Cardiac Notes
Cardiac Notes
Cardiac Notes
Four chambers
Heart valves
o Atrioventricular (A-V) valves (S1/SYSTOLE)
o Semilunar valves (S2/DIASTOLE)
Coronary arteries (Feed the heart)
Cardiac conduction system
Cardiac hemodynamics (pressure of blood/ fluid volume status)
Overview of Anatomy and Physiology – Heart
• Cardiac Cycle
• Systole (contraction)
• Diastole (relaxation)
• Cardiac Output= HR X SV
Anything that decreases cardiac output causes: dizziness, fatigue, LOC changes, and
shortness of breath
• HR
• SV
• Preload (diastole, relaxation, if there is a lot of fluid the preload will be increased and vice)
• Afterload (systole, contraction)
• Contractility
• Autonomic Nervous System (ANS)
• SNS (increase)
• PSNS (decrease)
Terms - Cardiac Output
• Stroke volume: amount of blood ejected with each heartbeat
• Cardiac output: amount of blood pumped by ventricle in liters per minute
• Preload: degree of stretch of cardiac muscle fibers at end of diastole
• Contractility: ability of cardiac muscle to shorten in response to electrical impulse
• After load: resistance to ejection of blood from ventricle
• Ejection fraction: percent of end diastolic volume ejected with each heart beat
CO = SV x HR
Control of heart rate
Autonomic nervous system, baroreceptors (located in aortic arch, right carotid, the
monitor pressure throughout the body, when the pressure is low, they send a
signal to speed the HR)
Control of stroke volume
Preload: Frank-Starling Law (AMOUNT THE HEART CAN STRETCH WHEN FILLING
UP)
After load: affected by systemic vascular resistance, pulmonary vascular resistance
Contractility increased by catecholamines, SNS, some medications (Epinephrine,
dopamine)
Decreased by hypoxemia, acidosis, some medications
Risk factors
Modifiable (diet, weight, drugs, smoking, exercises, stress management)
Nonmodifiable (age, gender, race, genetics)
Most Common Clinical Manifestations (MI, ANGINA, HF)
• Chest pain (due to lack of O2, hypovolemia or low BP, can also cause chest pain)
• Dyspnea (difficulty breathing)
• Peripheral edema, weight gain (retention of H2O.)
• Fatigue (not enough O2, pt gets tired)
• Dizziness, syncope, changes in level of consciousness
• Acute Coronary Syndrome (is prodromal(before) like S/S that there is a cardiac
problem.
-Shortness of breath
-Swell feet
- Tired
• Experience prodromal symptoms for a month to more prior to acute event
Assessment
Medications
Nutrition (Low Na, low cholesterol)
Elimination (avoid straining, to avoid increase pressure)
Activity, exercise
Sleep, rest
Self-perception, self-concept
Roles, relationships
Sexuality, reproduction
Coping, stress tolerance
Prevention strategies
Laboratory Tests
• Cardiac biomarkers
• Serum Enzymes:
- Creatinine Kinase (CK), CK-MB
Whenever there is injury to the heart muscle
• CK formerly known as (CPK)- elevation indicates muscle injury
• CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18 hours post
injury and returns to normal within 2-3 days.
• Useful in DX of MI
- Lactic dehydrogenase (LDH)
After an MI, LDH is always elevated. THIS TEST IS DONE AFTER TROPONIN I, AND CK-MB
• Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
• Useful for delayed DX of MI
- Troponin T and I (First to be drawn, bc is more specific)
Is released when there is damaged to cardiac muscle (is the most important to detect Heart attack,
mainly Troponin I which is specific for heart muscle, troponin T is heart muscle and skeletal muscle)
• Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks; provides
early sensitivity
• More specific to cardiac injury for DX of MI
Laboratory Tests
Lipid profile: to determine risk factors of developing atherosclerosis (to determine what
build up of plaque)
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL
Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL
Laboratory Tests
Brain (B-type) natriuretic peptide (BNP)
BNP, is secreted from the ventricules, it indicates, INCREASED PRELOAD, TOO
MUCH FLUID. IS TO RULE OUT CHF. If BNP is elevated then I need to look further
for CHF.
A neurohormone that helps regulate BP and fluid volume.
