1. Anatomy, Physiology &
Patophysiology of the
Cardiovascular System:
Anesthesia Approach
Prof. Karen Haddock
MSN, CRNA

2. Comprises
and
The• Heart four chambers, side,iseach
divided into a right and left
with an atrium and a ventricle.
•
The left ventricle generate greater
pressures than the right ventricle, and
so has a much thicker and more
muscular wall.
•
Four valves ensure that blood flows
only one way:
– tricuspid and mitral valves - from atria
to ventricle
– pulmonary and aortic valves - to the
arterial circulations
•
The myocardium consists of muscle
cells which can contract
spontaneously, also pacemaker and
conducting cells, which have a
specialized function.

3. Coronary Circulation
• Right coronary arterysupplies the right atrium, right
ventricle, inferior wall left
ventricle, SA node (60% of
individuals), AV node (8590% of individuals)
EKG: lead II, III y AVF
• Left coronary arterysupplies left atrium,
interventricular septum, the
left ventricle (septal, anterior
& lateral walls), SA node
(40% of individuals)
EKG: lead V3 yV5

4. • Circumflex artery (CX)supplies lateral wall.
EKG: lead I y AVL
• Left anterior descending
(LAD) - supplies
septum and anterior
wall
EKG: Lead V5

5. 1. left coronary artery
(left main artery)
2. circumflex artery
3. obtuse marginal
branch of the
circumflex artery
4. atrioventricular groove
branch of the
circumflex artery
5. anterior
interventricular artery
(left anterior
descending artery -

6. The Coronary Circulation
• Myocardial blood supply is from the right and left coronary
arteries.
• Venous drainage is mostly via the coronary sinus into the
right atrium, but a small proportion of blood flows directly
into the ventricles through the Thebesian veins, delivering
unoxygenated blood to the systemic circulation.
• Oxygen extraction by the tissues is dependent on
consumption and delivery.
• Myocardial oxygen consumption is higher than in skeletal
muscle (65% of arterial oxygen is extracted as compared to
25%).

7. • The sympathetic
nerves
– The SA node is an
increase in heart
rate.
– The effect on the
muscle is an
increase in rise of
pressure within the
ventricle, thus
increasing stroke
volume.
Α1, β1 & β2

8. Effect of sympathetic stimulation on
the heart:
• Increased sympathetic stimulation > release of
norepinephrine at SA node > decreased permeability
of SA node cell membranes to potassium >
membrane potential becomes less negative (closer
to threshold) > more action potentials (and more
contractions) per minute.

9. • The vagus provides
the parasympathetic
The effect of the
vagus at the SA
node is the opposite
of the sympathetic
nerves, it decreases
the heart rate.
acetilcoline (MU 2)

10. Effect of parasympathetic stimulation
on the heart
• Increased parasympathetic stimulation >
release of acetylcholine at the SA node >
increased permeability of SA node cell
membranes to potassium > 'hyperpolarized'
membrane > fewer action potentials (and,
therefore, fewer contractions) per minute.

11. • Depolarization is due to
the inward diffusion of
calcium (not sodium as in
nerve cell membranes).
• Depolarization begins
when:
– the slow calcium channels
open (4),
– then concludes (quickly)
when the fast calcium
channels open (0).
– Repolarization is due to the
outward diffusion of
potassium (3).

12. Cardiac Cycle
• The first stage is diastole, which
diastole
represents ventricular filling and a brief
period just prior to filling at which time the
ventricles are relaxing.
• The second stage is systole, which
systole
represents the time of contraction and
ejection of blood from the ventricles.

13. • P wave = caused by
atrial depolarization
• QRS complex =
caused by ventricular
depolarization
• T wave = caused by
ventricular
repolarization

15. Determinants of Ventricular
Performance
• Cardiac output (CO) is the product of heart rate
(HR) and stroke volume (SV):
CO = HR x SV
• Stroke volume is determined by three main
factors: preload, afterload and contractility.
• Preload is the ventricular volume at the end of
diastole.

16. Starling's law of the heart.
• The relationship
between ventricular
end-diastolic volume
and stroke volume is
known as Starling's
law of the heart.
• An increase in
preload (end-diastolic
volume) increases
stroke volume.

