Cardiac DiseasesCardiac Diseases

Prepared byPrepared by

Abed ShagoraAbed Shagora

In-service EducationIn-service Education

EGHEGH

Stroke VolumeStroke Volume

The amount of blood ejected by the The amount of blood ejected by the left ventricle each beat. left ventricle each beat.

PreloadPreload• The amount of stretch placed on the cardiac The amount of stretch placed on the cardiac

muscle just prior to systolemuscle just prior to systole• StarlingStarling’’s Laws Law

AfterloadAfterload• The force or pressure at which the blood is The force or pressure at which the blood is

ejected from the ventricleejected from the ventricle• Equated with systemic vascular resistance (SVR)Equated with systemic vascular resistance (SVR)

ContractilityContractility

Cardiac Output/IndexCardiac Output/Index

Cardiac outputCardiac output • CO = HR (beats/minute) X SV (liters/beat)CO = HR (beats/minute) X SV (liters/beat)• Normal adult: 4-8 liters/minute Normal adult: 4-8 liters/minute

Cardiac indexCardiac index• CI = CO(liter/minute)/Body surface area CI = CO(liter/minute)/Body surface area

(m(m22))• Normal adult: 2.8-4.2 liter/minute/mNormal adult: 2.8-4.2 liter/minute/m22

• Normalizes liter flow to body sizeNormalizes liter flow to body size

Myocardial InfarctionMyocardial Infarction

Myocardial infarction (MI) refers to a dynamic Myocardial infarction (MI) refers to a dynamic process which one or more regions of the heart process which one or more regions of the heart muscle experience a severe and prolonged decrease muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary in oxygen supply because of insufficient coronary blood flow; subsequently, necrosis or "death" to the blood flow; subsequently, necrosis or "death" to the myocardial tissue occurs. myocardial tissue occurs.

The onset of the myocardial infarction process may The onset of the myocardial infarction process may be sudden gradual, and the progression of the event be sudden gradual, and the progression of the event to completion takes approximately 3 to 6 hours. to completion takes approximately 3 to 6 hours.

Pathophysiology and EtiologyPathophysiology and Etiology

1. Acute coronary thrombosis (partial or total) -1. Acute coronary thrombosis (partial or total) -associate with 90% of MIs. associate with 90% of MIs.

a. Severe coronary artery disease (greater than 70% a. Severe coronary artery disease (greater than 70% narowing of the artery) precipitates thrombus narowing of the artery) precipitates thrombus formationformation

b. Intramural hemorrhage into atheromatous plaque b. Intramural hemorrhage into atheromatous plaque causes the lesion to enlarge and occlude the vessles causes the lesion to enlarge and occlude the vessles

c. The plaque ruptures into the vessel lumen, and a c. The plaque ruptures into the vessel lumen, and a thrombus forms on top of the ulcerated lesion, with thrombus forms on top of the ulcerated lesion, with resultant vessel occlusion.resultant vessel occlusion.

2. Other etiologic factors include coronary artery 2. Other etiologic factors include coronary artery spasm, coronary artery embolism, infectious spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart anemia, and severe exertion or stress on the heart in the presence of significant coronary artery in the presence of significant coronary artery disease (ie, surgical procedures). disease (ie, surgical procedures).

3. Different degrees of damage occur to the heart 3. Different degrees of damage occur to the heart musclemuscle

a. Zone of necrosis-death to the heart muscle a. Zone of necrosis-death to the heart muscle caused by extensive and complete oxygen caused by extensive and complete oxygen deprivation; _irreversible damage deprivation; _irreversible damage

b. Zone of injury-region of the heart muscle b. Zone of injury-region of the heart muscle surrounding the area of necrosis; inflamed and surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygenation injured, but still viable if adequate oxygenation can be restored' can be restored'

c. Zone of ischemia-region of the heart muscle c. Zone of ischemia-region of the heart muscle surrounding the area of injury, which is ischemic surrounding the area of injury, which is ischemic and viable; not endangered unless extension of and viable; not endangered unless extension of the infarction occurs the infarction occurs

4. According to the layers of the heart muscle involved, 4. According to the layers of the heart muscle involved, MIs can be classified as:MIs can be classified as:

A.A. Transmural (Q wave) infarction-area of necrosis Transmural (Q wave) infarction-area of necrosis occurs throughout the entire thickness of the heart occurs throughout the entire thickness of the heart muscle. muscle.

