2. Myocardial Innervation Flashcards
Innervation ANS
predominantly autonomic.
Efferent and afferent fibres originate from the cardiac plexuses,
which are aggregations of autonomic nerves and ganglia
superficial plexus lies below the arch of the aorta in front of the right pulmonary artery,
and the deep plexus lies anterior to the bifurcation of the trachea
and behind the arch of the aorta.
Parasympathetic supply
branches of the vagus nerves that enter the cardiac plexus
right vagus innervates the SAN, whereas the
left vagus innervates the AVN.
can be some overlap.
Vagal efferents supply atrial muscle but
innervate the ventricular myocardium only sparsely
. Vagal stimulation vasoconstricts the coronary arterial circulation
via muscarinic receptors
Sympathetic supply
sympathetic fibres originate mainly from the upper thoracic spinal cord
(segments T2–T4) and are
distributed through the middle cervical and
the stellate (cervicothoracic) ganglia as well as
through the first four ganglia of the thoracic sympathetic chain
Pass into the cardiac plexus and thence to the SAN and the cardiac muscle.
Ventricular sympathetic innervation is denser than atrial. Sympathetic
stimulation dilates coronary arteries via actions on beta-adrenoceptors
The Physiology of the Transplanted Heart
Autonomic denervation:
Sympathetic Denervation
Parasympathetic denerve
Starling mechanism
Autonomic denervation:
the transplanted heart loses both sympathetic and parasympathetic
efferent and afferent neurons.
This leads to a (predictable) alteration in
some aspects of cardiac physiology, including the absence of anginal pain.
Sympathetic denervation
Despite the lack of a direct neuronal supply,
the heart still responds normally to circulating catecholamines.
This humoral response is of relatively slow onset and takes some minutes to develop.
The response to exogenous catecholamines is similarly delayed.
Parasympathetic denervation
Parasympathetic denervation:
there may be some residual vagal activity associated with the vestigial
recipient right atrium which is part of the anastomosis, but this
does not extend to the donor atria.
Vagal effects are absent, and so drugs which
usually have muscarinic actions do not cause bradycardia,
and drugs which are vagolytic do not increase the heart rate.
In normal individuals, the resting heart rate
is governed by vagal tone.
In heart transplant patients therefore the rate is higher,
commonly around 100 beats per minute
Starling mechanism
: the myocardial response to stress is maintained,
with increases in contractility and cardiac output in response
to any rise in left ventricular enddiastolic volume (LVEDV).
It is important to avoid hypovolaemia in these patients.
Other considerations:
a discussion of anaesthetic problems is unlikely to feature at
this stage but is summarized briefly here for completeness.
Such problems include accelerated graft atherosclerosis owing to chronic rejection;
absence of warning symptoms of angina; and
immunosuppression by drugs, the commonest of which
are corticosteroids (with a wide range of side effects, from myopathy to hyperglycaemia),
cyclosporin (with effects on renal and hepatic function)
and azathioprine (myelosuppression).
Immune reactivity decreases with time, and so dose regimens
will be highest in the early months following transplantation
Cardiac Pain
The localization of somatic pain is usually precise, whereas visceral sensations are
limited to discomfort (due, for example, to distension) and to pain. There are many
fewer visceral sensory fibres than somatic sensory fibres in the dorsal roots, which
helps to explain why visceral pain is poorly localized.
Origin of cardiac pain:
In a normal heart the oxygen supply can be increased six- toeightfold
in response to increased demand, such as during exertion. At the point at
which demand exceeds supply there is an accumulation of lactate and other metabolites.
Exercise is then limited by fatigue and dyspnoea, but not by cardiac pain. In a
patient with coronary artery disease it is common for cardiac pain to precede fatigue
A number of substances (which include lactate, potassium,
adenosine, prostaglandins and bradykinins) are released from ischaemic areas of the
myocardium.
may sensitize sympathetic afferents, in
particular those neurons which have a so-called acid-sensing sodium channel.
Lactate increases the activity of these channels and enhances their excitability. This
increased sensitization is not an acute phenomenon, because systemic lactic acidosis
is not associated with chest pain
Nature of pain - mechanism
Pain is the only sensation that is evoked from the heart, but it too is more vaguely
localized.
Sympathetic afferents account for only around 2% of the total number of
afferents to the upper thoracic cord. Stimulation of these afferents leads to excitation
of spinothalamic tract cells (T1–T5) which also receive somatic input from
overlying structures.
This convergence onto a common pool of spinothalamic tract
cells helps account for the classic nature of anginal pain, which is frequently
referred to the arm and ches
The convergence is on tracts with afferents from
deep (muscle) rather than cutaneous (skin) structures. In addition, vagal afferents
transmit nociceptive information to the spinothalamic tract at the level of C1 and
C2, which explains referred pain in the neck and jaw. This vagal innervation is one
of the reasons why not all cases of refractory angina can be treated successfully by
sympathetic block
Other structures
Sympathetic afferents from viscera such as the gallbladder and the oesophagus also
converge on this pool of spinothalamic tracts; hence the similarity of symptoms that
these structures can evoke.
Angor animi’,
discussion is a simplification which does not include other ascending spinal
tracts that are involved, and does not entirely account for aspects such as the specific
emotional components of cardiac pain. ‘Angor animi’, for example, which is a
profound sense of impending death, is a sensation that is said to be unique to
myocardial pain, but one whose neural processing has not been elaborated
