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Cardiovascular Anatomy & Physiology. Objectives. Function Anatomy Cells Cardiac Output Oxygen Transport Pathologies. Cardiovascular Function. Deliver oxygenated blood to tissues- where diffusion and filtration occur

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objectives
Objectives
  • Function
  • Anatomy
  • Cells
  • Cardiac Output
  • Oxygen Transport
  • Pathologies
cardiovascular function
Cardiovascular Function
  • Deliver oxygenated blood to tissues- where diffusion and filtration occur
  • Transport blood back to lungs- where oxygen and carbon dioxide exchange occur
human heart
Human Heart

Surface anatomy of the human heart. The heart is demarcated by:

-1. A point 9 cm to the left of the midsternal line (lower left or apex of the heart)

-2. The seventh right sternocostal articulation (lower right side of heart)

-3. The upper border of the third right costal cartilage 1 cm from the right sternal line (upper right side of heart)

-4. The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line (upper left side of heart)

3.

4.

2.

1.

cells of the cardiovascular system
Cells of the Cardiovascular System
  • Cardiac cells
    • pacemaker cells
    • cardiac myocytes
  • Vascular cells
    • endothelial cells
    • smooth muscle cells
cardiac myocytes
Cardiac Myocytes
  • Conduct AP cell-to-cell via gap junctions
  • Are packed with contractile elements
  • Have well developed sarcoplasmic reticulum which sequesters calcium
  • Are dependent on extracellular calcium for contraction
how does membrane depolarization lead to mechanical contraction
How does membrane depolarization lead to mechanical contraction?

Action Potential

Calcium influx from ECF

Calcium release from SR

Increased intracellular free calcium

actin-myosin crossbridging

myocardial cell shortening

cardiac muscle cell
Cardiac Muscle Cell

Ca

Ca++

channel

Ach

receptor

ATP

Ca

beta

receptors

cAMP

Ca

Na

Ca

Na

ATP

K

Na channel

SR

Na

digoxin

K

K channel

ans effects on heart and vessels
ANS effects on heart and vessels

Heart SNS PSNS

  • inotropy + -
  • chronotropy + -
  • dromotropy + -
  • lusitropy + -

Vessels

  • pulmonary/coronary constrict dilate
  • most others constrict no effect
cardiac output
Cardiac Output

THE most important variable in cardiac function!

CO = HR x SV

oxygen transport
Oxygen Transport

pO2 lungs = 80-100 mm Hg

pO2 tissues = 30-40 mm Hg

SaO2 lungs = 95-100%

SaO2 tissues = 60-80%

slide14
PaO2

Saturation

100

90

80

70

60

50

40

98%

96%

94%

92%

89%

83%

75%

shifts in hb o 2 affinity
Shift to left: affinity

alkalemia

hypothermia

hypocarbia

decreased 2,3DPG

Shifts in Hb-O2 Affinity
  • Shift to right: affinity
    • acidemia
    • hyperthermia
    • hypercarbia
    • increased 2,3DPG
carbon dioxide transport
Carbon Dioxide Transport

Physical Solution: (5%)

PaCO2 X .06

Carbaminohemoglobin: (15%)

HB N H

COO-

Bicarbonate ion (80%)

CO2 + H2O H2CO3 H+ + HCO3-

red cell production
Red Cell Production
  • iron
  • folate
  • vitamin B12
  • erythropoietin
  • functional stem cells
cardiovascular pathology
Cardiovascular Pathology
  • Anemia
  • Heart Failure
  • Valvular Defects
  • Cardiomyopathies
  • Congenital Defects
  • Vascular Insufficiency
general signs and symptoms of anemia
General Signs and Symptoms of Anemia
  • Increased respiration
  • Increased heart rate
  • Fatigue
  • Decreased activity tolerance
  • Pallor
  • Murmur
heart failure
Heart Failure
  • Def: Inability to effectively PUMP the amount of blood delivered to the heart
  • Left ventricular ejection fraction (EF)
    • Normal values: 60-80%
    • Important measure of heart failure
  • Etiologies: Many, but 2 main causes are hypertension and ischemia
    • MI
    • CIHD
    • Valve Disease
    • Congenital Defects
    • Cardiomyopathy
figure 19 5 interdependence of left and right heart function
Figure: 19-5Interdependence of left and right heart function

