Diseases of the Cardiovascular

System
CONTENTS
1. Anatomy
2. Recap of basic physiology
3. Heart failure
4. Angina
5. MI
6. Development of the heart
7. Congenital defects
 Basic Anatomy

- Heart is in middle
mediastinum
- Surrounded by
pericardium
- 4 valves, 4 chambers
- Great vessels
Coronary Circulation

Functional end arteries = no

collateral supply
Most important = LAD!
 Basic physiology

• Double pump system

• Right side is deoxygenated  Lung
• Left side is oxygenated the body
• Closed circuit
– Any event in one part of the circuit will have
knock on effects on other parts of the circuit!
 Heart failure
• Clinical syndrome where the heart is unable to
maintain sufficient blood flow to meet the body’s
needs.

25

Percentage with definite heart failure

• Commonest cause for 20
emergency admissions
in over 65’s 15

• More common in men 10

than women 5
• Estimated to increase by
0
50% by 2030. 45-54 55-64 65-74 75-84 85+
Age group (years)
Men Women
 Risk Factors
• Smoking
• Previous MI
• Abnormal lipid
profile (high ApoB:
ApoA ratio)
• Hypertension
• Diabetes
• Abdominal obesity
• Psychosocial stress
Causes of left heart failure
 Classification of HF
• Reduced EF vs Preserved EF
• Acute vs Chronic
• Left ventricular failure vs Right Ventricular failure
• NYHA classification scale (Classes 1  4 )
• Class 1  No limitations
• Class 4  Breathless at rest and unable to carry out any
physical activity without discomfort
 Right HF Left HF
• RV fails • LV fails
• Increased back pressure • Increased back
 RA IVC & SVC pressure  LA 
• Increased pressure pulmonary veins 
causes oedema, pleural lungs = pleural
effusion, ascites effusion
• Examination: raised • Can build up on right
JVP side as well

Quite common to get both at the same time = CONGESTIVE HF

 What happens during HF?
Starling’s Law:
• Myocyte damage = reduced ability to contract
• Less blood pumped out into circulation so less coming back
• i.e. lower preload = Starling’s law breaks down

Laplace’s Law
• Reduced energy of contraction = afterload harder to overcome
• i.e. effect of laplace’s law increases as more pressure needed
to push blood out of heart
• Stroke volume and CO both decrease = low cardiac perfusion
= ischaemia = HF
 How does the Heart Compensate?

• Ventricular dilatation
• Muscle hypertrophy
• RAAS
• Increased sympathetic drive
 Ventricular Dilatation
• Muscle fibres stretch
• Increases contractility
 Starlings law
• Increases ventricular
volume  Increased
EDV

What is the problem with a dilated heart?

 La Place’s Law
• P = 2Sw / r or S = P x r / 2w
• States radius is proportional to wall stress
• i.e. increased radius = increased wall stress
• when heart is dilated, LaPlace’s law is at it highest value
• high opposition to ejection of blood out of heart
• Normally, Starling’s effect > LaPlace’s law
• however in heart failure, LaPlace’s effect is greater.

How does the heart overcome the effect of

LaPlace’s law?
 Myocardial hypertrophy
• The heart compensates by increasing its wall
thickness.
Increasing wall thickness

Reduces wall stress (remember Increases force of

that wall stress and wall thickness contraction as there are
are inversely proportional to each more sarcomeres present to
other) contract

Increases cardiac output

What is the problem
with increasing muscle
wall thickness?
What is the problem with hypertrophy?

• Hypertrophy  Increased metabolic demand!

• Makes it more difficult for the heart to sustain
its own supply  heart failure

Vicious cycle - Compensatory mechanism only

useful temporarily
 Neurohormonal compensations - RAAS

• Low BP activates RAAS

• Ang II = vasoconstriction
• Aldosterone = Na and H2O
retention
• Increases CO, good in the
short term
• Long term:
• Vasoconstriction increases
afterload,
• Increased CO = Increased
preload
• Both increases cardiac work
Neurohormonal compensation-
Increased sympathetic drive
Signs and symptoms of heart failure

