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Outline of > Chapter 35: Supporting Cardiovascular Function

Key Terms:

• Afterload>
Afterload can also be described as the pressure that the chamber of the heart has to
generate in order to eject blood out of the chamber.It is the final determinant of stroke
volume. It is the pressure against which the left ventricle pumps—partly determined by aortic
diastolic pressure. A higher aortic pressure forces the heart to work harder, and less blood is
ejected from the ventricles with each contraction.
• Antidiuretic Hormone (ADH)>
A hormone that decreases the production of urine by increasing the re-absorption of water by the
renal tubules. It is secreted by the cells of the hypothalamus and stored in the neurohypophysis.
It is released in the response to a decrease in blood volume, an increased concentration of
sodium or other substances in plasma, pain, stress, or the action of certain drugs. Another name
for ADH is Vasopressin.
• Atherosclerosis>
It is a pathological condition in which fat and plaque form deposits on the intimal (inner) surface of
the arteries.
• Baroreceptors>
These are specialized pressure receptor cells located in the aorta, the carotid, and other large
systemic arteries to detect pressure changes in the vascular system.
• Bradycardia>
Heart rate less than 60 beats per minute.
• Cardiac Output>
It is the amount of blood pumped by the ventricles in one minute.
• Claudication>
This is the cramping like pain caused in the calves due to inadequate blood flow to the leg
muscles.
• Diastole>
This refers to the relaxation of the ventricles.
• Dysrhythmia>
They are abnormalities of heart rate or rhythm.
• Edema>
This is an abnormal accumulation of fluid in the interstitial spaces of tissue , commonly known as
swelling.
• Inotropic Agent>
These are medications that increase the contractility of the heart muscle, thereby increasing
cardiac output.
• Ischemia>
A decreased supply of oxygenated blood to tissues.
• Necrosis>
Localized death of tissues caused by disease, oxygen deficit, or injury.
• Preload>
The amount of blood in the left ventricle immediately before contraction. Itis the main force
that stretches cardiac muscle fibers. Frank-Starling’s law statesthat eh force of contraction of the
cardiac muscle is proportional to its length at the beginning of contraction, at least up to the
physiological limits to muscle stretching. In other words, the muscle is stretched, the stronger the
contraction and the greater the cardiac output.
• Stroke Volume>
It is the amount of blood ejected from the heart with each contraction.

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• Systole>
This refers to the contraction of the ventricles.
• Tachycardia>
Heart rate greater than 100 beats per minute.
• Viscosity>
It is the relative ability of a fluid to flow measured as its resistance to flow. As the viscosity of
blood increases, the flow of blood slows. It is affected by the amount of protein in the plasma and the
tendency of the RBCs to clump together when blood flow is sluggish—but hematocrit is the major
factor that determines viscosity.
Concepts of Tissue Perfusion: 39.3% of deaths in the US are accounted for by cardiovasculardisease.
Need for O2 and nutrients are met by the cardiovascular system. Ischemia and Necrosis are due to
varying oxygen needs in impaired tissues (see key terms for def.)

Nursing Dx for cardiovascular problems:

Ineffective tissue perfusion

Decreased Cardiac Output

Risk for Peripheral Neurovascular Dysfunction.

The Cardiovascular System:

The heart is an organ that acts as a pump to create the pressure that causes the blood to flow
throughout the vascular system. It has four chambers: two atria above and two ventricles below.

The dynamics of blood flow are as follows: During diastole, blood enters the Right atrium fro the Venae
Cavae (superior and inferior). At the same time the blood enters the Left atrium from the pulmonary artery.
At the end of the diastole, the atria contract (atrial systole). Now during systole the ventricles contract and
oxygenated blood is sent from the Left Vent. to the body while the deoxygenated blood is sent by the
Right vent. to the Lungs for oxygenation/waste elimination.

Blood Vessels (Arteries and Veins):


Both have a :
• Tunica Media (smooth muscle layer)
• Tunica Adventitia (Connective tissue layer)
• Lumen (derived from the latin for “open place or light”) –it is the open space in the artery or vein
where we would see blood flow when it is functioning properly.

Arteries carry oxygenated blood away from the Heart. They have a thicker elastic tunica media, which
means they have more smooth muscle to control the diameter of the vessel and so the blood
pressure.The arterial blood pressure is 30-40mmHg at the arterioles.
Veins can be distended/dilated and rely on skeletal muscle in conjunction with one-way valves to provide
adequate blood flow. The venous pressure is 10-15mmHg at the venules.

• Blood flows from areas of higher pressure to lower pressure ( this is called Pressure Gradient).
Therefore when blood travels from the arterioles to the venules via the body capillaries the
colloidal pressure exerted upon the capillaries, in combination with the above state pressures
create a condition where oxygenation is provided to the surrounding tissues (near the
arterioles/body capillaries)while waste materials and deoxygenated blood is returned back (near
the venules /body capillaries).