Secreted from the ventricles in response to increased preload with elevated ventricular
pressure
Useful in the diagnosis of HF
Greater than 100 pg/mL
C-reactive protein (CRP)
A protein produced by the liver in response to inflammation. It is not specific for heart.
Anywhere where there is infection or injury to the body (Heart attack, plaque to heart, cut
in the toe anything that causes damage in the body elevates this protein)
Laboratory Tests
Homocysteine (not specific for heart attack)
An amino acid linked to the development of atherosclerosis (deposit of plaque in
arteries) because it can damage the endothelial lining of the arteries and cause thrombus
formation
A 12 hour fast is necessary before drawing a blood sample for an accurate serum
measurement
Optimal: less than 12 mol/L
Borderline: 12-15 mol/L
High risk: above 15 mol/L
Magnesium (Mg):
High Mg=Bradycardia
Low Mg= Tachycardia
Hypo: ventricular tachycardia and fibrillation
Hyper: bradycardia, hypotension, prolonged PR and QRS intervals
Electrocardiography
12 lead ECG
Continuous monitoring: hardwire, telemetry
Signal-averaged electrocardiogram
Continuous ambulatory monitoring (HOLTER)
Transtelephonic monitoring
Wireless mobile monitoring
Cardiac stress testing
Exercise stress testing (how heart work in stress, exercises)
Pharmacologic stress testing (how pt response under certain meds)
Diagnostic Tests
Radionuclide imaging
Myocardial perfusion imaging (if heart is perfussing well)
Test of ventricular function, wall motion
Computed tomography CT (Looking at structures)
Positron emission tomography
Magnetic resonance angiography
Diagnostic Tests
Echocardiography (ultrasound of the heart)
US of heart to evaluate the structure and function of chambers and valves
Phonocardiography (recording w/ a simutaneos ECG)
Graphic recording of heart sounds with simultaneous ECG
Coronary Angiography/Arteriography
Invasive procedure where cardiologist injects dye into coronary arteries and
immediately takes a series of x-ray films to assess structure of arteries
Cardiac Catherization
Invasive procedure study used to measure cardiac chamber pressures, assess patency of
coronary arteries
Requires ECG, hemodynamic monitoring; emergency equipment must be available
Assessment prior to test; allergies, blood work (PT, PTT)
Assessment of patient post-procedure; circulation, potential for bleeding, potential for
dysrhythmias
Activity restrictions
Patient education pre-, post-procedure
Hemodynamic Monitoring
• Central Venous Pressure (CVP) (volume status)
High fluid or hypervolemia= Increased CVP and vice
CVP is looking at the right side of the heart
• Appropriate for clients who require accurate monitoring of fluid volume status but
are not candidates for the more invasive pulmonary artery pressure monitoring
• Done by a central catheter with the tip in the SVC to measure the R heart filling pressure
• Provides data about right ventricular preload. Not for left heart pressures
• Normal CVP 2-8 cm H2O or 2-6 mm Hg
• Decreased CVP= decreased circulating volume
• Increased CVP= increased blood volume or right heart failure
Diagnostic Tests
• Pulmonary artery pressure (PAP)
PAP = left side of heart
High PAP = TOO MUCH FLUID and vice
• Appropriate for critically ill clients requiring more accurate assessments of left heart
pressures
• Pulmonary artery catheter (Swan-Ganz) has the tip in the pulmonary artery
• Pressure is obtained after the tip is wedged into a pulmonary capillary and is called
PCWP
• Good indicator of left ventricular preload also called left ventricular end diastolic pressure
(LVEDP)
Cardiovascular Conditions:
1.Coronary Atherosclerosis
Homocysteine is a test specific for atheroesclerosis
Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within
arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary vessels
reduce blood flow to the myocardium.
Cardiovascular disease is the leading cause of death in the United States for men and
women of all racial and ethnic groups.
CAD, coronary artery disease, is the most prevalent cardiovascular disease in
adults.