• Pulmonary
• SOB oedema
• Coughing • Ascites (Abdo
• Tachycardia swelling)
• Raised JVP • Ankle swelling
Heart failure – Diagnosis
• BNP
– Normal BNP  Look for other causes of SOB
– High BNP  Carry out an echocardiogram to
confirm heart failure or refute diagnosis
Heart failure - Treatment
• B Blockers e.g. atenolol
– Decrease BP = decrease afterload
– Decrease HR = less O2 demand, heart can rest &
recover
• ACE Inhibitors e.g. elanapril
• Angiotensin receptor blockers e.g. losartan
– Decrease vascular resistance = decrease BP
• Other options: biventricular pacing, transplant
 Q1
What is the biggest risk factor for cardiovascular
diseases?
a) Abnormal lipid profile
b) Hypertension
c) Abdominal obesity
d) Smoking
e) Psychological stress
 Q2
How do we diagnose heart failure?
a) BNP and Ultrasound
b) BNP and X ray
c) Computed Tomography
d) BNP only
e) BNP and Echocardiogram
 What happens to our coronary vessels
when we run?
R=19
R=1 (coronary artery) Total resistance = 20
(arterioles)

R=4
R=1 Total resistance = 5 (4x flow)

• During exercise, heart beast stronger and faster

• Increased cardiac demand
• Coronary vessels vasodilate to meet these demands
• More blood flow to heart tissue
 Angina Pectoris
• Crushing chest pain
• narrowing/blockage of coronary artery = O2
demand exceeds supply
• Types
– Stable = Predictable, chest pain on exertion
– Unstable = Chest pain due to thrombus formation
– Variant (Prinzmetal) = Vasospasm of coronary
arteries, causes chest pain at rest
 Stable Angina
R=10
R=10 Total resistance = 20
atheroma

R=4
R=10 Total resistance = 14 (1.5x  flow)

• At rest, coronary vessels maximally vasodilated

• further exertion will lead to an increase in cardiac demand
• Demand > Supply  Ischaemia
• Ischaemic products stimulate sympathetic nociceptive afferents =
chest pain
 RISK FACTORS AND TREATMENT
• Risk factors for angina
– High BP
– Tachycardia
– Increased force of contraction
– Cold weather
– Large meal
• Treatment for angina
– Nitrates
– Beta blockers
– Calcium channel blockers
– Antiplatelet drugs
Myocardial Infarction
• Tissue death as a result of vascular occlusion
• ST elevation on ECG
• As opposed to angina which has ST depression

ST elevation ST depression
Development of the heart

1)The four chambered heart tube forms

2)Cardiac looping
3)AV canal divides into right and left channels
4)Atrial septa forms
5)Conotruncal cushion forms leading to the
division of outflow tract

https://embryology.med.unsw.edu.au/embryology/index.php/Intermediate_-
_Heart_Tube_Looping
Patent Foramen Ovale
• In foetus, circulation does not need to go
through lungs, gets O2 from placenta instead
• Blood in a foetal heart shunted straight from
RA to LA
• Hole in inter-atrial wall called foramen ovale
allows for this
• Normally closes up after birth
• Patent foramen ovale = does not close
Ventricular Septal Defect
• Most common congenital
heart defect
• Hole in inter-ventricular
septum
• Left side of heart has
higher pressure than right
side
• Oxygenated blood from
left side passes to right
side, mixed with
deoxygenated blood
 Tetralogy of Fallot

Tetralogy of Fallot and VSD both common

in Down’s syndrome
Useful Equations
• CO = HR x SV
• SV = EDV – ESV
• EF = SV / ESV
• BP = CO x TPR
• Velocity = blood flow / CSA
• Pulse pressure = systolic - diastolic
• Mean arterial pressure = diastolic x (1/3 pulse pressure)
• Stroke work = change in ventricular pressure x change
in volume
 Q3
What is the most common congenital heart
defect?
a) Patent ductus arteriosus
b) Tetralogy of Fallot
c) Atrial septal defect
d) Ventricular septal defect
e) Dextrocardia
 Q4
Which of the following statements is not a sign
for the tetralogy of Fallot?
a) Overriding aorta
b) Aortic stenosis
c) Pulmonary stenosis
d) Ventricular septal defect
e) Right ventricular hypertrophy
QUESTIONS?
• References used:
– Heart Failure – Lisa Anderson
– Specialised Circulation – Anthony Albert
– Development of the CVS – James Moffat
• Talk hosted by iSoc Academics
• m1701330@sgul.ac.uk

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