This document summarizes cardiac physiology and considerations for anesthesia in cardiovascular diseases. It discusses cardiac reflexes like the baroreceptor reflex and effects of anesthetic agents. It notes that volatile anesthetics decrease heart rate and contractility by reducing calcium entry. For diseases like coronary artery disease, the goal is maintaining a favorable supply-demand relationship. For mitral stenosis, sinus rhythm and avoiding tachycardia are important. Congenital heart diseases require exclusion of air from IV fluids to prevent paradoxical embolism.

1. CARDIOVASCULAR
PHYSIOLOGY PART 2
Presenter- Maj Rishabh Mishra
Moderator- Lt Col Purushottam G

2. TOPICS
 Cardiac reflexes
 Effects of anaesthetic agents on
cardiovascular system
 Anaesthetic considerations in various
cardiovascular diseases

3. CARDIAC REFLEXES
 Baroreceptor reflex
 Chemoreceptor reflex
 Bainbridge reflex
 Bezold-Jarisch reflex
 Valsalva maneuver
 Cushing Reflex
 Oculocardiac Reflex

4. Baroreceptor reflex
 Maintains BP around a preset value
through a negative feedback loop
 Changes in BP are monitored by
circumferential and longitudinal stretch
receptors in carotid sinus and aortic
arch
 Stretch receptors afferents of
glossopharyngeal and vagus
nucleus solitarius in cardiovascular
centre of medulla

6.  Stretch receptors activated at BP >
170mm Hg
 Response includes decrease in cardiac
contractility, heart rate and vascular tone
 Activation of parasympathetic system
decreases HR and myocardial
contractility

7.  Important during acute blood loss and
shock
 Reflex arch loses functional capacity at
BP< 50 mm Hg
 Volatile anaesthetics (particularly
halothane) decrease the HR component
of this reflex

8.  Concomitant use of CCBs, ACE
inhibitors or PDE inhibitors decreases
the cardiovascular response of raising
BP
 Pts with chronic HTN often exhibit
perioperative cardiac instability due to
their decreased baroreceptor reflex
response

9. CHEMORECEPTOR
REFLEX
 Chemosensitive cells located in
carotid bodies and aortic body
 Respond to changes in pH and PO2
 Afferents: Sinus nv of Hering (br of
glossopharyngeal) and vagus
 Centre: chemosensitive area of
medulla
 Effects: 1. stimulates resp system 2.
increase ventilatory drive 3. reduction
in HR and myocardial contractility

12. BAINBRIDGE REFLEX
 Elicited by stretch receptors located in
Rt atrial wall and cavoatrial junction
 Increase in Rt sided filling pressure
sends vagal afferent signal to
cardiovascular centre in medulla
inhibiting parasympathetic activity
causing increase in HR

14. BEZOLD- JARISCH REFLEX
 Triggers: myocardial
ischemia/infarction, thrombolysis,
revascularisation and syncope
 This reflex responds to noxious stimuli
sensed by chemo and mechano
receptors within LV wall resulting in
hypotension, bradycardia and
coronary art dilatation
 Cardioprotective reflex

16. VALSALVA MANEUVER
 Forced expiration against a closed
glottis increases intrathoracic
pressure, increased CVP and
decreased venous return
 Cardiac output and BP are decreased
after this maneuver
 This is sensed by baroreceptors
resulting in sympathetic stimulation
causing increase in HR and
myocardial contractility

18. CUSHING REFLEX
 Occurs as a result of cerebral
ischemia caused by raised ICP
 Activates sympathetic system causing
rise in HR, BP and myocardial
contractility to improve cerebral
perfusion
 As a result of high vascular tone reflex
bradycardia mediated by baro
receptors will ensue

20. OCULOCARDIAC REFLEX
 Provoked by pressure applied to globe
of eye or traction on surrounding
tissues
 Stretch receptors in extraocular
muscles send afferent signals through
short and long ciliary nvs
 Ciliary nvs merge with trigeminal nv at
ciliary ganglion. Impulses carried to
gasserian ganglion resulting in
increased parasympathetic tone and

22. EFFECTS OF ANAESTHETIC
AGENTS ON
CARDIOVASCULAR SYSTEM
 Adrenergic agonists enhance the rate
of relaxation by enhancing calcium
reuptake by the Sarcoplasmic
reticulum
 Release of ACh following vagal
stimulation depresses contractility
through increased cGMP and

23.  Acidosis blocks slow calcium channels
and therefore also depresses cardiac
contractility by unfavourably altering
intracellular calcium kinetics