B. Subendocardial (nontransmural/non-Q) infarction- area B. Subendocardial (nontransmural/non-Q) infarction- area of necrosis is confined to the innermost layer of the of necrosis is confined to the innermost layer of the heart lining the chambers. heart lining the chambers.

5. Location of MI is identified as the location of the 5. Location of MI is identified as the location of the damaged heart muscle within the left ventricle: inferior, damaged heart muscle within the left ventricle: inferior, anterior, lateral, and posterior or right ventricle. anterior, lateral, and posterior or right ventricle.

a. Left ventricle is the most common and dangerous a. Left ventricle is the most common and dangerous location for an MI, because it is the main location for an MI, because it is the main pumping' chamber of the heart. pumping' chamber of the heart.

b. Right ventricular infarctions commonly occur in b. Right ventricular infarctions commonly occur in conjunction with damage to the inferior and/or conjunction with damage to the inferior and/or posterior wall of the left ventricle. posterior wall of the left ventricle.

6. Region of the heart muscle that becomes 6. Region of the heart muscle that becomes damaged- determined by the coronary artery damaged- determined by the coronary artery that becomes obstructed . that becomes obstructed .

7. The amount of heart muscle damage and the 7. The amount of heart muscle damage and the location of the MI-determine prognosis. location of the MI-determine prognosis.

Clinical ManifestationsClinical Manifestations 1. Chest pain 1. Chest pain a. Severe, diffuse steady substernal pain of a crushing a. Severe, diffuse steady substernal pain of a crushing

and squeezing nature and squeezing nature b. Not relieved by rest or sublingual vasodilator b. Not relieved by rest or sublingual vasodilator

therapy, but requires narcotics therapy, but requires narcotics c. May radiate to the arms (commonly the left), c. May radiate to the arms (commonly the left),

shoulders, neck, back, and/or jaw shoulders, neck, back, and/or jaw d. Continues for more than 15 minutes d. Continues for more than 15 minutes e. May produce anxiety and fear, resulting in an in- e. May produce anxiety and fear, resulting in an in-

crease in heart rate, blood pressure, and respiratory crease in heart rate, blood pressure, and respiratory rate rate

2. Diaphoresis, cool clammy skin, facial pallor 2. Diaphoresis, cool clammy skin, facial pallor

3. Hypertension or hypotension 3. Hypertension or hypotension

4. Bradycardia or tachycardia4. Bradycardia or tachycardia

5. Premature ventricular and/or atrial beats 5. Premature ventricular and/or atrial beats

6. Palpitations, severe anxiety, dyspnea 6. Palpitations, severe anxiety, dyspnea

7. Disorientation, confusion, restlessness 7. Disorientation, confusion, restlessness

8. Fainting, marked weakness . 8. Fainting, marked weakness .

9. Nausea, vomiting, hiccups 9. Nausea, vomiting, hiccups

10. Atypical symptoms: epigastric or abdominal distress, 10. Atypical symptoms: epigastric or abdominal distress,

dull aching or tingling sensations, shortness of breath, dull aching or tingling sensations, shortness of breath,

extreme fatigue extreme fatigue

Diagnostic EvaluationDiagnostic Evaluation

ECG Changes ECG Changes

1. Generally occur within 2 to 12 hours, but may 1. Generally occur within 2 to 12 hours, but may take 72 to 96 hours. take 72 to 96 hours.

