cardiac a&p review
TRANSCRIPT
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Cardiovascular Review: There’s Cardiovascular Review: There’s More Than Just a Beating Heart More Than Just a Beating Heart
Natalie Bermudez, RN, BSN, MSNatalie Bermudez, RN, BSN, MSClinical Educator for Cardiac TelemetryClinical Educator for Cardiac Telemetry
Telemetry
Course
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The Human HeartThe Human Heart
• Layers (3)
• Atria (2)
• Ventricles (2)
• Valves (4)
• Veins
• Arteries
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Layers of the HeartLayers of the Heart
1) Pericardium
2) Myocardium
3) Endocardium
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The PericardiumThe Pericardium
• Double-walled serous sac surrounding the heart
• Strengthened externally by a tough fibrous connective tissue layer
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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
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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
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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.
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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
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Myocardial Cardiac Cell TypesMyocardial Cardiac Cell Types
Fibroblasts
• Cells residing in the extracellular mix
Endotehlial & Smooth Muscle Cells
• Cells found in the blood vessels
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Atria & VentriclesAtria & VentriclesRight Atrium
Left Atrium
Right Ventricle
Left Ventricle
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Heart ValvesHeart Valves
Right:Tricuspid Pulmonic
Left:Bicuspid (Mitral)
Aortic
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Valvular StructuresValvular Structures
Leaflets
AV Valves(2 or 3)
Semilunar (3)
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Additional Valvular Additional Valvular StructuresStructures
Help to keep A-V valves closed during ventricular systole
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Blood VesselsBlood Vessels
Aorta (A & D)
SVC
IVC
Pulmonary Artery
Pulmonary Vein
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Coronary ArteriesCoronary ArteriesAnterior ViewAnterior View
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Coronary ArteriesCoronary ArteriesPosterior ViewPosterior View
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Coronary Blood FlowCoronary Blood Flow
Coronary filling occurs during
ventricular Diastole
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Coronary Blood FlowCoronary Blood Flow
An increase in heart rate shortens
diastole and can decrease
myocardial perfusion
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Coronary Blood FlowCoronary Blood Flow
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
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Coronary Blood FlowCoronary Blood Flow
LCA Blood Supply:Divides into the Anterior Descending
Artery & Circumflex Artery
• Left atrium
• Most of the left ventricle
• Most of the intraventricular septum
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Coronary Blood FlowCoronary Blood Flow
Cardiac veins lie superficially to the
arteries
The largest vein, the coronary sinus
empties into to the right atrium
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Coronary Blood FlowCoronary Blood Flow
Most of the major cardiac veins empty
into the coronary sinus
However, the anterior cardiac veins empty into the right atrium
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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
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Pumping Action of the HeartPumping Action of the Heart
Atrial Contraction → 10% to 20% left ventricular filling
Pulmonary Veins passively fill left ventricle while mitral
valve is open
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Pumping Action of the HeartPumping Action of the Heart
In elevated heart rates Atrial Contraction → 40% left
ventricular filling
A.K.A. Atrial KickA.K.A. Atrial Kick
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Pumping Action of the HeartPumping Action of the Heart
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
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Aortic Valve Opens Aortic Valve Closes
S1 S2AV
Valve Closes
AV Valve Opens
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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
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Pumping Action of the HeartPumping Action of the Heart
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)
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Pumping Action of the HeartPumping Action of the Heart
Cardiac OutputCardiac Output
The amount of blood discharged from the left or right ventricle per minute.
(Taber’s Medical On-line Dictionary)
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Pumping Action of the HeartPumping Action of the Heart
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
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Pumping Action of the HeartPumping Action of the Heart
Cardiac Output is Cardiac Output is determined by:determined by:
PreloadContractility
AfterloadHeart Rate
(Core Curriculum for Progressive Care Nurses, p. 138)
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Pumping Action of the HeartPumping Action of the Heart
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)
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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
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Frank-Starling MechanismFrank-Starling Mechanism
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.
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Frank-Starling MechanismFrank-Starling Mechanism
The Rubber Band Effect
The farther a rubber band is stretched, the farther it will go!!
