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Cardiovascular Case Study


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Title: Cardiovascular Case Study

Cardiovascular Case Study
Case Study
  • Mr. Alex Borg is a 70 year old retired black
    male, who presented to the emergency department
    at 1000 on Saturday September 23rd via ambulance.
    He was accompanied by his wife. His primary
    complaints were of chest pain and shortness of
    breath. This was the Mr. Borgs third visit to
    the emergency department in the last 2 weeks,
    with the same symptoms. On arrival, his chest
    pain was rated 9/10, and did not subside with

Vitals Upon Arrival
  • T 35.9 oC
  • P 118 bpm
  • R 30 rpm
  • BP 168/88 mm/Hg
  • SpO2 88 on RA

  • Oxygen was applied by nasal prongs at 4L/min
    which brought his oxygen saturation levels up to
    92. Further clinical assessments were performed
    in order to confirm suspected diagnosis and
    treatment. The patients lungs were auscultated
    for decreased air entry and exit, but were clear
    throughout. Heart sounds were auscultated and a
    third sound, S3, was heard. Blood was drawn and
    sent to the lab for cardiac workup and routine
    chemistry. Peripheral edema was noted with 1
    pitting around the ankles. Telemetry monitoring
    and a 12 lead ECG was performed. ECG results were
    obtained and showed the following rhythm.

(No Transcript)
Medications administered
  • All other systems had no significant findings. An
    IV was started in the R forearm, N/S TKVO.
  • Nitrospray spray q 5 minutes x3 doses under the
    tongue beginning at 1005
  • Aspirin 650mg PO given at 1005

  • Shortly after medications were administered, Mr.
    Borgs chest pain decreased to 5/10.
  • Mr. Borg was admitted to 4W Medical floor for
    observation. At that point a patient history was
    obtained with the following significant factors
  • His mother died from a heart attack at age 53.
  • His father had hypertension.
  • He smokes 1 pack of cigarettes a day
  • He consumes 4 or more alcoholic drinks a day
  • He is obese
  • Wt. 109kg and ht. 59
  • He has Type II Diabetes Mellitus

Doctors Orders Upon Admission
  • Vitals q4h
  • Keep SpO2 gt92 with 3L oxygen
  • Cardiac diet
  • AAT
  • IV TKVO NS 30mL/h
  • Daily in outs
  • Telemetry
  • CXR
  • Repeat cardiac profile
    in 12 hours.
  • Daily CBC, BUN, Cr, Lytes
  • EC ASA 325mg po daily
  • Metoprolol 100mg po daily
  • Norvasc 2.5mg po daily
  • Nitrospray spray prn

  • Coronary Artery Disease with Anginal Episode

What are coronary arteries?
Coronary Arteries Cont
  • High density lipoprotein (HDL)
  • A protein bound lipid that transports cholesterol
    to the liver for excretion in the bile.
  • Composed of a higher proportion of lipids than
    the LDLss.
  • Exerts a beneficial effect on the arterial wall.
  • Low density lipoprotein (LDL)
  • Protein bound lipids that transport cholesterol
    to tissues in the body.
  • Composed of a lower proportion of protein than
    the HDLs.
  • It exerts a harmful effect of the arterial wall.

Coronary Artery Disease (CAD)
  • LDLs travel through the blood stream and adhere
    to the walls of the coronary arteries.
  • Over time, a fibrous layer composed of platelets
    and other clotting factors envelope the fatty
    deposits and form a plaque.

Coronary Artery Disease (CAD)
  • Eventually the plaque buildup becomes so large
    that the coronary arteries become occluded and
    blood is unable to pass through. The lack of
    blood decreases the amount of oxygen that is
    being delivered to the myocardial cells and
    myocardial tissue become ischemic.
  • An occlusion can happen 2 ways
  • The vessel becomes totally occluded and blood is
    unable to pass through at all.
  • A piece of the plaque breaks off the vessel wall,
    called a thrombus, and occludes a smaller
    coronary artery.