2. Necrotic, injured, and ischemic tissue alters 2. Necrotic, injured, and ischemic tissue alters ventricular depolarization and repolarisation. ventricular depolarization and repolarisation.

a. S-T segment depression and T wave inversion a. S-T segment depression and T wave inversion indicate a pattern of ischemia. indicate a pattern of ischemia.

b. S- T elevation indicates an injury pattern. b. S- T elevation indicates an injury pattern.

c. Q waves indicate tissue necrosis and are c. Q waves indicate tissue necrosis and are permanent. permanent.

Elevation of-Serum Enzymes and IsoenzymesElevation of-Serum Enzymes and Isoenzymes

1. Enzymes are drawn in a serial pattern, usually on 1. Enzymes are drawn in a serial pattern, usually on ad- mission and every 6 to 24 hours until three ad- mission and every 6 to 24 hours until three samples are obtained; enzyme activity then is samples are obtained; enzyme activity then is correlated to the ex- tent of heart muscle damage. correlated to the ex- tent of heart muscle damage.

2. Enzymes commonly evaluated include creatinine 2. Enzymes commonly evaluated include creatinine kinase (CK), lactic dehydrogenase (LDH), and kinase (CK), lactic dehydrogenase (LDH), and aspartate amino- transferase (AST). aspartate amino- transferase (AST).

3. CK and LDH can be broken down further 3. CK and LDH can be broken down further into isoenzymes, which are more organ into isoenzymes, which are more organ specific. specific.

a. CK-MB is specific to heart muscle and a. CK-MB is specific to heart muscle and thus the most sensitive enzyme for thus the most sensitive enzyme for determining heart muscle damage.determining heart muscle damage.

b. LDH enzymes are specific to heart b. LDH enzymes are specific to heart muscle and they elevatedmuscle and they elevated

Other FindingsOther Findings

1. Elevated cardiac troponins 1. Elevated cardiac troponins 2. Elevated myoglobin 2. Elevated myoglobin 3. White blood cell count and sedimentation rate 3. White blood cell count and sedimentation rate

elevation due to inflammatory process associated elevation due to inflammatory process associated with the damaged heart muscle. with the damaged heart muscle.

4. Radionuclide imaging allows recognition of areas 4. Radionuclide imaging allows recognition of areas of decreased perfusion. of decreased perfusion.

5. PET determines the presence of reversible heart 5. PET determines the presence of reversible heart muscle injury and irreversible or necrotic tissue.muscle injury and irreversible or necrotic tissue.

6. Cardiac muscle dysfunction noted on 6. Cardiac muscle dysfunction noted on echocardiograph echocardiograph

ManagementManagement Therapy is aimed at the protection of ischemic and Therapy is aimed at the protection of ischemic and

injury of heart tissue to preserve muscle function, injury of heart tissue to preserve muscle function, reduce the infarction size, and prevent death. reduce the infarction size, and prevent death. Innovative modalities provide early restoration of Innovative modalities provide early restoration of coronary blood flow, and the use pharmacologic coronary blood flow, and the use pharmacologic agents improves oxygen supply and demand, agents improves oxygen supply and demand, reduces and/or prevents dysrhythmias, and inhibit reduces and/or prevents dysrhythmias, and inhibit the progression of coronary artery disease. the progression of coronary artery disease.

Oxygen Therapy Oxygen Therapy

• Improves oxygenation to ischemic heart muscle. Improves oxygenation to ischemic heart muscle.

ManagementManagement

Pain Control Pain Control Endogenous catecholamine release during pain Endogenous catecholamine release during pain

imposes increased workload on the heart muscle, imposes increased workload on the heart muscle, thus causing increase in oxygen demand. thus causing increase in oxygen demand.

1. Opiate analgesic therapy1. Opiate analgesic therapy a. Morphine is used to relieve pain, to improve a. Morphine is used to relieve pain, to improve

heart Hemodynamic by reducing preload and heart Hemodynamic by reducing preload and afterload and to provide anxiety relief. afterload and to provide anxiety relief.

b. Meperidine (Demerol) is useful for pain b. Meperidine (Demerol) is useful for pain management in those patients allergic to management in those patients allergic to morphine or sensitive( respiratory depression. morphine or sensitive( respiratory depression.

