1. Cardiovascular Disorders
Disease Models
Part 2

2. Objectives
See Part 1

3. Angina Pectoris
"Angina" meaning to choke.
• When the demand for myocardial oxygen exceeds the ability
of the coronary arteries to supply the heart, myocardial
ischemia occurs.
o The clinical manifestation of this is: Angina pectoris
o Can be caused by:
 An increase in demand for oxygen
 A decrease in oxygen transport in the blood
o Almost 90% of cases involve some level of
atherosclerosis
o symptoms don't develop until the lumen of the coronary
artery narrows 75%.

4. Why do we care about Angina and
Coronary syndromes?

5. Causes of Angina Pectoris
Lack of Supply to the myocardium:
• Blood flow factors or low blood pressure (hemodynamic
factors).
• Vasospasms
• Cardiac Factors
• Hematologic Factors
o low hgb/hct
Most often (>90%) of cases, lack of blood supply to the
myocardium is caused by atherosclerosis of a main coronary
artery

6. Causes of Angina Pectoris
Myocardium demands an increase in blood supply
(increased need for O2)
• High Systolic BP
• Increased Ventricular Volume
• Increased Heart Rate and Contractility

7. Risk Factors for Angina pectoris

8. Patterns of Angina
1. Stable Angina (Chronic Stable Angina)
2. Variant or Prinzmental's angina
3. Unstable Angina
4. Silent Ischemia

9. Stable Angina
This is caused by a fixed coronary obstruction that causes
intermittent decreases in blood flow and a lack of vessel
flexbility (the vessel can't dilate to allow more blood flow).
• symptomatic chest pain or pressure that is associated with
transient myocardial ischemia
• usually precipitated by some sort of activity or stress that
causes an increased need for oxygen in the myocardium
• usually resolves with rest or by alleviating the stressor, use
of nitrates to increase coronary blood flow also can reduce
the pain
• pain usually resolves within 3-5 minutes.

11. Variant or Prinzmental's Angina
This is an angina pain that occurs mainly at rest, and results
from vasospasm of the coronary arteries (strong contraction of
the smooth muscle in the coronary artery).
• Vasospasm can occur in individual who have no underlying
coronary disease, but can also confound the problem of
CAD in individuals.
• Seen in patients with a history of migraine headaches and
Raynaud's disease.
• Thought to occur due to increased myocardial demand and
increased levels of certain substances.
• Treated with nitrates and primarily calcium channel blockers
• Often see anginal pain and ST segment elevation

12. Unstable Angina
This form of angina, also called crescendo angina, is new onset
angina, angina that occurs at rest (but is not due to
vasospasm), or angina that is worsening in pattern (increased
frequency of events, increased intensity of events).
• s/s include: fatigue, SOB, anxiety, indigestion (and can also
include the chest pressure and pain associated with stable
angina), ST segment depression.
• A result of an unstable plaque (post rupture, where there is
platelet aggregation and thrombus formation).
• This is considered an emergency, and often is seen pre-
myocardial infarction

13. Silent Ischemia
This is ischemia that occurs in the absence of anginal pain.
• Diagnosed often with an EKG showing ischemic changes in
the heart.
• Thought to be the same pathophysiology as stable angina
(r/t atherosclerotic disease).
• Why don't they feel pain (different theories):
o these episodes may be shorter and involve less tissue
o the patient may have a defect in their pain threshold or
pain tolerance
 patients with diabetes mellitus have a higher incidence
of silent ischemia (have some cardiac autonomic nerve
dysfunction)

14. Comparison of the types of angina

16. Clinical manifestations of angina
pectoris
Think about what disease process may be causing these s/s?
• Substernal chest discomfort, described as squeezing,
constricting, or suffocating.
o usually steady, increasing in intensity at the beginning
and the end of the attack
• Can radiate to the left shoulder, jaw, arm, between the
shoulder blades, or other areas of the chest.
• May complain of indigestion or a burning sensation in the
epigastic region
• Can be associated with a feeling of apprehension,
impending doom

19. Potential Medical Complications
1. Myocardial Infarction
2. Arrhythmias
These are both worse case scenarios, as both have a high
mortality rate, especially when left untreated.

