University of Santo Tomas

THE GRADUATE SCHOOL

ADVANCED MEDICAL-SURGICAL NURSING I
CASE SCENARIO
THE CLIENT WITH CARDIOVASCULAR ALTERATIONS
Prepared by: John Henry O. Valencia, RN, RM
Master of Arts in Nursing Student

It is mid-morning in the medical ward where you work, and you are getting a new patient, M.A., a 60-
year-old, retired businessman, is married and has 3 grown children. As you take his health history, he tells you
that he began to feel palpitations and on and off chest discomfort about 10 days ago. He has hypertension and
a 5-year history of angina pectoris. He is 59 and weighs 200 lb. He is sedentary and gets no routine exercise.
During the past week, he has had more frequent episodes of midchest discomfort. During the week, he has also
experienced increased fatigue. He states I just feel crappy most of the time. He tells you a cardiac
catheterization done several years ago revealed 50% occlusion of the right coronary artery and 50% occlusion of
the LAD artery. He also tells you that both his parents had CAD. He is taking NTG, amlodipine, metoprolol, lipitor
and baby ASA.The MD writes his diagnosis as CAD, HPN.

At 1AM the following day, M.A. turns on his call light. When you respond, he is talking rapidly and
pointing to the bathroom. His speech pattern indicates he is short of breath. You assist him to the bathroom and
note that his skin feels clammy. While sitting on the commode he vomits. The resident MD comes and evaluates
M.A.s condition. He orders Furosemide 40 mg. IV push STAT. M.A. continues to experience vomiting and
diaphoresis inspite of medications and comfort measures. A STAT 12-lead ECG reveals ischemic changes
indicating ACS. M.A. is ordered to be transferred to the CCU.

Five days later his condition is stabilized and M.A. is taken to OR for CABG x3. When he arrives from
the OR, he has a Swan-Ganz catheter in place for hemodynamic monitoring and is intubated and put on a
ventilator at FiO2 70. His ABG reading is: pH 7.36; PCO2 46 mmHg; PO2 61 mmHg; SaO2 85% with a Hgb
10.3mg/dL. Hemodynamic values show that the pressures within his heart and lungs are slightly elevated and
that his cardiac output is low, indicating that the heart is not effectively pumping out the blood that is returned to it
or that he is experiencing a little fluid overload. M.A. receives continuous IV infusions of Nitroprusside and
Dobutamine. Close monitoring and intensive management of M.A.s condition is done. His condition improves
and is transferred to the Telemetry unit. Five days later, he is now preparing for discharge.

INSTRUCTIONS:
Identify the learning issues (at least 7) related to pathophysiology (Focus on CV) that you can draw out from
this case. Prepare to discuss these issues with the class on Tuesday, September 23, 2014. Your written answer
to your learning issues will be submitted next Tuesdays class.




Page 2 of 8

OLD AGE (60 YEARS OLD), OBESITY (97KGS OR 200LBS) AND SEDENTARY LIFESTYLE

Nonspecific Injury to endothelial lining

Desquamation of endothelial lining

Activation of tissue inflammatory response

Release of pro-inflammatory cytokines
(MCP-1, TNF-, Interleukins, CRP and Serum Amyloid A)











































Interleukin - 6
Leukocyte and
Endothelial cell
activation
Hepatic Acute-
phase reactants
production
Increased Liver
Enzymes (SGPT)
Monocyte
Chemoreactant Protein-1
Leukocyte-
Endothelium binding
Migration to site of
inflammation
Mononuclear
phagocyte activation
Increased
WBC count
Complete Blood
Count
Interleukin-18 and 10
Expression of
interferon-
Endothelial
adhesion molecule
activation
Intercellular
Adhesion Molecule
(ICAM) Formation
Vascular Cell
Adhesion Molecule
(VCAM)
E-selectin
Formation
Monocyte
Adhesion
Leukocyte diapedesis
into extravascular space
Adhesion of molecules
Increase von
Willebrand Factor
Developing fatty Streak Oxidative Stress
LDL Oxidation
Oxidized LDL attracts monocytes and
macrophages to the site
Plaques begin to form from cells which
embedded into the endothelium
Blood Tests
(Cardiac Enzymes
Test)



