Cardiac Combined Powerpoint

Disorders of the Cardiovascular System Fall 14
HCA Critical Care College
Assessment
Current or chief complaint

Past medical history
Diagnostic Studies
Vital signs
Cardiovascular inspection/auscultation
Murmurs, Extra heart sounds
Palpation of extremities
Skin turgor, edema, pulses
Chest Pain Assessment
PQRST Pneumonic:
= Precipitators
What were you doing when it started
Does it go anywhere
Q = Quality
What does it feel like?

Rate on scale of 0-10
R = Region/Radiation
Point to where else it hurts?
Chest Pain Assessment
= Signs/Symptoms
Have you had any other signs or symptoms?
= Time/Treatment
When did it start?
Does it come and go?
Is it worse when you take a deep breath?
How long does it last?
What makes it worse or better?
CP Assessment
Chief
complaints
If
patient has prior history of chest

pain or cardiac disease, assume it is
cardiac pain until proven otherwise
Assess for shortness of breath (SOB),
dyspnea on exertion, and dyspnea
when lying or sitting
Assess for history of CHF
Assessment
Syncope
Period
of unconsciousness
Due to decreased perfusion to head
Determine Cardiac vs. Neurologic
Palpitations
Awareness
of fluttering or racing heart

Determine if precipitated by
stress/anxiety
Assessment
Edema
Determine degree and how

long present
Cardiac related ascends from
feet and ankles upward toward
heart
May be dependent edema
seen in sacrum, posterior legs,
abdomen when lying in bed
JVD
Recent weight gain
Assessment
Heart
Sounds
S1-S2
are normal, lub-dub

S3 and S4 not normal
Murmurs
Systolic
or Diastolic
Whooshing sound
Assessment
Cardiac Output
Blood pressure
Peripheral pulse quality
Heart rate
Urine output
Lung Sounds:
Coarse breath sounds
Pulmonary edema
Assessment
General Appearance
Color of skin, lips, nail beds
Mucous membranes
Obvious shortness of breath
Level of consciousness
Peripheral Pulses
Rate, rhythm, strength (1+ to 4+)
Capillary Refill (<3 seconds normal)
Normal Lab Values

Serum
Chemistries:
Sodium
135-145 mEq/l
Potassium 3.5-5.0 mEq/l
Chloride
96-106 mEq/l
Calcium
8.5-10.5 mEq/l
Phosphorus 3.0-4.5 mEg/l
Magnesium 1.5-2.5 mEq/l or 1.8-2.4
mg/dl
Glucose
70-110 mg/dl
BUN
5-20 mg/dl
Creatinine 0.7-1.5 mg/dl
Lab Studies
Enzymes:
Total
CK (Creatine Kinase)
55-170
u/l for males

30-135 u/l for females
CKMB 0% of total
LDH 90-200 IU/L
Muscle
CK
Proteins:
Troponin
I <1.5 ng/ml
Lab Studies
Lipid
Profile:
Cholesterol
150-200 mg/dl
Triglycerides 40-150 mg/dl
Lipoprotein
Cholesterol fractionation
HDL
29-77 mg/
LDL 62-130 mg/dl
Lab Studies
Hematology:
Hematocrit:
Hemoglobin:
WBC:
Sed. Rate:
40%-52% for males

35%-47% for females
13-18 g/dl for males
12-16 g/dl for females
3,500-11,000 mm
<15 mm/hr or males
<20 mm/hr for females
Lab Studies
Clotting Profile:
Prothrombin time (PT/INR) 12-15 sec/<2.0

Therapeutic levels for
A-fib 1.5-2.5
DVT/PE 2.0-3.0
Prosthetic valves 2.5-3.5
Activated Partial Thromboplastin Time (PTT)
25-38 sec.
Therapeutic is 1.5-2.5 times normal
Platelets 150,000-400,000/mm
Cardiac Angiography
PTCA
Percutaneous Transluminal Coronary

Angioplasty (PTCA)
The physician inserts a balloon-tipped

catheter through the femoral artery up to the
heart. Once the balloon-tipped catheter is at
the site of the blockage, the balloon at the tip
of the catheter is inflated, pushing the plaque
in the artery back against the wall of the
artery.
Cardiac Stent
First performed in the mid-1980s and first

approved by the FDA in the mid 1990s
A stent (a small, expandable wire mesh tube) is

inserted into a diseased artery to hold it open
Drug eluding stents are coated with a drug that

dramatically reduces any reblockage of the stent
by inhibiting scar tissue formation within the stent
Currently, stenting is performed most often in

conjunction with other catheter-based procedures,
such as PTCA and atherectomy
Coronary Atherectomy
Atherectomy is performed with a catheter that

has a blade-like device on the end
The coronary atherectomy actually cuts away

or "debulks" some of that plaque
A physician is more likely to choose

atherectomy over angioplasty/stenting when
the plaque is very hard (due to calcification)
or presents other challenges.
Intervention
Coronary Re-Stenosis
To prevent restenosis, one of the following

antiplatelet medications may be administered prior
to or during intervention and continue for up to 12
hours after:
Integrelin
Reopro
Aggrastat
Angiomax
Post-stent or PTCA, patients usually take Plavix