Blood Components:
All cellular components develop from mother cells (stem cells) which differentiate or specialize
into WBC, RBC and Platelets. RBCs transport oxygen to tissues as oxyhemoglobin. WBCs fight
infections and maintain the body’s immune function. Platelets (Thrombocytes) are essential for

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coagulation or clotting to the blood. Plasma is the fluid in the blood—it carries the cellular elements,
electrolytes, protein, glucose, fats, billirubin and gases.

PRESSURE RECEPTORS:

Baroreceptors: are specialized cells located in the aorta, carotid and other large systemic arteries to
detect pressure changes in the vascular system. Higher pressure stretches the walls of the arteries,
triggering stretch. Low pressure receptors in the right atrium and the pulmonary artery minimize arterial
pressure changes in response to change sin blood volume. Both types send messages to the CNS which
activates the autonomic nervous system to adjust the circulation to changes I pressure—to maintain a
stable blood pressure. The Autonomic Nervous System has a sympathetic branch (adrenergic response)
that increases the heart rate, the strength of myocardial contraction and the constricting of the peripheral
vessels. The other branch of the ANS is the parasympathetic (cholinergic response) which decreases the
heart rate , decreases the strength of contraction and has no effect on the peripheral vessels.

Hormonal Controls:
• Hormones like Epinephrine (adrenaline), Norepinephrine, Acetylcholine are secreted by the
endocrine system for longer cardiovascular control than the Sympathetic-Parasympathetic
responses of the nervous system. These hormones have the same response but the effect lasts
5 to 10 times longer.
• Another hormonal control (we have already discussed) is the RAA—Renin-Angiotensis-
Aldosterone system. The Juxtaglomerular cells of the kdneys detect a drop in blood pressure so
the enxyme Renin is released. Renin buddys up with liver enzymes and makes Angiotensin I ( a
weak vasoconstrictor. This is sent up to the the Lungs where in the Lungs capillaries the
Angiotensis I is converted to Angiotensin II by the ACE (angiotensin converting enzyme) –which
increases the blood pressure due to the vasoconstriction. Also angiotensin stimulates the adrenal
cortex to release aldosterone, a hormone that stimulates the kidney to retai sodium and water—
increasing plasma volume and circulating blood volume. The increase in blood volume tells the
Kidneys to knock off the Renin.

• The ADH (Vasopressin) is a second hormal compensatory mechanism. It is produced in the


Hypothalmus an is screatedby the posterior pituitary gland when the sympathetic nervous system
is stimulated. It tells the kidneys to retain water, which increases circulating blood volume.

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REGULATION OF CARDIAC OUTPUT:

amount of blood ejected from the heart with each contraction.

 CARDIAC OUTPUT = STROKE VOLUME X HEART RATE

How may times the heart beats per minute.

 Average cardiac output for an adult is 5 to 6 L /min.

Factors affecting Tissue perfusion ad cardiac function:

 Life-Span Risk Factors:

✔ Heredity, lifestyle, psychological factors and underlying health


problems all influence circulatory functions.

✔ Modifiable risk factors: diet, exercise, smoking, stress, hypertension.

✔ Development of Atherosclerosis increases with age.

 Physiological Factors:

✔ Men are more likely to have heart attacks then women.

✔ Estrogen levels in premenopausal women maintain elasticity of blood


vessels and keep serum cholesterol levels low.

✔ Women, however have a poorer prognosis for recovery and experience


more complications once they develop coronary disease.

✔ RAYNAUD’S DISEASE: Peripheral vascular disease of women which


involves vasospasms.

✔ BUERGER’S DISEASE: Peripheral vascular disease in men that includes


an occlusive vascular condition.

✔ Obesity increases the workload on the heart. Excessive adipose tissue


requires the development of more blood vessels to nourish the tissue.
Heavy adipose can compress blood vessels.

✔ Hypertension= B/P is persistently higher than 140/90 mmHg.


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✔ Pregnancy= Growing fetus and amniotic fluid puts pressure on pelvic
veins, thus you have slow Venus return.

 Problems of Cardiovascular Function:

✔ Atherosclerosis—

 Targets the heart , brain, kidneys and peripheral vessels.

 Fat and plaque form deposits on the intimal surface of


arteries.

 These deposits narrow the lumen of artery, break loose,


traveling to a distant site where they cause obstruction.

 Disorders of Cardiac Output:

✔ Angina Pectoris: Chest pain resulting form inadequate oxygenation


to heart muscle, due to partially occluded coronary arteries.

✔ Myocardial Infarction: Necrosis of heart muscle resulting from


complete occlusion of a coronary artery.

