Terms in this set (125)

The heart is covered by the pericardium (two layers of the pericardium is the parietal and epicardium). The myocardium is the middle layer, and is the muscle of the heart. Then there is the innermost layer, the endocardium - which lines the inside of the heart's chambers and great vessels. There are four chambers; two upper - atria, two lower - ventricles. These are divided by septum and valves.
Right atrium receives deoxygenated blood => Right ventricle pumps blood into lungs => left atrium receives oxygenated blood from the lungs => left ventricle pumps oxygenated blood to the body => AV valve closure; S1 heart sound (lub) => semilunar valve closure; S2 heart sound (dub).

The Conducting System of the Heart It is a network of specialized cardiac muscle cells that (1)initiates and (2) distribute select electrical impulses. It is composed of the following:
•1-Sinoatrial (SA) node,
•2-Atrioventricular (AV) node,
•3-Bundle of His
•4-continues down the inter-ventricular septum through the right and left bundle branches, and out into the Perkinje Fibers in the ventricular walls.
At rest the myocardial cells are POLARIZED (negative charge). When the electrical impulse goes through 1-4, it causes ions to move across cell membranes, making the cells more positive. This is known as DEPOLARIZATION. The electrical impulse (also known as the Action Potential) and depolarization causes the muscle to contract. REPOLARIZATION begins immediately following DEPOLARIZATION. For a brief period before and after repolarization, the cells resist stimulation, which is known as the refractory period. This refractory period protects the heart from going into spasm or tetany.
Sinus Bradycardia: Sinus bradycardia occurs when the sinus node creates an impulse at a slower-than-normal rate. Causes include lower metabolic needs (eg, sleep, athletic training, hypothermia, hypothyroidism), vagal stimulation (eg, from vomiting, suctioning, severe pain, extreme emotions), medications (eg, calcium channel blockers, amiodarone, beta-blockers), increased intracranial pressure, and myocardial infarction (MI), especially of the inferior wall. All characteristics of sinus bradycardia are the same as those of normal sinus rhythm, except for the rate.

Sinus Tachycardia: Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rate. It may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia, congestive heart failure, pain, hypermetabolic states, fever, exercise, anxiety, or sympathomimetic medications. All aspects of sinus tachycardia are the same as those of normal sinus rhythm, except for the rate. As the heart rate increases, the diastolic filling time decreases, possibly resulting in reduced cardiac output and subsequent symptoms of syncope and low blood pressure. If the rapid rate persists and the heart cannot compensate for the decreased ventricular filling, the patient may develop acute pulmonary edema.

Sinus Arrhythmia: Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; the rate usually in- creases with inspiration and decreases with expiration. Non respiratory causes include heart disease and valvular disease, but these are rarely seen. Usually not treated.
Premature Atrial Contractions (PACs): A premature atrial complex (PAC) is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node. The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (as in hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states, or atrial ischemia, injury, or infarction. PACs are often seen with sinus tachycardia. PACs are common in normal hearts. The patient may say, "My heart skipped a beat." A pulse deficit (a difference between the apical and radial pulse rate) may exist.
If PACs are infrequent, no treatment is necessary. If they are frequent (more than 6 per minute), this may herald a worsening disease state or the onset of more serious dysrhythmias, such as atrial fibrillation. Treatment is directed toward the cause.

Atrial Flutter: Atrial flutter occurs in the atrium and creates im- pulses at an atrial rate between 250 and 400 times per minute. Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a ther- apeutic block at the AV node. This is an important feature of this dysrhythmia. If all atrial impulses were conducted to the ventri- cle, the ventricular rate would also be 250 to 400, which would result in ventricular fibrillation, a life-threatening dysrhythmia. Causes are similar to that of atrial fibrillation. Atrial flutter can cause serious signs and symptoms, such as chest pain, shortness of breath, and low blood pressure.

