Lecture notes

Lecture notes on cardiac output and blood pressure- clinical Medicine

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Module
Clinical Medicine

Institution
Queen Mary, University Of London (QMUL)

This document covers all the learning objectives on lecture 1 in Clinical Medicine Cardiology. It entails details of the cardiac cycle, cardiac output and factors affecting it. It also outlines how the heart is regulated by the autonomic nervous system. Finally, it explains how blood pressure works...

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Uploaded on February 4, 2024
Number of pages 9
Written in 2021/2022
Type Lecture notes
Professor(s) Dr mahenderan
Contains Lecture 1- cardiac output and blood pressure

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Lecture 1- Cardiac output and blood pressure

Cardiac output

1. Describe the phases of the
cardiac cycle

2. Define cardiac output and factors affecting it.

CARDIAC OUTPUT: the volume of blood being pumped by the heart/ minute- units: LITRES/ MIN

CO= heart rate (HR) x stroke volume (SV)
- CO normally 5-6 L/min. Exercise: CO can increase to 25-30 L/min.
- HR generally 75bpm, SV generally 70 ml/beat

- Stroke volume: volume of blood pumped from the ventricle in one beat- aka. ventricular stroke
volume.
 SV= EDV-ESV
 End diastolic volume: the amount of blood in the ventricles after ventricular diastole i.e. just
after atrial contraction when blood has filled into the ventricles. This is the max. volume of
blood in the ventricle for this cycle.
 End systolic volume: residual volume of blood left in ventricle after contraction.
- Ejection fraction (EF): measure of the pumping efficiency of the heart- used to indicate severity of
heart failure.
 EF= SV (volume of blood pumped from the ventricle per beat)/ end diastolic volume.

Factors affecting CO- any factors which affect HR and SV. Altogether, 4 main determinants of CO:

a) Heart rate
b) Preload: volume of blood entering ventricles- proportional rship
c) Afterload: resistance the ventricles must overcome (aortic pressure)- inversely proportional rship
d) Contractility
A. Heart rate
- Factors positively affecting heart rate i.e. increasing HR= positive chronotropic factors- cause
tachycardia (over 100bpm)
 Sympathetic NS stimulation (fight/ flight)- increases HR through adrenaline/ noradrenaline
release

,  Hypercapnia (high CO2)
 Hypocalcemia (low calcium)
 Drug atropine
- Factors negatively affecting HR i.e. decreases heart rate= negative chronotropic factors- cause
bradycardia (below 60bpm).
 Parasympathetic stimulation- acetylcholine neurotransmitter
 Hypoxia
 Hypercalcemia

3.

Describe: preload, afterload, inotropic chronotrope, vasoconstrictor and vasodilator.

Stroke volume

B. Preload: volume of blood entering ventricle at the end of diastole, stretching ventricular walls
- The EDV that enters the ventricle and stretches it under physiological demand.
- If more blood enters= greater stretch= increased preload= increased SV

Frank-Starling mechanism: the amount of blood entering the ventricles will be the amount of blood
ejected by ventricles to the body i.e. EDV ~ stroke volume.

C. Afterload: The resistance ventricles must overcome to circulate blood around the body
- Resistance= the aortic/pulmonary arterial pressure
- When ventricles contract, they must generate enough pressure to EXCEED the BP in the
aorta/pulmonary artery, so that the semilunar valves can be forced open.
- SO, the aortic BP is called afterload since it imposes a workload on the heart after contraction has
begun.
- Therefore, if arterial BP is too high or valve is stenotic, centrical will need to generate MORE pressure
to eject the blood
- =increase in afterload= decreased amount of blood pumped from ventricles i.e. SV, due to high
pressure in front (in the aorta).
- Decreased afterload= increased SV (inversely proportional relationship).

D. Contractility: how hard the myocardium (cardiac muscle) contracts for a given preload i.e. how
hard the heart contracts to pump blood out of the heart

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