20. Myocardial Infarctions
This occurs as a result of sustained ischemia. Heart muscle
can tolerate 20 minutes of sustained hypoxia. Then cellular
death begins to occur. After 4-6 hours, if the ischemia persists,
there entire thickness of the myocardium can become
necrosed.
• This is a worst case scenario

21. Clinical manifestations of an MI
• Pain: Severe, immobilizing chest pain that is not relieved by
rest, position change, or nitrate administration
o commonly in the early morning hours
o pain is from the buildup of toxic metabolites in the heart
cells
• Sympathetic Nervous System activation: epinephrine and
norepinephrine are released in large amounts from the
damaged myocardial cells. Activates the sympathetic
nervous system and causes peripheral vasoconstriction and
diaphoresis. Patient will appear pale and feel cool, and
clammy to the touch.
• Nausea and Vomiting: there is reflex stimulation of the
vomiting center in the medulla by the severe pain

22. Clinical Manifestations of an MI
• Cardiovascular Manifestations: the release of the epi/norepi
can initially increase the BP and HR. but the BP eventually
drops due to decreased cardiac output. May decrease renal
perfusion and ARF and decreased renal output. Left
ventricular dysfunction may cause blood to back up in the
lungs causing crackles.
• Fever: Temperature increase up to a week post MI due to
the systemic manifestation of inflammation from myocardial
cell death.

25. Potential complications of an MI
• Dysrhythmias: Occur in 80% of patients post acute MI. Life
threatening dysrhythmias often occur with anterior wall
infarctions. Ventricular fibrillation is a common cause of
sudden cardiac death and often occurs within 4 hours of an
acute MI
• Heart Failure: the pumping power of the heart is diminished.
• Cardiogenic shock: occurs when the heart is not perfusing
the tissues because of severe Left ventricular failure.
o very emergent if it occurs
• Ventricular Aneurysms: the infarcted myocardial wall thins
and develops an outpouching that doesn't function with
normal contractile properties.

26. http://www.hrt.org/ecghome.html

28. Medical Management of Angina/MI
1. Diagnostics
2. Pharmacologic
3. Surgical
4. Pre-hospital emergency management of suspected MI.

29. Diagnostic Studies
1. EKG/ECG
2. Serum enzyme level test
3. Serum lipid level test
4. Exercise stress test
5. Nuclear imaging
6. Coronary Angiography

30. EKG/ECG
There are classic ECG changes that can occur with Angina and
MI.
• T-wave inversion
• ST-segment elevation
• Development of an abnormal Q-wave
These findings can vary based on the duration of the ischemic
event (acute vs. evolving), extent of ischemia (subendocardial
vs. transmural), and the location.
Findings may "disappear" when the angina isn't occuring, need
to check ECG with the anginal pain.

32. Serum Enzyme Level Tests
The damaged heart muscle will often release proteins into the
bloodstream that are indicative of cardiac damage.
• These levels can be checked with a blood test
• There are varying levels of specificity for cardiac vs. general
muscle damage.
o CK-MB
o Troponin I, Troponin T
o Myoglobin
o Beta type Natiuretic peptide (BNP)
• Albumin Cobalt Binding Test

33. Serum Enzyme Level Tests
CK-MB: Troponin:
• Creatinine Kinase MB is • This protein regulates the
an intracellular enzyme Ca++ mediated Actin-
found in the muscle cells Myosin contractile process
• increases outside the • Troponin I/T begin to rise
normal range within 4-8 within 3 hours after the
hours post myocardial onset of MI and may
injury remain elevated for 3-4
• there are 3 bands of CK days post MI
enzymes • More sensitive then CK-
• CK-MB is very specific MB
for cardiac muscle
damage

34. Serum Enzyme Level Tests
Myoglobin:
• oxygen carrying protein, which is normally present in cardiac
and skeletal muscle.
• It is a small molecule, so it is released into the system
quickly
• Starts rising 1 hour post cardiac damage, peaks 4-8 hours
post MI
• myoglobin is rapidly excreted in the urine, so blood levels
return to normal within 24 hours post MI
• Not Cardiac Specific

36. Serum Enzyme Level Tests
Cobalt Albumin binding Beta-type Natriuretic
test: peptide:
• in an MI, albumin • this is used for diagnosis,
molecules in the blood are assessment of severity
altered, and unable to bind and prognosis of
cobalt properly congestive heart failure.
• Helpful to determine if the • peptide that is produced by
patient didn't have a heart the ventricular myocardium
attack if their ECG and • studies are showing that
troponins are negative. it can predict the risk for
• negative predictive value cardiac death in patients
post MI