How CAD Causes Ischemia
Coronary Artery Disease Risk Factors
  • Modifiable
  • Dyslipidemia
  • Hypertension
  • Smoking
  • Diabetes Type II
  • Obesity
  • Sedentary Lifestyle
  • Alcoholism
  • Non-Modifiable
  • Advanced age
  • Males under 60
  • Race
  • Genetics
  • Diabetes Type I

  • Diabetic dyslipoproteinemia includes
  • increased LDL
  • increased triglycerides
  • deceased HDL
  • Glycation of LDL protein decreases uptake by the
    liver, increases hepatic synthesis of LDL, and
    increases LDL oxidation.
  • Smoking and diabetes also increase LDL oxidation.
  • Oxidized LDL is toxic to endothelial cells and
    causes smooth muscle proliferation and abnormal

  • Mr. Borg is currently in a hypertensive state.
    He has never been diagnosed with hypertension but
    may have unknowingly had it for years.
  • Hypertension causes hypertrophy of the myocardial
    cells which increases the myocardial need for
    coronary flow.

  • Mr. Borg has been a smoker for 40 years. He
    smokes approximately 1 pack a day.
  • Nicotine in the cigarettes stimulates the
    release of catecholamines which increases heart
    rate and vascular constriction. This causes
    blood pressure to rise and the cardiac workload
    and need for oxygen to increase.

  • Mr. Borg is an obese man (112 kg). He has lived
    with obesity for many years.
  • HDL (good cholesterol) levels decrease with
    obesity. Obesity also causes the heart to
    increase in size, and therefore increases the
    workload of the heart. This makes it more
    difficult to pump blood to the body.

  • Mr. Borg has been ingesting 4 or more alcoholic
    drinks each day for the past 35 years.
  • Alcohol ingestion increases body weight, LDL
    levels, and blood pressure which are all other
    leading causes of CAD.

Clinical Manifestations
  • Chest pain from myocardial ischemia (angina)
  • Feels like heaviness or pressure
  • May radiate to the neck, jaw, left arm, shoulder,
    back, or right arm
  • Pallor
  • Diaphoresis
  • Dyspnea

  • When a blood vessel becomes occluded for a long
    period of time, blood flow is limited and
    myocardial tissue becomes ischemic.
  • Length of occlusion time is approx. 10-20
  • The thrombus then breaks apart or vasodilation
    occurs and myocardial perfusion returns before
    significant tissue necrosis occurs.

Nursing Interventions
  • Improving respiratory function
  • Monitor vital signs
  • Bedrest or sitting until pain subsides
  • Oxygen if SpO2 levels are low.
  • Reducing anxiety
  • Develop a trusting relationship
  • Provide privacy
  • Reassure patient
  • Improving cardiac flow
  • Elevate head of the bed
  • Monitor fluid volume status
  • Monitor peripheral pulses

Treatment and Evaluation
  • 3rd heart sound, S3 was heard on auscultation
  • This indicates left ventricle failure
  • ECG and telemetry
  • Laboratory tests

  • The process of continuous electrocardiographic
    monitoring by the transmission of radiowaves from
    a battery-operated transmitter worn by the
  • Anagram
  • L Smoke (black) over fire (red)
  • M White on the right
  • R Bear (Brown, on bottom) in the bush (green, on

Nitrates - Nitrospray
  • Side Effects
  • Headaches from vasodilation
  • Hypotension
  • Dizziness and weakness
  • Faintness
  • Be careful when using with other vasodilators,
    Viagra and alcohol because together they can
    enhance the effects of hypotension.
  • Act on the blood vessels in venous circulation
    and the coronary arteries
  • Cause generalized vascular and coronary
    vasodilation which causes
  • Increased blood flow through the coronary
    arteries into the myocardial cells.
  • Decreased cardiac preload and afterload
  • Decreased myocardial oxygen demand