Atrial Fibrillation: trialfibrillationcausesarapid,disorganized, and uncoordinated twitching of atrial musculature. It is the most common dysrhythmia that causes patients to seek medical atten- tion. It may start and stop suddenly. Atrial fibrillation may occur for a very short time (paroxysmal), or it may be chronic. Atrial fibrillation is usually associated with advanced age, valvular heart disease, coronary artery disease, hypertension, cardiomyopathy, hyperthyroidism, pulmonary disease, acute moderate to heavy in- gestion of alcohol ("holiday heart" syndrome), or the aftermath of open heart surgery. A rapid ventricular response reduces the time for ventricular filling, resulting in a smaller stroke volume. Because this rhythm causes the atria and ventricles to contract at different times, the atrial kick (the last part of diastole and ventricular filling, which accounts for 25% to 30% of the cardiac output) is also lost. This leads to symptoms of irregular palpitations, fatigue, and malaise. There is usually a pulse deficit, a numerical difference between apical and radial pulse rates. The shorter time in diastole reduces the time available for coronary artery perfusion, thereby increas- ing the risk for myocardial ischemia. The erratic atrial contraction promotes the formation of a thrombus within the atria, increas- ing the risk for an embolic event. There is a two- to five-fold increase in the risk of stroke (brain attack).
Premature Ventricular Complex (PVC): Premature ventricular com- plex (PVC) is an impulse that starts in a ventricle and is con- ducted through the ventricles before the next normal sinus impulse. PVCs can occur in healthy people, especially with the use of caffeine, nicotine, or alcohol. They are also caused by car- diac ischemia or infarction, increased workload on the heart (eg, exercise, fever, hypervolemia, heart failure, tachycardia), digitalis toxicity, hypoxia, acidosis, or electrolyte imbalances, especially hypokalemia.
In the absence of disease, PVCs are not serious. In the patient with an acute MI, PVCs may indicate the need for more aggressive therapy.

Ventricular Tachycardia (V-Tach): Ventricular Tachycardia. Ventricular tachycardia (VT) is de- fined as three or more PVCs in a row, occurring at a rate exceed- ing 100 beats per minute. The causes are similar to those for PVC. VT is usually associated with coronary artery disease and may precede ventricular fibrillation. VT is an emergency because the patient is usually (although not always) unresponsive and pulseless. The patient's tolerance or lack of tolerance for this rapid rhythm depends on the ventricular rate and underlying disease. If the patient is stable, continuing the assessment, especially ob- taining a 12-lead ECG, may be the only action necessary. Cardio- version may be the treatment of choice, especially if the patient is unstable. VT in a patient who is unconscious and without a pulse is treated in the same manner as ventricular fibrillation: immediate defi- brillation is the action of choice.

Ventricular Fibrillation (V-Fib): Ventricular fibrillation is a rapid but dis- organized ventricular rhythm that causes ineffective quivering of the ventricles. There is no atrial activity seen on the ECG. Causes of ventricular fibrillation are the same as for VT; it may also re- sult from untreated or unsuccessfully treated VT. Other causes include electrical shock and Brugada syndrome, in which the pa- tient (frequently of Asian descent) has a structurally normal heart, few or no risk factors for coronary artery disease, and a family his- tory of sudden cardiac death. This dysrhythmia is always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations. Because there is no coordinated cardiac activity, cardiac arrest and death are im- minent if ventricular fibrillation is not corrected. Treatment of choice is immediate defibrillation and activation of emergency services. After defibrillation, eradicating causes and administering vaso- active and antiarrhythmic medications alternating with defibrillation are treatments used to try to convert the rhythm to normal sinus rhythm.