Pathophysiology of Atherosclerosis
Inflammation (red and swollen area)
Coagulation (stop bleeding)
Bradikinin, which causes the pain
Non-Modifiable
Family Hx of CAD
Older than 45 years old
Gender (men earlier than women)
Race
Modifiable
Hyperlipidemia
Smoking
HTN
DM
Obesity
Physical inactivity
Laboratory Tests
Lipid profile: to determine risk of developing atheroclerosis
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL
Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL
Medications
HMG-COA Reductase Inhibitors
“Statins”- Atorvastatin ( Lipitor)
Nicotinic Acids
“Niacins” (flushing, like a tomato)
Fibric Acids
Gemfibrozil ( Lopid)
Bile Acid Sequestrants
Cholestyramine ( Questran)
Cholesterol Absorption Inhibitors
Ezetimibe (Zetia)
Omega-3-acid
Fish oils
The main goal of all this categories is to lower cholesterol
The main side effect of this meds is
- Myalgia (muscle pain)
- GI – bloating, constipation, dispepcia (GERD)
- Myositis (inflammation of muscle)
Clinical Manifestations
Symptoms are due to myocardial ischemia
Symptoms and complications are related to the location and degree of vessel obstruction
-Angina pectoris (Ischemia)
-Myocardial infarction (if the ischemia wasn’t corrected then MI happens)
-Heart failure
-Sudden cardiac death (heart suddenly stops beating)
Clinical Manifestations
The most common symptom of myocardial ischemia is chest pain; however, some
individuals may be asymptomatic or have atypical symptoms such as weakness, dyspnea,
and nausea.
Atypical symptoms are more common in women and in persons who are older,
or who have a history of heart failure or diabetes. (nausea, weight gain)
2. Angina Pectoris
CAD (the buildup of plaque in the arteries lead to angina pectoris)
• A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior
chest caused by insufficient coronary blood flow.
• Physical exertion or emotional stress increases myocardial oxygen demand and the coronary
vessels are unable to supply sufficient blood flow to meet the oxygen demand.
- 3 types of Angina
a) Stable angina: exertional (predictable response to increased activity)
With stable angina, the pt take the nitro, and pain goes away.
With angina the main med is nytroglicerin (1 SL) and if after 5 min if still hurts, go to ER
COSTOCHONDRIATIS (MUSCLE PAIN) is often confused with chest pain
(GERD, PNEUMONIA, PANIC ATTACKS) can be confused with heart attack
For Angina the main thing is re-perfuse !!!
Treatment
Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply
Medications
-Beta-blockers & Ca Channel blocker (for long term/chronic angina) these 2 meds are also
used for HTN and Dysrhythmias.
- Nitrates (nitroglycerin) for acute/immediate angina
Oxygen
Reduce and control risk factors
Reperfusion therapy may also be done
Medications
Nitroglycerin
Beta-adrenergic blocking agents (to decrease the heart and the demand of O2)
Calcium channel blocking agents (to decrease the heart and the demand of O2)
Antiplatelet and anticoagulant medications
Aspirin
Clopidogrel and ticlopidine (Plavix)
Heparin
Glycoprotein IIB/IIIa agents
Patient Teaching
Lifestyle changes and reduction of risk factors
Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of
ischemia
Teaching regarding disease process
Medications
Stress reduction (bc stress increase
SNS)
When to seek emergency care
Angina Pectoris Review
Warning sign of impending MI
Women and older adults present atypically
3 types
Stable angina: exertional
Unstable angina:( preinfarction) exertional- with exercise or stress
Variant angina: (prinzmetals) spasms of coronary artery
Pain unrelieved by rest or nitro and lasting more than 15 min differentiate
angina from MI
Precipitated by exertion or stress
Relieved by rest or nitro
Symptoms last < 15 min
Angina Review
Client education:
Stop activity and rest
Place nitro under tongue
Should be a bite to the med
3 in 15 minutes if not go to ER
HEADACHE is most common s/e of nitro
Encourage patient to sit and lie down slowly
Encourage smoking cessation
Diet and lifestyle modification
Get cholesterol and B/P checked regularly
Remain physically active
Myocardial Infarction
An area of the myocardium is permanently destroyed. Usually caused by reduced blood
flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent
occlusion of the artery by a thrombus.
In unstable angina, the plaque ruptures but the artery is not completely occluded.
Unstable angina and acute myocardial infarction are considered the same process but at
different point on the continuum.
The term acute coronary syndrome includes unstable angina and myocardial infarction.