Beta-Adrenergic Blockers Metoprolol
  • Act on the B1 receptor sites and decrease the
    effects of the SNS by blocking the release of
    catecholamines (epi norepi) causing
  • Decreased heart rate
  • Decreased blood pressure
  • Decreased myocardial oxygen demand
  • Decreased anginal pain
  • Side Effects
  • Decreased pulse
  • Decreased blood pressure
  • Bronchospasm
  • Behavioural repsonses

Calcium Channel Blocker - Norvasc
  • Calcium activates the myocardial cells to
    contract, increasing cardiac workload and oxygen
  • When these channels are blocked the heart rate
    slows and the demand for oxygen is decreased.
  • Side Effects
  • Headache
  • Hypotension
  • Dizziness
  • Flushing of the skin
  • Reflex tachycardia
  • Liver and kidney changes

Anti-Coagulants - Aspirin
  • Aspirin will also help to reduce the pain a
    patient is experiencing because it is also a
    non-opioid analgesic.
  • Side Effects
  • GI bleeding
  • Increased bleeding time
  • Anemia from bleeding
  • Anaphylaxis
  • Heartburn, N V, abdominal pain
  • Hepatotoxicity
  • Aspirin prevents platelet activation and is used
    to inhibit clot formation.
  • Aspirin reduces the incidence of MI and death in
    patients with CAD.
  • Aspirin does not dissolve clots that are already
    present, but it works prophylactically to prevent
    clots from forming or enlarging.

  • While on the floor for the past 2 days, Mr. Borg
    has been stable with no complaints of chest pain
    or shortness of breath. Lab reports and CXR came
    back with no significant findings. Mr. Borg is
    ready to be discharged tomorrow if no
    complications occur.

  • At 1235, Monday September 25th, Mr. Borgs wife
    approaches the nursing station in a frantic
  • She states My husband doesnt feel very well. He
    says he feels like he is dying.

Signs and Symptoms
  • What do we see?
  • Mr. Borg is sitting at the side of his bed,
    clutching his chest.
  • He is diaphoretic and cyanotic around his lips
    and nail beds.
  • He has obvious dyspnea because he is gasping for
    his breath
  • He seems quite anxious and restless
  • Upon palpation, his skin is cool and clammy.

  • T 37.9
  • P 180 bpm
  • R 30 rpm
  • BP 120/70
  • SpO2 90 on 3L/min

Assessments and Interventions
  • Oxygen is increased to 5L/min
  • Heart auscultated a third and fourth heart
    sound are heard, S3 and S4
  • Lung ausculation decreased air entry and exit,
    chest is clear.
  • Elevate the head of the bed to 45 degrees,
    semi-fowlers position

  • Nitrospray spray sl q5min x3
  • After nitrospray has been administered, Mr.
    Borgs chest pain is not relieved
  • His ECG shows the following

ST elevation
Altered Q waves
Inverted T waves
  • Altered Q waves
  • When a thrombus becomes permanently lodged in the
    coronary artery the infarct (tissue necrosis)
    spreads from the endocardium through to the
    epicardium. This results in altered Q waves.
  • ST Elevation
  • Myocardial injury also causes ST segment changes.
    The injured myocardial cells depolarized
    normally, but repolarize more rapidly then normal
    cells, causing the ST segment to rise at least
    1mm above the isoelectric line.
  • Inverted T Waves
  • Myocardial injury causes the T wave to become
    enlarged and symmetric. As the area of injury
    becomes ischemic, myocardial repolarization is
    altered and delayed, causing the T wave to

  • Acute Myocardial Infarction

Myocardial Infarction
  • Plaque progression, disruption, and subsequent
    clot formation is the same for myocardial
    infarction as it is for other acute coronary
    syndromes, such as angina and coronary artery
  • The same process occurs, but happens along a
    different point of the continuum.
  • In an acute MI, the thrombus is lodged for a
    prolonged period of time, depriving the cells of
    oxygen and causing cellular injury. The longer
    the deprivation of oxygen, there is more tissue
    necrosis that occurs.

