Case Scenario Cv (1)

8/11/2019 Case Scenario Cv (1)

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University of Santo Tomas

THE GRADUATE SCHOOL

ADVANCED MEDICAL-SURGICAL NURSING I

CASE SCENARIOTHE 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 5’9” 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 cardiaccatheterization 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 order s 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 Tuesday’s class.



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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-α, Interleukins, CRP and Serum Amyloid A)

Interleukin - 6

Leukocyte andEndothelial cell

activation

Hepatic Acute-phase reactants

production

Increased LiverEnzymes (SGPT)

MonocyteChemoreactant Protein-1

Leukocyte-Endothelium binding

Migration to site ofinflammation

Mononuclearphagocyte activation

IncreasedWBC count

Complete BloodCount

Interleukin-18 and 10

Expression ofinterferon-γ

Endothelialadhesion molecule

activation

Intercellular Adhesion Molecule(ICAM) Formation

Vascular Cell Adhesion Molecule

(VCAM)

E-selectinFormation

Monocyte Adhesion

Leukocyte diapedesisinto extravascular space

Adhesion of molecules

Increase vonWillebrand Factor

Developing fatty StreakOxidative Stress

LDL Oxidation

Oxidized LDL attracts monocytes andmacrophages to the site

Plaques begin to form from cells whichembedded into the endothelium

Blood Tests(Cardiac Enzymes

Test)

COMPREHENSIVE

PATHOPHYSIOLOGIC BASIS OF

CLIENT’s CONDITION



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Development of Foamcells

Lipids are engulfed by the foam cells

Development of smooth muscle cells

ATHEROSCLEROTIC PLAQUE FORMED

Increased inflammatorystress

Continuousinflammatory response

ANGIOGENESISVascular endothelial growth factor (VEGF), Placental Growth Factor (PlGF),

and hepatocyte growth factor (HGF)

Intraplaque Hemorrhage

Conversion of Stable plaqueto unstable plaque

Intraplaque Inflammation

Degradation of fibrous

cap

Plaque Instability

Platelet Activation

Plaque Erosion

THROMBUS FORMATION

Thrombus occluding vessel

Prevention of myocardialperfusion

Decreased Myocardial

Oxygen Supply

Anaerobic Metabolism ofGlycogen

Failure of Sodium-Potassium and Calcium

pump

Accumulation of hydrogenions and lactate

Acidosis

Altered electrical conduction

Altered Repolarization

Inverted T-wave

Ischemic PhaseMyocardial cells are sensitive to

acidic pH

Myocardial Injury

ST Segment ElevationMyocardial Ischemia

Myocardial Cell

Necrosis

Absence ofdepolarization current

from dead tissues

Presence of opposing

currents from otherareas of the heart

Abnormal Q Wave

Injury Phase

InfarctionPhase

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)

CardiacBiomarkers

NTG or Morphineto Control pain

FibrinolyticTherapy

Lipitor



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Inflammatory Response toNecrotic Myocardial Cell

Impaired MyocardialContractility

Increased WBC

Released ofEndogenous Pyrogens

Release ofProstaglandins

Prostaglandins willreset hypothalamic

thermostat

FEVER

Scar Tissues replacinghealthy tissues

Decrease CardiacOutput

Decrease Blood Pressure

Release of Epinephrine andNorepinephrine

Increased BloodPressure

IncreasedHeart Rate

Increased Afterload

Stimulation ofBaroreceptors

PeripheralVasoconstriction

Increased Pumping Action of Heart

DecreasedRenal Perfusion

RAAS Activation

Increased Myocardialoxygen Demand

ADH and Aldosterone Release

Sodium and Waterreabsorption

Increased BloodVolume

Increased Preload

Increased Myocardial

Workload

Cardiomegaly Chest X-Ray and 2DEcho with Doppler

studies

Deterioration of

Heart’s ability to pump

Moderate LeftVentricular 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

BreathWidespread

CracklesOcassional

Wheeze(“Cardiac Asthma”)

Increased RightVentricular Pressure

(Above Systolic-20-30 mmHgDiastolic 0-5 mmHg)

HemodynamicMonitoring

Increased CVP(Above 2-6mmHg)



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Fluids leak intoalveolar space

Lymphatic system drains excessinterstitial fluid volume

Additional fluid in the pleural spacedrains into titer lymph nodes

Fluid moves from the interstitial spacein the alveolar walls

Damaged to alveolarepithelium

Further fluid accumulation in thealveolar space

Alveolar Edema

Impaired gas exchange

H oxemiaHypercarbia

Decrease lung complianceDecrease oxygen diffusion

Use of Accessory Muscle Bradypnea

Poor cerebral

oxygenation

tered Level ofonsciousness

Agitation /

Restlesness

Poor Peripheraloxygenation

Pallor Sweaty coolperiphery

Reducedcapillaryreturn

Increased work

of breathing

Exhaustion

Fatigue

Decreased PO2 (PO2 61mmHg)

Increased Pulmonary Artery

Pressure(Above 25mmHg)

andPulmonary Artery Wedge Pressure(PAWP) (Above 4-12mmHg)

Decreased SaO2 (SaO2 85%)

HemodynamicMonitoring

Arterial Blood GasAnalysis



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Identify the learning issues (at least 7) related to pathophysiology (Focus on CV) that you can draw out

from this case.