Blockage of one or more of the coronary arteries
Causes:
Arteriosclerosis, emboli, thrombus, shock, hemorrhage, hypoxia leading to necrosis
Classic sign: substernal pain or feeling of heaviness on chest
Patients may report:
Substernal pain or pain over pericardium ↑ 15 min
Pain that is heavy and radiating down left arm
Spontaneous pain not relived by nitro or rest
Pain that radiates to jaw
Pain accompanied by SOB, pallor, diaphoresis, N/V
↑HR, ↓ B/P, ↑ temp, ↑ RR
When the pain is not relieved by nitro, most probably is not an angina anymore
but an MI. This is when MONA comes into play
Aspirin prophylactic: 81 mg
Aspirin Acute MI: 325-650 mg
Diagnosis
EKG
Angina= ST depression and/or T wave inversion (ischemia)
MI= T wave inversion (ischemia), ST elevation (injury), and abnormal Q wave
(necrosis)
When cardiac muscle suffers ischemic injury, cardiac enzymes are released into the blood
stream providing specific markers
Myoglobin
CK-MB
Troponin I
Troponin T
Thallium scans: (Look at the coronary arteries)
Cardiac Cath: evaluates blockage
Laboratory Tests
• Cardiac biomarkers
• Serum Enzymes:
• Creatinine Kinase (CK), CK-MB
• CK formerly known as (CPK)- elevation indicates muscle injury
• CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18
hours post injury and returns to normal within 2-3 days.
• Useful in DX of MI
• Lactic dehydrogenase (LDH)
• Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
• Useful for delayed DX of MI
• Troponin T and I
• Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks;
provides early sensitivity
• More specific to cardiac injury for DX of MI
Management
Monitoring
V/S q15 until stable (q 5min when the pt first come in)
EKG continuous monitoring (within 10 min in ER)
Location, severity, quality of pain
Hourly output (kidneys need O2 and fluid etc, if pt have decreased cardiac output, there is decreased
perfusion to kidneys and they don’t work, therefore there will be minimal output)
Labs
MONA
When B/P falls rapidly= dopamine
Thrombolytics= streptokinase, retavase
Promote energy conservation
Medications
Vasodilators (nitro, hydrolazine)
Nitroglycerin
Analgesics
Morphine
Beta-blockers/ Calcium Channel Blockers (to slow HR, decrease O2 demand)
Lopressor (Metoprolol), Norvasc (Amlodipine) Cardizem (Diltiazem)
Thrombolytic agents
-Streptokinase
Antiplatelet
-Aspirin, Clopidogrel
Anticoagulants
-Heparin, Lovenox
Glycoprotein inhibitors
Integrillin (blocks binding of fibrinogen=blocked platelet aggregation)
Complications
Heart failure and cardiogenic shock
Ischemic mitral regurgitation
Ventricular aneurysm/rupture
Dysrhythmias
Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock (main problem is decreased BP, bc shock means low)
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade (right side failure)
Postoperative
Assessing the patient
Monitoring for complications
Restoring cardiac output (BP, HR, I/O, Shortness of breath, increased energy. This shows pt
perfussess well)
Promoting adequate gas exchange
Maintaining fluid and electrolyte balance (Na, K, Mg, Ca)
Relieving pain (watch for respiration !!)
Maintaining adequate tissue perfusion
Maintaining normal body temperature
Heart Failure
• The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen
and nutrients.
- (MI, HTN, Cardiac tamponade can lead to HF)
• A syndrome characterized by fluid overload or inadequate tissue perfusion.
• The term heart failure indicates myocardial disease, in which there is a problem with the
contraction of the heart (systolic failure) or filling of the heart (diastolic failure).
• Some cases are reversible.
• Most heart failure is a progressive, lifelong disorder managed with lifestyle changes and
medications.
Clinical Manifestations
• Right-sided failure
• RV cannot eject sufficient amounts of blood and blood backs up in the venous system.
This results in peripheral edema, hepatomegaly, ascites, anorexia, nausea,
weakness, and weight gain.
• Left-sided failure
• LV cannot pump blood effectively to the systemic circulation. Pulmonary venous pressures
increase and result in pulmonary congestion with dyspnea, cough, crackles, and
impaired oxygen exchange.