Clinical presentation of CHF

Differs for left, right, or both ventricle failure

Left Ventricular Failure (LVF)Right Ventricular Failure (RVF)

Forward Failure

Poor cardiac pumping = reduced CO

Backward Failure

Congestion of blood behind the heart

figure 19 7 manifestations of left heart failure
Figure: 19-7Manifestations of left heart failure

Clinical presentation of LVF

most common presentation for CHF

Often leads to RVF (biventricular failure)

Common causes

Left ventricular infarction

Cardiomyopathy

Aortic and mitral valvular disease

Systemic hypertension

Forward effects – reduced CO leads to hypoxia

Brain hypoxia – restlessness, mental fatigue,

confusion, anxiety, impaired memory

Cardinal symptom – dyspnea (early sign)

Hypoxemia results from impaired gas exchange

Cyanosis results from deOxyHgb (late sign)

Arterial Blood Gas analysis

Cyanotic

Elevated Left arterial pressure

Acute cardiogenic pulmonary edema – life threatening

Bolt-upright posture

Dyspnea and anxiety

Lungs are congested but systemic venous system is not

summary
Summary
  • Anemia
  • Heart Failure
  • Valvular Defects
  • Cardiomyopathy
  • Congenital Defects
  • Vascular Insufficiency
valvular disorders
Valvular Disorders
  • Abnormalities of Valve function:
    • Stenosis & Regurgitation
  • Etiology
    • congenital
    • rheumatic
    • degenerative calcification
    • infective
  • Diagnostic Evaluation: Echo-doppler
common valve disorders
Common Valve Disorders
  • Mitral Stenosis
  • Mitral Regurgitation
  • Aortic Stenosis
  • Aortic Regurgitation

Mitral valve lies between the left atrium and left ventricle.

Stenosis – obstruction to blood flow thru cardiac valves that are

not opening completely

Regurgitation – retrograde blood flow through a cardiac valve

when the valve is closed

differential diagnosis of murmur
Differential Diagnosis of Murmur
  • Mitral Stenosis
    • Increased Left Arterial Pressure
    • Loud S1 opening snap at apex
    • Murmur rare, if present, short diastolic
    • atrial fibrillation is common
mitral stenosis
Mitral Stenosis

120

90

60

30

LA/LV

gradient

0

differential diagnosis of murmur1
Differential Diagnosis of Murmur
  • Mitral Regurgitation
    • Systolic Murmur
    • Radiates to left axilla
    • Pansystolic, blowing
    • Prominent S3
mitral regurgitation
Mitral Regurgitation

120

90

60

large regurgitant V-wave

30

0

differential diagnosis of murmur2
Differential Diagnosis of Murmur
  • Aortic Stenosis
    • Mid systolic
    • Crescendo-decrescendo
    • Radiates to neck
    • S4 prominent
    • Angina, syncope common
aortic stenosis
Aortic Stenosis

180

LV/Aortic

pressure gradient

120

90

40

0

differential diagnosis of murmur3
Differential Diagnosis of Murmur
  • Aortic Regurgitation
    • Diastolic murmur
    • Bounding Pulse “waterhammer”
    • Wide pulse pressure
aortic regurgitation
Aortic Regurgitation

180

aortic pressure

with Aortic

Regurgitation

120

90

normal

aortic

pressure

40

0

cardiomyopathy
Cardiomyopathy
  • Dilated
    • enlarged heart chambers
    • poor contractility
  • Hypertrophic
    • outflow obstruction
    • ischemia
  • Restrictive
    • impaired diastolic filling
congenital heart defects
Acyanotic