1. 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.

A.

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.

B.

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.



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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 fromvascular 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.

C. 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.

D. 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



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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 canpromote lesion fibrosis and luminal encroachment.

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.

E. 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, themyocardium 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, andelectrical 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.



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CAD

CLINICAL MANIFESTATIONS

CHRONIC STABLE ANGINA PECTORIS UNSTABLE ANGINA PECTORIS (Preinfarction)

Chest pain or discomfort provoked by EXERTION or

EMOTIONAL STRESS. Relieved by REST or

NITROGLYCERIN.

Characteristics

substernal chest pain, pressure, heaviness or

discomfort

pain may be mild or severe

gradual buildup of discomfort and subsequent

gradual fading

numbness or weakness in arms, wrists, or

hands

diaphoresis

tachycardia

increased BP

Location

Behind middle or upper third of sternum

+ Levine Sign

Radiation

Radiates to neck, jaw, shoulders, arms, hands,

and posterior intracapsular area

Duration

2-15 minutes (after stopping activities)

1 minute after NITROGLYCERINE

Other Precipitating Factor

Exposure to hot or cold weather

Eating heavy meal

Coitus (increase workload of the heart, increase

oxygen demand)

Chest pain occurring at REST, no OXYGEN

DEMAND is placed on the heart, but an ACUTE

LACK of BLOOD FLOW to the HEART occurs

because of:

Coronary artery spasm

Presence of an enlarge plaque

Hemorrhage / ulceration of a complicated lesion

Critical narrowing of the vessel lumen occurs

A change in FREQUENCY, DURATION, and

INTENSITY of stable angina symptoms Pain lasts longer than 10 MINUTES

Pain UNRELIEVED by rest or Nitroglycerine

Mimics S&S of MI

CAN CAUSE SUDDEN DEATH OR RESULT IN

MI.

SILENT ISCHEMIA

Absence of chest pain with documented evidence of

an imbalance between myocardial oxygen supply

and demand (ST DEPRESSION of 1mm or more). CIRCADIAN EVENT (occurs during the first few

hours after awakening due to an increase in

sympathetic nervous system activity) o Increase heart rate

o Increase BP

o Increase coronary vessel tone

o Increase blood viscosity

2. Significant clinical presentation of the disease presented by the patient:



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3. Possible Complications of Acute Coronary Syndrome.

The complications of acute coronary syndromes depend on how much, how long, and where a

coronary artery is blocked. If the blockage affects a large amount of heart muscle, the heart will notpump effectively. If the blockage shuts off blood flow to the electrical system of the heart, the heart

rhythm may be affected.

Pumping problems:

In a heart attack, part of the heart muscle dies. Dead tissue, and the scar tissue that eventually

replaces it, does not contract. The scar tissue sometimes even expands or bulges when the rest of

the heart contracts. Consequently, there is less muscle to pump blood. If enough muscle dies, the

heart's pumping ability may be so reduced that the heart cannot meet the body's need for blood

and oxygen. Heart failure, low blood pressure, or both develop. If more than half of the heart tissueis damaged or dies, the heart generally cannot function, and severe disability or death is likely.

Drugs such as beta-blockers and especially angiotensin-converting enzyme (ACE) inhibitors

can reduce the extent of the abnormal areas by reducing the workload of and the stress on the

heart. Thus, these drugs help the heart maintain its shape and function more normally.

The damaged heart may enlarge, partly to compensate for the decrease in pumping ability (a

larger heart beats more forcefully). Enlargement of the heart makes abnormal heart rhythms more

likely.

Rhythm problems:

Abnormal heart rhythms (arrhythmias) occur in more than 90% of people who have had a heart

attack. These abnormal rhythms may occur because the heart attack damaged part of the heart's

electrical system. Sometimes there is a problem with the part of the heart that triggers the

heartbeat, so heart rate may be too slow. Other problems can cause the heart to beat rapidly or

irregularly. Sometimes the signal to beat is not conducted from one part of the heart to the other,

and the heartbeat may slow or stop.

In addition, areas of heart muscle that have poor blood flow but that have not died can be very

irritable. This irritability can cause heart rhythm problems, such as ventricular tachycardia orventricular fibrillation. These rhythm problems greatly interfere with the heart's pumping ability and

may cause the heart to stop beating (cardiac arrest). A loss of consciousness or death can result.

These rhythm disturbances are a particular problem in people who have an imbalance in blood

chemicals, such as a low potassium level.

