compliant ventricle - always pathological in adults (hypertrophy, ischemia, hypertension)

6. Right Heart vs Left Heart (mention briefly)

The right ventricle goes through the identical sequence of phases simultaneously, but because pulmonary artery pressure (~8-25 mmHg systolic) is much lower than aortic pressure, the right ventricle:

Develops much lower peak systolic pressure (~25 mmHg vs 120 mmHg)
Isovolumetric contraction/relaxation periods are shorter
Pulmonary valve opens slightly before and closes slightly after the aortic valve

How to score full marks on this LAQ

Definition + duration of cycle, systole vs diastole (2 marks)
Well-labeled Wiggers diagram with all 5 tracings (6-8 marks - this is the single biggest scoring element)
Phase-by-phase description with valve status and pressure-volume correlation (6-8 marks)
Heart sounds mechanism correlated to phases (3-4 marks)
Normal values: EDV, ESV, SV, EF, pressures (2 marks)

Source: Guyton and Hall Textbook of Medical Physiology, Ch. 9 (The Cardiac Cycle) and Ch. 23 (Heart Sounds); Costanzo Physiology 7th Edition, Ch. 4, Fig. 4.25 and Table 4.5.

Ready for the next one whenever you are - Cardiac Output, Coronary Circulation, ECG, or Circulatory Shock.

Make a visual Wiggers diagram poster I can print and study

Generating Image

An educational physiology poster titled "The Cardiac Cycle - Wiggers Diagram" for exam study. It shows five vertically stacked graph panels sharing the same horizontal time axis (one cardiac cycle, in seconds), divided into 7 labeled vertical phase bands: 1) Atrial Systole, 2) Isovolumetric Ventricular Contraction, 3) Rapid Ventricular Ejection, 4) Reduced Ventricular Ejection, 5) Isovolumetric Ventricular Relaxation, 6) Rapid Ventricular Filling, 7) Diastasis (Reduced Filling). Panel 1 (top): ECG waveform showing P wave, QRS complex, T wave aligned with the correct phases. Panel 2: Aortic pressure curve (oscillating between about 80 and 120 mmHg) with a labeled dicrotic notch (incisura) where the aortic valve closes. Panel 3: Left ventricular pressure curve (rising from near 0 to about 120 mmHg and back down), overlapping conceptually with the aortic pressure curve during ejection, with labeled points for "Mitral valve closes", "Aortic valve opens", "Aortic valve closes", "Mitral valve opens". Panel 4: Left atrial pressure curve, small waveform showing labeled a wave, c wave, and v wave. Panel 5: Left ventricular volume curve, a loop-like curve showing decrease during ejection to end-systolic volume (~50 mL) and increase during filling to end-diastolic volume (~120 mL), with those two volumes labeled with dashed reference lines. Bottom panel: a phonocardiogram / heart sounds track showing labeled S1, S2, S3, and S4 marks positioned at the correct time points in the cycle. All panels are vertically aligned so the phase boundaries line up across every graph with thin dashed vertical guide lines. Clear axis labels (Pressure in mmHg, Volume in mL, Time in seconds). Clean textbook medical diagram style, black and white line-art with light color accents distinguishing each curve, suitable for printing on a single page as a study poster.

Here's your printable Wiggers diagram poster covering the full cardiac cycle:

It has all five stacked panels lined up on the same time axis, exactly how you'd want to reproduce it in your exam:

ECG (P, QRS, T waves)
Aortic pressure with the dicrotic notch
LV pressure with mitral/aortic valve open-close points marked
LA pressure with a, c, v waves
LV volume with end-diastolic and end-systolic volumes marked
Heart sounds (S1-S4) at their correct time points

All 7 phases (atrial systole through diastasis) are marked as vertical bands so you can see exactly which ECG wave, pressure change, and heart sound line up in each phase - that's the same phase breakdown from the written explanation I gave you earlier.

Practical tip for using it: print it out, then cover the labels and try to redraw/label it from memory a few times before your exam - that's usually how this diagram gets tested (either "draw and label" or "identify what's happening at point X").

Let me know when you're ready to move to Cardiac Output, Coronary Circulation, ECG, or Circulatory Shock.

Incorporate this diagram in the answer above of the cardiac cycle.

Here's the full Cardiac Cycle answer again with the Wiggers diagram embedded right at the top, where you'd draw/reference it:

THE CARDIAC CYCLE

1. Definition

Duration: Total duration of one cardiac cycle = 60/heart rate (seconds). At a normal heart rate of 72 beats/min: cycle duration = 60/72 = 0.8 second. Of this, roughly systole = 0.3 sec and diastole = 0.5 sec at rest - diastole is longer, which is why tachycardia shortens filling time proportionally more than contraction time. At 3x normal heart rate, systole occupies about 65% of the cycle instead of 40%.

Initiation: Each cycle begins with spontaneous depolarization at the SA node, spreading through the atria, then delayed at the AV node (~0.1 sec), allowing the atria to contract and act as "primer pumps" before the ventricles contract.

Wiggers Diagram (draw this - it's the highest-scoring element of this LAQ)

Wiggers Diagram - Cardiac Cycle Poster showing ECG, aortic pressure, LV pressure, LA pressure, LV volume, and heart sounds across the 7 phases

This single diagram plots, on one shared time axis: the ECG (P-QRS-T), aortic pressure, left ventricular pressure, left atrial pressure (a, c, v waves), left ventricular volume, and the heart sounds (S1-S4) - all lined up against the 7 phases of the cycle described below. Reproduce it with all six tracings stacked and the phase boundaries marked as vertical dashed lines - that's exactly how examiners expect it drawn.