• Chronic heart failure is frequently biventricular. (Congestive HF)
Classification of Heart Failure (Once the heart is damage is difficult to go back)
• NYHA classification of heart failure
• Classification I: no symptoms w/activity
• Classification II: symptoms w/ordinary exertion
• Classification III: displays symptoms with minimal exertion
• Classification IV: symptoms at rest (means cardiac arrest is coming)
• Treatment guidelines are in place for each stage
Stages of Heart Failure
• ACC/AHA classification of heart failure
• Stage A: high risk but no structural disease or S/S
• Stage B: LV dysfunction or heart disease no S/S
• Stage C: LVD or structural disease- prior S/S
Stage D: End stage HF requiring interventions (pt is waiting for transplant)
- In this stage pt is given Milrinone & Inamrinone (only used short term for end stage HF, have
the same function as Digoxin)
Common Medications
• Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors)
• Angiotensin II Receptor Blockers (ARBS)
• Beta-blockers (decrease the HR, RELAX SMOOTH MUSCLE AROUND THE VEINS)
• Diuretics
• Digitalis (Digoxin, decrease HR, Increase contractility, slow conduction to AV)
• Hydralazine (vasodilator)
• Isosorbide Dinitrate (nitrate)
BNP (indicator of HF, send message that there is too much fluid)
– ↓100= no heart failure
– b/t 100-300= heart failure present
– ↑300= mild heart failure
– ↑600= moderate heart failure
– ↑900= severe heart failure
• CO (Cardiac Output)
– Decreased
Assessment
• Health history
• Sleep and activity (Paroxismal Nocturnal Dyspnea)
Waking up at night and can’t breath
• Knowledge and coping
• Physical exam
– Mental status
– Lung sounds: crackles and wheezes (Dyspnea, Orthopnea)
– Heart sounds: S3
– Fluid status/signs of fluid overload
• Daily weight (gain) and I&O (weight a pt at the same time, same scale, same
cloth, if gain 5 lb in 1 week is fluid retention)
• Assess responses to medications
• Lab test:
– Human B-type natriuretic peptides (hBNP): elevated in heart failure
– Used to differentiate dyspnea r/t heart failure versus respiratory problems
Collaborative Problems/Potential Complications
• Cardiogenic shock (heart not working, not perfusing, BP is on the floor)
• Dysrhythmias
• Thromboembolism (if the heart is not pumping well there is stasis of blood, and clot
forms)
• Pericardial effusion and cardiac tamponade (too much fluid in heart, accumulation, not
working)
Planning
• Goals may include
• Promoting activity and reducing fatigue.
• Relieving fluid overload symptoms.
• Decreasing anxiety or increasing the patient’s ability to manage anxiety.
• Encouraging the patient to make decisions and influence outcomes.
• Teaching the patient about the self-care program.
Activity Intolerance
• Bed rest for acute exacerbations
• Encourage regular physical activity; 30–45 minutes daily
• Exercise training
• Pacing of activities
• Wait 2 hours after eating for physical activity
• Avoid activities in extreme hot, cold, or humid weather
• Modify activities to conserve energy
• Positioning; elevation of the HOB to facilitate breathing and rest, support of arms
Hypertension
• High blood pressure
• Defined by the Seventh Report of the Joint National Commission on the Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) as a systolic pressure
greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg. based on
the average of two or more accurate blood pressure measurements taken during two or more
contacts with a health care provider
Patient Assessment
• History and Physical
• Laboratory tests
• Urinalysis
- Protein
- Specific gravity if is high the urine will look concentrated and vice)
• Blood chemistry
• Cholesterol levels (the cholesterol accumulates in the lumen of the arteries
makes them narrow, increasing risk for HTN)
• Elevated BUN, Creatinine
- To determine kidney function, mainly Creatinine, bc BUN can change due to
dehydration or if the person workout for hours.
• Elevated glucose
• ECG: shows left ventricular hypertrophy (left ventricle working hard)
CXR: cardiomegaly (enlarged heart)
Lifestyle Modifications
• Weight loss
• Reduced alcohol intake
• Reduced sodium intake
• Regular physical activity
• Diet: high in fruits, vegetables, and low-fat dairy
• DASH diet (dietary approaches to stop hypertension) No Na, fat, low cholesterol.