Other problems:

Pericarditis (inflammation of the membranes enveloping the heart) may develop in the first day

or two after a heart attack or about 10 days to 2 months later. Pericarditis is more common in

people who have not had the blocked artery opened by percutaneous coronary intervention (PCI)or coronary artery bypass grafting (CABG). People seldom notice symptoms of early developing



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Acute CoronarySyndromes

Rupture, fissuring, orulceration

Exposing

Highly thrombogenicplaque constituents

Underlyingsubendothelial

basement membrane

Hemorrhage into thecore of plaques

Expansion of plaquevolume

Worsening of theluminal occlusion

Plaque rupture

Intrinsic factors

• Large atheromatous core

• Thickness of the fibrous cap

Extrinsic factors

• Adrenergic stimulation

• Intense emotional stress

collagen

synthesis

collagen

degradation

pericarditis because their heart attack symptoms are more prominent. However, pericarditis

produces a scratchy rhythmic sound that can sometimes be heard through a stethoscope 2 to 3

days after a heart attack. Sometimes, the inflammation causes a small amount of fluid to collect in

the space between the two layers of the pericardium (pericardial effusion). Later developing

pericarditis is usually called Dressler (post-myocardial infarction) syndrome. This syndrome causes

fever, pericardial effusion, inflammation of the membranes covering the lungs, pleural effusion(extra fluid in the space between the two layers of the pleura), and joint pain.

Other complications after a heart attack include malfunction of the mitral valve,rupture of the

heart muscle, a bulge in the wall of the ventricle (ventricular aneurysm), blood clots (emboli), and

low blood pressure (hypotension). Nervousness and depression are common after a heart attack.

Depression after a heart attack may be significant and may persist.

4. Triggering factors for Myocardial infarction from Acute Coronary Syndrome

Role of Acute Plaque Changes

In most patients, unstable angina, infarction, and many cases of SCD all occur because of

abrupt plaque change followed by thrombosis. Hence the term acute coronary syndrome.

A. Events that trigger the abrupt plaque changes

Rupture reflects the inability of a plaque to withstand mechanical stresses.

Triggers may be intrinsic or extrinsic

B. Integrity of the Plaque Fibrous caps are continuously remodeling



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Collagen produced by smooth muscle cells

Collagen degraded by the action of metalloproteinases (macrophages)

InflammationNeutrophilinfiltration

Release ofmetalloprotein

ases

Breakdown ofcollagen in the

fibrous cap

Plaquedestabilization

& rupture

Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel

Vasospasm (platelet aggregation and mediator release)

Other mediators activate the extrinsic pathway of coagulation

Release potent secondary aggregators(thromboxane A2, adenosine diphosphate, and serotonin)

Platelets adhere, aggregate, become activated

A sudden disruption of an atheromatous plaque

Role of Inflammation

Inflammation plays an essential role at all stages of atherosclerosis.

What’s the contribution of Inflammation to acute coronary syndromes…?

Role of Thrombus

o Formation of a thrombus on a disrupted atherosclerotic plaqueo Significant rapid stenosis

o Complete occlusion of the coronary arteries

o Mural thrombus in a coronary artery can also embolize

o Small fragments of thrombotic material

o Small infarcts

5. Myocardial infarction as a result of continues necrosis of heart muscles

• Ischemic necrosis of a part of the myocardium

•

In a typical MI ,



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Ischemia Death of myocardium

Electrical instability of themyocardium

Arrhythmias (ventricularfibrillation)

Reduction in thecontractility of the

myocardiumReduction in the ejectionfraction & increase in end

systolic volume &pressure (Heart failure)

Or a fatal mechanicalfailure

6.

Role of Ischemia in development of Myocardial Infarction and significant signs and symptoms.

Please see the above comprehensive pathophysiologic basis of the client’s condition for furtherexplanation.

7. Likelihood that signs & symptoms represent an ACS secondary to CAD

Normal Normal Elevated cardiac TnI,TnT or CK-MB

CardiacMarker

T wave flattening orinversion in leads withdominant R wave

Normal EKG

Fixed Q waves

Abnormal ST segmentsor T waves notdocumented to be new

New or presumablynew, transient STsegment deviation(≥0.05mV) or T waveinversion (≥0.2mV)with symptoms

EKG

Chest discomfortreproduced bypalpation or respiration

Extracardiac vasculardisease

Transient MR,hypotension,diaphoresis, pulmonaryedema or rales

Exam

Probable ischemicsymptoms in absence

of the intermediatelikelihoodcharacteristics

Recent cocaine use

Chest or left arm painor discomfort as chief

symptom Age > 70

Male gender

Diabetes mellitus

Chest or left arm painor discomfort as chief

symptom reproducingprior documentedangina

Known history of CAD,including MI

History

Low Intermediate High Feature



References:

McPhee SJ, Hammer GD, et al. Pathophysiology of Disease: an Introduction to Clinical

Medicine 6th

Edition; 2013; 26:985-998

Huether S, McCance K, Parkinson C, et al. Understanding Pathophysiology 5th

edition; 2012;

22:782-892

Carol JR, Mattson JH, Porth JB, et al. Essentials of Pathophysiology: Concepts of Altered

Health States; 2014; 18:865-872

Corwin EJ, West BJ, Lilly LS, et al. Pathophysiology of Heart Disease: A Collaborative Project

of Medical Students and Faculty 5th

Edition; 2013; 8:345-356

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