Page 3 of 8























































Development of Foam
cells
Lipids are engulfed by the foam cells
Development of smooth muscle cells
ATHEROSCLEROTIC PLAQUE FORMED
Increased inflammatory
stress
Continuous
inflammatory response
ANGIOGENESIS
Vascular endothelial growth factor (VEGF), Placental Growth Factor (PlGF),
and hepatocyte growth factor (HGF)
Intraplaque Hemorrhage
Conversion of Stable plaque
to unstable plaque
Intraplaque Inflammation
Degradation of fibrous
cap
Plaque Instability
Platelet Activation
Plaque Erosion
THROMBUS FORMATION
Thrombus occluding vessel
Prevention of myocardial
perfusion
Decreased Myocardial
Oxygen Supply
Anaerobic Metabolism of
Glycogen
Failure of Sodium-
Potassium and Calcium
pump
Accumulation of hydrogen
ions and lactate
Acidosis
Altered electrical conduction
Altered Repolarization
Inverted T-wave
Ischemic Phase
Myocardial cells are sensitive to
acidic pH
Myocardial Injury
ST Segment Elevation Myocardial Ischemia
Myocardial Cell
Necrosis
Absence of
depolarization current
from dead tissues
Presence of opposing
currents from other
areas of the heart
Abnormal Q Wave
Injury Phase
Infarction
Phase
ECG
ECG
CHEST PAIN
Cardiac Catheterization
(Reveals 50% Occlusion of Right Coronary
Artery and 50% Occlusion of Left Anterior
Descending Artery)

Increased Troponin I and T;
Mrocardium-Specific
Creatinine Kinase (CK-MB)
Cardiac
Biomarkers
NTG or Morphine
to Control pain
Fibrinolytic
Therapy
Lipitor



Page 4 of 8






















































Inflammatory Response to
Necrotic Myocardial Cell
Impaired Myocardial
Contractility

Increased WBC
Released of
Endogenous Pyrogens
Release of
Prostaglandins
Prostaglandins will
reset hypothalamic
thermostat
FEVER
Scar Tissues replacing
healthy tissues
Decrease Cardiac
Output
Decrease Blood Pressure
Release of Epinephrine and
Norepinephrine
Increased Blood
Pressure
Increased
Heart Rate
Increased
Afterload
Stimulation of
Baroreceptors
Peripheral
Vasoconstriction
Increased Pumping
Action of Heart
Decreased
Renal Perfusion
RAAS Activation
Increased Myocardial
oxygen Demand
ADH and
Aldosterone Release
Sodium and Water
reabsorption
Increased Blood
Volume
Increased Preload
Increased Myocardial
Workload
Cardiomegaly Chest X-Ray
Deterioration of
Hearts ability to pump
Moderate Left
Ventricular Failure
Continuous blood flow to the lungs
from Right side of the heart
Left Ventricle unable
to pump out blood
Pulmonary back flow
of the blood
Pulmonary Congestion
Dyspnea Shortness of
Breath
Widespread
Crackles
Ocassional
Wheeze
(Cardiac Asthma)
Increased Right
Ventricular Pressure



Page 5 of 8



Fluids leak into
alveolar space
Lymphatic system drains excess
interstitial fluid volume

Additional fluid in the pleural space
drains into titer lymph nodes
Fluid moves from the interstitial space
in the alveolar walls
Damaged to alveolar
epithelium
Further fluid accumulation in the
alveolar space
Alveolar Edema
Impaired gas exchange
Hypoxemia
Hypercarbia
Decrease lung compliance Decrease oxygen
diffusion
Use of Accessory Muscle
Bradypnea
Poor cerebral
oxygenation
Altered Level of
consciousness
Agitation /
Restlesness
Poor Peripheral
oxygenation
Pallor
Sweaty cool
periphery
Reduced
capillary
return
Increased work
of breathing
Exhaustion
Fatigue
Decreased PO2
(PO2 61mmHg)
Increased Pulmonary Artery
and Pulmonary Artery
Wedge Pressure (PAWP)
Decreased SaO2
(SaO2 85%)



Page 6 of 8

STAGES OF PATHOPHYSIOLOGIC BASIS OF CORONARY ARTERY DISEASE


Coronary artery disease (CAD) also known as atherosclerotic heart disease, coronary heart
disease, or ischemic heart disease (IHD),is the most common type of heart disease and cause of heart
attacks.The disease is caused by plaque building up along the inner walls of thearteries of the heart,
which narrows the arteries and reduces blood flow to the heart.
Atherogenesis in humans typically occurs over a period of many years, usually many decades.
Growth of atherosclerotic plaques probably does not occur in a smooth, linear fashion but
discontinuously, with periods of relative quiescence punctuated by periods of rapid evolution. It
undergoes different steps; Initiation, Leukocyte recruitment and Foam Cell formation.