Ventricle Asystole: Commonly called flatline, ventricular asystole is characterized by absent QRS complexes, al- though P waves may be apparent for a short duration in two different leads. There is no heartbeat, no palpable pulse, and no respiration. Without immediate treatment, ventricular asystole is fatal. Cardiopulmonary resuscitation and emergency services are necessary to keep the patient alive. lyte imbalance, drug overdose, or hypothermia. Intubation and establishment of intravenous access are the first recommended ac- tions. Transcutaneous pacing may be attempted. A bolus of intra- venous epinephrine should be administered and repeated at 3- to 5-minute intervals, followed by 1-mg boluses of atropine at 3- to 5-minute intervals. Because of the poor prognosis associated with asystole, if the patient does not respond to these actions and others aimed at correcting underlying causes, resuscitation efforts are usually ended ("the code is called") unless special circumstances (eg, hypothermia) exist.
Calcium Channel Blockers - Calcium channel blockers decrease the workload of the heart and decrease the heart's oxygen demands and are used to treat variant angina pectoris, HTN, and dysrhythmias.
S&S: hypotension, bradycardia, may precipitate AV block, HA, constipation, nausea, peripheral edema
NI: administer before meals to reduce GI upset, check liver/renal function tests, weigh patient and report wt gain, avoid grapefruit, increase fiber.
ie Veropamil, Nifedipine, Diltiazem

Potassium Channel Blockers (Class III) - delays repolarization of fast potentials, prolong action potential duration and effective refractory period.
S&S: pulmonary toxicity, visual impairment, hypotension, fatigue, bradycardia
ie Amiodarone

Sodium Channel Blockers -
Reduces automatically in ventricles and bundle of HIs-Purkinje system
IA: Slows conduction; prolongs repolarization
S&S Toxicity for Lidocaine: (SAMS) Slurred/Difficult speech (paresthesias, numbness of lips/tongue), Altered CNS (drowsiness, dizziness, dysrhythmias, restlessness, confusion), Muscle twitching (tremors), Seizures (convulsions, respiratory depression, respiratory and cardiac arrest).
S&S cinchonism, cardiotoxicity, arterial embolism, tinnitus, HA, N/V/D dizziness, hypotension, fatigue, bradycardia
NI: assess LOC, pulse checks, seizure precautions, VS frequently, monitor ECG, assess respiratory system and gas exchange, never give IV if prepared with epinephrine - can cause severe hypertension and life-threatening dysrhythmias.
ie Lidocaine (Lidocaine used for local anesthesia often contains epinephrine), Quinidine, Procainamide

Beta Blockers -
blocks beta-receptors in the heart causing decreased HR, decreased force of contraction, decreased rate of AV conduction, and reduces contractibility in the atria and ventricles.
S&S: bradycardia, lethargy, GI upset, CHF r/t AV block, hypotension, depression, bronchospasm
NI: assess for symptoms of heart failure,evalute BP and pulse for significant changes: hold if systolic BP is below 90mmHg, monitor pts with diabetes. 1st, 2nd, and 3rd generations of drugs, no urinary retention issues.
ie Inderal, Tenormin, Bystolic, metroprolol

Cardiotonic Glycosides - decrease conduction through the AV node and reduce automaticity of the SA node. used for heart failure, a-fib/flutter.
S&S: dizziness, HA, malaise, fatigue, muscle weakness, visual disturbances, anorexia, hypokalemia, dysrhythmias, bradycardia
NI: monitor digoxin serum levels, monitor apical pulse: report below 60 in adults and 90 in children and hold the dose, administer IV slowly over 5 minutes, do not double up with missed doses, teach patients about early signs of hypokalemia and digitalis toxicity (N/V/D, blurred or yellow disturbances).
ie Digoxin, Adenosine