L to R shunt

Atrial Septal Defect

Ventricular Septal Defect

Patent Ductus Arteriosus

Cyanotic

R to L shunt

Transposition

Tetralogy of Fallot

Congenital Heart Defects
shock
Shock
  • Defining Characteristic: Oxygen Delivery to one or more tissues is below basal requirements leading to hypoxic and immunologic injury.
  • Types of Shock:
    • Hypovolemic
    • Cardiogenic
    • Distributive (e.g. anaphylactic, septic, neurogenic)
  • Manifestations: Signs and symptoms of tissue ischemia and death.
diagnosis of shock
Diagnosis of Shock
  • Tachycardia
  • Hypotension (orthostatic)
  • Peripheral hypoperfusion (slow capillary refill, cool, mottled)
  • Oliguria or anuria
  • Metabolic acidosis
  • In septic shock: fever, chills
general treatment measures
General Treatment Measures
  • Supine position
  • Oxygen
  • Analgesics
  • Labs: CBC, ABG, Renal panel, Type & X, UA
  • Cardiac Monitoring
  • CVP Monitoring (at least)
  • Volume replacement (colloid vs crystalloid vs blood)
  • Vasoactive Drugs
septic shock
Septic Shock
  • Usually caused by gram negative bacteria. Monoclonal antibody to endotoxin may be used.
  • Don’t be fooled by high cardiac output, still have insufficient blood volume to fill the tank.
  • Oxygen consumption is often low due to abnormal distribution and shunt. Look for increased consumption with treatment.
  • Mortality is high: 40-80%
vascular system

Vascular System

Arterial Insufficiency

Venous Insufficiency

risks for vascular insufficiency
Arterial

smoking

atherosclerosis

inflammatory:Buergers

trauma

DIC

emboli from LV

vasospasm

diabetes mellitus

Venous

stasis of bloodflow

immobility

R heart failure

prolonged standing

obesity

pregnancy

trauma

hypercoagulable

high platelets

high hematocrit

Risks for Vascular Insufficiency
pathophysiology of insufficiency
Heart Pump

venous

arterial

ischemia

edema

capillary

Pathophysiology of Insufficiency
arterial insufficiency
Arterial Insufficiency

Flow Downstream

ischemia

chronic

acute

Pain

Pallor

Pulselessness

Paresis

Paralysis

Poikilothermy

Intermittent claudication

Atrophy (skin, hair)

Thickening of nails

venous insufficiency
Venous Insufficiency

Obstruction of Venous Drainage

capillary hydrostatic pressure

edema, stasis

pain

risk of pulmonary

embolus

stasis ulcers

and skin changes

thrombophlebitis
Deep Vein (DVT)

Extremity Edema

General leg pain

Fever

High Risk of PE

Treatment

immobilize

anticoagulate

treat risk factors

Superficial

local Inflammation

warm

tender

red

swollen

Collateral veins minimize edema

Low Risk of PE

Thrombophlebitis
assessment of cardiac function

Assessment of Cardiac Function

Electrical Function

Contractile Function

ecg assessment
ECG Assessment
  • Rate?
  • Conduction Abnormality?
    • Dysrhythmias
    • Conduction blocks
  • Ischemia/Infarction?
  • LVH?
cardiovascular pathophysiology

Cardiovascular Pathophysiology

Afterload – The resistance that must be overcome to eject blood

from a cardiac chamber. Left ventricular afterload is correlative with

the resistance in the systemic vasculature.

Preload – The volume of blood that remains in the cardiac chamber

prior to systole.

classification of hypertension
Classification of Hypertension

RecommendedFollowup

Category

SBP

DBP

Normal <130 <85 Recheck in 2 years

High Normal 130-139 85-89 Recheck in 1 year

Hypertension

Stage 1 (mild) 140-159 90-99 Confirm within 2 mo

Stage 2 (mod) 160-179 100-109 Eval or refer 1 mo

Stage 3 (severe) 180-209 110-119 Eval or refer 1 week

Stage 4 (very sev) >210 >120 Eval or refer immediately

differential diagnosis of hypertension
Differential Diagnosis of Hypertension
  • Primary Hypertension (95%)
  • Secondary Hypertension
    • Contraceptive use
    • Renal disease
    • Renal artery stenosis
    • Cushing’s syndrome
    • Pheochromocytoma
    • Pregnancy induced hypertension
treatment
Treatment?
  • Diuretics, beta blockers, ACE inhibitors, calcium channel blockers, alpha blockers
  • Consider age, ethnicity, coexisting disorders, cost, lipid profile
figure 18 2 lipoprotein transport
Figure: 18-2Lipoprotein transport

Chylomicron

85% triglyceride

5% cholesterol

VLDL

55% triglyceride

20% cholesterol

LDL

5% triglyceride

55% cholesterol

20% protein

HDL

5% triglyceride

20% cholesterol

50% protein

figure 18 3 type i iv atherosclerotic plaques
Figure: 18-3Type I - IV atherosclerotic plaques

