Upload
twiggypiggy
View
500
Download
2
Embed Size (px)
Citation preview
Cardiovascular DisordersDisease Models
Part 2
Objectives
See Part 1
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 pectoriso 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%.
Why do we care about Angina and Coronary syndromes?
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
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
Risk Factors for Angina pectoris
Patterns of Angina
1. Stable Angina (Chronic Stable Angina)
2. Variant or Prinzmental's angina
3. Unstable Angina
4. Silent Ischemia
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.
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
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
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 tissueo 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)
Comparison of the types of angina
Clinical manifestations of angina pectorisThink 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
Potential Medical Complications
1. Myocardial Infarction2. Arrhythmias
These are both worse case scenarios, as both have a high mortality rate, especially when left untreated.
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
Clinical manifestations of an MI
• Pain: Severe, immobilizing chest pain that is not relieved by rest, position change, or nitrate administrationo commonly in the early morning hourso 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
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.
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.
http://www.hrt.org/ecghome.html
Medical Management of Angina/MI
1. Diagnostics
2. Pharmacologic
3. Surgical
4. Pre-hospital emergency management of suspected MI.
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
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.
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-MBo Troponin I, Troponin To Myoglobino Beta type Natiuretic peptide (BNP)
• Albumin Cobalt Binding Test
Serum Enzyme Level Tests
CK-MB:• Creatinine Kinase MB is
an intracellular enzyme found in the muscle cells
• increases outside the normal range within 4-8 hours post myocardial injury
• there are 3 bands of CK enzymes
• CK-MB is very specific for cardiac muscle damage
Troponin:• This protein regulates the
Ca++ mediated Actin-Myosin contractile process
• Troponin I/T begin to rise within 3 hours after the onset of MI and may remain elevated for 3-4 days post MI
• More sensitive then CK-MB
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
Serum Enzyme Level Tests
Cobalt Albumin binding test:• in an MI, albumin
molecules in the blood are altered, and unable to bind cobalt properly
• Helpful to determine if the patient didn't have a heart attack if their ECG and troponins are negative.
• negative predictive value
Beta-type Natriuretic peptide:• this is used for diagnosis,
assessment of severity and prognosis of congestive heart failure.
• peptide that is produced by the ventricular myocardium
• studies are showing that it can predict the risk for cardiac death in patients post MI
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
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.
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
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
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
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)
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
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
Chronic Anginal Prophylaxis
Long-Acting Nitrates:• Extended release
tablets/capsules• Taken every 8 to 12 hours• work to reduce the
incidence of anginal attacks
• Imdur and Isordil (both isosorbide base)
Sublingual Nitroglycerin:• take a pill or a nitrospray
5-10 minutes before engaging in a activity that could precipitate anginal attack
• Better to use before the pain develops
• increases exercise tolerance and stress tolerance
Chronic Anginal Prophylaxis
Beta-Adrenergic Blockers:• These are the preferred
drugs to help manage chronic stable angina
• decrease myocardial contractility
• decrease HR, SVR, and BP (dec. renin secretion)
• can decrease morbidity and mortality in patients who are s/p MI
• Counsel patients not to stop beta-blockers abruptly
Calcium Channel Blockers:• Drug of choice for
prinzmental's angina• Inhibits the transport of
calcium into the myocardial and smooth muscle vasculature inhibiting muscle contraction
• cause systemic vasodilation, decreased myocardial contractility, and coronary vasodilation
Chronic Anginal Prophylaxis/ManagementAspirin (ASA):• Inhibits cyclooxygenase,
which decreases the productions of thromboxane A2, a potent platelet activator
• 81mg po qd
Clopidogrel (Plavix):• Inhibits platelet
aggregation (ADP Blocker)• Alternative for patients
who can't tolerate ASA• indicated in combination
with aspirin in patients who've had a heart attack or ACS
• 75mg po qd
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, ECGo 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.
Invasive and Surgical Treatment
1. Percutaneous Transluminal Coronary Angioplasty (PTCA)
2. Intracoronary Stents
3. Laser Angioplasty
4. Atherectomy
5. Coronary Artery bypass grafting (CABG)
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 functiono V/S and continuous monitoring of pulse ox and ECG
before, during and post procedure.
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.