37. Serum Lipid Panels
Elevated serum lipids are one of the most firmly established
risk factors for coronary artery disease.
• Trigylcerides
• Total Cholesterol
• Cholesterol Fractionation: This usually includes HDL/LDL
and total cholesterol.
• C-reactive protein- inflammatory marker that is associated
with recurrent cardiovascular events
• N-High Sensitivity C-Reacitve Protein-tested with
Cholesterol to help manage atherosclerosis

38. Exercise Stress Test
• Treadmill exercise testing is an important diagnostic test
done for the patient with chronic stable angina.
• Patient is on a treadmill (or is injected with adenosine if they
can't tolerate exercise) with a ECG/EKG hooked up and a
BP cuff on. The patient then walks for however long they
can tolerate it, and they are to stop and report chest pain or
pressure if it occurs.
• ST segment and T-wave abnormalities are used as an
INDIRECT MEASURE of CORONARY PERFUSION
• Can differentiate anginal chest pain from other chest pain.

39. Nuclear Cardiology Imaging
A small amount of blood is removed and a radionucleotide dye
is mixed and the "tagged" blood is returned to the body. The
radiologic machine can then scan the body and assess:
• Blood flow
• Ventricular structures/Motion of the ventricles
• Areas darkness where infarctions have occured ("cold
spots")
• Perfusion of the myocardium

40. Coronary Calcium Scan
This is a specialized CT scan that is able to assess the amount
of calcium that has built up in the arteries of the heart:
• A score is attached to the amount of calcifications seen
• Can help determine amount of atherosclerosis in the
coronary vessels
• INDIRECT MEASURE OF CORONARY BLOOD FLOW

41. Coronary Angiography
A catheter is inserted into one of the larger arteries of the heart
and is advanced to the coronary arteries, where dye is injected.
• DIRECT EVALUATION OF CORONARY BLOOD FLOW
• helps to evaluate collateral circulation
• can assess the extent of the coronary vascular disease
• only way to evaluate if the angina is variant type or due to
obstruction
• Need to assess platelets, PT, INR, PTT, and kidney function
prior...why?
• Also, can engage in therapeutic management during PCI

43. Pharmacologic Therapy
Acute Attacks:
• Nitroglycerine SL
Chronic Anginal Prophylaxis
• Nitroglycerin ointment
• Transdermal Nitrates
• Long-acting Nitrates
• SL nitroglycerine prior to activity
• Beta-Adrenergic Blockers
• Calcium Channel Blockers
• Antithrombotic Therapy...Aspirin (ASA), Clopidogrel (Plavix)

45. Acute Attacks
Short acting nitrates are the first line therapy for anginal
attacks, the drug works by:
1. dilating peripheral blood vessels (decreases SVR, increased
blood return to the heart)
2. dilating coronary arteries and collateral vessels (increases
coronary artery circulation, increases O2 to the heart)
Sublingual Nitroglycerin:
for an acute attack: give 0.4-0.6mg sublingual x1, may repeat
2 more times every 5 minutes if no pain relief.
o 1 pill sublingual, or 1 metered spray sublingual

46. Chronic Anginal Prophylaxis
Nitroglycerin Ointment:
• Nitropaste is a 2% nitroglycerin topical ointment.
• Dosed by inch
• place on the skin, in an area free of hair and scars.
• lasts 3-6 hours, especially good for nocturnal and unstable
angina
Transdermal Nitrates:
• Small, thin adhesive patch
• Apply to a intact, hairless skin q24hours
• Allows for a steady state of drug

47. Chronic Anginal Prophylaxis
Long-Acting Nitrates: Sublingual Nitroglycerin:
• Extended release • take a pill or a nitrospray
tablets/capsules 5-10 minutes before
• Taken every 8 to 12 hours engaging in a activity that
• work to reduce the could precipitate anginal
incidence of anginal attack
attacks • Better to use before the
• Imdur and Isordil (both pain develops
isosorbide base) • increases exercise
tolerance and stress
tolerance

48. Chronic Anginal Prophylaxis
Beta-Adrenergic Blockers: Calcium Channel Blockers:
• These are the preferred • Drug of choice for
drugs to help manage prinzmental's angina
chronic stable angina • Inhibits the transport of
• decrease myocardial calcium into the
contractility myocardial and smooth
• decrease HR, SVR, and muscle vasculature
BP (dec. renin secretion) inhibiting muscle
• can decrease morbidity contraction
and mortality in patients • cause systemic
who are s/p MI vasodilation, decreased
• Counsel patients not to myocardial contractility,
stop beta-blockers abruptly and coronary vasodilation