Types I-III

Asymptomatic

Arterial wall narrowing

Types IV-VI

Predispose to ischemic

episodes

ischemic heart disease
Ischemic Heart Disease
  • Etiology:
    • Coronary Atherosclerosis
  • Risks:
  • Clinical Syndromes:
    • angina pectoris
    • myocardial infarction
    • chronic ischemic heart disease
    • sudden cardiac death
pathogenesis of atherosclerosis
Pathogenesis of Atherosclerosis

Lipid accumulates in vascular wall

Macrophages infiltrate the wall and

oxidize the lipids

Cell injury and release of local growth factors

(Angiotensin II)

Plaque formation on intimal wall

demand supply angina
Demand > Supply: Angina

Perfusion pressure

fixed stenosis

oxygen content

afterload

contractility

preload

heart rate

SUPPLY

DEMAND

How to increase supply? How to decrease demand?

pathogenesis of ischemia
Pathogenesis of Ischemia

Plaque Disruption or Breakdown

Tissue Thromboplastin Exposed

Platelet Aggregation and Clotting Cascade Activated

Thrombus Formation

Acute Ischemia

ischemic syndromes
Ischemic Syndromes

StableAngina

UnstableAngina

MI

Patho: Fixed stenosis Thrombus Thrombus

>75% + lysis with occlusion

Pain: predictable unpredictable unpredictable

relieved by not relieved not relieved

rest (3-5 min) rest rest (>15-30)

Serum Enz: not elevated not elevated elevated

ecg changes with ischemia
ST elevation

Q

ECG Changes with Ischemia
  • Indicative Leads show:
  • Ischemia: ST elevation or depression

T-wave peaking, flattening, inversion

Bigger than normal Q-waves

sequela of myocardial infarction
Decreased Myocardial Perfusion

Partially ischemic cells

Totally ischemic cells

Anaerobic metabolism

and lack of ATP

No ATP

Cell rupture and death

Ion leak across

cell membrane

Elevated

Enzymes

ST changes

Dysrhythmias

Q-waves

Sequela of Myocardial Infarction
figure 18 8 time course of serum marker elevations after mi
Figure: 18-8Time course of serum marker elevations after MI

Serum markers

released from damaged

cardiac cells

Cardiac isozymes – MI indicators

creatine kinase (CK-MB)

only present up to 72 hrs

troponin I (present longer)

troponin T (present longer)

compensatory response to decreased stroke volume
Compensatory Response to Decreased Stroke Volume

Decreased Stroke Volume

IMMEDIATE HOURS WEEKS

baroreceptor

activation

Increased LV

wall tension

RAS activity

fluid retained

ventricular

hypertrophy

SNS

preload

SV, CO

SV, CO

SV, CO

differential diagnosis of chest pain
Differential Diagnosis of Chest Pain
  • Cardiac ischemia
  • Chest wall trauma, costochondritis
  • Pleural pain - pneumonias
  • Pneumothorax
  • Gastrointestinal (GERD)
treatment of cardiac ischemia
Treatment of Cardiac Ischemia
  • Stable angina
    • SL nitroglycerin
    • Platelet inhibitor (e.g. ASA 325mg qod)
    • beta blocker
    • add long acting nitrate (remove at night)
    • add calcium channel blocker (not verapamil)
treatment of cardiac ischemia1
Treatment of Cardiac Ischemia
  • If ECG shows signs of current ischemia
    • Continuous ECG monitoring, Labs
    • Oxygen
    • Give ASA
    • Relieve pain with SL nitro, morphine
    • Evaluate for thrombolytic therapy
    • Decrease MVO2: bedrest, pain relief, etc
    • Manage dysrhythmias, hemodynamics
slide71
Heart Failure
  • Pathophysiological state
  • Abnormality of cardiac function to supply blood to meet demand
  • Pumps only from abnormally elevated diastolic filling pressure
  • Etiology
  • Myocardial failure
  • High demand on heart with near normal cardiac function
  • Inadequate adaptation of cardiac myocytes to increased wall stress
  • Causes circulatory failure but converse is not always true
  • Adaptations
  • Frank-Starling mechanism – increased preload sustains cardiac performance
  • Myocardial hypertrophy – mass of contractile tissue increases
  • Neurohumoral Activation –
    • Adrenergic cardiac nerves causes release of NE
    • Positive inotropy
    • Activation of RAA system – salt and water retention (increased preload, increased energy expense)
    • Release vasoconstrictive agents which increase afterload
  • Increased cAMP causes increased calcium entry
  • Positive inotropy, negative lusitropy
  • Increased energy expenditure and reduced CO which further stimulates RAA system
  • Calcium overload may cause arrythmia and sudden death
  • Cardiac AngII may cause negative lusitropy, positive inotropy, positive afterload, increased myocardial energy
  • expense
slide72
Congestive Heart Failure

