cardiac a&p review - bmh/tele

Cardiovascular ReviewCardiovascular Review

Natalie Bermudez, RN, BSN, MSNatalie Bermudez, RN, BSN, MSClinical Educator for Cardiac TelemetryClinical Educator for Cardiac Telemetry

Telemetry

Course

The Human HeartThe Human Heart

• Layers (3)

• Atria (2)

• Ventricles (2)

• Valves (4)

• Veins

• Arteries

Layers of the HeartLayers of the Heart

1) Pericardium

2) Myocardium

3) Endocardium

The PericardiumThe Pericardium

• Double-walled serous sac surrounding the heart

• Strengthened externally by a tough fibrous connective tissue layer

The Pericardium: Three LayersThe Pericardium: Three Layers

• Fibrous pericardium (outer)– Pericardiophrenic

ligament• Blends with the outer

fibrous layer or adventitia of all the great vessels except the IVC

– Sternopericardial ligaments

• Keeps heart in its place; attaches to the sternum

The Pericardium: Three LayersThe Pericardium: Three Layers

• Parietal Pericardium– Lines the inner surface

of the fibrous pericardium

• Visceral Pericardium– Aka epicardium– Serous fluid secreted

by these cells forms a thin lubricating film in the pericardial cavity that provides a friction-free environment for the beating heart

Cardiac TamponadeCardiac Tamponade• It is a potentially fatal condition that occurs when fluid

rapidly accumulates in the pericardial cavity as a result of trauma, aortic aneurysm, or cardiac surgery.

• The increased fluid causes external compression of the heart, which decreases venous return and CO.

The MyocardiumThe Myocardium

P Cells • Pacemaker cells

– Responsible for generation of action potentials

– electrical activity

Cardiomyocytes• Myocardial Cells

– Contractile cells that generate force– Mechanical activity

Myocardial Cardiac Cell TypesMyocardial Cardiac Cell Types

Fibroblasts

• Cells residing in the extracellular mix

Endotehlial & Smooth Muscle Cells

• Cells found in the blood vessels

Atria & VentriclesAtria & VentriclesRight Atrium

Left Atrium

Right Ventricle

Left Ventricle

Heart ValvesHeart Valves

Right:Tricuspid Pulmonic

Left:Bicuspid (Mitral)

Aortic

Valvular StructuresValvular Structures

Leaflets

AV Valves(2 or 3)

Semilunar (3)

Additional Valvular Additional Valvular StructuresStructures

Help to keep A-V valves closed during ventricular systole

Blood VesselsBlood Vessels

Aorta (A & D)

SVC

IVC

Pulmonary Artery

Pulmonary Vein

Coronary ArteriesCoronary ArteriesAnterior ViewAnterior View

Coronary ArteriesCoronary ArteriesPosterior ViewPosterior View

Coronary Blood FlowCoronary Blood Flow

Coronary filling occurs during

ventricular Diastole


An increase in heart rate shortens

diastole and can decrease

myocardial perfusion


RCA Blood Supply:(a) Originates behind the right

coronary cusp of the aortic valve

(b) Supplies• Right atrium and Right ventricle• SA Node and AV node• Inferior-posterior wall of the LV

(in 90% of hearts)• Inferior-posterior third of the

intraventricular septum


LCA Blood Supply:Divides into the Anterior Descending

Artery & Circumflex Artery

• Left atrium

• Most of the left ventricle

• Most of the intraventricular septum


Cardiac veins lie superficially to the

arteries

The largest vein, the coronary sinus

empties into to the right atrium


Most of the major cardiac veins empty

into the coronary sinus

However, the anterior cardiac veins empty into the right atrium

Pumping Action of the HeartPumping Action of the Heart

Diastole:Diastole:

Atrial Contraction (ventricular muscle relaxation)

Pressure Greater in the Atria

A-V Valves Open

Ventricles Fill


Atrial Contraction → 10% to 20% left ventricular filling

Pulmonary Veins passively fill left ventricle while mitral

valve is open


In elevated heart rates Atrial Contraction → 40% left

ventricular filling

A.K.A. Atrial KickA.K.A. Atrial Kick


End-Diastolic Volume End-Diastolic Volume (EDV)(EDV)

Amount of blood in ventricular volume right before systole

occurs

Left Ventricular EDV is approximately 120 ml

Aortic Valve Opens Aortic Valve Closes

S1 S2AV

Valve Closes

AV Valve Opens

Pumping Action of the HeartPumping Action of the HeartVentricular Contraction

Systole:Systole:

(relaxation of atrial muscles)

Pressure Greater in Ventricles than Aortic & Pulmonic Blood Vessels

Aortic & Pulmonic Valves Open

Blood Ejected into Vessels


Stroke Volume Stroke Volume

The amount of blood ejected by the left or right ventricle at each heartbeat.

The amount varies with age, sex, and exercise but averages 60 to 80 ml.

EDV = LVEDV - LVESV

(Taber’s Medical On-line Dictionary)


Cardiac OutputCardiac Output

The amount of blood discharged from the left or right ventricle per minute.