General Nursing Implications: take apical + radial pulse, blood pressure, baseline respiratory rate, while beginning medication take VS q1hrs-4hrs, skin color monitoring, LOC change monitoring, any subjective complaints from pt needs to be followed up, monitor labs - electrolytes, CBCs, liver enzymes, DVTs
The primary presenting symptoms of infective endocarditis are fever and a heart murmur. The fever may be intermit- tent or absent, especially in patients who are receiving an- tibiotics or corticosteroids, in those who are elderly, or those who have heart failure or renal failure. A heart murmur may be absent initially but develops in almost all patients. Murmurs that worsen over time indicate progressive damage from vegetations or perforation of the valve or the chordae tendineae.
In addition to the fever and heart murmur, clusters of pe- techiae may be found on the body. Small, painful nodules (Osler nodes) may be present in the pads of fingers or toes. Irregular, red or purple, painless, flat macules (Janeway le- sions) may be present on the palms, fingers, hands, soles, and toes. Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi of the eyes. Splinter hemorrhages (ie, reddish-brown lines and streaks) may be seen under the fingernails and toenails, and petechiae may appear in the conjunctiva and mucous membranes. Cardiomegaly, heart failure, tachycardia, or splenomegaly may occur.
Central nervous system manifestations of infective endocarditis include headache; temporary or transient cerebral ischemia; and strokes, which may be caused by emboli to the cerebral arteries. Embolization may be a presenting symptom, and it may occur at any time and may involve other organ systems. Embolic phenomena may occur, as dis- cussed in the previous section on rheumatic endocarditis.
Heart failure, which may result from perforation of a valve leaflet, rupture of chordae, blood flow obstruction due to vegetations, or intracardiac shunts from dehiscence of prosthetic valves, indicates a poor prognosis with medical therapy alone and a higher surgical risk (Libby, et al., 2008). Valvular stenosis or regurgitation, myocardial damage, and mycotic (fungal) aneurysms are potential cardiac complica- tions. First-degree, second-degree, and third-degree atri- oventricular blocks may occur and are often a sign of a valve ring abscess. Emboli, immunologic responses, abscess of the spleen, mycotic aneurysms, cerebritis, and hemodynamic deterioration may cause complications in other organs.
The objective of treatment is to eradicate the invading organism through adequate doses of an appropriate antimicrobial agent. Antibiotic therapy is usually administered parenterally in a continuous IV infusion for 2 to 6 weeks. Parenteral therapy is administered in doses that produce a high serum concentration for a significant period to ensure eradication of the dormant bacteria within the dense vege- tations. This therapy is often delivered in the patient's home and is monitored by a home care nurse. Serum levels of the antibiotic are monitored. If there is insufficient bactericidal activity, increased dosages of the antibiotic are prescribed or a different antibiotic is used. Numerous antimi- crobial regimens are in use, but penicillin is usually the medication of choice. Blood cultures are taken periodically to monitor the effect of therapy. In fungal endocarditis, an antifungal agent, such as amphotericin B (eg, Abelcet, Amphocin, Fungizone), is the usual treatment.
In addition, the patient's temperature is monitored at regular intervals because the course of the fever is one indication of the effectiveness of treatment. However, febrile reactions also may occur as a result of medication. After adequate antimicrobial therapy is initiated, the infective organism is usually eliminated. The patient should begin to feel better, regain an appetite, and have less fatigue. During this time, patients require psychosocial support because although they feel well, they may find themselves confined to the hospital or home with restrictive IV therapy.
Patients are given specific treatment for the underlying cause if it is known (eg, penicillin for hemolytic streptococci) and are placed on bed rest to decrease cardiac workload. Bed rest also helps decrease myocardial damage and the complica- tions of myocarditis. In young patients with myocarditis, ac- tivities, especially athletics, should be limited for a 6-month period or at least until heart size and function have returned to normal. Physical activity is increased slowly, and the pa- tient is instructed to report any symptoms that occur with increasing activity, such as a rapidly beating heart. If heart failure or dysrhythmia develops, management is essentially the same as for all causes of heart failure and dysrhythmias (see Chapters 27 and 30), except that beta-blockers are avoided because they decrease the strength of ventricular contraction (have a negative inotropic effect).