Can result from most cardiac disorders.

Most common causes of CHF is myocardial ischemia from coronary artery disease, hypertension and dilated cardiomyopathy

Systolic dysfunction

Reduced myocardial contractility

Congestion is result of fluid backup in heart

Common cause is myocardial cell death – MI (neg inotropy)

EF less than 50%

Chronic overexcitation of b receptor SNS may be exacerbate condition

B receptor blockers – treatment

Heart failure –

Signs, symptoms CHF

Reduced stroke volume

Reduced cardiac output

Reduced EF (typically < 40%; severe if EF<20%)

slide73
Congestive Heart Failure

Diastolic dysfunction

Reduced myocardial relaxation

Ventricle is not compliant and does not fill effectively

Ventricle filling dependent on Ca2+ uptake (active phase of diastolic relaxation)

Passive phase (myocardial stretch) impaired

Common cause is myocardial cell death – MI (neg inotropy)

Heart failure –

Signs, symptoms CHF (congestion; edema)

Reduced stroke volume

Reduced cardiac output

Near normal EF > 50%

factors affecting cardiac output
Factors Affecting Cardiac Output
  • Heart Rate (chronotropy)
  • Contractility (inotropy)
  • Preload
  • Afterload
how is heart rate regulated
How is Heart Rate Regulated?
  • Intrinsic pacemaker rate = 100 bpm
  • Autonomic Influences
    • SNS------> B1 receptor-------> Increased HR
    • PSNS-> Muscarinic (Ach)--> Decreased HR
  • Stretch Reflex (Bainbridge): Increased filling------> Increased HR
  • Drugs: ANS drugs, digitalis
what factors affect contractility
What Factors Affect Contractility?
  • Anything that increases Ca++ availability in the heart muscle cell will increase Contractility.
  • Anything that decreases Ca++ availability in the heart muscle cell will decrease Contractility.
  • What would be the effect of:
    • SNS
    • PSNS
    • Digoxin
    • Ca++ channel blocker
    • B1 blocker
preload volume work of the heart
Preload: Volume Work of the Heart

S.V.

preload

The Frank-Starling Law of the Heart: Increased preload increases force of contraction

afterload pressure work of the heart
Afterload: Pressure work of the Heart
  • Increased Afterload occurs with increased resistance to ejection of blood from the ventricle
    • Increased Systemic Vascular Resistance
    • Increased Diastolic Blood Pressure
    • Aortic Stenosis
  • Increased Afterload: Decreased stroke volume
how can the different types of anemia be differentiated
How can the different types of anemia be differentiated?
  • Laboratory Diagnosis of Anemia
    • Low Hematocrit
    • Low Hemoglobin
    • Low RBC count
  • Red Cell Indices
    • MCV (size) microcytic, normocytic macrocytic
    • MCHC (color) hypochromic, normochromic
slide83
MCV

low

high

normal

Microcytic

  • iron deficiency
  • hemoglobinopathy
  • chronic disease
  • lead poisoning

Normocytic

  • acute bleeding
  • aplastic
  • hemolytic
  • low erythropoietin
  • malignancy

Macrocytic

  • low Vit B12
  • low folate
MCV
polycythemia
red cell mass

normal

increased

check erythropoietin

Relative

polycythemia

high

low

Secondary

Vera

- hydrate

- assess lung and kidney function

- assess

wbc, platelets

Polycythemia

Polycythemia

figure 19 2 compensatory mechanisms in heart failure
Figure: 19-2Compensatory mechanisms in heart failure

