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. Borg’s
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 rest.
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 patient’s 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.
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.
Borg’s 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. 5’9”
– He has Type II Diabetes Mellitus
Doctors Orders Upon Admission
• Vitals q4h
• Keep SpO2 >92%
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
Diagnosis?
Coronary Artery
Disease with Anginal
Episode
What are coronary arteries?
Coronary Arteries Cont’
Cholesterol
• 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
Diabetes
• 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 vasoconstriction.
Hypertension
• 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.
Smoking
• 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.
Obesity
• 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.
Alcohol
• 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
Angina
• 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
minutes.
• 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
Telemetry
• The process of continuous
electrocardiographic
monitoring by the transmission
of radiowaves from a batteryoperated transmitter worn by
the patient.
• Anagram:
– L: Smoke (black) over fire
(red)
– M: White on the right
– R: Bear (Brown, on bottom) in
the bush (green, on top)
Nitrates - Nitrospray
• 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
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.
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 demand.
• 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 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.
• 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
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.
Borg’s wife approaches the nursing station
in a frantic state.
• She states “My husband doesn’t 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.
Vitals
• 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
Medications
• Nitrospray spray sl q5min x3
• After nitrospray has been administered,
Mr. Borg’s chest pain is not relieved
• His ECG shows the following:
ECG
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 invert.
Diagnosis?
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
disease.
– 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.
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 acidosis.
• After 8 – 10 seconds of decreased blood flow the
affected myocardium becomes cyanotic and cooler.
• After 30 – 60 seconds of hypoxia, ECG changes are
visible.
• 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
– <100 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 postdamage.
• Normal Values
– <0.1 ng/mL
• Patient Values
– 0.15 ng/mL
Laboratory Findings
Serum Glucose
Electrolytes
• 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.
• Oxygen deprivation is
accompanied by electrolyte
disturbances
• Normal values
• Normal Values
– 3.9 – 6.1
• Patient Values
– 7.8
–
–
–
–
Loss of K
Loss of Ca
Loss of Mg
These electrolytes are
released into the blood stream
and are evident on lab results.
– Na: 125 - 145
– K: 3.5 – 5.0
– Mg: 0.74 – 1.23
• Patient Values
– Na: 152
– K: 5.3
– Mg: 1.36
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
Interventions
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.
rPA
• 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.
rPA
• 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 can’t get
thrombolytic therapy?
– Active internal bleeding
– Recent CVA
– Uncontrolled hypertension
• Adverse reaction
–
–
–
–
Bleeding
Arrhythmias
Hypotension
Cholesterol embolism
rPA
• What are the
contraindications?
– Recent major surgery
– Recent gastrointestinal
bleeding
– Recent trauma needing
CPR
– Hypertension
>180/>110mmHg
– Age >75
– Pregnancy
– Bleeding conditions
Streptokinase
Route
Dosage
Intravenous infusion
1, 500, 000 IU within 60
minutes
Nursing Interventions
• Ineffective cardiopulmonary
tissue perfusion related to
reduced coronary blood flow
– The patient’s 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 environment
• 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 perscription
• 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.
ICU
• Mr. Borg is transferred to ICU following his
MI and is placed under close monitoring
• His condition deteriorates…
Mr. Borg’s 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. Borg’s 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 well.
SVT
• 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.
Drugs
• 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 work
In ICU, Mr. Borg’s 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 What’s 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 What’s 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
artery
• Pericardial tamonade:
– accumulation of blood in the pericardial space
compresses the myocardium and interferes with
the myocardium’s 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
client’s 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
Assess
Chest pain:
Location
Duration
Quality
Intensity
Presence
Radiation
Precipitation
Alleviation
Scale 1-10
Diagnosis Plan/Goal Intervene
Altered pain
level related to
discomfort due
to myocardial
infarction as
evidenced by
patient
describing pain
3-10 and
holding chest
Evaluate
Patient will be Administration
Patient
free of chest
of
verbalized that
pain within 15 nitroglycerine,
pain had
to 20 minutes
lasix,
subsided from
after
adenosine
a 8/10 to a
administration
3/10 within 15
of drug therapy
minutes of
medication
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 Ringer’s 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. Borg’s 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 13:00 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. Borg’s
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.
Dopamine
• To raise blood pressure by increasing
peripheral resistance
• Acts on norepinephrine and dilates
vessels in kidneys to maintain perfusion
(can be detrimental to the kidneys if used
for long periods of time).
Digoxin
• 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?
Lasix
• 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 heart
• May promote the loss of K+
Benazepril
(Ace inhibitors = pril, Beta blockers = lol)
• Blocks angiotensin I to angiotensin II
which vasoconstricts leading to decreased
BP
Misc.
• 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 build-up
– 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 phases
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 he’s a ticking time bomb?
• What impact does that have on his family
and state of mind?