Invasive Management of Angina/ACS
Laser Angioplasty:• A laser tipped angio
catheter is introduced via a large peripheral vessel
• the laser vaporizes the plaque and creates 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
Atherectomy:• Plaque is shaved off using
a rotational blade• removes atheromas• Can embolize the
atheroma
Coronary Artery Bypass GraftThis 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
Prehospital Emergency Care of Chest PainFor person with Unknown CHD:• Recognize symptoms-
Chest pain, SOB, nausea, weakness
• Stop activity and sit or lie down
• If pain persists for 5 minutes or more, activite the EMS
For Person with Known CHD:• Recognize symptoms-
Chest pain, SOB, Nausea, weakness
• Stop Activity, sit or lie down
• place 1 nitro-tab under your tongue or dispense one spray SL, repeat at 5 minute intervals x3 doses
• If symptoms persist, activate EMS
Congestive Heart Failure
Impaired cardiac function rendering the heart unable to maintain proper
output (PUMP FAILURE)
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
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
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
Diastolic Dysfunction
This accounts for 40% of all cases of CHFCharacterized 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
Compensatory Mechanisms in Heart FailureVentricular Dilation:• Chambers stretch and
dilate to allow more blood in the ventricle
• The ventricle can dilate to the point of overstretching where the actin and myosin fibers are unable to contract properly and allow for a proper ejection of blood
• Frank Starling Law...page 605 Porth
Ventricular Hypertrophy:• there is an increase in the
muscle mass and cardiac wall thickness in response to overwork and strain
• occurs slowly and over time
• allows for initial increases in CO, but demands more Oxygen, has poor contractility, is poorly vascularized, and is prone to dysrhythmias
Compensatory Mechanisms in Heart FailureSympathetic Nervous System Activation:• decreased CO causes a
release of catecholamines (epinephrine and norepinephine)
• initially increases HR, myocardial contractility, and peripheral vasoconstriction
• Overtime, causes an overload on the failing heart (inc. O2 needs, inc. preload)
Neurohormonal Response:• Renin-Angiotensin-
aldosterone mechanism with low CO to kidney
• Low CO to the brain causes increase ADH secretion, which increases preload
• Vascular endothelium releases endothelin which causes vasoconstriction (inc. SVR)
• Inflammatory cytokines are released
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 outputo Increase in Left Atrial and left ventricle end diastolic
pressureso Congestion in the pulmonary circulationo Pulmonary edema
• Most common cause is Acute Myocardial Infarction and Cardiomyopathy
Right Sided Heart Failure
This is the failure of the right of side of the heart.• S/S:
o Jugular Venous Distentiono Hepatomegalyo Splenomegalyo Vascular congestion of the GI tract
get N/V/Reflux/hematemesiso Peripheral Edema
• Caused by (most commonly) Left sided heart failure, 2nd primary pulmonary HTN , 3rd Right ventricle AMIo Lung disease can cause hypertrophy of the right ventricle
called Cor Pulmonale
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
Clinical Manifestations of Heart Failure:Fluid Retention and EdemaEdema: • Common sign and usually
appears in the dependent areaso peripheral edemao livero abdominal cavityo lungs
• Can be pitting (can indent the skin with a finger tip)
• Acute development of edema or wt. gain of >3lbs in 2 days is a sign of decompensation
Nocturia:• During the day, the
decreased CO causes decreased urine production
• At night, with the patient lying back, the fluid from the interstitial space moves back into the circulation where the kidneys are able to process it and make urine
• Can be 6-7 times per night
Clinical Manifestations of Heart Failure:Respiratory Manifestations Pulmonary Edema:• Sign of ADHF, caused by
increased pulmonary venous pressure caused by the decreased efficiency of the LV
• the lungs are less compliant and there is increased resistence in the small airways
• see dyspnea, anxiety, cool, pale, diaphoretic skin, cough with frothy sputum, orthopnea
• Hear crackles, wheezes, and rhonchi
Paroxysmal Nocturnal Dyspnea:• Occurs in the middle of the
night when the patient is recumbant
• Fluid from the dependent body areas are reabsorbed
• often wake up in a panic with a feeling of suffocation
Cough:• often persistent, dry, hacking
cough• sputum +/-
Clinical Manifestations of Heart Failure:Fatigue and Limited Exercise ToleranceFatigue:• caused by decreased CO• fatigue occurs in activities
that were not previously tiring
• Anemia is often associated with CHF and compounds the fatigue
Tachycardia:• Early clinical sign• SNS response to
decreased CO• Beta-blockers can mask
this
Anxiety and Restlessness:• Secondary to poor gas
exchange in the lungs and impairment in cerebral circulation
• Family may report anxiety, restlessness, confusion and decreased attention span
Clinical Manifestations of Heart Failure:Weight Loss and MalnutritionWeight Loss:• Cardiac Cachexia is a
condition hallmarked by tissue wastingo caused by fatigue and
depressiono also hepatomegaly and
congestion of GI vasculature contributes to feeling of fullness
o inflammatory mediators suppress hunger
Malnutrition:• closely linked to the
cardiac cachexia
Clinical Manifestations of Heart Failure:CyanosisThis 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
Complications of Heart Failure
1. Pleural Effusion
2. Arrhythmias
3. Left Ventricular Thrombus
4. Hepatomegaly
Management of Heart Failure
1. Chest Xray
2. EKG
3. Echocardiogram
4. Radionuclide Angiography
5. Labs
Pharmacologic Therapy
ACE Inhibitor:• Angiotensin Converting
Enzyme Inhibitors• Prevents the conversion of
angiotensin I to angiotensin II and also inhibits the subsequent release of aldosterone
• Decreases both SV and PVR (preload and afterload)
• Decreases mortality due to heart failure
Inotropics:• Digitalis Glycosides
o good at reducing symptoms but doesn't improve survival
o Increase the force of cardiac contraction while decreasing the rate of contraction
• Beta-Adrenergic Agonistso Dopamine/dobutamine
• Calcium Sensitizers: in clinical trials here
Pharmacologic Therapy
Diuretics:• Utilized in CHF to mobilize
edematous fluid and decrease pulmonary venous pressure
• Reduces vascular volume/preload
• Different types of diuretic available, and they work in the different areas of the kidneyo Potassium sparing vs.
potassium wasting
Vasodilators:• Class of drugs clearly
shown to improve survival in CHF
• Work to increase venous capacity, improve EF by improving contractility, slowing ventricular dysfunction, decreasing heart size, and avoiding the neurohormonal changes of CHF
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)
Supportive Care of Heart Failure
Oxygen:• 2-6 lpm, increase amount
of available Oxygen to the heart and the tissues
Rest: • decrease cardiac demand
Daily Weights:• Check for fluid retention• Call provider if there is a
weight gain of >3lbs in 2 days or 3-5lbs gain in 1 week
Sodium Restricted Diet:• DASH diet
o <2.4gm sodium a dayo normal american diet is
7-10gms of sodium/day Fluid Restrictions:• In acute cases• want to be careful in
emergency situations