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Cardiac Tissue Surrounding the Infarct
  • Myocardial stunning
  • Temporary loss of contractile functioning
  • Hibernating myocardium
  • Tissue that is persistently ischemic and
    undergoes metabolic adaptation
  • Myocardial remodeling
  • Causes myocyte hypertrophy and loss of
    contractile function

Functional Changes Post MI
  1. Decreased cardiac contractility with abnormal
    wall motion
  2. Altered left ventricular compliance
  3. Decreased stroke volume
  4. Decreased ejection fraction
  5. Increased left ventricular end diastolic pressure
  6. SA node malfunction
  7. Dysrhythmias and heart failure often follow MI

Time is Muscle!
  • Within 8 seconds oxygen reserves of the
    myocardial cells are used up, glycogen stores are
    decreased, and anaerobic metabolism begins. This
    can put the patient into a state metabolic
  • After 8 10 seconds of decreased blood flow the
    affected myocardium becomes cyanotic and cooler.
  • After 30 60 seconds of hypoxia, ECG changes are
  • Even if cells are metabolically altered and
    dysfunctional, they can be saved if blood flow
    returns within 20 minutes.
  • Within an hour, tissue necrosis results in the
    release of certain intracellular enzymes through
    the damaged cell membranes. These enzymes are
    evident on the laboratory results.

Laboratory Findings
  • Creatinine Kinase (CK-MB)
  • This is a cardiac specific enzyme found mainly in
    cardiac cells and, therefore, rises only when
    there is damage to these cells.
  • It is the most specific index for the diagnosis
    of an MI
  • Levels start to increase within a few hours and
    peak within 24 hours of an acute MI
  • Normal values
  • 5 100 IU/L
  • Patient value
  • 152 IU/L
  • This level is elevated, clearly indicating Mr.
    Borg has had an MI

Laboratory Findings
  • Myoglobin (Myo)
  • Heme protein that is found in cardiac and
    skeletal muscle that helps to transport oxygen.
  • Levels begin to increase within 1 3 hours, and
    peak within 12 hours from the onset of symptoms.
  • If these values are negative it is a good
    indicator that the patient has not had an acute MI
  • If the first test is negative, repeat the test in
    3 hours. If the second test is negative it is
    confirmed that the patient did not have an MI
  • Normal Values
  • lt100 ng/mL
  • Patient Value
  • 154 ng/mL

Laboratory Findings
  • Troponins
  • Cardiac and skeletal muscle is controlled by
    intracellular calcium concentrations.
  • When calcium levels rise, the muscles contract,
    and when the levels fall the muscles relax.
  • Long filament that calcium binds to.
  • There are 3 types of trops
  • Trop T
  • Trop I
  • Trop C
  • Trop levels are normally quite low so even slight
    elevations are indicative of heart damage.
  • Levels of TropT will begin to elevate within 4
    hours of myocardial damage and are normally
    elevated for 1 2 weeks post-damage.
  • Normal Values
  • lt0.1 ng/mL
  • Patient Values
  • 0.15 ng/mL

Laboratory Findings
  • Electrolytes
  • Oxygen deprivation is accompanied by electrolyte
  • Loss of K
  • Loss of Ca
  • Loss of Mg
  • These electrolytes are released into the blood
    stream and are evident on lab results.
  • Normal Values
  • Na 125 - 145
  • K 3.5 5.0
  • Mg 0.74 1.23
  • Patient Values
  • Na 152
  • K 5.3
  • Mg 1.36
  • Serum Glucose
  • Arterial occlusion causes the myocardial cells to
    release catecholamines.
  • Catecholamines mediate the release glycogen,
    glucose, and stored fat from body cells.
  • These levels are increased on lab values.
  • Normal values
  • 3.9 6.1
  • Patient Values
  • 7.8

Laboratory Findings
  • White Blood Cells
  • WBC levels increase with tissue necrosis and
    inflammation of the heart.
  • Specifically the neutrophils will have the
    greatest increase.
  • Normal Findings (Neutrophils)
  • 0.54 0.75
  • Patient Value
  • 0.97