75mg po qd for several months or for life to assist
with antiplatelet activity and decrease risk of restenosis
Post-Intervention Care
ECG: for signs of abrupt re-occlusion

Pedal Pulses
Bleeding at groin site/Hematoma formation
Coronary dissection
Postural or vasovagal syncope (during sheath
removal)
Pseudoaneurysm formation (auscultate site
for a bruit)
Retroperitoneal bleed
Femoral Sheath Removal

Orders for type of removal:
Femostop
Manual
Vascular closure devices (i.e.
Perclose,
Vasoseal, Angioseal, Starclose)
On
hand items to include fluids and

atropine
4-8 hours bedrest post-sheath removal
Pedal pulse checks
Femoral Sheath Removal
Consider pre-med with pain medicine prior to

sheath removal (Morphine systemically or
Lidocaine locally at the site)
PAR:
P = Pressure
A = Application of Pressure
R = Release (slow) of Pressure
Module II: Care of the Post-op

CABG Patient
Care of the Post-op CABG and Valve Replacement
Patient
CABG Care
Concerns in the early postoperative period:

Hemodynamics
Bleeding
Heart rhythm
Urine Output
Labs
Respiratory status
Incisions
CABG Care
Record/Monitor Hourly:
Arterial BP, HR, RR (q 15 min.
till patient is extubated)
PAP, CVP, EDV, REF
CO/CI
SVR
SaO2, SVO2
I/O: Urine, CT, JP
Hemodynamic Monitoring
Report CI <2, SBP <90
Treat BP >150 mmHg
Maintain volume status:
CVP/PCWP ~ 10-12
EDV ~ 160
UO > 30ml/hr
JP/CT <100-200 ml/hr
Hemodynamic Monitoring
Report EKG Changes:
PVCs
PACs
AFib
Bradycardia
Post-op Monitoring
Maintain SaO2 >90-92%
Monitor CO2
Maintain K+ >4.0 and <5.0
Maintain Mag++ >2
Monitor H/H
VIA ABGs
Post-op Monitoring
Monitor incisions:
Radial artery grafts

Sternotomy
Vein grafts
Chest Tubes
Dressing Changes
Pain Control
Post-Op Pulmonary Management
Accurate & frequent physical assessment

Arterial blood gas analysis
Continuous pulse oximetry
Pulmonary care (including suctioning while pt.
is intubated, coughing & incentive spirometry
after extubation)
Early mobilization
Control of pain and shivering
Post-Op Pulmonary Management
Chest X-ray to determine placement of ETT,

thermodilution catheter, and nasogastric tube,
as well as information about the width of the
mediastinum, amount of atelectasis, presence
of hemothorax or pneumothorax, and size of
the heart.
Assess patient for readiness for extubation
Considered if pt. is arousable, able to follow

commands, hemodynamically stable, and
initiating spontaneous ventilations without
excessive respiratory effort
Extubation Weaning Parameters
Post-Op Management of Hemodynamics
Cuff BP is taken to provide correlation of BP

from arterial line
Monitor the interrelationship between:
Heart rhythm and rate

Preload
Afterload
Contractility
Myocardial compliance
Monitor volume within the system: RAP, PAWP

If
BP is too low:
There
is either too little volume

(preload)
OR the SVR is too low (patients blood
vessels are dilated)
Volume is generally replaced with a
colloid such as Albumin or Hetastarch,
unless hematocrit is low, then volume
may be replaced with PRBC
If BP and CO are low, but the PCWP is high:
Patient may be experiencing decreased

contractility and inotropic support may be
instituted with an agent such as Dopamine or
Dobutamine
If the BP is low & the CO is adequate or

elevated:
The SVR may be low & the patient may need a

constrictive agent, such as Phenylephrine
Low BP can also be temporarily increased by

turning off PEEP (to decrease intrathoracic pressure
and augment preload) nad by position changes.
The patient should be put in the supine position
with legs elevated to allow the BP to increase until
the cause of the low BP can be determined and
corrective measures are taken.
Trendelenberg position (not universally utilized) can
also offer symptomatic relief, by shifting volume
from the legs to the chest & increasing preload.
Provide only temporary improvement in clinical picture
If BP becomes too high, esp. in the early post

op period, surgical anastomoses may be
disrupted
Can cause significant intrathoracic bleeding,

hemodynamic instability, poor tisse perfusion, and
necessitate return to the operating room
RN needs to quickly intervene for high BP per
institution protocol or MD orders
Nitroprusside (vasodilator) is often administered to
lower BP to the ordered parameter
Nitroglycerine (a nitrate) is given to cause

vasodilation and lower BP
These medications need to be started slowly, so
patient response can be evaluated.
Patients must be monitored closely as the BP may
drop as the patients body temperature increases.
Rewarm patient
after surgery if
hypothermia persists
Use of warm blankets