2. Vasodilator therapy2. Vasodilator therapy

a. Nitroglycerin (sublingual, IV, paste) promotes a. Nitroglycerin (sublingual, IV, paste) promotes venous (low-dose) and arterial (high-dose) venous (low-dose) and arterial (high-dose) relaxation as well as relaxation of coronary relaxation as well as relaxation of coronary vessels and prevention of coronary spasmvessels and prevention of coronary spasm

b. Myocardial oxygen demand is reduced with b. Myocardial oxygen demand is reduced with subsequent pain relief. c. Persistent chest pain subsequent pain relief. c. Persistent chest pain requires prompt action (IV nitroglycerin) requires prompt action (IV nitroglycerin)

3. Anxiolytic therapy3. Anxiolytic therapy

a. Benzodiazepines are used with analgesics a. Benzodiazepines are used with analgesics when anxiety complicates chest pain and its when anxiety complicates chest pain and its relief. relief.

Pharmacologic TherapyPharmacologic Therapy

1. Thrombolytic agents, such as tissue plasminogen 1. Thrombolytic agents, such as tissue plasminogen activator (Activase), streptokinase (Streptase), and activator (Activase), streptokinase (Streptase), and reteplase (Retavase), reestablish blood flow in reteplase (Retavase), reestablish blood flow in coronary vessels by dissolving obstructing coronary vessels by dissolving obstructing thrombus. thrombus.

a. No effect on the underlying stenosis that a. No effect on the underlying stenosis that precipitated the thrombus to form.precipitated the thrombus to form.

b. Administered IV or intracoronary.b. Administered IV or intracoronary.

2. Adjunctive therapy aimed to prevent platelet 2. Adjunctive therapy aimed to prevent platelet activation, aspirin.activation, aspirin.

3. Anticoagulation therapy is useful as an adjunct 3. Anticoagulation therapy is useful as an adjunct to thrombolytic therapy. Also used in situations to thrombolytic therapy. Also used in situations of prolonged bed rest, pulmonary embolism, of prolonged bed rest, pulmonary embolism, deep vein thrombosis, mural thrombi, deep vein thrombosis, mural thrombi, cardiogenic shock, and patients with atrial cardiogenic shock, and patients with atrial fibrillation. fibrillation.

4. Beta-adrenergic blocking agents improve oxygen 4. Beta-adrenergic blocking agents improve oxygen supply and demand, decrease sympathetic supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the stimulation to the heart, promote blood flow in the small vessels of the heart, and have small vessels of the heart, and have antidysrhythmic effects. antidysrhythmic effects.

a. Appears to lower mortality and decrease chance a. Appears to lower mortality and decrease chance of reinfarction and sudden death post-MI. of reinfarction and sudden death post-MI.

5. Antidysrhythmic therapy-lidocaine (Xylocaine) 5. Antidysrhythmic therapy-lidocaine (Xylocaine) decreases ventricular irritability, which commonly decreases ventricular irritability, which commonly occurs after MI. occurs after MI.

6. Calcium channel blockers improve the balance 6. Calcium channel blockers improve the balance between oxygen supply and demand by decreasing between oxygen supply and demand by decreasing heart rate, blood pressure, and dilating coronary heart rate, blood pressure, and dilating coronary vessels. vessels.

a. Diltiazem has been shown to decrease the a. Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-incidence of reinfarction in patients with non-Q-wave MIs and is currently the only calcium blocker wave MIs and is currently the only calcium blocker proven to be beneficial. proven to be beneficial.

