Introduction to the Cardiovascular System

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<h1>Introduction to the Cardiovascular System</h1>
<h2>Lecture 2: The Heart & Integrated Control | Dr. Robert Hunter</h2>

.callout-question[
**A question for you:** A 19-year-old medical student runs a marathon.  Her cardiac output rises from 5 L/min at rest to over 20 L/min at peak effort.  What causes this?
]

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**Timing overview:**
- Brief recap of muddiest points from Lecture 1, then open with the hook (~3 min)
- Section 4: The Heart (~15 min)
- Section 5: Integrated Control (~20 min)
- Close: Summary and signposting (~5 min, folded into closing sequence below)

---

.left-panel.left-panel.amber[

#### Yesterday:

1) body fluids  
2) capillary exchange  
3) blood vessels

#### Today:

4) the heart  
5) cardiac output  
6) integrated control  
]

# Learning outcomes

1. **Describe** the cardiac cycle and **define** systole and diastole
2. **State** the determinants of cardiac output (CO = SV × HR) and **apply** this
   equation to simple physiological scenarios
3. **Explain** the Frank-Starling law and its molecular basis
4. **Outline** the key intrinsic and extrinsic mechanisms controlling blood
   pressure and blood flow
5. **Apply** the relationship ABP = CO × TPR to explain simple clinical scenarios

<br>

.callout[
**Context:** these lectures form a skeleton of knowledge you will build in in semester 2 ("Sustaining Life") and year 2 ("Renal & Urology")
]

.callout-ref[
**Primers:** the heart | haemodynamics | integrated control of the cardiovascular system | the renin-angiotensin-aldosterone system  
]

---

# Part 4
## The Heart

???

**Aim:** Signpost start of Section 4 (~15 minutes).

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# Anatomy

.pull-right-66[
- **Four chambers:** right atrium (RA), right ventricle (RV), left atrium (LA),
  left ventricle (LV)
- **Four valves**, all functioning to **prevent backflow**:
  - Atrioventricular: **tricuspid** (right), **mitral** (left)
  - Semilunar: **pulmonary**, **aortic**
  
  <br>
  
.callout[
The left ventricle wall is far thicker than the right.
The **LV pumps against systemic resistance (~120 mmHg)**; the **RV pumps against
pulmonary resistance (~25 mmHg)**. Same output; very different workload .
]
]

???

Link explicitly back to yesterday's "two circulations in series"
diagram — this is the same circuit, now with the pump itself opened up. Point out
the LV/RV wall thickness difference directly on the diagram.

---

# The cardiac cycle

1. **Diastole** — ventricles relax and fill passively via open AV valves
2. **Atrial systole** — atria contract, contributing the final **~20% of
   ventricular filling** (the "atrial kick")
3. **Isovolumetric contraction** — AV valves close (producing the **1st heart
   sound**); ventricular pressure rises sharply; no blood flows yet, because
   pressure hasn't yet exceeded the aortic/pulmonary pressure
4. **Ventricular systole (ejection)** — semilunar valves open; blood is ejected
   into the aorta (left) and pulmonary trunk (right)

<br>

.callout[
**Systole** — the phase of the cardiac cycle during which the
ventricles **contract** and eject blood (**S**ystole = **S**queezing). **Diastole** — the phase during which the ventricles **relax** and fill with blood.
]

.callout-warn[
**The atrial kick can matter clinically.** Lose coordinated atrial contraction (as in
atrial fibrillation) and you lose roughly a fifth of ventricular filling — enough
to matter in patients with limited cardiac reserve.
]

---

# The conduction system

.pull-left[
1. **SA node** (right atrium) — the natural pacemaker; sets heart rate
2. Electrical impulse spreads through the atria → **atrial contraction**
3. **AV node** — a deliberate **conduction delay**
4. **Bundle of His** → left and right bundle branches → **Purkinje fibres** →
   coordinated **ventricular contraction**

<br>

.callout[
**Why the AV delay matters.** It allows the atria to **finish emptying into the
ventricles** before the ventricles contract. Without it, the atrial kick would be
lost entirely.
]
]

---

# The ECG

.pull-left[
| Wave | Event |
|:---|:---|
| **P wave** | Atrial depolarisation |
| **QRS complex** | Ventricular depolarisation |
| **T wave** | Ventricular repolarisation |

]

.callout-ref.callout-bottom[
Learning to interpret an ECG takes many years. You will learn how to interpret cardiac rhythm in semester 2.  For now, you only need to link each wave to the underlying electrical event.
]

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![:scale_c 75%](images/wiggers.svg)

???