INITIATION
Studies of human atherosclerosis suggests that the "fatty streak" represents the initial lesion of
atherosclerosis. These early lesions most often seem to arise from focal increases in the content of
lipoproteins within regions of the intima. Our patient being a smoker without exercise and with a
susceptible age predisposes him to atherosclerotic plaque formation which is heralded by the Fatty
streak formation from lipoprotein accumulation. This accumulation of lipoprotein particles may not result
simply from increased permeability, or "leakiness," of the overlying endothelium. Rather, the lipoproteins
may collect in the intima of arteries because they bind to constituents of the extracellular matrix,
increasing the residence time of the lipid-rich particles within the arterial wall.
Lipoproteins that accumulate in the extracellular space of the intima of arteries often associate
with glycosaminoglycans of the arterial extracellular matrix, an interaction that may slow the egress of
these lipid-rich particles from the intima. Lipoprotein particles in the extracellular space of the intima,
particularly those retained by binding to matrix macromolecules, may undergo oxidative modifications.
Considerable evidence supports a pathogenic role for products of oxidized lipoproteins in
atherogenesis. Lipoproteins sequestered from plasma antioxidants in the extracellular space of the
intima become particularly susceptible to oxidative modification, giving rise to hydroperoxides,
lysophospholipids, oxysterols, and aldehydic breakdown products of fatty acids and phospholipids.
Considerable evidence supports the presence of such oxidation products in atherosclerotic lesions.

LEUKOCYTE RECRUITMENT
Accumulation of leukocytes characterizes the formation of early atherosclerotic lesions. Thus,
from its very inception, atherogenesis involves elements of inflammation, a process that now provides a
unifying theme in the pathogenesis of this disease. The inflammatory cell types typically found in the
evolving atheroma include monocyte-derived macrophages and lymphocytes. A number of adhesion
molecules or receptors for leukocytes expressed on the surface of the arterial endothelial cell probably
participate in the recruitment of leukocytes to the nascent atheroma. Constituents of oxidatively modified
low-density lipoprotein can augment the expression of leukocyte adhesion molecules. This example
illustrates how the accumulation of lipoproteins in the arterial intima may link mechanistically with
leukocyte recruitment, a key event in lesion formation.

Once captured on the surface of the arterial endothelial cell by adhesion receptors, the
monocytes and lymphocytes penetrate the endothelial layer and take up residence in the intima. In
addition to products of modified lipoproteins, cytokines (protein mediators of inflammation) can regulate
the expression of adhesion molecules involved in leukocyte recruitment. For example, interleukin 1 (IL-
1) or tumor necrosis factor (TNF-) induce or augment the expression of leukocyte adhesion molecules
on endothelial cells. Because products of lipoprotein oxidation can induce cytokine release from



Page 7 of 8

vascular wall cells, this pathway may provide an additional link between arterial accumulation of
lipoproteins and leukocyte recruitment. Chemoattractant cytokines such as monocyte chemoattractant
protein 1 appear to direct the migration of leukocytes into the arterial wall.

FOAM-CELL FORMATION
Once resident within the intima, the mononuclear phagocytes mature into macrophages and
become lipid-laden foam cells, a conversion that requires the uptake of lipoprotein particles by receptor-
mediated endocytosis. One might suppose that the well-recognized "classic" receptor for LDL mediates
this lipid uptake; however, humans or animals lacking effective LDL receptors due to genetic alterations
(e.g., familial hypercholesterolemia) have abundant arterial lesions and extraarterial xanthomata rich in
macrophage-derived foam cells. In addition, the exogenous cholesterol suppresses expression of the
LDL receptor; thus, the level of this cell-surface receptor for LDL decreases under conditions of
cholesterol excess. Candidates for alternative receptors that can mediate lipid loading of foam cells
include a growing number of macrophage "scavenger" receptors, which preferentially endocytose
modified lipoproteins, and other receptors for oxidized LDL or very low-density lipoprotein (VLDL).
Monocyte attachment to the endothelium, migration into the intima, and maturation to form lipid-laden
macrophages thus represent key steps in the formation of the fatty streak, the precursor of fully formed
atherosclerotic plaques.