Warm, humidified
oxygen
Convective air
mattresses
Other individual
institutional
approaches
Negative effects of
hypothermia:
Depression of the
myocardium
Ventricular
dysrhythmias
Vasoconstriction
Depression of clotting
factors (increasing the
risk of bleeding post
operatively)
Carefully monitor the PAPs & the CO, as well

as BP when interventions are instituted to
assess the effect.
Need to maintain effective CO after CABG to
provide adequate tissue perfusion
Need to regularly perform neurovascular
assessments of the lower extremities to
provide information about the effectiveness of
the CO
Continuously monitor the cardiac rate and

rhythm
Ventricular dysrhythmias are common in the early

post op period and SVT are more likely 24 hours to
5 days post operatively.
Incidence of A Fib is from 10 to 65% depending on
patients history
Factors in post op dysrhythmias:
Hypothermia
Inhaled anesthetics
Electrolyte disturbances (hypo-/hypercalcemia,
hypomagnesemia, hypokalemia)
Metabolic disturbances (Acidosis)
Manual manipulation of the heart
Myocardial ischemia
Increase in catecholamine levels due to pain,
anxiety, inadequate sedation
Management of dysrhythmias:
Treat patient, not the monitor

Consider effectiveness of BP & CO when
evaluating dysrhythmias
Cardiac surgeons place epicardial wires on the
atrium and/or ventricles during surgery
Temporary pacing can be instituted to override
slow, rhythmic rhythm to maintain BP and CI
Atropine may be given to increase the HR in the
absence of epicardial pacing wires
Tachydysrhythmias can be controlled
pharmacologically depending on physicians orders
and hospital protocols
Post-Op Management of Bleeding
Monitor patient for signs of bleeding from the

chest tubes and surgical sites, as well as clinical
signs of hypovolemia related to blood loss
HH should be monitored at regular intervals
during post op period according to hospital
protocol
Nurse must be cognizant of the potential for
cardiac tamponade, blood could accumulate
in the pericardium
Signs: Lack of CT drainage, decreased BP,

narrowed pulse pressure, and muffled heart
sounds
Post-Op Management of Bleeding
If bleeding is an issue:
Protamine sulfate may be given to reverse the

effects of heparin
Or antifibrinolytic agents (DDAVP) may be ordered
Blood products such as FFP and platelets may also
be ordered
Post-Op Neurologic Management
Pupils should be assessed initially
Normal size & reactivity may not return until agents

utilized intraoperatively have been metabolized.
Over the 1st few hours, the results of neuro
assessments should improve gradually
By the time patient is ready for extubation, pt.
should follow commands & have equal movement
and strength of the extremities
Neuro status cannot be completely assessed until
patient is fully awake & extubated
Continue neurologic assessments on a regular

basis
Post-Op Renal Management
Monitor urinary output, at least, hourly

Assess urine for color & characteristics, as
well as amount
Potassium level should be monitored every 46 hours for the 1st 24 hours, potassium is lost
with diuresis
IV potassium replacement should be
administered to keep potassium level within
normal limits
Other lab values should be monitored daily:
BUN and Creatinine
Post-Op GI Management
Monitor the patient for bowel sounds,

abdominal distention, and nausea and
vomiting
Intubated patient will have nasogastric tube to
low intermittent suction
Placement & patency should be assessed, as
well as amout, color, and characteristics of the
drainage.
Antiemetic agents should be administered for
nausea
Post-Op Pain Management
Factors contributing to pain
Median sternotomy incision, leg incisions

Manipulattion of chest cavity
Use of retractors during surgery
Electrocautery
Positioning in the operating room table
Length of time of the surgery
Poorly controlled pain can stimulate the

sympathetic nervous system & lead to CV
consequences
The HR and BP can increase and the blood
vessels can constrict
Causes increase in cardiac workload and

myocardial oxygen demand
Nurses must individualize pain assessment

and control for each patient as responses vary
among individuals
Opioid analgesics, positioning, mobilization,

distraction, and relaxation techniques are
among some methods of pain control.
Ketoralac is an nonsteroidal anti-inflammatory
agent, can be administered IV in the early post
op period
Need to monitor renal status of patients taking