The nurse assesses for resolution of tachycardia, fever, and any other clinical manifestations. The cardiovascular as- sessment focuses on signs and symptoms of heart failure and dysrhythmias. Patients with dysrhythmias should have con- tinuous cardiac monitoring with personnel and equipment readily available to treat life-threatening dysrhythmias. Patients with myocarditis are sensitive to digitalis. Nurses must closely monitor these patients for digitalis toxicity, which is evidenced by dysrhythmia, anorexia, nausea, vomiting, headache, and malaise.
Anti-embolism stockings and passive and active exer- cises should be used because embolization from venous thrombosis and mural thrombi can occur, especially in patients on bed rest.
Myocarditis: Cardiac MRI with contrast may be diagnostic and can guide clinicians to sites for endocardial biopsies, which may be diagnostic for an organism or its genome, immune process, or a radiation reaction causing the myocarditis. Pa- tients without any abnormal heart structure (at least initially) may suddenly develop dysrhythmias or ST-T-wave changes. If the patient has structural heart abnormalities (eg, systolic dys- function), a clinical assessment may disclose cardiac enlarge- ment, faint heart sounds (especially S1), a gallop rhythm, or a systolic murmur. The WBC count and ESR may be elevated.

Pericarditis: An echocardiogram may detect in- flammation, pericardial effusion or tamponade, and heart failure. It may help confirm the diagnosis and may be used to guide pericardiocentesis (needle or catheter drainage of the pericardium). TEE may be useful in diagnosis but may underestimate the extent of pericardial effusions. Com- puted tomography (CT) may be the best diagnostic tool for determining the size, shape, and location of pericardial ef- fusions and may be used to guide pericardiocentesis. MRI may assist with detection of inflammation and adhesions. Occasionally a video-assisted pericardioscope-guided biopsy of the pericardium or epicardium is performed to obtain tis- sue samples for culture and microscopic examination. Be- cause the pericardial sac surrounds the heart, a 12-lead ECG may show concave ST elevations in many, if not all, leads (with no reciprocal changes) and may show depressed PR segments or atrial dysrhythmias.

Endocarditis: A definitive diagnosis is made when a micro-organism is found in two separate blood cultures, in a vegetation, or in an abscess. Three sets of blood cultures (with each set including one aerobic and one anaerobic cul- ture) drawn over a 24-hour period (or every 30 minutes if the patient's condition is unstable) should be obtained be- fore administration of any antimicrobial agents. Negative blood cultures do not definitely rule out infective endo- carditis. Patients may have elevated white blood cell (WBC) counts. Doppler echocardiography may assist in the diagnosis by demonstrating a mass on the valve, prosthetic valve, or sup- porting structures and by identifying vegetations, abscesses, new prosthetic valve dehiscence, or new regurgitation. The echocardiogram may reveal the development of heart failure. TEE may provide better data than transthoracic imaging.
Lipid Profile - should be preformed fasting for 12 hours before testing, and to avoid alcohol 24 hours before testing.
C-Reactive Protein - none
Serum Cardiac Monitors - some drugs may interfere. must be obtained necessitating blood draws every 12-24 hours for several days.
12-lead ECG - noninvasive - very tense muscles and movement can interfere with results
Stress ECG - have resuscitation supplies available
TTE - noninvasive; performed at the client's bedside. conductive gel may be cold. provide a washcloth or wash the chest wall following the exam for comfort.
TEE - the client is sedated and the throat anesthetized to allow passage of the endoscope into the esophagus. Monitor breathing, cough, and gag reflexes following the exam. Keep NPO until the gag reflex returns and the client is fully awake.
Echocardiogram - same as stress ECG
Doppler - monitor BPs
X-Rays/CT/EBCT - if contract is injected, ask about allergies (iodine, seafood) before exam; ensure good hydration before and after the exam to reduce the risk of kidney damage. exposes to radiation.
Angiography/cardiac catheterization - closely monitor the client, the insertion site, and the extremity after the procedure. Immediately report evidence of bleeding, pain, or a pale, pulseless extremities.
MRI - the client is not exposed to radiation, ask about implantable metal or electronic devices.
Radionuclear scans - the amount of radioisotope injected is very small; no special radiation precautions needed. encourage increased fluid intake.
General Anemia S&S: Pallor, Angina, Fatigue, Dyspnea on exertion, Night cramps, Bone pain, HA, Dizziness, Dim vision, Petechiae, Purpura