ComplicationsComplications

1. Rhythm disturbances 1. Rhythm disturbances 2. Cardiac failure 2. Cardiac failure

a. Infarct expansion (thinning and dilation of the a. Infarct expansion (thinning and dilation of the necrotic zone) necrotic zone)

b. Infarct extension (additional heart muscle b. Infarct extension (additional heart muscle necrosis occurring after 24 hours of acute necrosis occurring after 24 hours of acute infarction) infarction)

c. CHF (with 20% to 35% left ventricle damage) c. CHF (with 20% to 35% left ventricle damage) d. Cardiogenic shock .d. Cardiogenic shock .f. Reinfarction f. Reinfarction g. Ischemic cardiomyopathy – g. Ischemic cardiomyopathy –

ComplicationsComplications

3. Cardiac rupture3. Cardiac rupture

4. Ventricular mural thrombus 4. Ventricular mural thrombus

5. Thromboemboli 5. Thromboemboli

6. Ventricular aneurysm 6. Ventricular aneurysm

7. Cardiac tamponade 7. Cardiac tamponade

8. Pericarditis (2 to 3 days after MI) 8. Pericarditis (2 to 3 days after MI)

9. Psychiatric problems-depression, personality9. Psychiatric problems-depression, personality

changeschanges

Nursing AssessmentNursing Assessment 1. Gather information regarding the chest pain: 1. Gather information regarding the chest pain:

a. Nature and intensity-describe the pain in patient's a. Nature and intensity-describe the pain in patient's own words and compare it with pain experienced in own words and compare it with pain experienced in the past. the past.

b. Onset and duration-exact time pain occurred, as b. Onset and duration-exact time pain occurred, as well as the time pain relieved or diminished .well as the time pain relieved or diminished .

c. Location and radiation-point to the area where the c. Location and radiation-point to the area where the pain is located and to other areas where the pain pain is located and to other areas where the pain seems to travel. seems to travel.

d. Precipitating and aggravating factors-describe the d. Precipitating and aggravating factors-describe the activity performed just before the onset of pain .activity performed just before the onset of pain .

2. Ask patient about other symptoms experienced 2. Ask patient about other symptoms experienced associated with the pain. Observe patient for associated with the pain. Observe patient for diaphoresis, facial pallor, dyspnea, guarding diaphoresis, facial pallor, dyspnea, guarding behaviors, rigid body posture, extreme weakness, behaviors, rigid body posture, extreme weakness, confusion. confusion.

3. Evaluate cognitive, behavioral, and emotional 3. Evaluate cognitive, behavioral, and emotional status. status.

4. Ask patient regarding prior health status with 4. Ask patient regarding prior health status with emphasis on current medications, allergies (opiate emphasis on current medications, allergies (opiate analgesics, iodine, shellfish), recent trauma or analgesics, iodine, shellfish), recent trauma or surgery, aspirin ingestion, peptic ulcers, fainting, surgery, aspirin ingestion, peptic ulcers, fainting, drug and alcohol use. drug and alcohol use.

5. Analyze information for contraindications 5. Analyze information for contraindications for thrombolytic therapy and/or PTCA. for thrombolytic therapy and/or PTCA.

6. Gather information on presence or absence 6. Gather information on presence or absence of cardiac risk factors. of cardiac risk factors.

7. Identify patient's social support system and 7. Identify patient's social support system and potential caregivers. potential caregivers.

8. Identify significant other's reaction to the 8. Identify significant other's reaction to the crisis situation. crisis situation.

Nursing InterventionsNursing Interventions

Reducing PainReducing Pain

1. Handle patient carefully while providing initial 1. Handle patient carefully while providing initial care, starting IV infusion, obtaining baseline vital care, starting IV infusion, obtaining baseline vital signs, and attaching electrodes for continuous signs, and attaching electrodes for continuous ECG monitoring. ECG monitoring.

2. Administer oxygen by nasal cannula if 2. Administer oxygen by nasal cannula if prescribed, and encourage patient to take deep prescribed, and encourage patient to take deep breaths-may decrease incidence of dysrhythmias breaths-may decrease incidence of dysrhythmias by allowing the heart to be less ischemic and less by allowing the heart to be less ischemic and less irritable; may reduce infarct size, decrease irritable; may reduce infarct size, decrease anxiety, and resolve chest pain. anxiety, and resolve chest pain.