  • Medications
  • Anti-Platelet/Anti-Coagulant Aspirin 650mg PO
  • ACE Inhibitor Altace 5mg PO
  • Beta - Adrenergic Blocker Metoprolol 100mg IV
  • Calcium Channel Blocker Norvasc 2.5mg PO
  • Analgesic Morphine
  • Streptokinase or rPA as per protocol

Streptokinase or rPA
  • What is it?
  • Sterile, purified preparation of the bacteria
    protein group C (beta)-hemolytic streptococci.
  • What does it do?
  • Acts with plasminogen to produce an activator
    complex that converts plasminogen to plasmin.
  • Plasmin degrades fibrin clots, fibrinogen , and
    other plasma proteins.

  • Goal of the therapy
  • The goal of thrombolytic therapy is to dissolve
    and lyse the thrombus in the coronary artery.
  • This allows blood to reperfuse through the
    coronary arteries, minimizing the size of the
    infarction and preserving ventricular function.

  • Why is it needed?
  • Lysis of intracoronary thrombi
  • Improvement of ventricular function
  • Reduction of mortality associated with MI
  • Reduction of the size of the infarct
  • Reduction of CHF related to MI
  • Who cant get thrombolytic therapy?
  • Active internal bleeding
  • Recent CVA
  • Uncontrolled hypertension
  • Adverse reaction
  • Bleeding
  • Arrhythmias
  • Hypotension
  • Cholesterol embolism

  • What are the contraindications?
  • Recent major surgery
  • Recent gastrointestinal bleeding
  • Recent trauma needing CPR
  • Hypertension gt180/gt110mmHg
  • Age gt75
  • Pregnancy
  • Bleeding conditions

  • Route
  • Intravenous infusion
  • Dosage
  • 1, 500, 000 IU within 60 minutes

Nursing Interventions
  • Potential ineffective peripheral tissue perfusion
    related to decreased cardiac output
  • Observe for hypotension, tachycardia, activity
    intolerance, reduced urine output, cool, moist,
    cyanotic extremities.
  • Anxiety related to fear of death, change is
    health status.
  • Assess patients level of anxiety
  • Assess need for spiritual counseling
  • Allow patient to express anxiety and fear
  • Allow for flexible visiting hours
  • Encourage active participation in cardiac rehab
  • Teach stress reduction techniques.
  • Ineffective cardiopulmonary tissue perfusion
    related to reduced coronary blood flow
  • The patients description of chest discomfort and
    other symptoms
  • Obtain a 12 lead ECG during the symptomatic event
  • Administer oxygen
  • Administer medication therapy
  • Ensure physical rest and ensure a restful
  • Potential ineffective air exchange related to
    fluid overload
  • Assess for abnormal heart sounds, and abnormal
    breath sounds
  • Teach patient to adhere to diet and activity

  • Mr. Borg is transferred to ICU following his MI
    and is placed under close monitoring
  • His condition deteriorates

Mr. Borgs heart rhythm changes and he suddenly
goes into SVT (supraventricular tachycardia) with
a rate of 186 beats per minute (bpm). The
physician orders adenosine (Adenocard) 6 mg IV.
After no change in his heart rate or rhythm, the
doctor orders an additional dose of adenosine of
12 mg. This bolus of adenosine administered IV
push converts him briefly to normal sinus rhythm
but then Mr. Borgs rhythm changes back to SVT.
Mr. Borg reports increased chest pain and
shortness of breath. He is cyanotic with no
palpable blood pressure. A Diltiazem drip is
ordered and initiated. Blood gases are drawn as
  • Supra above
  • Ventricle is contracting too soon. There is not
    enough blood in the ventricle dec. card output
    also the heart needs more oxygen to accommodate
    the increased HR.
  • The use of extra fibres in and around the AV node
  • The impulse travels from the SA to the AV and
    down into the ventricles but then back up via
    these extra fibres causing more contractions then
    is necessary.