Bloss Loss Anemia - Increased reticulocyte level; normal Hgb and Hct if measured soon after bleeding starts, but levels decrease thereafter. Acute/chronic bleeding

Iron Deficiency Anemia - Decreased reticulocytes, iron, ferritin, iron saturation. Patients with iron deficiency primarily have symptoms of anemia. If the deficiency is severe or prolonged, they may also have a smooth, sore tongue; brittle and ridged nails; and angular cheilosis. These signs subside after iron re- placement therapy. The health history may be significant for multiple pregnancies, GI bleeding, and pica.

Pernicious Anemia (B12) - Decreased vitamin B12 level. Paresthesias = numbness, tingling, altered proprioreception. Smooth, beefy red tongue - glossitis. Diarrhea.

Folic Acid Anemia - Decreased folate level. Glossitis, cheilosis, diarrhea. Can lead to spinal tube defects in fetus.

Anemia of Chronic Disease - similar to iron deficiency anemia - pts with chronic kidney disease have pallor of conjunctiva

Hemolytic Anemia - Decreased MCV; fragmented RBCs; increased reticulocyte level

Sickle Cell Anemia - characterized by abnormal HbS in the RBC - affects how they react to stressors.
Crisis: sudden onset of INTENSE pain usually in the abdomen, chest, back, joints, multiple infarctions, may become jaundiced.

Aplastic Anemia - Aplastic anemia is a rare disease caused by a decrease in or damage to marrow stem cells, damage to the microenviron- ment within the marrow, and replacement of the marrow with fat. pancytopenia, tachycardia
1. decreased cardiac output
> assess patient's condition> monitor and record vital signs> encourage patient to verbalize concerns
> encourage patient to change position every two hours
> encourage patient to do relaxation techniques
> encourage patient to engage in divertional activities such as chatting with family and friends.

2. ineffective tissue perfusion
>assess pt.'s condition.
>monitor and record v/s.
>note color and temperature of the skin.
>monitor peripheral pulse.
>provide a warmth environment.
>encourage active rom.

3. acute pain
>assess pt.'s condition.
>monitor and record v/s.
>assess pains location and intensity/severity arising with.
>provide comfort measures like stretching of linens and assisting in position.
> provide diversional activities like having conversation w/ the pt.
>stress to pt the importance of providing adequate rest period to the pt.
>administer meds as ordered.
>monitor urine output.
> reinforced low salt and low fat diet

4. activity intolerance
> monitor and record vital signs
> teach method to increase activity level
> plan care with rest periods between activities
> provide positive atmosphere
> assist with activities
> promote comfort measures
> encourage participation and diversion of activities

5. fatigue
> monitor vital signs
>determine ability to participate in activities/level of mobility.
>establish realistic activity goals with client
>plan care to allow individually adequate rest periods, schedule activities for periods when client has the most energy
>provide environment conducive
>give medication as doctors ordered
Nurses and other health care professionals need to be aware that "atypical" symptoms of angina and myocardial infarction, such as shortness of breath or left-sided chest pain, are common, especially among African Americans. Any patient with shortness of breath or left-sided chest pain should be assessed for other symptoms of CAD.
Assess the pain: location, character, intensity, radiation, timing, duration, etc. obtain hx of meds and family history of heart disease. assess for risk factors like HTN, diabetes, high blood cholesterol levels, smoking/alcohol use, high stress levels, menopause, hormone replacement therapy, or oral contraceptives.
Obtain VS and ECG tracing during chest pain within 10 minutes of report of the pain. Measure the effectiveness of the relief measures (oxygen, NTG, rest), obtain labs: cardiac enzyme levels, serum cholesterol and glucose, hemoglobin and hematocrit.