17. Determinants of Ventricular
Performance
• Afterload is the resistance to ventricular
ejection. This is caused by the resistance to flow
in the systemic circulation and is the systemic
vascular resistance.
– Is affected mainly by:
• ventricular volume (size)
• arterial vasomotor tone (arterial resistance)
• ventricular wall thickness
– Afterload is increased by:
• increase in ventricular volume
• increase in arterial vasomotor tone
• decrease in ventricular wall thickness
– Afterload is decreased by the opposite changes

18. Determinants of Ventricular
Performance
• Contractility describes the ability of the myocardium to
contract in the absence of any changes in preload or
afterload.
• In the sympathetic nervous system, Beta-adrenergic
receptors are stimulated by noradrenaline released from
nerve endings, and contractility increases.
• A similar effect is seen with circulating adrenaline and
drugs such as ephedrine, digoxin and calcium.
• Contractility is reduced by acidosis, myocardial ischemia,
and the use of beta-blocking and anti-arrhythmic agents.

19. Hemodynamics
Monitoring Values and Equations
1. Systemic Vascular Resistance (SVR) =
[(MAP-PAWP)/CO]x80 → SVR=1170
dynes/sec/cm-5 (range 700-1200).
2. MAP=mean arterial pressure=1/3(SBP-DBP)+DBP or
MAP
(1) SBP+ (2) DBP / 3
3. CO (cardiac output)= SV x HR → 5 - 6L/m
4. SV (Stroke Volume)= CO/HR
4. PAWP or PCWP=pulmonary artery wedge pressure.
PCWP
5. Cardiac Index (CI)=CO/BSA → CI=2.5-3.5 L/min/m2
(CI)
6. BSA=body surface area.
BSA

20. Swan-Ganz Catheter pressures
• RA - 0-8 mmHg
• RV -15-30/2-8 mmHg
• PA –
– Systolic 20-30 mmHg,
Diastolic 8-12 mmHg,
Mean 25 mmHg
• PAWP or PCWP6-12 mmHg (measured
at end-expiration)

21. Cardiovascular
Disorders: Anesthesia
Management

23. Heart failure
• Is the inability of the heart to supply
adequate blood flow and therefore oxygen
delivery to peripheral tissues and organs.
Under perfusion of organs leads to
reduced exercise capacity, fatigue, and
shortness of breath.
• It can also lead to organ dysfunction (e.g.,
renal failure) in some patients.

24. Path physiology of Heart Failure
• Systolic heart failure occurs when the heart
is unable to pump a sufficient amount of
blood to meet the body's metabolic
requirements.
• Clinical manifestations usually reflect the
effects of the low cardiac output on tissues
(eg, fatigue, oxygen debt, acidosis), the
damming up of blood behind the failing
ventricle (systemic or pulmonary venous
congestion), or both.
• The left ventricle is most commonly involved,
often with secondary involvement of the right
ventricle. Isolated right ventricular.

25. Path physiology of Heart Failure
• Diastolic dysfunction can also cause
symptoms of heart failure as a result of
atrial hypertension.
• Common causes include hypertension,
coronary artery disease, hypertrophic
cardiomyopathy, and pericardial
disease.
• Although diastolic dysfunction can
cardiac output is reduced in most
forms of heart failure. Inadequate
oxygen delivery to tissues is reflected.

27. Anesthesia Management in
presence of CHF
•
•
•
•
Not deshydration or fluids overload
Ketamine, Etomidate & Opioids
Isoflurane in low MAC
Positive Pressure ventilation may
decrease pulmonary congestion
• Invasive monitoring
• Regional anesthesia is acceptable

28. Hypertension
• Essential hypertension accounts for 80-95% of
cases and may be associated with an abnormal
baseline elevation of cardiac output, systemic
vascular resistance (SVR), or both.
• The chronic increase in cardiac afterload results
in concentric LVH and altered diastolic function.
• Hypertension also alters cerebral autoregulation
in the range of mean blood pressures of 110180 mm Hg.

29. Hypertension
• In the perioperative period, poorly
controlled hypertension is associated with
an increased incidence of ischemia, left
ventricular dysfunction, arrhythmia, and
stroke.
• The goal should be a systolic blood
pressure less than 140 mm Hg and a
diastolic blood pressure lower than 90 mm
Hg before proceeding with elective
surgery.

30. Hypertension
• In any patient with stage 3 hypertension (ie,
>180/110 mm Hg), blood pressure should be
well controlled prior to surgery.
• Intravenous esmolol, hidralazine, labetalol,
nitroprusside, or nitroglycerin may be used for
acute episodes of intraoperative hypertension,
whereas calcium channel blockers or
angiotensin-converting enzyme (ACE) inhibitors
may be used in less acute situations.