Ketoralac
Discontinued if creatinine level is elevated
Teach client to splint incision when coughing &

moving improves pain control
Treatment Hemodynamic Changes
Beta Blockers
Decreases
myocardial workload
and myocardial oxygen demand
by decreasing HR and contractility
Rhotral, Sectral
Tenormin
Zebeta, Monocor
Brevibloc
Lopressor (also beta-2 at high doses)
Ace Inhibitors
Work by suppressing the renin-angiotensinaldosterone system, which results in fluid loss

and BP
May get CO
When ACE inhibitors are started, it may take
weeks to achieve optimal results
ACE inhibitors work well with diuretics to BP
and may work well for some heart failure
patients
Renin-AngiotensinAldosterone System
So what happens
if you suppress the action
of the angiotensinconverting
enzyme?
You prevent the production

of angiotensin II which then
blocks the production of
Aldosterone and therefore
decreases the preload and
the afterload, important in
patients with CHF.
Ace Inhibitors
Examples:
Lotensin
Capoten
Vasotec
Monopril
Prinivil
Zestril
Accupril
Altace
Calcium Channel Blockers

Calcium
Channel Blockers inhibit the

influx of Ca++ through the cell
membrane resulting in depression of
automaticity and muscle contraction
Indications:
Hypertension
Angina from vasospasm
Dysrhythmias
Calcium Channel Blockers

Examples:
Calan
Procardia
Cardene
Plendil
Cardizem
Norvasc
Angiotensin Receptor Blocker (ARB)

Act
by blocking the angiotensin

receptor, which controls the
physiologic effects of angiotensin on
blood pressure
Indications:
Hypertension
Heart
Failure
So what happens if you

suppress angiotensin II?
Aldosterone production
is reduced and
therefore preload and
afterload are reduced.
ARBs
Examples
of ARBs:
Atacand
Avapro
Benicar
Cozaar
Diovan
Micardis
Teveten
Anticoagulants
Heparin or Low Molecular Weight Heparin

(LMWH)
Coumadin
For patients with high risk for systemic emboli

Large anterior MI
Atrial fibrillation
LV thrombus
Valve replacement
Use with fibrinolytics

PTCA or CABG surgery
Thrombolytics
Indications:
ST segment elevation >1 mm in two related leads

Chest Pain with new onset, LBBB
Clinical suspicion of acute MI even if chest pain is
absent
AMI Core Measures recommends thrombolytics be
given within 30 min of arrival to hospital.
t-PA,
Activase, Retivase
Plasminogen activator causes transient, systemic

fibrinogen depletion
Weight based dosing (see Policy and standing
orders)- administered in the ER
Contraindications for Thrombolytics
Hemorrhagic stroke
Intracranial neoplasm
Active internal bleeding
Pregnancy
Suspected aortic dissection
Complications from Thrombolytics

Bleeding:
Cerebral
hemorrhage
GI bleed
Epitaxis
Hematuria
Puncture sites
Dysrhythmias
Hypotension
Other Interventions
Electrophysiology
Study):
Studies (EP
A procedure in which a thin tube catheter

is inserted into a vein or artery (e.g., in the
groin) and guided to the heart, where it
can perform specific, essential
measurements of the hearts electrical
activity and pathways
These measurements are particularly
helpful in the diagnosis of the origin of
tachycardias, or bradycardias
Other Interventions
Ablation
is a procedure in which a physician

destroys very small, carefully selected parts of
the heart that are causing tachycardia
Allows
the heart to beat more slowly and

normally
Usually
used for A-Fib, A-flutter, WPW, AT, SVT,

junctional tachycardia, and ventricular
tachycardia
Cardiovascular System: Mitral Valve Stenosis
The mitral valve is located between the left

atrium and left ventricle and is also referred to
as the atrioventricular valve
Mitral valve stenosis is the obstruction of blood
flow from the left atrium into the left ventricle
most often caused by Rheumatic Endocarditis
Pathophysiology:
Since the left atrium has difficulty moving blood into the
left ventricle, the blood backs up into the pulmonary veins,
overloading the pulmonary circulation.
The right ventricle must contract against a very high

pulmonary arterial pressure causing strain and eventual
failure of the right ventricle.
Clinical
manifestations
Diagnostics
dyspnea
fatigue
hemoptysis
cough
repeated respiratory
infections
weak, often irregular

pulse
diastolic murmur
EKG
cardiac catheterization
Medical Management
antibiotic prophylaxis
treat Congestive Heart Failure
anticoagulants
treat anemia
surgical intervention
valvuloplasty
mitral valve replacement
Nursing Care
same as post-op needs as other patients experiencing

cardiac surgery
Cardiovascular System: Mitral Valve Prolapse
Definition
mitral valve prolapse is deformity that usually has no signs

and symptoms
although rare, it can progress and lead to sudden death
occurs more frequently in women
Pathophysiology:
a portion of the mitral valve leaflet balloons back into

the atrium during systole
occasionally the valve does not stay closed during

systole, blood then backs into the left atrium from the
left ventricle
Clinical
Manifestations
Diagnostics
many are asymptomatic

