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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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Cardiovascular anatomy physiology

Cardiovascular Anatomy & Physiology


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


Cardiovascular system

Cardiovascular System


Cardiovascular structures

Cardiovascular Structures


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 SNSPSNS

  • inotropy+-

  • chronotropy+-

  • dromotropy+-

  • lusitropy+-

    Vessels

  • pulmonary/coronaryconstrictdilate

  • most othersconstrictno 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%


Cardiovascular anatomy physiology

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


Figure 13 15 the oxyhemoglobin dissociation curve

Figure: 13-15The oxyhemoglobin dissociation curve


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


Figure 13 17 the erythropoietin response to anemia hypoxia polycythemia

Figure: 13-17The erythropoietin response to anemia, hypoxia, polycythemia


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


Is electrical conduction normal

R

P

T

Q S

Is Electrical Conduction Normal?


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<85Recheck in 2 years

High Normal130-13985-89Recheck in 1 year

Hypertension

Stage 1 (mild)140-15990-99Confirm within 2 mo

Stage 2 (mod)160-179100-109Eval or refer 1 mo

Stage 3 (severe)180-209110-119Eval or refer 1 week

Stage 4 (very sev)>210>120Eval 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 stenosisThrombus Thrombus

>75% + lysiswith occlusion

Pain:predictableunpredictableunpredictable

relieved bynot relievednot relieved

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

Serum Enz: not elevatednot elevatedelevated


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 9 summary of events following mi

Figure: 18-9Summary of events following MI


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


Cardiovascular anatomy physiology

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


Cardiovascular anatomy physiology

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%)


Cardiovascular anatomy physiology

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


Cardiovascular anatomy physiology

ANEMIAS


Cardiovascular anatomy physiology

ANEMIAS


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


Cardiovascular anatomy physiology

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


Cardiovascular system physiology

Cardiovascular System Physiology


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 (-)


Cardiovascular anatomy physiology

CO2 transport in Blood

Also see

Fig 13-16

  • Dissolved CO2

  • Carbaminoglobin

  • Bicarbonate ion

Chloride

shift


Cardiovascular system1

Cardiovascular System


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


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