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Summary Diseases of the heart and large blood vessels
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  • Course
  • Blok 3.1
  • Institution
  • Rijksuniversiteit Groningen (RuG)
  • Book
  • Kumar and Clark\'s Clinical Medicine

Summary of diseases of the heart and large blood vessels. Based on many books: - Kumar & Clark’s Clinical Medicine - Kumar, 9th edition - Textbook of Medical Physiology - Guyton & Hall, 13th edition - Robins and Coltran Pathologic Basis of Disease - Kumar, 9th edition - Essential surgery - Quick...

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  • No
  • Chapter 23
  • September 28, 2019
  • October 3, 2019
  • 22
  • 2018/2019
  • Summary

Subjects

  • heart
  • pericariditis
  • cardiac tamponade
  • myocardial infarction
  • aneurysm
  • aortic rupture
  • aortic dissection
  • mesenteric ischaemia
  • ecg
  • clinical medicine
  • guyton

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By Nerea Campillo




Diseases of the heart and large bloodvessels
Clinical Medicine1: Chapter 23 (p. 933-946, 1042-1046)
Basic pathology of disease2: Chapter 12 (p. 523-526, 538-549)
Essential Surgery3: Chapters 42,48 (p. 510-515, 518-522, 539-540)
Medical Physiology4: Chapter 11 (p. 131-139)
Powerpoints 2018
Farmacotherapeutisch Kompas “Coronairlijden”

Content:
1. The heart and heart diseases p. 2
a. Basic pathology of disease: Chapter 12 (p. 523-526) and Clinical Medicine:
Chapter 23 (p. 933-946)
2. Acute pericarditis and tamponade p. 7
a. PowerPoint “Acute pericarditis and tamponade” on Nestor & Clinical
Medicine: Chapter 23 (p. 1042-1046)
3. Myocardial infarction p. 9
a. PowerPoints “Anatomy and (patho)physiology” & “ECG in ACS” & “ACS
2015” & “Collapse” on Nestor & Farmacotherapeutisch Kompas
“Coronairlijden” & Pathologic basis of disease: Chapter 12 (p. 538-549)
4. Arterial disorders p. 16
a. Essential Surgery: Chapter 42 (p. 510-515 & 518-522) & Chapter 44 (p. 539-
540) & PowerPoints: “Aneurysm”, “Traumatic aortic rupture” “Aortic
dissection”
5. ECG p. 20
a. Medical Physiology: Chapter 11 (p. 131-139) & Clinical Medicine: Chapter 23
(p. 944-946)




1
Kumar & Clark’s Clinical Medicine - Kumar (9 ed.)
2
Robins and Coltran Pathologic Basis of Disease - Kumar (9 ed.)
3
Essential surgery - Quick & Reed (5 ed.)
4
Textbook of Medical Physiology - Guyton & Hall (13 ed.)

1

,By Nerea Campillo




The heart and heart diseases
Basic pathology of disease: Chapter 12 (p. 523-526) and Clinical Medicine: Chapter 23
(p. 933-946)

The heart in general
The heart weighs about 250-320 grams (females) and 300-360 grams (males).
Hypertrophy is characterised by an increase in weight or ventricular thickness. Dilation is
characterised by an increased size of the atrium/ventricle. Cardiomegaly is an increase in
weight and/or size (due to hypertrophy and/or dilation).
Myocardium
The cardiac myocytes together form the myocardium. In the left ventricle, this myocardium is
organised in a spiral so the blood gets efficiently ejected in one direction. In the right
ventricle, this organisation is less structured. The atria are even less well organised.
A bit of stretching of the myocardium during diastole helps increase the force of the
contraction (Frank-Starling mechanism) but there is a limit to that. Too much stretching
makes the contraction less strong and can lead to heart failure.
Valves
The part of the valve that is near the outflowing blood is made of a dense collagen core
(fibrosa). In the middle of the valve is loose connective tissue (spongiosa) and at the inflow
side there is elastin. Because the valves are so thin, they can get their nutrients from the
blood that flows past them.
In all layers, valvular interstitial cells can be found. These cells synthesise extracellular
matrix.
Problems with valves:
● Weakening collagen: e.g. mitral valve prolapse
● Calcification, beginning in interstitial cells: e.g. calcific aortic stenosis
● Fibrotic thickening: e.g. rheumatic heart disease
Conduction system
The cells in the heart that depolarise the fastest, set the pace of the heart and make other
cells join them. This is normally the SA node.
Blood supply
The coronary arteries start from just above the aortic valve (left and right aortic sinus) and
course along the surface of the heart (epicardial coronary arteries) till they penetrate the
myocardium (intramural arteries) where they branch into arterioles.
Blood flow to the myocardium happens during diastole when the blood flows back on the
aortic valves and into the coronary arteries. Besides, during diastole, the heart is relaxed and
the coronary arteries are not compressed.
Cardiac stem cells
There are some cardiac stem cells present in the myocardium. These can produce all the
cells present in the myocardium but they proliferate very slowly. The rate of proliferation gets
even slower with increasing age. When myocardial cells are lost (for example during an
infarct), not much of this is recovered by cardiac stem cells.

Sinus node
The sinus node (SA node) lies on the wall of the right atrium behind the opening of the
superior vena cava.



2

, By Nerea Campillo




The sinus node hyperpolarizes rhythmically thanks to the influx of sodium into the cells of the
SA node. There is an always-present inward flow of sodium and there is a ‘funny’ inflow.
This ‘funny’ inflow enters the cell through channels that get activated with hyperpolarization
(instead of depolarization).

Contraction of ventricles
The signal from the SA node travels to the AV node and after a pause is conducted through
the His bundle in the annulus fibrosus of the heart. The His bundle splits into a right and left
branch.
The right bundle branch travels to the apex and then forms a Purkinje network in the sub-
endocardial surface of the right ventricle. The main left bundle branch is short and spreads
into many side branches. The anterior hemi-bundle supplies the anterior and superior parts
of the left ventricle. The posterior hemi-bundle supplies the inferior and posterior part of the
left ventricle.

Excitation-contraction coupling
Myocytes contain myofibrils that run parallel. Thanks to the intercalated discs, the electrical
signals can be passed on easily. Myocytes have lots of mitochondria because they need a
lot of oxygen for all the contractions.
Tropomyosin moves away from the actin band when troponin binds to calcium. The calcium
enters the cell during the plateau phase of the signal and it is then also released from the
sarcoplasmic reticulum.
The Frank-Starling mechanism describes how the stroke volume (ventricular output)
increases when there is a larger diastolic volume (volume before contraction).
Increased volume → stretch of myocytes → increased contraction.

Nerve supply
The vagus nerve (parasympathetic) innervates the SA and AV node. It tries to maintain a
slow heart rate. It uses acetylcholine as a neurotransmitter and muscarinic-receptors in the
heart.
Sympathetic nervous system uses epinephrine and norepinephrine as neurotransmitters and
beta1-receptors. Adrenaline and noradrenaline work on the beta1-receptors on myocytes to
activate calcium channels. The increased influx of calcium increases contractility of the
heart. Beta1-receptor stimulation also increases the relaxation speed of the heart due to
phosphorylation of phospholamban. So there is increased contractility and increased
relaxation.
-adrenergic stimulation = vasoconstriction. β-adrenergic stimulation = vasodilation.

Coronary arteries
The coronary arteries fill during diastole.
● Left anterior descending coronary artery (LAD):
The left anterior descending artery runs in the anterior interventricular groove.
○ Left ventricle: anterior wall
○ Ventricular septum: anterior side
○ Apex
● Right coronary artery (RCA):




3

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