ARTERIAL REMODELING DURING ATHEROGENESIS
During the initial part of the life history of an atheroma, growth is often outward, preserving the
caliber of the lumen. This phenomenon of "compensatory enlargement" accounts in part for the
tendency of coronary arteriography to underestimate the degree of atherosclerosis. Rupture of the
plaque's fibrous cap causes thrombosis. Physical disruption of the atherosclerotic plaque commonly
causes arterial thrombosis by allowing blood coagulant factors to contact thrombogenic collagen found
in the arterial extracellular matrix and tissue factor produced by macrophage-derived foam cells in the
lipid core of lesions. In this manner, sites of plaque rupture form the nidus for thrombi. The normal artery
wall has several fibrinolytic or antithrombotic mechanisms that tend to resist thrombosis and lyse clots
that begin to form in situ. Such antithrombotic or thrombolytic molecules include thrombomodulin,
tissue- and urokinase-type plasminogen activators, heparan sulfate proteoglycans, prostacyclin, and
nitric oxide. When the clot overwhelms the endogenous fibrinolytic mechanisms, it may propagate and
lead to arterial occlusion.
The consequences of this occlusion depend on the degree of existing collateral vessels. In a
patient with chronic multivessel occlusive coronary artery disease (CAD), collateral channels have often
formed. In such circumstances, even a total arterial occlusion may not lead to myocardial infarction (MI),
or it may produce an unexpectedly modest or a non-ST-segment elevation infarct because of collateral
flow. In a patient with less advanced disease and without substantial stenotic lesions to provide a
stimulus for collateral vessel formation, sudden plaque rupture and arterial occlusion commonly
produces an ST-segment elevation infarction. These are the types of patients who may present with MI
or sudden death as a first manifestation of coronary atherosclerosis. In some cases, the thrombus may
lyse or organize into a mural thrombus without occluding the vessel. Such instances may be clinically
silent.
The subsequent thrombin-induced fibrosis and healing causes a fibroproliferative response
that can lead to a more fibrous lesion that can produce an eccentric plaque that causes a
hemodynamically significant stenosis. In this way, a nonocclusive mural thrombus, even if clinically
silent or causing unstable angina rather than infarction, can provoke a healing response that can
promote lesion fibrosis and luminal encroachment.



Page 8 of 8

Such a sequence of events may convert a "vulnerable" atheroma with a thin fibrous cap that is
prone to rupture into a more "stable" fibrous plaque with a reinforced cap. Angioplasty of unstable
coronary lesions may "stabilize" the lesions by a similar mechanism, producing a wound followed by
healing.

MYOCARDIAL ISCHEMIA AS CAUSE OF PATIENTS CHEST PAIN
Central to an understanding of the pathophysiology of myocardial ischemia is the concept of
myocardial supply and demand. In normal conditions, for any given level of a demand for oxygen, the
myocardium will control the supply of oxygen-rich blood to prevent underperfusion of myocytes and the
subsequent development of ischemia and infarction. The major determinants of myocardial oxygen
demand are heart rate, myocardial contractility, and myocardial wall tension (stress).The normal
coronary circulation is dominated and controlled by the heart's requirements for oxygen. This need is
met by the ability of the coronary vascular bed to vary its resistance (and, therefore, blood flow)
considerably while the myocardium extracts a high and relatively fixed percentage of oxygen. By
reducing the lumen of the coronary arteries, atherosclerosis limits appropriate increases in perfusion
when the demand for flow is augmented, as occurs during exertion or excitement.
During episodes of inadequate perfusion caused by coronary atherosclerosis, myocardial
tissue oxygen tension falls and may cause transient disturbances of the mechanical, biochemical, and
electrical functions of the myocardium. Coronary atherosclerosis is a focal process that usually causes
nonuniform ischemia. During ischemia, regional disturbances of ventricular contractility cause
segmental hypokinesia, akinesia, or, in severe cases, bulging (dyskinesia), which can reduce
myocardial pump function.