Wiggers diagram (Carl Wiggers, Iowa 1940s).  Revisit in semester 2.

---

# Part 5
## Cardiac output

---

# Cardiac output

`$$CO = SV \times HR$$`
<br>

`$$CO = 70\text{ mL} \times 70\text{ bpm} \approx 5\text{ L/min}$$`

.callout.callout-bottom[
**Definitions:**
- **SV** = stroke volume: volume ejected from the ventricle per cardiac cycle  
- **HR** = heart rate: number of cardiac cycles per minute  
]

---

# 76 yo female with a fast pulse

**History**
- sudden onset of palpitation (senstation of heart beating fast)  
- then quickly developed chest pain and shortness of breath

<br>

**Examination findings**
- looks unwell  
- tachycardic (HR 220 bpm)  
- hypotensive (systolic BP 70 mmHg)  
- cool hands
- oliguric (not peeing)

.callout-bottom.callout-question[
**Apply your knowledge.** Why is her cardiac output so low when her heart rate is so high?  Remember CO = SV `$\times$` HR.  
]

---

# Cardiac output

![:scale_l 75%](images/CO_vs_HR.png)

---

# The Frank-Starling Law

.pull-left-33[
- **CO = VR.**  Cardiac output matches venous return, beat by beat.  This is an intrinsic property of the heart (i.e. no external / nervous input required).

- **Elegant molecular basis.**  At resting sarcomere length, actin–myosin overlap is only
  about **70% of optimal**. Stretching the myocyte (increased preload) improves
  this overlap, producing a **stronger contraction**
]

.callout.callout-bottom[
**Two consequences.** (1) It **balances output** of the left and right hearts
automatically. (2) It allows cardiac output to **match physiological demand**
without conscious or autonomic control.
]

---

# Determinants of stroke volume

Stroke volume is governed by three factors:

- **Preload** — the degree of ventricular filling at end-diastole (≈ left
  ventricular end-diastolic volume; clinically approximated by right atrial
  pressure)
- **Afterload** — the resistance against which the ventricle must pump (≈ total
  peripheral resistance)
- **Contractility** — the intrinsic strength of myocardial contraction,
  **independent of loading conditions**; increased by sympathetic stimulation

.callout.callout-bottom[
**Definitions:** 
- inotropy = change in *force* of contraction  
- chronotropy = chainge in *rate* of contraction  
- ejection fraction = proportion of ventricular volume ejected with each systole  
]

---

# Part 6
## Integrated Control

???

**Aim:** Signpost start of Section 5 (~20 minutes), the longest and most
integrative section of the two-lecture arc.

**Script cue:** "We now have a pump and we know what determines its output.
Zooming out one final time: how does the body decide, moment to moment, what blood
pressure should actually be?"

---

# The master equation

#### The master equation

`$$BP = CO \times TPR$$`

Where **BP** = arterial blood pressure, **CO** = cardiac output, **TPR** = total
peripheral resistance.

.callout[
**Metaphor.** This is the haemodynamic equivalent of **Ohm's law** (`$V = IR$`):
pressure is the product of flow and resistance. Every mechanism of cardiovascular
control you will ever learn acts by altering **CO**, **TPR**, or both.
]

<br>

#### Mean arterial pressure (MAP)

`$$MAP \approx DBP + \frac{1}{3}(SBP - DBP)$$`
Where **DBP** = diastolic blood pressure, **SBP** = systolic blood pressure.

MAP is the pressure that actually drives tissue perfusion, and is what "BP" refers to in the equation above.

---

# Intrinsic (local) control

Blood vessels can regulate their own tone **without any external signal** —
tailoring local blood flow to local tissue need:

- **Metabolic (functional) hyperaemia** — active tissues generate CO₂, H⁺,
  lactate, adenosine, and K⁺; these cause local arteriolar **vasodilation**,
  increasing blood flow precisely where metabolic demand has risen
- **Myogenic response (autoregulation)** — a rise in perfusion pressure stretches
  vascular smooth muscle, triggering reflex **contraction**; keeps flow roughly
  constant despite changing pressure — particularly important in the **kidney**
  and **brain**
- **Flow-mediated vasodilation** — increased shear stress on the endothelium
  triggers release of **nitric oxide (NO)**, causing smooth muscle relaxation and
  vasodilation