49. Chronic Anginal
Prophylaxis/Management
Aspirin (ASA): Clopidogrel (Plavix):
• Inhibits cyclooxygenase, • Inhibits platelet
which decreases the aggregation (ADP Blocker)
productions of • Alternative for patients
thromboxane A2, a potent who can't tolerate ASA
platelet activator • indicated in combination
• 81mg po qd with aspirin in patients
who've had a heart attack
or ACS
• 75mg po qd

50. Fibrinolytic Therapy
This is a rapid and available method to break up a blockage in
a coronary artery.
• Aimed at dissolving the thrombus in the coronary artery and
reperfusing the heart.
• IV infusion of a thrombolytic agent
• Will break down any clot...not just in the heart, need to
watch for bleeding.
• Nursing Management:
o Assess V/S, pulse Ox, ECG
o heart and lung assessments
• Should see an improvement in the ST segment changes
• Watch for reperfusion arrhythmias
• Likely start heparin drip in the immediate post fibrinolytic
period to prevent reocclusion.

52. Invasive and Surgical Treatment
1. Percutaneous Transluminal Coronary Angioplasty (PTCA)
2. Intracoronary Stents
3. Laser Angioplasty
4. Atherectomy
5. Coronary Artery bypass grafting (CABG)

53. Percutaneous Transluminal Coronary
Angioplasty (PTCA)
• Catheter is inserted through a large peripheral vessel and
advanced to the coronary vessels where a dye is injected
(see previous slides)
• Allows for a direct assessment of coronary blood flow
• The atherosclerotic plaques can be shaved off and
circulation to the coronary myocardium improved.
• Need to assess:
o PT/INR, PTT, Platelets, Kidney function
o V/S and continuous monitoring of pulse ox and ECG
before, during and post procedure.

55. Intracoronary Stents
• PTCA with intravascular stent over a balloon
• The catheter that is advanced to the coronary arteries had a
balloon that can push aside the plaque and a stent is placed
holding open the vessel.

57. Invasive Management of Angina/ACS
Laser Angioplasty: Atherectomy:
• A laser tipped angio • Plaque is shaved off using
catheter is introduced via a a rotational blade
large peripheral vessel • removes atheromas
• the laser vaporizes the • Can embolize the
plaque and creates atheroma
channels between the left
ventricle and
microcirculation
• used in patients who are
not a CABG Candidate
and who have failed
maximal medical treatment
for their angina

58. Coronary Artery Bypass Graft
This is the construction of new passages for block around a
blocked coronary vessel
• Traditional CABG involves a stenotomy and the use of
cardiopulmonary bypass
• A vessel is harvested from the saphenous vein area or
internal mammary artery and are grafted from the aorta or
left subclavian to an area beyond the occlusion (bypassing
it)
• Significant morbidity and recovery period (6-8 weeks off
work)
MIDCABG: (minimally invasive) thorascopic approach to the
heart and beta-blockers or adenosine are used to slow the
heart and allow for suturing of the bypass

60. Prehospital Emergency Care of Chest
Pain
For person with Unknown For Person with Known
CHD: CHD:
• Recognize symptoms- • Recognize symptoms-
Chest pain, SOB, nausea, Chest pain, SOB, Nausea,
weakness weakness
• Stop activity and sit or lie • Stop Activity, sit or lie
down down
• If pain persists for 5 • place 1 nitro-tab under
minutes or more, activite your tongue or dispense
the EMS one spray SL, repeat at 5
minute intervals x3 doses
• If symptoms persist,
activate EMS

61. Congestive Heart Failure
Impaired cardiac function rendering
the heart unable to maintain proper
output (PUMP FAILURE)

62. Cardiac Failure:
High Output Failure: (not common) caused by an excessive
need for cardiac output. The function of the heart may be
normal to even excessive, but the body needs are higher.
• severe anemia, thyroxicosis, conditions that cause
arteriovenous shunting, and Paget's disease
• Treatment involves treating the underlying disease
Low Output Failure: (common) caused by failure of the heart
as a pump
• ischemic heart disease, cardiomyopathy, long standing
hypertension
• Treatment is focused on symptom management and slowing
the natural disease state