If the patient reports pain (or the person's prodromal symp- toms suggest anginal ischemia, which may include sensa- tions of indigestion or nausea, choking, heaviness, weakness or numbness in the upper extremities, dyspnea, or dizziness), the nurse takes immediate action. When a patient experiences angina, the patient is directed to stop all activ- ities and sit or rest in bed in a semi-Fowler's position to re- duce the oxygen requirements of the ischemic myocardium. The nurse assesses the patient's angina, asking questions to determine whether the angina is the same as the patient typically experiences. A change may indicate a worsening of the disease or a different cause. The nurse then continues to assess the patient, measuring vital signs and observing for signs of respiratory distress. If the patient is in the hospital, a 12-lead ECG is usually obtained and scrutinized for ST- segment and T-wave changes. If the patient has been placed on cardiac monitoring with continuous ST-segment monitoring, the ST segment is assessed for changes.
Nitroglycerin is administered sublingually, and the patient's response is assessed (relief of chest pain and effect on blood pressure and heart rate). If the chest pain is unchanged or is lessened but still present, nitroglycerin administration is repeated up to three doses. Each time blood pressure, heart rate, and the ST segment (if the patient is on a monitor with ST-segment monitoring capability) are as- sessed. The nurse administers oxygen therapy if the patient's respiratory rate is increased or if the oxygen saturation level is decreased. Oxygen is usually administered at 2 L/min by nasal cannula, even without evidence of respiratory distress, although there is no documentation of its effect on out- come. If the pain is significant and continues after these in- terventions, the patient is further evaluated for acute MI and may be transferred to a higher-acuity nursing unit.
The patient with suspected MI is given aspirin, nitroglycerin, morphine, an IV beta-blocker, and other medications as indicated while the diagnosis is being confirmed. Patients should continue the beta-blocker throughout hospitalization and after discharge because long-term therapy with beta- blockers can decrease the incidence of future cardiac events. Unfractionated heparin or an LMWH is prescribed along with platelet-inhibiting agents to prevent further clot formation. Nonsteroidal anti-inflammatory drugs (NSAIDS) may be discontinued because of their association with adverse cardiac event.

Beta Blockers - blocks beta-receptors in the heart causing decreased HR, decreased force of contraction, decreased rate of AV conduction.
S&S: bradycardia, lethargy, GI upset, CHF r/t AV block, hypotension, depression, bronchospasm
NI: assess for symptoms of heart failure,evalute BP and pulse for significant changes: hold if systolic BP is below 90mmHg, monitor pts with diabetes. 1st, 2nd, and 3rd generations of drugs.
ie Inderal, Tenormin, Bystolic, metroprolol

ACE Inhibitors - suppress formation of angiotensin II from the renin-angiotensin-aldosterone system, reduces peripheral resistance, and improves cardiac output.
S&S: HA, angioedema, postural hypotension, altered sense of taste, hyperkalemia, nonproductive cough
NI: monitor VS especially for two hours after first dose, administer on empty stomach
It is important to ensure that a patient is not hypotensive, hyponatremic, hypovolemic, or hyper- kalemic before administering ACE inhibitors. Blood pressure, urine output, and serum sodium, potassium, and creatinine levels need to be monitored closely.


antidysrhythmics meds


-angioplasty with STENT (In angioplasty, a balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. After angioplasty, the area that has been treated may close off partially or completely, a process called restenosis. The in- tima of the coronary artery has been injured and responds by initiating an acute inflammatory process. This process may include release of mediators that leads to vasoconstriction, clotting, and scar tissue formation. A coronary artery stent may be placed to overcome these risks.)

-intra-aortic balloon pump

-ventricular assistive device
Dysrhythmias - The major goals for the patient may include eradicating or decreasing the incidence of the dysrhythmia (by decreasing contributory factors) to maintain cardiac output, minimizing anxiety, and acquiring knowledge about the dysrhythmia and its treatment.