(Taber’s Medical On-line Dictionary)


Ejection FractionEjection FractionThe percentage of the blood emptied

from the ventricle during systole

The left ventricular ejection fraction averages 60% to 70% in healthy

hearts(Taber’s Medical On-line Dictionary)

Normal LV EF = 50% to 75%

EF = Ventricular EDV/EDV x 100


Cardiac Output is Cardiac Output is determined by:determined by:

PreloadContractility

AfterloadHeart Rate

(Core Curriculum for Progressive Care Nurses, p. 138)


PreloadPreloadStretching of the muscle fibers in the

ventricle. Results from blood volume in the ventricles at diastole

(EDV).(Comerford & Mayer, 2007, p. 15)

…Refers to the degree of stretch of the cardiac muscle fibers at the

end of diastole(Smeltzer et al, 2008, p. 786)

Frank-Starling MechanismFrank-Starling Mechanism

Preload is described by the Frank-Starling Mechanism

A.K.A.Frank-Starling Law of the Heart

orStarling’s Law


In the intact heart, this means that the force of contractions will

increase as the heart is filled with more blood and is a direct

consequence of the effect of an increasing load on a single muscle

fiber.


The Rubber Band Effect

The farther a rubber band is stretched, the farther it will go!!

PreloadPreloadIncreased Preload Occurs With:• Increased circulating volume• Venous constriction (decreases venous

pooling and increases venous return to the heart)

• Drugs: Vasoconstrictors

PreloadPreloadDecreased Preload Occurs With:• Hypovolemia• Mitral stenosis• Drugs: Vasodilators• Cardiac Tamponade• Constrictive Pericarditis


ContractilityContractility

Refers to the inherent ability of the myocardium to contract normally

It is directly influenced by preload

The greater the stretch, the more forceful the contraction

(Comerford & Mayer, 2007, p. 15)

ContractilityContractilityIncreased Contractility Occurs With:• Drugs: Positive inotropic agents

– digoxin, milrinone, epinephrine, dobutamine

• Increased heart rate– Bowditch’s phenomenon

• Sympathetic stimulation – via ß1-receptors

ContractilityContractilityDecreased Contractility Occurs

With:• Drugs: Negative inotropic agents

– Type 1A antiarrhythmics, ß-Blockers, CCBs, barbituates

• Hypoxia• Hypercapnia• Myocardial ischemia• Metabolic acidosis


AfterloadAfterload

Refers to the pressure that the ventricular muscles must

generate to overcome the higher pressure of the aorta to the blood

out of the heart(Comerford & Mayer, 2007, p. 15)

AfterloadAfterloadIncreased Afterload Occurs With:• Aortic stenosis• Peripheral arteriolar

vasoconstriction• Hypertension• Polycythemia• Drugs: Arterial vasoconstrictors

AfterloadAfterloadDecreased Afterload Occurs With:• Hypovolemia• Sepsis• Drugs: Arterial vasodilators

Heart RateHeart RateInfluenced By Many Factors:• Blood volume status• Sympathetic & Parasympathetic Tone• Drugs• Temperature• Respiration• Dysrhythmias• Peripheral Vascular Tone• Emotions• Metabolic Status (includes hyperthyroidism)

Heart RateHeart RateDeterminant of Myocardial O2

Supply & Demand:• Increased heart rates increase myocardial

oxygen demand• Fast heart rates (> 150 bpm) decrease

diastolic coronary blood flow (shorter diastole)

Ventricular Function Curve


Systemic Vascular Systemic Vascular Resistance Resistance

Also affects cardiac output…

The resistance against which the left ventricle must pump to move

blood throughout systemic circulation

(Comerford & Mayer, 2007, p.13)



Can be affected by:• Tone and diameter of the blood

vessels• Viscosity of the blood

• Resistance from the inner lining of the blood vessels

(Comerford & Mayer, 2007, p.13)



SVR has an inverse relationship to CO

If SVR decreases, CO increasesIf SVR increases, CO decreases

SVR = mean arterial pressure – central venous pressure x 80cardiac output

(Comerford & Mayer, 2007)



Conditions that cause an increase in SVR:

• Hypothermia• Hypovolemia

• Pheochromocytoma• Stress response

• Syndromes of low CO



Conditions that cause a decrease in SVR:

• Anaphylactic and neurogenic shock• Anemia

• Cirrhosis• Vasodilation


• About 60,000 miles of arteries, aterioles, capillaries, venules, and veins keep blood circulating to and from every functioning cell in the body!