63. General clinical features of heart failure
The failure of the compensatory mechanisms of the heart
results in heart failure:
• heart rate fails to compensate for inadequate cardiac output
• dilation of the heart fails to compensate for inadequate
cardiac output
• hypertrophy of the heart fails to compensate for inadequate
cardiac output
• kidneys, sensing decreased circulation, increase the
production of renin, causing increased angiotensin
II/increased SVR and Aldosterone/increasing blood volume

64. Systolic Dysfunction
Involves a decrease in cardiac contractility and ejection fraction
• Caused by:
o conditions that impair the contractile performance of the
heart (ischemic heart disease and cardiomyopathy)
o produce a volume overload (valvular insufficiency and
anemia)
o generate a pressure overload (hypertension and valvular
stenosis) on the heart
Symptoms result from reduction in ejection fraction and cardiac
output

65. Diastolic Dysfunction
This accounts for 40% of all cases of CHF
Characterized by:
• smaller ventricular chamber
• ventricular hypertrophy
• poor ventricular compliance (ability to stretch)
• Symptoms:
o because impaired filling, congestive symptoms
predominate
o symptoms increase in situations where the heart rate
increases
CHF is often a combination of systolic and diastolic
dysfunction

66. Compensatory Mechanisms in Heart
Failure
Ventricular Dilation: Ventricular Hypertrophy:
• Chambers stretch and • there is an increase in the
dilate to allow more blood muscle mass and cardiac
in the ventricle wall thickness in response
• The ventricle can dilate to to overwork and strain
the point of overstretching • occurs slowly and over
where the actin and time
myosin fibers are unable to • allows for initial increases
contract properly and allow in CO, but demands more
for a proper ejection of Oxygen, has poor
blood contractility, is poorly
• Frank Starling Law...page vascularized, and is prone
605 Porth to dysrhythmias

67. Compensatory Mechanisms in Heart
Failure
Sympathetic Nervous Neurohormonal Response:
System Activation: • Renin-Angiotensin-
• decreased CO causes a aldosterone mechanism
release of catecholamines with low CO to kidney
(epinephrine and • Low CO to the brain
norepinephine) causes increase ADH
• initially increases HR, secretion, which increases
myocardial contractility, preload
and peripheral • Vascular endothelium
vasoconstriction releases endothelin which
• Overtime, causes an causes vasoconstriction
overload on the failing (inc. SVR)
heart (inc. O2 needs, inc. • Inflammatory cytokines are
preload) released

69. Left Sided Heart Failure
The left side of the heart moves blood from a low pressure
circuit (the lungs) to a high pressure circuit (the peripheral
circulation).
• S/S:
o Decrease in cardiac output
o Increase in Left Atrial and left ventricle end diastolic
pressures
o Congestion in the pulmonary circulation
o Pulmonary edema
• Most common cause is Acute Myocardial Infarction and
Cardiomyopathy

71. Right Sided Heart Failure
This is the failure of the right of side of the heart.
• S/S:
o Jugular Venous Distention
o Hepatomegaly
o Splenomegaly
o Vascular congestion of the GI tract
 get N/V/Reflux/hematemesis
o Peripheral Edema
• Caused by (most commonly) Left sided heart failure, 2nd
primary pulmonary HTN , 3rd Right ventricle AMI
o Lung disease can cause hypertrophy of the right ventricle
called Cor Pulmonale

73. Clinical Manifestations of Heart Failure
1. Fluid Retention and edema
2. Respiratory manifestations
3. Fatigue and limited exercise tolerance
4. Cachexia and malnutrition
5. Cyanosis

74. Clinical Manifestations of Heart Failure:
Fluid Retention and Edema
Edema: Nocturia:
• Common sign and usually • During the day, the
appears in the dependent decreased CO causes
areas decreased urine
o peripheral edema production
o liver • At night, with the patient
o abdominal cavity lying back, the fluid from
o lungs the interstitial space
• Can be pitting (can indent moves back into the
the skin with a finger tip) circulation where the
• Acute development of kidneys are able to
edema or wt. gain of >3lbs process it and make urine
in 2 days is a sign of • Can be 6-7 times per night
decompensation