Nursing InterventionsNursing Interventions

3. Offer support and reassurance to patient that 3. Offer support and reassurance to patient that relief of pain is apriority.relief of pain is apriority.

4. Administer sublingual nitroglycerin as directed; 4. Administer sublingual nitroglycerin as directed; recheck blood pressure (BP), heart rate (HR), recheck blood pressure (BP), heart rate (HR), and respiratory rate and respiratory rate

Nursing InterventionsNursing Interventions

5. Discuss with patient and family member the 5. Discuss with patient and family member the anticipate nursing and medical regimen. anticipate nursing and medical regimen.

a. Explain visiting hours and need to limit a. Explain visiting hours and need to limit number of visitors at one time. number of visitors at one time.

b. Offer family members preferred times to b. Offer family members preferred times to phone to check on patient's status. phone to check on patient's status.

6. Observe for autonomic signs of anxiety such as 6. Observe for autonomic signs of anxiety such as increases in heart rate, BP, respiratory rate. increases in heart rate, BP, respiratory rate.

7. Administer antianxiety agents as prescribed. 7. Administer antianxiety agents as prescribed.

a. Explain to patient the reason for sedation: und a. Explain to patient the reason for sedation: und anxiety can make the heart more irritable and anxiety can make the heart more irritable and require more oxygen. require more oxygen.

b. Assure patient that the goal of sedation is to b. Assure patient that the goal of sedation is to promote comfort and, therefore, should be promote comfort and, therefore, should be requested anxious, excitable.requested anxious, excitable.

c. Observe for adverse effects of sedation such as c. Observe for adverse effects of sedation such as lethargy, confusion, and/or increased agitation. lethargy, confusion, and/or increased agitation.

8. Maintain consistency of care with one or two 8. Maintain consistency of care with one or two nurse regularly assisting patient, especially if nurse regularly assisting patient, especially if severe anxiety is present. severe anxiety is present.

9. Offer back massage to promote relaxation, 9. Offer back massage to promote relaxation, decrease muscle tension, and improve skin decrease muscle tension, and improve skin integrity. integrity.

10. Use techniques such as guided imagery to relieve 10. Use techniques such as guided imagery to relieve tension and anxiety. tension and anxiety.

Nursing InterventionsNursing Interventions

Maintaining Hemodynamic StabilityMaintaining Hemodynamic Stability

1. Monitor BP every 2 hours or as directed-1. Monitor BP every 2 hours or as directed-hypertension increases afterload of the heart, hypertension increases afterload of the heart, elevating oxygen demand; hypotension causes elevating oxygen demand; hypotension causes reduced coronary an tissue perfusion. reduced coronary an tissue perfusion.

2. Monitor respirations and lung fields every 2 to 4 2. Monitor respirations and lung fields every 2 to 4 hours or as prescribed. hours or as prescribed.

a. Auscultate for normal and abnormal breath sound a. Auscultate for normal and abnormal breath sound (crackles may indicate left ventricular failure; (crackles may indicate left ventricular failure; diffuse crackles indicate pulmonary edema). diffuse crackles indicate pulmonary edema).

Congestive Heart FailureCongestive Heart Failure

Basic DefinitionBasic Definition

Heart failure is a Heart failure is a medical term that medical term that describes an describes an inability of the inability of the heart to keep up heart to keep up its work load of its work load of pumping blood to pumping blood to the lungs and to the lungs and to the rest of the the rest of the body.body.

StatisticStatistic

It is estimated that as many as two It is estimated that as many as two million Americans suffer from million Americans suffer from congestive heart failure and that up to congestive heart failure and that up to 29, 000 die annually from this chronic 29, 000 die annually from this chronic disorder.disorder.