2. The Seven Phases of the Cardiac Cycle (correlate with the diagram above)

Phase A: Atrial Systole

Triggered by the P wave (atrial depolarization) + PR interval
Left atrium contracts, atrial pressure rises slightly, pushes final ~20-30% of blood into the already-filling ventricle (atrial kick)
Mitral valve open; aortic valve closed
Produces the a wave of the atrial/venous pressure pulse
S4 may coincide here - not normally audible in healthy adults, heard in reduced ventricular compliance (e.g., ventricular hypertrophy)

Phase B: Isovolumetric Ventricular Contraction

Begins with the QRS complex (ventricular depolarization)
Ventricular pressure rises steeply, exceeds atrial pressure -> mitral valve closes
Ventricular pressure still less than aortic pressure, so aortic valve remains closed too
All 4 valves closed -> volume constant while pressure rises rapidly ("isovolumetric")
Mitral valve closure produces the first heart sound (S1) - "lub"

Phase C: Rapid Ventricular Ejection

ST segment on ECG
Ventricular pressure exceeds aortic pressure -> aortic valve opens
Blood ejected rapidly into the aorta; ventricular volume falls sharply
Both ventricular and aortic pressures rise together and reach their peak/maximum here
No heart sound normally audible in this phase

Phase D: Reduced Ventricular Ejection

Coincides with the T wave (ventricular repolarization)
Ejection continues but at a slower rate
Ventricular volume reaches its minimum (= end-systolic volume, ~50 mL)
Aortic pressure begins to fall as blood runs off into the peripheral arteries faster than it's being added

Phase E: Isovolumetric Ventricular Relaxation

Ventricle relaxes, pressure falls rapidly
Once ventricular pressure drops below aortic pressure -> aortic valve closes
Produces the second heart sound (S2) - "dub" - and the dicrotic notch (incisura) on the aortic pressure curve
Mitral valve still closed -> all 4 valves closed again, volume constant while pressure falls steeply

Phase F: Rapid Ventricular Filling

Ventricular pressure falls below atrial pressure -> mitral valve opens
Blood pooled in the atria rushes rapidly into the relaxed ventricle
Ventricular volume rises quickly; pressure stays low
May produce a third heart sound (S3) - physiological in children/young adults, pathological (volume overload/heart failure) in older adults

Phase G: Reduced Ventricular Filling (Diastasis)

Longest but "quietest" phase - passive filling slows as ventricular and atrial pressures equalize
Ventricle fills slowly until the next P wave restarts the cycle

3. Summary Table

Phase	Ventricular volume	Valves	ECG event	Heart sound
Atrial systole	Slight increase	Mitral open, Aortic closed	P wave	S4 (if present)
Isovolumetric contraction	Constant	All closed	QRS	S1
Rapid ejection	Decreases sharply	Aortic open	ST segment	-
Reduced ejection	Decreases (to minimum)	Aortic open	T wave	-
Isovolumetric relaxation	Constant	All closed	-	S2
Rapid filling	Increases sharply	Mitral open	-	S3 (if present)
Diastasis	Increases slowly	Mitral open	-	-

4. Pressure and Volume Values to Quote

Left ventricular pressure: rises from ~0-8 mmHg (diastole) to ~120 mmHg (peak systole)
Aortic pressure: oscillates between ~80 mmHg (diastolic) and ~120 mmHg (systolic)
Left atrial pressure: low throughout, ~2-10 mmHg, with a, c, v waves (a = atrial contraction; c = AV valve bulging into atrium during isovolumic contraction; v = atrial filling against closed mitral valve)
End-diastolic volume (EDV): ~110-120 mL
End-systolic volume (ESV): ~50 mL
Stroke volume (EDV - ESV): ~70 mL
Ejection fraction (SV/EDV): ~60-65% (links directly to Cardiac Output)

5. Heart Sounds (mechanism)

S1 ("lub"): closure of mitral and tricuspid valves at start of systole; vibration of tensed valve leaflets/chordae tendineae as back-surging blood abruptly stops them; duration ~0.14 sec, lower pitch
S2 ("dub"): closure of aortic and pulmonary valves at end of systole; vibration of taut semilunar valves and elastic recoil of arterial walls; duration ~0.11 sec, higher pitch
S3: rapid ventricular filling phase - physiological in youth, pathological if loud in adults
S4: atrial contraction against a stiff, non-compliant ventricle - always pathological in adults

6. Right Heart vs Left Heart (brief mention)

The right ventricle goes through the identical phase sequence simultaneously, but since pulmonary artery pressure (~8-25 mmHg systolic) is much lower than aortic pressure, the right ventricle develops much lower peak systolic pressure, shorter isovolumetric periods, and the pulmonary valve opens slightly before and closes slightly after the aortic valve.

How to score full marks on this LAQ

Definition + duration of cycle, systole vs diastole (2 marks)
Well-labeled Wiggers diagram, all 6 tracings (6-8 marks - biggest scoring element)
Phase-by-phase description with valve status and pressure-volume correlation (6-8 marks)
Heart sounds mechanism correlated to phases (3-4 marks)
Normal values: EDV, ESV, SV, EF, pressures (2 marks)

Source: Guyton and Hall Textbook of Medical Physiology, Ch. 9 (The Cardiac Cycle) and Ch. 23 (Heart Sounds); Costanzo Physiology 7th Edition, Ch. 4, Fig. 4.25 and Table 4.5.

Ready for the next one - Cardiac Output, Coronary Circulation, ECG, or Circulatory Shock?

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