• There is approximately 5 liters of total circulating blood volume in the adult body


Five Types:

ArteriesArteriolesCapillaries

VenulesVeins

ArteriesArteries• Strong, compliant elastic-

walled vessels that branch off the aorta, carry blood away from the heart, and distribute it to capillary beds throughout the body

• A high-pressure circuit• Able to stretch during systole

and recoil during diastole because of the elastic fibers in the arterial walls

Arterial BaroreceptorsArterial Baroreceptors• These are receptors that

are sensitive to arterial wall stretching

• Located in the aortic arch and near the carotid sinuses

• Responsible for modulation of vascular resistance and heart rate in order to maintain appropriate BP

• Keep MAP constant

Arterial BaroreceptorsArterial BaroreceptorsVasomotor Center: • In high blood pressures,

the aortic arch and carotid sinus stretch

• When stretching is sensed, a message is sent via the vagus nerve (aortic arch) and the glossopharyngeal nerve (carotid sinus)

Arterial BaroreceptorsArterial Baroreceptors

• Inhibition of SNS outflow to the peripheral blood vessels & Stimulates the PNS

• Blood Pressure Decrease by:– Vasodilation of peripheral

vessels– Decrease in HR & contractility– Decrease SVR

Arterial BaroreceptorsArterial Baroreceptors

• Responsible for short-term adjustment of BP

• Respond to abrupt fluctuations in BP (postural changes)

• Less effective in long-term regulation of BP– Reset or become

insensitive when subjected to prolonged elevated BP

Arterial BaroreceptorsArterial BaroreceptorsIn low blood pressures:

• SNS is stimulated & PNS is inhibited

• Blood Pressure Increased by:– Increased HR & Contractility– Peripheral Arterial & Venous

Constriction• Preserves blood flow to the brain

& heart

ArteriolesArterioles• Control systemic

vascular resistance and thus arterial pressure

• Lead directly into capillaries

• Have strong smooth muscle walls innervated by the ANS

ArteriolesArteriolesAutonomic Nervous System

• Adrenergic (Stimulatory) System– 2 Neurotransmitters

•Epinephrine: stimulates β-receptors which increases heart rate and contractility and causes arteriolar vasodilation

•Norepinephrine: stimulates α-receptors which results in vasoconstriction

ArteriolesArteriolesAutonomic Nervous System

• Cholinergic (Inhibitory) System– 1 Neurotransmitter

•Acetylcholine: Decreases heart rate; releases nitric oxide causing vasodilation

CapillariesCapillaries

Microscopic

Walls are composed of only a single layer of endothelial cells

CapillariesCapillaries

Capillary pressure is extremely low to allow for exchange of

nutrients, oxygen, and carbon dioxide with body cells

SphinctersSphincters

At the ends of the arterioles and beginning of capillaries

• Dilate to permit blood flow• Constrict to increase blood pressure

• Close to shunt blood

VenulesVenules

Gather blood from capillaries

Walls are thinner than

those of arterioles

VeinsVeins

Thinner walls than arteries

Large diameters because of the

low blood pressure of

venous return to the heart

VeinsVeins

Valves prevent backflow

Pooled blood in each valve segment is

moved toward the heart by pressure from the moving volume of blood in the previous

valve segment

VeinsVeins

Most veins return

blood to the right atrium of the heart

Blood pressure regulation is maintained

via vasodilation

or vasoconstricti

on of the arterial vessels

Function of Blood Vessels

What is the function of blood vessels???• Distribution of blood throughout the body

– Supplies all cells w/ O2 & nutrients– Removes metabolic waste & CO2

• Provides a conduit for hormones, cells of the immune system, & regulation of body temperature

FYI – The lymphatic system is a parallel circulatory system that functions to return excess interstitial fluid to the heart

Blood Pressure Regulation

Resistance Vessels

Dilation of arteries (resistance vessels) = decrease in cardiac afterload

Arteriolar dilators reduce cardiac workload while causing cardiac output and tissue perfusion to

increase

Blood Pressure Regulation

Capacitance Vessels

Dilation of veins (capacitance vessels) = reduced force of blood return to the heart thus decreasing preload

Results in decreased force of ventricular contraction and oxygen

consumption, decreased cardiac output and tissue perfusion

Renin-Angiotensin-Aldosterone Renin-Angiotensin-Aldosterone SystemSystem

Blood Pressure Regulatory Mechanism

R-A-A-SR-A-A-S

ReninRenin

a.k.a. angiotensinogenase

Converts angiotensinogen to angiotensin I

R-A-A-SR-A-A-S

Angiotensin IAngiotensin I

Has no biological activity

Exists solely as a precursor to angiotensin II

R-A-A-SR-A-A-SAngiotensin IIAngiotensin II

Angiotensin I is converted into angiotensin II by the

angiotensin-converting enzyme

Potent vasoconstrictor

Also acts on the adrenal cortex in releasing aldosterone

R-A-A-SR-A-A-SAldosteroneAldosterone

Regulates sodium and potassium in the blood – retain sodium & excrete

potassium

Release triggered by increased levels of angiotensin II, ACTH,

and potassium

ReferencesReferencesComerford, K.C., & Mayer, B.H. (Eds.). (2007). Hemodynamic

monitoring made incredibly visual. Ambler, PA: Lippincott, Williams, and Wilkins.

Donofrio, J., Haworth, K., Schaeffer, L., & Thompson, G. (Eds.). (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott, Williams, and Wilkins.

Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

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