SymptomsSymptoms(involving gravity/exhaustion of heart)(involving gravity/exhaustion of heart)

Swelling of the ankles, legs, and handsSwelling of the ankles, legs, and hands

Orthopnea, or the shortness of breath Orthopnea, or the shortness of breath when lying flat when lying flat

Shortness of breath during exertionShortness of breath during exertion

SymptomsSymptoms(involving circulation)(involving circulation)

Cyanosis, or a bluish color that is seen in the Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygenlips and fingernails from a lack of oxygen

Fatigue or weaknessFatigue or weakness

Rapid or irregular heart beatRapid or irregular heart beat

Changes of behavior such as restlessness, Changes of behavior such as restlessness, confusion, and decreased attention spanconfusion, and decreased attention span

SymptomsSymptoms(involving congestion)(involving congestion)

Unexplained or unintentional weight gainUnexplained or unintentional weight gain

Chronic coughChronic cough

Increased urinationIncreased urination

Distended neck veinsDistended neck veins

Loss of appetite or indigestionLoss of appetite or indigestion

Congestive heart failure is a syndrome that can be Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such ascaused by multiple underlying diseases such as::

Congenital heart diseaseCongenital heart disease AtherosclerosisAtherosclerosis Rheumatic feverRheumatic fever CardiomyopathyCardiomyopathy Valve disordersValve disorders Ventricular failureVentricular failure Left or right-sided failureLeft or right-sided failure HypertensionHypertension Prolonged alcohol or drug addictionProlonged alcohol or drug addiction Previous heart attackPrevious heart attack DiabetesDiabetes Chronic rapid heartbeatsChronic rapid heartbeats

CardiomyopathyCardiomyopathy

Cardiomyopathy is the stretching Cardiomyopathy is the stretching and enlarging of the heart cavity and enlarging of the heart cavity that occurs making the heart weak that occurs making the heart weak so it does not pump correctlyso it does not pump correctly

Ventricular FailureVentricular Failure

Ventricular failure occurs when there Ventricular failure occurs when there are weak spots in the ventricular are weak spots in the ventricular walls causing a bulge, or an walls causing a bulge, or an aneurysm.aneurysm.

AtherosclerosisAtherosclerosis

Atherosclerosis is the gradual clogging Atherosclerosis is the gradual clogging of the arteries by fatty, fibrous deposits. of the arteries by fatty, fibrous deposits. A tiny lump of fibrous tissue grows as A tiny lump of fibrous tissue grows as the artery tries to repair the damage. the artery tries to repair the damage. Cholesterol accumulates and more Cholesterol accumulates and more tissue builds up. tissue builds up.

The arteries are thickened and hardened The arteries are thickened and hardened making a loss of elasticity causing making a loss of elasticity causing congestion.congestion.

Left-sided/Right-sided FailureLeft-sided/Right-sided Failure

Blood backs up causing congestion Blood backs up causing congestion and thus swelling of extremities and and thus swelling of extremities and internal organsinternal organs

Other ContributorsOther Contributors

HypertensionHypertension

Prolonged Alcohol or Drug AddictionProlonged Alcohol or Drug Addiction

Previous Heart AttackPrevious Heart Attack

Diabetes Diabetes

Chronic Rapid Heart BeatsChronic Rapid Heart Beats

TreatmentTreatment

When a treatable underlying cause ofWhen a treatable underlying cause of

congestive heart failure exists, congestive heart failure exists,

correcting the cause may resolve, or at correcting the cause may resolve, or at

least greatly improve, the degree of least greatly improve, the degree of

heart failureheart failure

Valve SurgeryValve Surgery

If a defective heart valve is If a defective heart valve is

responsible for heart failure, it may responsible for heart failure, it may

be treated by heart valve surgerybe treated by heart valve surgery

AngioplastyAngioplasty Angioplasty, which is catheterization using a Angioplasty, which is catheterization using a

balloon to flatten fatty deposits, can be used balloon to flatten fatty deposits, can be used to treat atherosclerosis or other conditions to treat atherosclerosis or other conditions with blocked arteries.with blocked arteries.

An artery of an arm or leg is used to guide An artery of an arm or leg is used to guide the catheter through to the blocked artery.the catheter through to the blocked artery.