31. Hypertension
General Anesthesia
•
•
•
Intravenous Agent : all except Ketamine.
Volatile anesthetics are secure.
Neuromuscular Blocking Agent: all except
pancuronium.
• Narcotics: secure
Narcotics
Regional anesthesia is acceptable.

32. Ischemic Heart Disease
• Otherwise known as Coronary Artery Disease, is
a condition that affects the supply of blood to the
heart. The blood vessels are narrowed or
blocked due to the deposition of cholesterol
plaques on their walls.
• This reduces the supply of oxygen and nutrients
to the heart musculature, which is essential for
proper functioning of the heart.

33. Angina pectoris
• The myocardial ischemia of unstable angina, like
all tissue ischemia, results from excessive
demand or inadequate supply of oxygen,
glucose, and free fatty acids.
• Stable Angina -is chest pain or discomfort that
typically occurs with activity or stress.
• Instable Angina- chest pain happens
unexpectedly after light activity or occurs at rest.

34. Myocardial Infarction
•
The pathogenesis can include:
– Occlusive intracoronary thrombus
– Vasospasm
– Emboli
•
Complications can include:
• Arrhythmias and conduction defects, with possible "sudden death"
• Extension of infarction, or re-infarction
• Congestive heart failure (pulmonary edema)
• Cardiogenic shock
• Pericarditis
• Mural thrombosis, with possible embolization
• Myocardial wall rupture, with possible tamponade
• Papillary muscle rupture, with possible valvular insufficiency
• Ventricular aneurysm formation

35. Anesthesia Management in Patient
with MI
• Goal: Avoid the activation of
Sympathetic nervous system all the
time.
• Preoperative preparation
– Sedation
– Antihypertensive drugs

36. Anesthesia Management in Patient
with MI
• Intraoperative management
Avoid increase the heart rate
(>110beats/min) & systemic pressure
more than 20%.
Invasive monitoring ( arterial line & PA
cath if required)
Lead II & V
Short duration on direct laryngoscopy (<15
sec.)

37. Anesthesia Management in Patient
with MI
• Intraoperative management
In patients with normal left ventricular
functionvolatile anesthetics with or without nitrous oxide
(Forane is the best)
In patients with severely impaired left
ventricular functionthe use of short-acting opioids (fentanyl, 50-100
/Lg/kg IV, or equivalent doses of other opioids)
Etomidate is the best

38. •
Drugs Intended to Attenuate the
Systemic Blood Pressure and/or
Heart Rate Response to Tracheal
Intubation
Laryngotracheal lidocaine
•
Lidocaine 1.5 mg/kg IV 90 seconds before beginning direct
laryngoscopy
•
Nitroprusside 1-2 /Lg/kg IV 15 seconds before beginning direct
laryngoscopy
•
Esmolol 100-300 /Lg/kg/min IV before and during direct laryngoscopy
•
Fentanyl 1-3 /Lg/kg IV 90-120 seconds before beginning direct
laryngoscopy
•
Nitroglycerin 0.25-1.00 /Lg/kg/min IV to decrease the pressor response
(no evidence that the incidence of intraoperative myocardial ischemia is
decreased)

39. Cardiac Tamponade
•
Cardiac tamponade is a clinical syndrome
caused by the accumulation of fluid in the
pericardial space, resulting in reduced
ventricular filling and subsequent
hemodynamic compromise.
• Cardiac tamponade is a medical
emergency.

40. Clinical Manifestations of Cardiac
Tamponade
• Increased central venous pressure
• Activation of the sympathetic nervous system (tachycardia
and vasoconstriction)
• Equalization of right and left atrial pressures and right
ventricular end-diastolic pressures at about 20 mmHg
(exception may be accumulation of blood and clots over the
right ventricle, as may follow cardiac surgery)
• Paradoxical pulse (decrease> 10 mmHg in systolic blood
pressure during inspiration)
• Hypotension (low cardiac output)

41. Cardiac Tamponade

42. Anesthesia management in Cardiac
Tamponade
• Treatment
– Removal of fluid (pericardiocentesis)
– Temporizing measures are designed to maintain stroke
volume until definitive surgical treatment of cardiac
tamponade.
– Intravenous infusion of colloid or crystalloid solutions
– Catecholamines
– Correction of metabolic acidosis

43. Anesthesia Management in Cardiac
Tamponade
• Pericardiocentesis performed with local anesthesia is
often preferred for the initial management of patients
who are hypotensive owing to low cardiac output
produced by cardiac tamponade.
• The goal is to maintain cardiac output. Ketamine is
useful for induction and maintenance of anesthesia, as it
increases myocardial contractility, systemic vascular
resistance, and heart rate.
• Continuous intravenous infusions of catecholamines,
such as isoproterenol, dopamine, or dobutamine, may be
isoproterenol dopamine
useful for maintaining cardiac output until the cardiac
tamponade can be relieved by surgical drainage.