75. Clinical Manifestations of Heart Failure:
Respiratory Manifestations
Pulmonary Edema: Paroxysmal Nocturnal
• Sign of ADHF, caused by Dyspnea:
increased pulmonary venous • Occurs in the middle of the
pressure caused by the night when the patient is
decreased efficiency of the LV recumbant
• the lungs are less compliant • Fluid from the dependent
and there is increased body areas are reabsorbed
resistence in the small • often wake up in a panic with
airways a feeling of suffocation
• see dyspnea, anxiety, cool, Cough:
pale, diaphoretic skin, cough • often persistent, dry, hacking
with frothy sputum, orthopnea cough
• Hear crackles, wheezes, and • sputum +/-
rhonchi

76. Clinical Manifestations of Heart Failure:
Fatigue and Limited Exercise Tolerance
Fatigue: Anxiety and Restlessness:
• caused by decreased CO • Secondary to poor gas
• fatigue occurs in activities exchange in the lungs and
that were not previously impairment in cerebral
tiring circulation
• Anemia is often associated • Family may report anxiety,
with CHF and compounds restlessness, confusion
the fatigue and decreased attention
Tachycardia: span
• Early clinical sign
• SNS response to
decreased CO
• Beta-blockers can mask
this

77. Clinical Manifestations of Heart Failure:
Weight Loss and Malnutrition
Weight Loss: Malnutrition:
• Cardiac Cachexia is a • closely linked to the
condition hallmarked by cardiac cachexia
tissue wasting
o caused by fatigue and
depression
o also hepatomegaly and
congestion of GI
vasculature contributes
to feeling of fullness
o inflammatory mediators
suppress hunger

78. Clinical Manifestations of Heart Failure:
Cyanosis
This is the bluish discoloration of the skin and mucous
membranes caused by excess desaturated hemoglobin in the
blood. Often a late sign of heart failure.
Central Cyanosis: caused by conditions that impair
oxygenation of the arterial blood like pulmonary edema
• Lips and mucous membranes
Peripheral Cyanosis: caused by conditions that cause low-
output failure that cause delivery of poorly oxygenated blood to
the peripheral tissues.
• finger tips and toes

79. Complications of Heart Failure
1. Pleural Effusion
2. Arrhythmias
3. Left Ventricular Thrombus
4. Hepatomegaly

80. Management of Heart Failure
1. Chest Xray
2. EKG
3. Echocardiogram
4. Radionuclide Angiography
5. Labs

82. Pharmacologic Therapy
ACE Inhibitor: Inotropics:
• Angiotensin Converting • Digitalis Glycosides
Enzyme Inhibitors o good at reducing
• Prevents the conversion of symptoms but doesn't
angiotensin I to improve survival
angiotensin II and also o Increase the force of
inhibits the subsequent cardiac contraction
release of aldosterone while decreasing the
• Decreases both SV and rate of contraction
PVR (preload and • Beta-Adrenergic Agonists
afterload) o Dopamine/dobutamine
• Decreases mortality due to • Calcium Sensitizers: in
heart failure clinical trials here

84. Pharmacologic Therapy
Diuretics: Vasodilators:
• Utilized in CHF to mobilize • Class of drugs clearly
edematous fluid and shown to improve survival
decrease pulmonary in CHF
venous pressure • Work to increase venous
• Reduces vascular capacity, improve EF by
volume/preload improving contractility,
• Different types of diuretic slowing ventricular
available, and they work in dysfunction, decreasing
the different areas of the heart size, and avoiding
kidney the neurohormonal
o Potassium sparing vs. changes of CHF
potassium wasting

85. Beta-Adrenergic Blocking Agents
Marked improvement in patient survival is seen in patients on
beta-blockers
• Specifically Carvedilol (Coreg) and metorprolol (Toprol XL)
• Blocks the negative effects of the SNS on the failing heart
• Use in combination with other drugs and increase the dose
slowly (because there can be a decrease in myocardial
contractility)

86. Supportive Care of Heart Failure
Oxygen: Sodium Restricted Diet:
• 2-6 lpm, increase amount • DASH diet
of available Oxygen to the o <2.4gm sodium a day
heart and the tissues o normal american diet is
7-10gms of sodium/day
Rest:
• decrease cardiac demand Fluid Restrictions:
• In acute cases
Daily Weights: • want to be careful in
• Check for fluid retention emergency situations
• Call provider if there is a
weight gain of >3lbs in 2
days or 3-5lbs gain in 1
week