.callout.callout-bottom[
**The endothelium is not a passive lining.** It is an active signalling organ,
constantly sensing shear stress and releasing vasoactive mediators like NO in
response.
]

---

# Extrinsic control — sensors

![:scale_c 50%](images/baroreceptors.png)

- **Baroreceptors** — stretch receptors in the **aortic arch** and **carotid sinus** > relay to brainsten vasomotor centre
- **Chemoreceptors** — located in the **carotid body**; sense O₂ and CO₂ levels
- **Renal volume sensor** (juxtaglomerular apparatus) > triggers the **RAAS**
  cascade

.callout[
**Clinical application.** In patients with tachyarrythmias, we can slow the heart down by massaging the carotids to "fool" these pressure sensors.  
]

---

# Extrinsic control — effectors

- **Heart:** ↑ contractility (+ve inotropy) and ↑ heart rate (+ve chronotropy) →
  ↑ CO
- **Arterioles:** vasoconstriction → ↑ TPR → ↑ ABP
- **Veins:** venoconstriction → ↑ venous return → ↑ preload → ↑ CO via
  Frank-Starling
]

- Acts mainly on the **SA and AV nodes**
- → ↓ heart rate (−ve chronotropy)
- Counterbalances sympathetic tone at rest
]

.callout.callout-bottom[
Sympathetic activation **raises** ABP by acting on almost every
variable in our master equation simultaneously; parasympathetic activation acts
far more narrowly, **lowering** heart rate alone.
]

---

# Extrinsic control — RAAS cascade

- **kidney** releases **renin**    
- cleaves **angiotensinogen** to **Angiotensin I**  
- **ACE** (in the lung) converts this to **Angiotensin II**  
- Angiotensin II has two effects:  
  1. **vasoconstriction** (↑ TPR)
  2. stimulates  **adrenal gland** to release **aldosterone** > ↑ renal Na⁺ and
     water retention > ↑ blood volume > ↑ preload > ↑ CO

]

.callout.callout-bottom[
The RAAS is particularly powerful because it acts on **both** CO and TPR:<br>
`$BP = CO \times TPR$`
]

---

# 19 yo medical student

**Runs a marathon**:  
- pulse rate increases from 50 bpm to 170 bpm
- systolic blood pressure increases from 120 to 150 mmHg  
- diastolic blood pressure falls from 70 to 60 mmHg  
- CO increases from 5L/min to 20L/min

.callout-bottom.callout-question[
**Apply your knowledge.**<br>
What causes the increase in her cardiac output?
]

---

# 19 yo medical student

<br>

1) muscle metabolism > functional hyperaemia > arteriolar vasodilation > `$\downarrow$` TPR

2) muscle & respiratory pumps > `$\uparrow$` venous return > `$\uparrow$` CO

3) (-) parasympathetic | (+) sympathetics > `$\uparrow$` HR > `$\uparrow$` contractility > `$\uparrow$` CO

4) (+) sympathetics > venoconstriction > mobilises blood > `$\uparrow$` VR > `$\uparrow$` CO

---

# BP = CO `$\times$` TPR | worked examples

???

**Aim:** Fourth active learning intervention — an unresolved clinical scenario that
students must solve using the equation just taught (this is the "unresolved story"
active learning format).

**Script cue after pause:** "If ABP is low despite a *high* CO, the arithmetic only
works if TPR has fallen dramatically — this is the haemodynamic signature of
distributive shock, most commonly septic shock. High output, collapsed resistance,
low pressure."

**Signpost:** "So — how does the body normally control CO and TPR to keep ABP
steady? There are two broad systems: local, intrinsic control, and body-wide,
extrinsic control."

---

# Summary — lecture 2

#### Equations to know

- `$CO = SV \times HR$`
- `$BP = CO \times TPR$`

<br>

#### Key facts

- Cardiac cycle: understand the Wiggers diagram  
- Frank-Starling: **the heart outputs what it receives**
- Control hierarchy: **intrinsic** (metabolic, myogenic) → **extrinsic** (SNS,
  PSNS, RAAS)

.callout-ref.callout-bottom[
**Remember**:
- all of this will be fleshed out in more detail (Sustaining Life, Semester 2)  
- see primers  
]

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# Reflection

.callout-question[
Take 🕐 60 seconds for each of these three questions. <br>
Write down, in your own words...
]

<br>

- The most important thing I learned today

<br>

- One thing I am still unclear on

<br>

- One specific thing you will do to enhance your learning by the end of the week

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# Thank You

## Any questions?

???