24. • Volatile anaesthetics depress cardiac
contractility by decreasing calcium
entry into cells during depolarization
• This blockade is potentiated by
hypocalcemia, ß-adrenergic blockade
and calcium channel blockers

26.  Potent inhaled anaesthetics decrease
SA node automacity
 Modest direct effects on AV node,
prolonging conduction times and
increasing refractoriness
 Explains junctional tachycardias when
an anticholinergic is administered for
sinus bradycardia during inhalation
anaesthesia

27.  Mechanism of cardiac depression by
IV anaesthetics is not well established
 Ketamine has the least depressant
effect on cardiac contractility
 Local anaesthetics also depress
cardiac contractility by reducing
calcium influx and release in dose-
dependant fashion

28.  Opioids, particularly fentanyl and
sufentanyl can depress cardiac
conduction, increasing AV node
conduction and the refractory period
and prolonging the duration of
Purkinje fibre action potential

29.  Lignocaine, due to its
electrophysiological effects, in low
doses can be therapeutic
 However, at high blood
concentrations, it depresses
conduction by binding to sodium
channels and at extremely high
concentrations it also depresses the
SA node

30.  Bupivacaine binds open or inactivated
sodium channels and dissociates from
them slowly.
 It can cause profound sinus
bradycardia and sinus node arrest and
malignant ventricular arrhythmias. It
can also depress left ventricular
contractility

31. ANAESTHETIC
CONSIDERATIONS
 Cardiovascular complications account
for 25-50% deaths following non
cardiac surgeries
 Perioperative MI, pulmonary edema,
CHF, arrhythmias, and
thromboembolism are most commonly
seen in patients with preexisting
cardiovascular disease

32.  Holter monitoring, exercise ECG,
myocardial perfusion scans and 2D
ECHO are important in determining
pre op risk and the need for coronary
angiography
 Patients with extensive ( three-vessel
or left main) coronary artery disease, a
history of MI or ventricular dysfunction
are at greatest risk of cardiac
complications

33.  Regardless of the level of pre op BP
control many pts with HTN display an
accentuated hypotensive response to
induction of anaesthesia followed by
an exaggerated hypertensive
response to intubation
 These pts display an exaggerated
response to both endogenous
catecholamines(intubation or surgical
stimulus) and exogenously
administered sympathetic agonists

34.  Sudden withdrawal of antianginal
medication preop- particularly ß
blockers- can precipitate sudden,
rebound increase in ischaemic
episodes

35.  Priority in managing ischaemic heart
disease is maintaining a favourable
myocardial supply- demand
relationship
 Autonomic- mediated increases in
heart rate and BP should be controlled
by deep anaesthesia or adrenergic
blockade and excessive reductions in
coronary perfusion pressure or arterial
oxygen content are to be avoided

36. Intra op detection of ischaemia:
1. Recognition of ECG changes
2. Hemodynamic manifestations
3. Regional wall motion anomalies on
TEE

37. MITRAL STENOSIS
Principal goal is maintainence of sinus
rhythm (if present preop) and to avoid
tachycardia, large increases in cardiac
output and both hypovolemia and fluid
overload by judicious administration of
IV fluids

38. MITRAL REGURGITATION
Tailored to severity of regurgitation and
to underlying left ventricular function
Exacerbating factors such as slow heart
rate and acute increases in afterload
should be avoided
Excessive volume expansion can also
worsen regurgitation by dilating LV

39. AORTIC STENOSIS
Maintainence of normal sinus rhythm,
heart rate, vascular resistance and
intravascular volume are critical
Loss of normally timed atrial systole
often leads to rapid deterioration
particularly when associated with
tachycardia
Spinal and epidural anaes are relatively
contraindicated in severe AS

40. AORTIC REGURGITATION
Bradycardia and increase in SVR
increase regurgitant volume in pts with
AR whereas tachycardia can contribute
to myocardial ischaemia
Compensatory increase in preload
should be maintained but excessive
fluid replacement may lead to
pulmonary edema

41. CONGENITAL HEART DISEASE
Presence of shunt flow between right
and left hearts, regardless of direction,
mandates the meticulous exclusion of
air bubbles or particulate matter from IV
fluids to prevent paradoxical embolism
into cerebral or coronary circulations

42.  Goal in management of TOF should
be to maintain intravascular volume
and SVR
 Increase in PVR, such as might occur
from acidosis or excessive airway
pressure should be avoided
 Right-to-left shunting tends to slow the
uptake of inhalational anaesthetics; in
contrast, it may accelerate the onset
of IV anaesthetics

43. THANK YOU