Medication Treatment
• Usually initial medication treatment is a thiazide diuretic.
• Low doses are initiated and the medication dosage is increased gradually if blood pressure
does not reach target goal.
• Additional medications are added if needed.
• Multiple medications may be needed to control blood pressure.
Lifestyle changes initiated to control BP must be maintained
Medication Therapy for Hypertension
• Diuretic and related drugs
• Thiazide diuretics
• Loop diuretics {Furosemide, bumex (is more potent than furosemide)}
• Potassium sparing diuretics (spironolactone, triamterene, amiloride, epleronone)
• Aldosterone receptors blockers
• Central alpha2-agonists and other centrally acting drugs (clonidine)
• Beta-blockers (HTN, ANGINA, DYSRHYTHMIAS)
• Beta-blockers with intrinsic sympathomimetic activity
• Alpha and beta blockers (ZOSIN)
• Vasodilators (HYDRALAZINE, NITROPRAZIDE)
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotenisin II antagonists (ARBS)
• Calcium channel blockers (HTN, ANGINA, DYSTHRYTHMIAS)
DON’T GIVE SPIRONOLACTONE WITH ACE INHIBITORS
CAN GIVE A SPARING AND A LOOP DIURETIC
Hypertensive Urgency
• Patient requires close monitoring of blood pressure and cardiovascular status.
• Assess for potential evidence of target organ damage.
• Medications
• Fast-acting oral agents: beta adrenergic blocker— labetalol; angiotensin-
converting enzyme inhibitor— captopril; or alpha2-agonist—clonidine (SL is very
fast)
Peripheral Disorders
Nonmodifiable
• Age
• Gender
• Familial predisposition/genetics
Modifiable
• Nicotine
• Diet
• Hypertension
• Diabetes
• Obesity
• Stress
• Sedentary lifestyle
• C-reactive protein (for inflammation or any injury can cause elevation of the
CRP)
• Hyperhomcysteinemia
Peripheral Arterial Insufficiency—Assessment
Health history
Medications
Risk factors
Signs and symptoms of arterial insufficiency
Extremities are cool and pale with cyanotic color on elevation
Nails thick and opaque
Bruits may be auscultated
Claudication and rest pain
Color changes (SHINY SKIN NOT ENOUGH OF HAIR)
Weak or absent pulses
Skin changes ( shiny with sparse hair) and skin breakdown (Ulcers)
Arterial Embolism
• Usually arise from thrombi that developed in the heart as a result of AFIB, MI,
prosthetic valves or CHF
• Assessment: 5 P’s
• Pain
• Pallor
• Pulselessness (↓ or absent)
• Parasthesias (altered local sensations)
• Paralysis (weakness or inability to move extremity)
• Poikilothermia ( body temp that varies with environment)
Arterial Embolism
• Medication therapy
• Thrombolytic therapy with streptokinase
• T-Pa
• Heparin
• Warfarin at home
Arterial ulcer are usually dry and necrotic and in the upper part, the venous ulcers
are moist and in the lower part in the malleolar.
Venous Insufficiency
• Inadequate venous return over a long period of time that causes pathologic changes as
a result of ischemia in the vasculature, skin and supporting tissues
• Venous insufficiency occurs:
• After prolonged venous HTN-stretches the veins and damages the valves
preventing blood return
• After thrombus formation or when valves are not functioning correctly
• In time stasis results in edema of the lower limbs, discoloration to the skin of the legs and
feet and venous stasis ulcer
Venous Insufficiency-Assessment
• Past HX of thrombophlebitis, HTN, variscosities
• Past HX of long periods of sitting or standing
• Edema to lower legs, may extend to the knee
• Thick coarse, brownish skin around ankles and feet
• Stasis ulcers, usually in the malleolar area (ruddy base, uneven edges)
Venous Insufficiency
Increase blood return, decrease venous pressure
Bedrest
Keep legs elevated above heart
Avoid long periods of standing
Wear elastic support or compression stockings
Treat venous stasis ulcer(s)
Open lesions are treated with hydrocolloid dressings and compression wraps
May apply low-dose hydrocortisone, zinc or antifungal to area
Ulcers may be treated with an UNNA boot or other compression wrap that is changed
every 1-2 weeks and is usually applied over a base dressing
May need surgical debridement