(No Transcript)
(No Transcript)
  • Adenosine
  • Antiarrythmic
  • Slows AV conduction
  • Diltiazem
  • Ca channel blocker
  • Inhibits movement of Ca across membrane of heart
    muscle cells resulting in depression of impulse,
    slowing HR
  • Also dilates coronary arteries which dec. heart

In ICU, Mr. Borgs hypotension and tachycardia
persisted and a low-dose dopamine drip is
initiated at 2 ug/kg/min. Mr. Borg becomes more
hypotensive, tachycardic, and hypoxic. He is
then intubated and placed on a ventilator with
100 oxygen. Furosemide (Lasix) 80 mg and
Procanamide (Pronestyl) 500 mg IV bolus are
administered. What diagnosis would you give
poor Mr. Borg?
Cardiogenic Shock
Cardiogenic Shock
  • 80 of those who develop, will die.
  • What is it?
  • impaired muscle action
  • blood is inadequately pumped through the heart
  • This results in back-up of blood.
  • Cardiogenic shock occurs when 40 or more of
    myocardium is damaged (usually left ventricular).

So Whats the Problem?
  • Right sided heart interference
  • When the shock is due to right-sided heart
    failure, back-up will be evidenced as
  • jugular venous distention
  • increased CVP

So Whats the Problem Cont?
  • Left sided heart interference
  • When the shock is due to left-sided failure,
    blood backs up into the pulmonary circulation
    resulting in
  • pulmonary edema
  • crackles in the lungs

Cardiogenic Shock Cont
  • Causes
  • Mechanical
  • Obstructive

Mechanical Causes
  • MI
  • systolic dysfunction inability of heart to pump
    blood forward
  • Valvular insufficiency due to disease or trauma
    (e.g. stenosis, regurgitation)
  • Cardiac dysrhythmias
  • These events cause the following which lead to
    cardiogenic shock
  • decreased myocardial contraction
  • diminished cardiac output

Obstructive Causes
  • Pulmonary emboli
  • travels through venous system
  • lodges in right side of heart in the pulmonary
  • Pericardial tamonade
  • accumulation of blood in the pericardial space
    compresses the myocardium and interferes with the
    myocardiums ability to expand
  • inability of heart to fill during diastole
  • Tension pneumothorax
  • significant amount of air in the pericardial
    space compresses heart and great vessels

Cardiogenic Shock Cont
  • What do you think this patient will look like?
  • Clinical Manifestation
  • systolic blood pressure significantly below
    clients normal blood pressure
  • diaphoresis
  • tachycardic
  • tachypneic
  • signs of peripheral hypoperfusion (cyanosis,
    pallor, decreased capillary refill time, cold
    clammy skin)

Clinical Manifestations Cont
  • decreased renal perfusion will result in sodium
    and water retention and therefore decreased
    urinary output
  • signs of decreased cerebral perfusion
    (restlessness, delirium, anxiety)

So What Do You Want To Do For This Patient?
  • Overall goal?
  • to restore blood flow to the myocardium

Nursing Interventions
  • Assess
  • chest pain
  • vital signs
  • 12 lead ECG
  • monitor response to medications given
  • be calm and provide care efficiently to reassure
    patient/reduce anxiety
  • limit visitors

Nursing Care Plan For Mr. Borg
So What Do You Want To Do For This Patient?
  • Some laboratory values
  • Cardiac Enzymes
  • Chest X-ray
  • ECG
  • Echocardiogram
  • IV, vitals, foley, meds (including something for
    pain usually Morphine) but why must we be
    careful with how much Morphine we give Mr. Borg???

So What Do You Want To Do For This Patient?
  • Angioplasty with stenting
  • Until these can be done, the heart must be
    supported to optimize stroke volume and cardiac
    output by...