44. Mitral Stenosis
• The clinical manifestations of mitral stenosis are
caused by the mechanical obstruction that impairs
ventricular filling through the narrowed mitral orifice.
• This obstruction results in the development of a
pressure gradient across the valve in diastole and
causes an elevation in left atrial and pulmonary
venous pressure.
• Avoid atrial fibrillation & tachycardia. The gradient
tachycardia
(and left atrial pressure) can be elevated by an
increase in cardiac output, a decrease in diastolic
filling time (which occurs with faster heart rates), or
the development of atrial fibrillation.

45. Mitral Stenosis
• The characteristic findings of mitral stenosis on
auscultation are an accentuated first heart sound
(diastolic), an opening snap, and a mid-diastolic
rumble, which is best heard at the cardiac apex.
• Reduced cardiac output from the restricted filling of
the left ventricle.
• Mitral stenosis is usually
secondary to rheumatic disease.
• Most patients are female

46. Anesthetic Management in
Mitral Stenosis
• The goals of anesthetic management are to
maintain cardiac output through the tight
mitral valve while avoiding pulmonary
congestion.
• Patients already in atrial fibrillation should
have the rate controlled aggressively.
aggressively
• The pulmonary vasculature is sensitive to
hypoxemia or hypercarbia so meticulous
attention should be paid to these values.
While epidural and spinal anesthesia can be
safely performed in patients with MS,

47. Mitral regurgitation
• Is leakage of blood from the left
ventricle into the left atrium during
systole.
• The characteristic finding in a patient
with mitral regurgitation is a blowing
systolic murmur that is heard best at
the cardiac apex.
• The pathophysiology of MR is volume
overload of the LV, similar to AR.

48. Mitral Valve Replacement

49. Anesthesia Management in
Mitral Regurgitation
• Cardiac output is best when the heart is full and
reasonably fast, and the blood pressure is lownormal.
• Bradycardia is associated with an increase in
ventricular size; avoid.
• The need for a low “afterload” as determined by
blood pressure is explained avoidance of myocardial
depression within reason should be a goal.
• Patients with MR often require inotropic assistance
to accomplish these hemodynamic goals in the face
of general anesthesia.

50. Aortic Stenosis
• The gradual process of narrowing of
the aortic orifice leads to concentric
left ventricular.
• Hypertrophy and a reduction in left
ventricular compliance – the
myocardium become thick, the enddiastolic pressure (LVEDP) rises, but
there is no dilatation. Concentric
hypertrophy.

51. Aortic Stenosis
• The gradual process
of narrowing of the
aortic orifice leads
to concentric left
ventricular
hypertrophy and a
reduction in left
ventricular
compliance – the
myocardium
becomes thick, the
end-diastolic

52. Anesthesia Management
• Invasive monitoring with an arterial catheter
is probably indicated for most procedures;
the use of a pulmonary artery catheter (PAC)
or transesophageal echo (TEE).
• Hypotension and dysrhythmias must be
treated early and aggressively.
aggressively
• Conversely, hypertension should be treated
very cautiously.
• The anesthetic was planned accordingly, in
some cases including spinal or epidural

53. Aortic Regurgitation
• The commonest causes of AR in the
adult are rheumatic fever, bacterial
endocarditits, trauma, and aortic
dissection.
• Congenital diseases such as Marfan
syndrome.
• The pathophysiology of AR is volume
overload of the left ventricle, with
dilatation and eccentric hypertrophy
rather than the concentric hypertrophy

54. The Anesthetic Management in
Aortic Regurgitation
• Maintaining an adequate preload to
assure filling of the hypertrophied,
dilated LV (maintaining cardiac output).
• High-normal heart rate to reduce the
proportion of time spent in diastole.
• Low-normal systemic blood pressure
to encourage forward rather than
regurgitant flow (decrease afterload)
afterload