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PreloadPreloadIncreased Preload Occurs With:• Increased circulating volume• Venous constriction (decreases venous
pooling and increases venous return to the heart)
• Drugs: Vasoconstrictors
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PreloadPreloadDecreased Preload Occurs With:• Hypovolemia• Mitral stenosis• Drugs: Vasodilators• Cardiac Tamponade• Constrictive Pericarditis
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Pumping Action of the HeartPumping Action of the Heart
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)
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ContractilityContractilityIncreased Contractility Occurs With:• Drugs: Positive inotropic agents
– digoxin, milrinone, epinephrine, dobutamine
• Increased heart rate– Bowditch’s phenomenon
• Sympathetic stimulation – via ß1-receptors
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ContractilityContractilityDecreased Contractility Occurs
With:• Drugs: Negative inotropic agents
– Type 1A antiarrhythmics, ß-Blockers, CCBs, barbituates
• Hypoxia• Hypercapnia• Myocardial ischemia• Metabolic acidosis
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Pumping Action of the HeartPumping Action of the Heart
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)
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AfterloadAfterloadIncreased Afterload Occurs With:• Aortic stenosis• Peripheral arteriolar
vasoconstriction• Hypertension• Polycythemia• Drugs: Arterial vasoconstrictors
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AfterloadAfterloadDecreased Afterload Occurs With:• Hypovolemia• Sepsis• Drugs: Arterial vasodilators
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Heart RateHeart RateInfluenced By Many Factors:• Blood volume status• Sympathetic & Parasympathetic Tone• Drugs• Temperature• Respiration• Dysrhythmias• Peripheral Vascular Tone• Emotions• Metabolic Status (includes hyperthyroidism)
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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)
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Ventricular Function Curve
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Pumping Action of the HeartPumping Action of the Heart
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)
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Pumping Action of the HeartPumping Action of the Heart
Systemic Vascular Systemic Vascular Resistance Resistance
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)
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Pumping Action of the HeartPumping Action of the Heart
Systemic Vascular Systemic Vascular Resistance Resistance
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)
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Pumping Action of the HeartPumping Action of the Heart
Systemic Vascular Systemic Vascular Resistance Resistance
Conditions that cause an increase in SVR:
• Hypothermia• Hypovolemia
• Pheochromocytoma• Stress response
• Syndromes of low CO
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Pumping Action of the HeartPumping Action of the Heart
Systemic Vascular Systemic Vascular Resistance Resistance
Conditions that cause a decrease in SVR:
• Anaphylactic and neurogenic shock• Anemia
• Cirrhosis• Vasodilation
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Blood VesselsBlood Vessels
• 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
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Blood VesselsBlood Vessels
Five Types:
ArteriesArteriolesCapillaries
VenulesVeins
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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
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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
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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)
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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
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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
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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
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ArteriolesArterioles• Control systemic
vascular resistance and thus arterial pressure
• Lead directly into capillaries
• Have strong smooth muscle walls innervated by the ANS
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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
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ArteriolesArteriolesAutonomic Nervous System
• Cholinergic (Inhibitory) System– 1 Neurotransmitter
•Acetylcholine: Decreases heart rate; releases nitric oxide causing vasodilation
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CapillariesCapillaries
Microscopic
Walls are composed of only a single layer of endothelial cells
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CapillariesCapillaries
Capillary pressure is extremely low to allow for exchange of
nutrients, oxygen, and carbon dioxide with body cells
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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
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VenulesVenules
Gather blood from capillaries
Walls are thinner than
those of arterioles
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VeinsVeins
Thinner walls than arteries
Large diameters because of the
low blood pressure of
venous return to the heart
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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
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VeinsVeins
Most veins return
blood to the right atrium of the heart
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Blood pressure regulation is maintained
via vasodilation
or vasoconstricti
on of the arterial vessels
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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
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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
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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
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Renin-Angiotensin-Aldosterone Renin-Angiotensin-Aldosterone SystemSystem
Blood Pressure Regulatory Mechanism
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R-A-A-SR-A-A-S
ReninRenin
a.k.a. angiotensinogenase
Converts angiotensinogen to angiotensin I
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R-A-A-SR-A-A-S
Angiotensin IAngiotensin I
Has no biological activity
Exists solely as a precursor to angiotensin II
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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
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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
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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.