These mechanisms attempt to improve cardiac output

SNS activation – early response to reduced CO

Increased heart rate

Increased contractility

Increased arterial vasoconstriction

Increased renin release

Chronic SNS activation

Increased afterload

Increased workload = Reduced CO

Decreased CO reduces kidney perfusion

Activates RAA system ultimately leading to increased fluid retention

Decreased EF = Increased Preload = Reduced CO = Reduced GFR =

Increased Fluid Retention = Increased RAS activation =

Increased Blood volume= Increased Chamber volume =

Increased Contraction (myocardial stretching)

Higher Preload = Increased Contractility = Increased CO

left heart failure
Forward Failure

Poor cardiac pumping = reduced CO

Backward Failure

Congestion of blood behind the heart

Left Heart Failure

LVF

Forward

effects

Backward

effects

EF

CO

Tissue

perfusion

RAS

activation

Left Ventricular

preload

Fluid

retention

Left atrial

pressure

Pulmonary

Congestion & edema

(dysfunction)

Pulmonary

Pressure

Right ventricular

afterload

Right ventricular

hypertrophy

right heart failure
Forward Failure

Poor cardiac pumping = reduced CO

Backward Failure

Congestion of blood behind the heart

Right Heart Failure

RVF

Forward

effects

Backward

effects

Output to LV

EF

Right Ventricular

preload

Left ventricular

CO

Fluid

retention

Tissue

perfusion

Right atrial

pressure

RAS

activation

Systemic Venous

Congestion

figure 19 9 manifestations of right heart failure
Figure: 19-9Manifestations of right heart failure

Clinical presentation of RVF

Often results from LVF

Common causes

LVF

Right MI

Pulmonary disorders that increase pulmonary resistance

increased right ventricular afterload

reduce lung vascularization

hypoxemia, emphysema, embolus

RV compensates by increasing preload and

hypertrophy

Cardiomyopathy

Aortic and mitral valvular disease

Systemic hypertension

Forward effects – reduces CO via action on LV

Backward effects – congestion of systemic venous system

Impaired function of liver, portal system, spleen,

kidneys, peripheral subcuatenous tissues, brain

Edema apparent in lower extremities

Systemic system is congested but pulmonary system is not

In biventricular heart failure – both systemic venous and pulmonary systems are congested

principles of heart failure treatment
Principles of Heart Failure Treatment
  • GOAL: Optimize Cardiac Output and Minimize Cardiac Workload
    • Management of Preload
    • Management of Afterload
    • Management of Contractility

Drugs used in the management of Heart Failure (table 19-3)

phases of the ventricular action potential
Phases of the Ventricular Action Potential

1

Hyperpolarized (+)

2

K+ out

Ca++ in

0

3

K+ out

Na+ in

4

-70 mV

Depolarized (-)

slide92
CO2 transport in Blood

Also see

Fig 13-16

  • Dissolved CO2
  • Carbaminoglobin
  • Bicarbonate ion

Chloride

shift

cardiovascular structures1
Cardiovascular Structures

Structure diagram of the human heart from an anterior view. Blue components indicate de-oxygenated blood pathways and red components indicate oxygenated pathways.

pacemaker cells
Pacemaker Cells
  • SA node, AV node, Purkinje fibers
  • Spontaneously generate action potentials
  • Vary rate in response to ANS
  • Action potentials are associated with opening of slow calcium ion channels
  • Almost no contractile elements
what is the basis of automaticity
What is the basis of automaticity?

Spontaneous Phase 4 depolarization

K out

Ca

threshold

-40 mV

-60 mV

Na

RMP

pacemaker cells are leaky to sodium at rest

ans influences on ion flux
ANS Influences on Ion Flux
  • Sympathetic: NE, E stimulates Beta receptors leading to opening of Na/Ca channels. The cell depolarizes faster.
  • Parasympathetic: acetylcholine stimulates muscarinic receptors leading to opening of K channels. Potassium leak out offsets sodium influx. The cell depolarizes slower.
autonomic nerves
SNS (T1-L2)

a1, a2

b1, b2, b3

Ach

N1

NE

receptor

nicotinic

PSNS (Cn IX, X)

Ach

M1 to M5

Ach

N1

muscarinic

receptor

nicotinic

alpha-MN

N2 (nicotinic)

Ach

muscle

Autonomic NERVES
ad