An uninflated balloon on the top of a smaller An uninflated balloon on the top of a smaller tube is threaded through the larger tube and tube is threaded through the larger tube and centered in the plaque narrowed area.centered in the plaque narrowed area.

The balloon inflates compressing the plaque The balloon inflates compressing the plaque against the walls and increasing the open against the walls and increasing the open area.area.

DrugsDrugs

Digitalis-strengthen the heartDigitalis-strengthen the heart’’s s contractions increasing blood flowcontractions increasing blood flow

Diuretic-increase the output of salt and Diuretic-increase the output of salt and water in urinewater in urine

Vasodilators-relax blood vessels which Vasodilators-relax blood vessels which lowers the resistance to blood flow. lowers the resistance to blood flow. More blood reaches the tissues and the More blood reaches the tissues and the heart works no harder than before.heart works no harder than before.

In conclusion, congestive heart In conclusion, congestive heart failure is often assumed to be a failure is often assumed to be a

disease when in fact it is a disease when in fact it is a syndrome caused by multiple syndrome caused by multiple

disorders.disorders.

Cardiogenic ShockCardiogenic Shock

Systemic hypoperfusion secondarySystemic hypoperfusion secondary to to

severe depression of cardiac output and severe depression of cardiac output and

sustained systolic arterial hypotension sustained systolic arterial hypotension

despite elevated filling pressures.despite elevated filling pressures.

Cardiac output is inadequate to meet Cardiac output is inadequate to meet

tissue demandstissue demands

EtiologiesEtiologies

Acute myocardial infarction/ischemiaAcute myocardial infarction/ischemia  

LV failureLV failure  

VSRVSR  

Severe mitral regurgitation (MR)Severe mitral regurgitation (MR)

Cardiac TamponadeCardiac Tamponade  

Clinical FindingsClinical Findings

Physical Exam:Physical Exam: elevated JVP, +S3, rales, elevated JVP, +S3, rales, oliguria, acute pulmonary edemaoliguria, acute pulmonary edema

Hemodynamics:Hemodynamics: CO, SVR, SvO2 CO, SVR, SvO2

Initial evaluation:Initial evaluation: hemodynamics (PA hemodynamics (PA catheter), echocardiography, catheter), echocardiography, angiographyangiography

<90 mmHg

<2.2 li/min.m2

>15 mmHg

ManagementManagement

PressorsPressors Intra-aortic Balloon Pump (IABP)Intra-aortic Balloon Pump (IABP) FibrinolyticsFibrinolytics Revascularization: CABG/PCIRevascularization: CABG/PCI

Refractory shock: ventricular assist Refractory shock: ventricular assist device, cardiac transplantationdevice, cardiac transplantation

PressorsPressors DopamineDopamine

• <2 renal vascular dilation<2 renal vascular dilation• <2-10 +chronotropic/inotropic (beta effects)<2-10 +chronotropic/inotropic (beta effects)• >10 vasoconstriction (alpha effects)>10 vasoconstriction (alpha effects)

DobutamineDobutamine –– positive inotrope, vasodilates, positive inotrope, vasodilates, arrhythmogenic at higher dosesarrhythmogenic at higher doses

NorepinephrineNorepinephrine (Levophed): (Levophed): vasoconstriction, inotropic stimulant. Should vasoconstriction, inotropic stimulant. Should only be used for refractory hypotension with only be used for refractory hypotension with dec SVR. dec SVR.

VasopressionVasopression –– vasoconstriction vasoconstriction VASO and LEVO should only be used as a VASO and LEVO should only be used as a

last resortlast resort

IABP is a temporizing measureIABP is a temporizing measure

Augments coronary blood flow in Augments coronary blood flow in diastolediastole

Balloon collapse in systole creates a Balloon collapse in systole creates a vacuum effect vacuum effect decreases afterload decreases afterload

Decrease myocardial oxygen Decrease myocardial oxygen demand demand

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