✔ Dysrhythmias are abnormalities of heart rate or rhythm.

 They may shorten the time available for the heart to fill with
blood which in turn decreases stroke volume and cardiac
output.

✔ Bacterial and Viral Infections: They can cause inflammation and


scarring(scar tissue doesn’t have the contractility like muscle and
so that can decrease contractility overall) of the heart, valves, and
pericardial sac.

✔ Congestive Heart Failure: The heart fails as a pump, so decreased


output and swelling at extremeties (edema) is a prominent
symptom of Right-Sided heart failure. Also, for Left sided Heart
Failure—fluid in the lungs is a big sign.

✔ Peripheral Neurovascular Dysfunction:

 In situations where circulation to extremities are disrupted


neurovascular damage occurs—If it in not detected early, it
may become permanent.

 Examples: Severe tissue edema, excessive pressure on blood


vessels from a cast, splint, tourniquet. Clots or occlusions
within blood vessels , trauma to blood vessels due to invasive
procedures like surgery.

 Assessment:

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✔ Health History—Ask patient about signs and symptoms of
cardiovascular problems, ask about activity level, rate severity,
discuss possible treatments.

✔ Physical Exam—Use the subjective data above to verify and


substantiate with objective assessment.

✔ Diagnostic Tests:

 CBC—Complete Blood Count—to evaluate blood loss, anemia


and hydration.

 Coagulation Studies—addresses the body’s ability to form


blood clots and to monitor drug therapy via PT, INR and aPTT.

 Lipid profile—Cholesterol, triglycerides and lipids are


checked.

 Electrocardiogram—Graphic recording of heart rate, rhythm,


electrical conduction.

 Angiography—A radio-opaque , iodine based contrast dye is


injected into a blood vessel while the heart is viewed by a
fluoroscope.

 Doppler Blood Flow Studies—Use sound waves to evaluate


the patency of peripheral blood vessels.

 Ineffective Tissue Perfusion:

✔ Pain and impaired organ function are cues to this.

 Poor renal perfusion= poor renal output ; Renal Faliure=


<30ml/hr

 Poor cerebral perfusion= Confusion, paralysis or other


neurological symptoms.

 GI symptoms include abdominal pain, slowed/absent bowel


sounds, abdominal distention.

 Cardiac symptoms include substernal chest pain, radiating to


the right arm, neck and dysrhythmias.

 Peripheral perfusions issues can include: Claudication


(cramping pain in the calves) and Edema (abnormal
accumulation of fluid in interstitial soaces of tissues—
swelling).

 Assess for Decreased Cardiac Output:


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✔ Mean Arterial pressure= [ (2 x diastolic) + systolic] ÷3

Mean Arterial pressure= < 70 mm Hg or > 130 mmHg

✔ Heart Rate = < 45 or > 125 bpm

✔ Resp Rate= < 10 or > 30 per min.

✔ C/O Chest pain.

✔ Change in mentation.

 Assess for Risk for Peripheral Neurovascular Dysfunction:

✔ This involves situations where pressure is exerted on blood vessels


and nerves.

✔ Arterial Occlusion:look for decreased pulses, pallor, cool skin, slow


capillary refill, numbness, tingling, burning, decreased movement of
the affected limb and pain in the affected limb. This means
possible O2 deprivation in the tissues and nerves of the involved
extremity.

✔ Venus Occlusion: Look for engorgement in the extremity producing


warm skin, red skin, edema, slow cap refill.

 Assess for SHOCK:

✔ Shock is life threatening circulatory collapse due to severe volume


deficit, cardiac pump failure or redistribution of blood.

✔ Look for :

 Tachycardia—In initial stages you may see only this.

 Hypotension—body can’t keep up the cardiac output so the


b/p falls.

 Weakened peripheral pulses

 Changes in neurological status—lack of oxygen, cerebral


hypoxia—in early stages seen as restlessness, agitation and
confusion. In later stages of shock person becomes
progressively less alert.

 Skin changes—Pale, cold, clammy skin due to blood going to


the center rather than the periphery.

 Decreased Urinary output—Hypotension=↓kidney filtration.

 CARDIOGENIC SHOCK: When heart failure results due to ↓contractility or


↓ stroke volume it is called cardiogenic shock.

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 HYPOVOLEMIC SHOCK: ↓circulating blood volume due to blood or plasma
loss in cases of hemorrhage, severe burns, extensive vomiting or diarrhea
can trigger hypovolemic shock.

 DISTRIBUTIVE SHOCK: Distributive shock is caused by an insufficient


intravascular volume of blood. This form of relative hypovolemia is the
result of blood vessel dilation. Septic shock is usually the major cause.
Septic shock is an overwhelming infection leading to vasodilatation, such
as by Gram negative bacteria i.e. Escherichia coli.

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