others will have:
dyspnea, fatigue, lightheadedness,
palpitations, dizziness,
syncope, chest pain and
anxiety
Mitral click
murmur of mitral valve
regurgitation
Rarely patient will have
signs and symptoms of
heart failure
Medical Management
eliminate caffeine, avoid alcohol, smoking, oxygen,

antiarrhythmic medications, diuretics, AngiotensinConverting Enzyme Inhibitors, Angiotensin II Receptor
Blockers, Hydralazine and Isosorbide Dinitrate, Beta
Blockers and Calcium Channel Blockers
Surgical intervention: mitral valve repair or

replacement
Nursing Management
Education
diagnosis, hereditary condition

prophylactic antibiotics
dietary and lifestyle changes
Cardiovascular System: Rheumatic Endocarditis
Rheumatic Endocarditis is a potential sequel

seen in patients who have had Rheumatic Fever.
Rheumatic Fever occurs most often in children
who have had a case of group A beta hemolytic
streptococcal pharyngitis (strep throat). With
prompt treatment with antibiotics the numbers
of people afflicted with Rheumatic Fever has
declined in the United States.
Pathophysiology
The damage to the heart is not directly related to the

streptococci but to the leukocytes that accumulate in
the tissue which leads to the formation of scar tissue.
Initially tiny translucent growths are seen on the valve
flaps. Over time the valve leaflets thicken, preventing
them from closing completely
Pathophysiology cont.
The myocardium can compensate for quite a while, but

eventually the condition will lead to heart failure
It is the mitral valve that is most often affected
The severity of symptoms is directly related to the location

and size of the lesion
Assessment
murmur, shortness of breath, crackles and wheezes to lung

fields
there may also be emboli phenomena to the lung, kidney,

heart, spleen or brain
* the key is prevention
Medical Management
eradicate the cause

antibiotic therapy
risk for embolitic event
Nursing Management
teaching: medications,
symptom monitoring &
management
lifestyle changes:
diet
activity
CPR
birth control (female)
Cardiovascular System: Infective Endocarditis
Definition
Infection of the valves and endothelial surface of the

heart, especially seen in people with valve disorders
more common in the elderly

high incidence among IV drug users
others at risk
invasive procedures can cause a bacteremia which leads to
Infective Endocarditis
Pathophysiology
caused by direct invasion of the endocardium by a

microbe, fungi or rickettsiae
leads to deformity of the valve leaflets, can also affect

other structures, such as: chordae tendineae
Assessment
malaise
anorexia
weight loss
cough
fever
joint pain
Oslers nodes
Roths spots
petechiae
murmurs
emboli
Diagnostics
microorganism is
identified in 2 separate
blood cultures
echocardiogram reveals
a moving mass on the
heart valves or
supporting structures
Medical Management
prevention
complications
antibiotic therapy
heart failure, cerebral vascular, other organ complications
related to septic or non septic emboli
treatment
Long-term antibiotics
surgical management: to replace severely damaged valves
Nursing Management
monitor the patients temperature

assess for new murmurs
assess for signs and symptoms of organ damage
education:
antibiotics for treatment & prophylactic

emotional
post-op care if indicated
Myocarditis
Etiology:
Inflammation of myocardium
as a response to invading organisms,
chemicals or drugs
Causes:
Viral, bacterial, fungal,

protozoal, autoimmune, toxins
Effects:
Decreased contractility,
decreased cardiac output, and
decreased LV function leading to failure
Cardiovascular System: Pericarditis
Definition:
an inflammation of the pericardium, the membranous

sac enveloping the heart
may be a primary illness, or develop during the course
of another medical or surgical disorder
it may be classified by what accumulates in the sac:
blood, purulent drainage, clotting proteins
Pericarditis
Inflammation
of the pericardium
Chronic vs. Acute

Pericardial Effusion
Cardiac Tamponade
Constrictive
Chronic scarring
Stiff pericardium
Pathophysiology
there are many underlying causes associated with

pericarditis
leads to a buildup of fluid in the pericardium which can
cause cardiac tamponade
can lead to thickening & decreased elasticity preventing
the heart to fill properly
can become calcified further restricting ventricular
expansion during diastole
leads to decreased cardiac output, heart failure and
hepatic failure
Cardiovascular System:
Pericarditis
Pericarditis
Patient presents with chest pressure and
shortness of breath that is worse when lying
down
Symptoms are somewhat relieved when
sitting upright and forward
Usually follows a bacterial or viral infection or
acute MI ~ 2 weeks later
12 Lead EKG follows no consistent ischemia
pattern
Commonly have ST elevation in multiple leads
Assessment
pericardial rub
chest pain
fever
Diagnostics
echocardiogram
CXR
12 lead ECG: ST
changes
WBC
ESR
Medical Management
determine cause
administer therapy:
NSAIDs, corticosteroids, Colchicine
Pericardiocentesis
Pericardectomy
Pericarditis
Treatment:
NSAIDs
Steroids
Pericardial Drain
Potential Complications
Development of pericardial effusion
Hemodynamic instability
Nursing Management
monitor for cardiac tamponade

pain management
activity restriction
emotional support
monitor for heart failure
Endocarditis
Acute or chronic infection of the

endocardium, including valves, chordae
tendinae, and septum.
Usually bacterial
Forms vegetations that destroy valve tissue,

mainly tricuspid and pulmonic
Organisms lead to bacteremia/sepsis
Can lead to cardiac failure