Management of Cardiogenic Shock
  • Fluid challenge
  • 300ml of NS or Ringers to rule out hypovolemia
    (unless CHF or pulmonary edema)
  • Insert CVP catheter to monitor
  • cardiac output, pulmonary artery pressure,
    pulmonary capillary wedge pressure
  • Administer inotropics (e.g. dopamine)
  • Administer vasodilators (e.g. nitro, calcium
    channel blockers, morphine)

Management of Cardiogenic Shock Cont
  • Administer Diuretics (lasix)
  • Beta blockers (propranolol)
  • Intra-aortic balloon pump or external
    counterpulsation device

Prevention of Cardiogenic Shock
  • Primary
  • teach patients the importance of diet and
    exercise to minimize risk factors
  • Secondary
  • provide oxygen
  • administer inotropics and vasodilators
  • Tertiary
  • provide intra-aortic balloon pump
  • administer inotropics and vasodilators

  • Mr. Borgs heart eventually improves a little.
    His heart rate is 140 bpm and the systolic BP is
    around 100 mm Hg while he is on 9 ug/kg/min of
    dopamine. A repeat ECG reveals that the distal
    two thirds of the left ventricle is akinetic.
    Mr. Borg is scheduled to have a right and left
    heart catheterization at 1300 today.

The results of the cardiac catheterization
reveal 100 occlusion of the left coronary artery
and severe diffuse disease of the left anterior
descending coronary artery. The physicians have
determined that he is a poor surgical candidate
and plan to treat him medically.
Over the next several days, Mr. Borgs blood
pressure stabilizes and he is weaned off the
dopamine. The Furosemide is changed to an oral
dose and the potassium is reduced to 10 mEq po
tid. Mr. Borg is also digitalized and will be
maintained on Digoxin 0.25 mg qd. His resting
heart rate has been approximately 70 bpm. Mr.
Borg is also extubated and placed on a no added
salt, low fat diet. He is to begin a cardiac
rehabilitation program. The physician is
planning to discharge him tomorrow following a
recovery treadmill test.
  • To raise blood pressure by increasing peripheral
  • Acts on norepinephrine and dilates vessels in
    kidneys to maintain perfusion (can be detrimental
    to the kidneys if used for long periods of time).

  • Better blood flow in the microcirculation
  • To treat CHF, increase the force of contractility
  • Always check apical pulse for 1 minute

Why was Mr. Borg intubated?
  • Loop diuretic
  • Inhibits the resorption of Na and Cl from
    proximal and distal loops of henle
  • Fluid may settle in the lungs due to back up from
  • May promote the loss of K

  • (Ace inhibitors pril, Beta blockers lol)
  • Blocks angiotensin I to angiotensin II which
    vasoconstricts leading to decreased BP

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  • Rhonchi dry rattle
  • Rales crackle (non-musical)
  • Thiamine Vitamin B1
  • Breakdown carbs for use

Cardiac Rehab
  • When the patient is free of symptoms cardiac
    rehab is initiated.
  • What is it?
  • Targets risk reduction by
  • Education
  • Individual and group support
  • Physical activity

Cardiac Rehab
  • Goal?
  • For a patient with an MI to extend and improve
    quality of life.
  • Limit the effects and progression of plaque
  • Return patient to pre-MI lifestyle
  • Prevent another cardiac episode
  • How will it happen?
  • Encouraging activity and physical conditioning
  • Education
  • Counseling
  • Behavioural interventions

Cardiac Rehab
  • Phases of rehab
  • Phase 1 diagnosis of MI
  • Low level activities and initial patient and
    family education
  • Ex when to call 911, medications, activity-rest
    balance, follow-up appointments.
  • Phase 2 After discharge
  • Supervised, ECG monitored, exercise training
  • Counseling re lifestyle changes
  • Phase 3 maintaining cardiovascular stability
  • Self directed
  • Build on the accomplishments of the previous

What lifestyle changes can he make?
  • When did the patient change from a stable state
    to an unstable state?

  • How can you imagine he feels going home knowing
    that hes a ticking time bomb?
  • What impact does that have on his family and
    state of mind?