Endocarditis
Treatment:
Generally
long term IV antibiotics

Possible need to remove infected
valve and replace with new valve
after infection under control
Potential
complications:
Migration
of vegetation to brain or
other parts of body
Overwhelming sepsis
Cardiomyopathy
Chronic or subacute disorder of

the heart muscle
Dilated
Hypertrophic
Restrictive
Dilated
Restrictive
Hypertrophic
Dilated Cardiomyopathy
Dilated Ventricle without Hypertrophy
Etiology: viral, idiopathic, alcoholism
Clinical Findings:
Right and left heart failure

Ventricular arrhythmias
Murmur
End-stage dilated Cardiomyopathy is the #1

indication for heart transplant.
Chamber Enlargement
Impaired Systolic and
Diastolic Dysfunction
Heart Failure
Refractory to
Treatment
Death
Treatment:
Fluid
Restriction
ACE Inhibitors
Beta-blockers
Diuretics
Antidysrhythmic
s
ICD
Hypertropic Cardiomyopathy
Significant increase in myocardial
mass with decreased chamber size
Diastolic dysfunction results
May be related to genetics
Clinical findings:
Malignant ventricular dysrhythmias

Systemic embolization and stroke
Restrictive Cardiomyopathy
Least common form
Decreased chamber size, rigid
ventricle, and right and left side
failure, decreased cardiac output
Etiology:
Radiation
Sarcoidosis
Idiopathic
Cardiomyopathy
Shock
An
acute, widespread process of

impaired tissue perfusion resulting in
cellular, metabolic and hemodynamic
derangements
Hypovolemic: Occurs from inadequate fluid

volume in intravascular space
Cardiogenic: Result of failure of heart to pump
blood forward effectively
Septic: Overwhelming infection of usually
bacterial origin
Cardiovascular System: Cardiogenic Shock
Definition:
Occurs when the heart cant pump enough blood to

supply the amount of oxygen needed by the tissues
Occurs when: >40% of the myocardium is necrotic, due

to a ruptured ventricle, valve dysfunction, trauma to
the myocardium, end stage of heart failure, pulmonary
emboli, cardiac tamponade, cardiomyopathy and
dysrhythmias
Pathophysiology
cardiogenic shock is circular in nature. The degree of

shock is related to the amount of left ventricular
dysfunction
damage to the myocardium results in a decreased CO2

which reduces arterial B/P and tissue perfusion to vital
organs
Pathophysiology cont..
As the flow to the coronary arteries is decreased, there

is less O2 to the myocardium increasing ischemia and
reducing the hearts ability to pump
inadequate emptying of ventricles causes pulmonary

edema, making the hypoxia and tissue perfusion even
worse
Assessment:
tissue hypo-perfusion
low B/P
rapid, weak pulse
cold, clammy skin
respiratory crackles
decreased urinary
output
hypoactive bowel
sounds
respiratory alkalosis
Diagnostics
pulmonary artery
catheter to measure left
ventricular pressure
and cardiac output
continued central
venous oximetry
blood lactic acid levels
Medical Management
correct underlying problem

restore tissue perfusion
prevent further damage
pharmacologic therapy: vasopressors, diuretics,
vasodilators, positive inotropic medications

other treatments: intra aortic balloon pump {IABP}decreases the workload of the heart by inflating during
diastole and deflating just before systole
Nursing Management
Assessment
cardiac rhythm
hemodynamic parameters: tissue perfusion
intake & output
reduce anxiety of patient & family
safety due to confusion, anxiety
Cardiovascular: Cardiac Tamponade
Definition
An increase in the intra-pericardial pressure due to:
fluid accumulation in the pericardial sac

direct or metastatic tumor invasion in the pericardial sac, or
fibrosis of the sac due to radiation therapy
Pericardial Tamponade
Risk Factors:
Primary tumors of the heart

Metastatic tumors to the pericardium:
Lung
Breast
Gastro-intestinal
Leukemia
Hodgkins & Non-Hodgkins Lymphomas
Sarcoma
Melanoma
other
Risk Factors cont
Patients who have received > 4000 cGy to a field which

includes the heart
Patients with Acquired Immunodeficiency Syndrome

(AIDS) related Karposis Sarcoma
Drug related
Pathophysiology
As the intra-pericardial pressure increases:
left ventricular filling decreases

the ability of the heart to pump decreases
cardiac output decreases
impaired systemic perfusion occurs
Clinical Manifestations:
Small effusions do not usually cause any symptoms

Large effusions especially with rapid accumulation of
fluid causes: epigastric or retro-sternal chest pain which is
often relieved when sitting or leaning forward
dysphagia, cough, dyspnea, hoarseness, increased JVD,
muffled heart sounds, pericardial friction rub, tachycardia,
and pulsus paradoxus
complications
Pericardial Tamponade
Cardiac tamponade usually occurs within the

first 12 hours post-op but may occur up to 3
weeks post-op
Signs/Symptoms:
Fever
Pericardial friction rub
Lethargy
Oliguria
Epigastric or sternal pain
Pulsus Paradoxus
Decreased chest tube output
Chest pain
Cardiac Tamponade
Hemodynamic Implications:
Early: Normal CO, HR, normal to low BP
Middle to Late:
CO, BP, JVD, HR, CVP/PCWP, UO
Diastolic pressure, Narrowed pulse pressure, pulsus
paradoxus, widened mediastinum
Late: Shock, PEA, death
Cardiac Tamponade
Diagnostic Findings
CXR: Widened mediastinum
Pulsus Paradoxus
Flattening of arterial waveform by
>10mmHg pressure on expiration
Pericardial Friction Rub
Widened Mediastinum
Medical Management:
Diagnostics:
CXR, EKG, Echocardiogram, CT, MRI
Treatment:
Symptom management
pericardiocentesis
sclerosing
radiation Therapy
chemotherapy
corticosteroids
Cardiac Tamponade
Treatment
Fluid Challenge for low BP or low
CO
Inotropic medications
Re-exploration of mediastinum
Nursing Management
Supportive Strategies:
emotional support
O2
repositioning to promote circulation
assist with activities
administer medications as prescribed
Cardiovascular: Potassium 3.5-5.5 mEq/L
The major intracellular electrolyte
important for neuromuscular, skeletal and cardiac muscle

functioning
98% in cells; 2 % in extracellular fluid
potassium is regulated by the sodium potassium pump
Requires intact renal system
80% of K+ excreted daily
aldosterone also increases excretion of K+ by the kidneys
Cardiovascular: Hypokalemia
Potassium below 3.5 mEq/L

common electrolyte imbalance
Related to:
deficit in potassium stores

metabolic alkalosis
loss of intestinal contents
prolonged intestinal suctioning
recent illeostomy
villous adenoma
Causes of Hypokalemia cont
Hyperaldosteronism
potassium wasting diuretics
medications: corticosteriods
PCN, Carbenicillin, Amphotericin B
patients with long term insulin
secretion
magnesium depletion
Clinical
Manifestations
Diagnostics
fatigue, muscle
weakness, leg cramps,
constipation, anorexia,
nausea, vomiting,
numbness, tingling,
dysrhythmias
EKG changes
flat T waves, inverted T

waves, depressed ST
segment, elevated U
wave
24 hour urine
potassium excretion
Medical Management
Oral / IV potassium
replacement
Monitor EKG
Nursing Management
monitor for s/s in

patients at risk
administer medications
as directed
diet
Cardiovascular: Hyperkalemia
Potassium level over 5.5 mEq/L
seen in patients with poor renal function

Leukocytosis
Thrombocytosis
False Hyperkalemia
Medications: Potassium, Heparin, Ace inhibitors,
Captopril, NSAIDS, potassium sparing diuretics
Acidosis: K+ move out of cells into ECF:
tumor lysis syndrome

extensive injury or burns
Clinical
Manifestations
Diagnostics
peaked, narrow T waves,

ST segment depression,
shortened QT interval,
disappearance of P waves
cardiac arrest
muscle weakness,
paralysis, GI disturbances
EKG changes
Arterial blood gases
potassium levels
Medical
Management
restrict dietary
potassium
kayexelate
calcium gluconate
Insulin
Beta 2 Antagonists
Dialysis
D/C potassium
sparing diuretics
Nursing
Management
observe for muscle

weakness and
dysrhythmias
accurate blood
sample
teach about
foods/salts with
potassium
Cardiovascular: Calcium 8.5-10.5 mg/dL
99% in the skeletal system; 1% in blood stream

Level is controlled mainly by the parathyroid hormone
which releases calcium from bone
Regulates:
muscle contractions
transmitting of nerve impulses
blood coagulation
absorbed from the GI tract in the presence of gastric acid

and Vitamin D
excreted mainly in feces; some in urine
Cardiovascular: Hypocalcemia
Calcium level below 8.5 mg/dL
Causes:
Osteoporosis
immobility
Hypoparathyroidism
Pancreatitis
Renal failure
Hyperphosphatemia
Inadequate Vit. D absorption
Magnesium deficiency
Low serum albumin
Causes cont
alkalosis
alcohol abuse
Medications: aluminum containing antacids,
caffeine, Aminoglycosides, Cisplatin, Corticosteroids,
Mithramycin, loop diuretics, Phosphates and
Isoniazid
Clinical
Manifestations
Diagnostics
tetany
pain due to spasms
Trosseaus sign
Chvosteks sign
Seizures
EKG changes
low albumin
(corrected serum
calcium)
other lab values:
magnesium,
phosphorous, PTH
Medical Management
IV or p.o. calcium
Vit. D
dietary supplements
Nursing Management
safety precautions:
seizures, airway,
confusion
Teaching
risk for falls
dietary intake of
calcium
medications:
Fosamax, Evista,
Calcitonin
Cardiovascular: Hypercalcemia
Calcium level greater than 10.5 mg/dL
mortality 50 % if not treated

Malignancies
Hyperparathyroidism
Immobility
Thiazide diuretics
Vit. A or D intoxication
Lithium
Alkaline antacids
Excessive milk intake
Clinical
Manifestations
muscle weakness
incoordination
anorexia
constipation
paralytic ileus
confusion
cardiac standstill
Diagnostics
calcium level
albumin
EKG
PTH Levels
xrays
Sulkowitch urine test:
measures amount of
calcium in urine
Medical Management
decrease calcium:
Chemotherapy
partial parathyroidectomy
dialysis
medications:
Lasix, IV fluids: NS, IV phosphate, Calcitonin, Aredia,

Didronel, Mithramycin, Neutra-phos
Nursing Management
monitor for s/s of Hypercalcemia

push oral fluids with sodium
safety
teaching
Cardiovascular: Sodium 135-145 mEq/L
Mostly located in the extracellular fluid

controls water distribution throughout the body
functions
muscle contraction
transmission of nerve
impulses
Cardiovascular: Hyponatremia
Sodium less than 135 mEq/L
ratio of body sodium to body water

can be related to fluid volume excess or deficit
sodium can be loss via:
vomiting, diarrhea, fistulas, sweating
diuretics
deficiency of aldosterone
types of Hyponatremia
SIADH:
Dilutional Hyponatremia
Clinical Manifestations
depends on cause/rate of occurrence
dry mucosa
decreased saliva
poor skin turgor
low B/P
nausea
abdominal cramping
confusion
muscle twitching to seizures
hemiparesis
papilledema
Diagnostics
sodium levels
urine sodium
urine specific gravity
Medical Management
careful administration
of sodium( no > 12
mEq/L every 24 hours
SIADH- Lasix is added
restrict fluid
Nursing Management
monitor patients at risk

monitor for s/s of
hyponatremia
teach:
dietary restrictions
medications
safety
Cardiovascular: Hypernatremia
Sodium level greater than 145 mEq/L
gain of sodium in excess of water

or loss of water in excess of sodium
fluid deprivation
hypertonic enteral feedings
Diabetes Insipidus
heat stroke
excess of sodium bicarbonate or a hypertonic saline
near drowning in sea water
malfunction of hemodialysis or peritoneal dialysis
Clinical
Manifestations
neurologic
Diagnostics
delusions,
disorientation
flushed skin
dry, swollen tongue
increased muscle tone
pulmonary edema
postural hypotension
sodium level > 145

osmolarity level urine
osmolarity
urine specific gravity
Medical Management
gradually administer a
hypotonic or isotonic
nonsaline solution to
avoid cerebral edema
Diuretics
Desmopressin Acetate
(DDAVP): treat: Diabetes
Insipidus
Nursing Management
strict I&O
teach
diet
medications
monitor for s/s of

Hypernatremia

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Disorders of the Cardiovascular System Fall 14

HCA Critical Care College

Current or chief complaint

Murmurs, Extra heart sounds

Skin turgor, edema, pulses

HCA Critical Care College

HCA Critical Care College

Chest Pain Assessment

What does it feel like?

Point to where else it hurts?

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Chest Pain Assessment

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patient has prior history of chest

of fluttering or racing heart

Determine degree and how

are normal, lub-dub

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Normal Lab Values

Creatinine 0.7-1.5 mg/dl

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u/l for males

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40%-52% for males

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Prothrombin time (PT/INR) 12-15 sec/<2.0

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Percutaneous Transluminal Coronary

The physician inserts a balloon-tipped

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First performed in the mid-1980s and first

A stent (a small, expandable wire mesh tube) is

Drug eluding stents are coated with a drug that

Currently, stenting is performed most often in

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Atherectomy is performed with a catheter that

The coronary atherectomy actually cuts away

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To prevent restenosis, one of the following

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ECG: for signs of abrupt re-occlusion

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Femoral Sheath Removal

hand items to include fluids and

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Femoral Sheath Removal

Consider pre-med with pain medicine prior to

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Module II: Care of the Post-op

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Concerns in the early postoperative period:

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Report EKG Changes:

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