-Cardiogenic shock - o2 therapy, pain control, hemodynamic monitoring, lab marker monitoring (BNP, cardiac enzymes, ECG), fluid therapy (never IV bolus due to risk of acute pulmonary edema with pts with cardiac failure), med therapy:
Dobutamine enhances the strength of cardiac contraction, improving stroke vol- ume ejection and overall cardiac output.
Nitroglycerin IV nitroglycerin in low doses acts as a venous vasodilator and therefore reduces preload. At higher doses, nitroglycerin causes arterial vasodilation and therefore re- duces afterload as well. These actions, in combination with dobutamine, increase cardiac output while minimizing car- diac workload. In addition, vasodilation enhances blood flow to the myocardium, improving oxygen delivery to the weakened heart muscle.
Dopamine is a sympathomimetic agent that has varying vasoactive effects depending on the dosage. It may be used with dobutamine and nitroglycerin to improve tissue perfusion.
Additional vasoactive agents that may be used in managing cardiogenic shock include norepinephrine, epinephrine, milrinone, vasopressin, and phenylephrine. Each of these medications stimulates different receptors of the sympathetic nervous system. A combination of these medications may be prescribed, depending on the pa- tient's response to treatment. All vasoactive medications have adverse effects, making specific medications more useful than others at different stages of shock. Diuretics such as furosemide may be administered to reduce the workload of the heart by reducing fluid accumulation.
Antiarrhythmics - Multiple factors, such as hy- poxemia, electrolyte imbalances, and acid-base imbalances, contribute to serious cardiac dysrhythmias in all patients with shock.

Pericarditis - reduce activity, watch for signs of cardiac tamponade, analgesics, NSAIDS

Risk of extensions of an MI

Ventricular Aneurysms
mitral stenosis - Mitral stenosis is a heart valve disorder that involves the mitral valve. This valve separates the upper and lower chambers on the left side of the heart. Stenosis refers to a condition in which the valve does not open fully, restricting blood flow.

mitral regurgitation - Mitral regurgitation is a disorder in which the heart's mitral valve suddenly does not close properly, causing blood to flow backward (leak) into the upper heart chamber when the left lower heart chamber contracts.

mitral valve prolapse - Mitral valve prolapse (MVP) occurs when one of your heart's valves doesn't work properly. MVP is one of the more common heart valve conditions. Most often, it's a lifelong condition that a person is born with. Most people with MVP have no symptoms or problems, need no treatment, and are able to lead normal, active lives. Its incidence declines with age.

aortic stenosis - The aorta is the main artery carrying blood out of the heart. When blood leaves the heart, it flows through the aortic valve, into the aorta. In aortic stenosis, the aortic valve does not open fully. This decreases blood flow from the heart. As the aortic valve becomes more narrow, the pressure increases inside the left heart ventricle. This causes the left heart ventricle to become thicker, which decreases blood flow and can lead to chest pain. As the pressure continues to rise, blood may back up into the lungs, and you may feel short of breath. Severe forms of aortic stenosis prevent enough blood from reaching the brain and rest of the body. This can cause light-headedness and fainting.

aortic regurgitation - is a condition that occurs when your heart's aortic valve doesn't close tightly. Aortic valve regurgitation allows some of the blood that was just pumped out of your heart's main pumping chamber (left ventricle) to leak back into it.
The leakage of blood may prevent your heart from efficiently pumping blood out to the rest of your body. As a result, you may feel fatigued and short of breath.
Echocardiogram. This test uses sound waves to produce an image of your heart. In an echocardiogram, sound waves are directed at your heart from a wand-like device (transducer) held on your chest. The sound waves bounce off your heart and are reflected back through your chest wall and processed electronically to provide video images of your heart. An echocardiogram helps your doctor get a close look at your aortic valve. A specific type of echocardiogram, a Doppler echocardiogram, may be used. It allows measurements of the volume of blood flowing backward through an aortic valve. This volume is expressed in cubic centimeters per beat.

Chest X-ray. With an X-ray of your chest, your doctor can study the size and shape of your heart to determine whether your left ventricle is enlarged — a possible sign of damage to the aortic valve.
Electrocardiogram (ECG). In this test, patches with wires (electrodes) are attached to your skin to measure the electrical impulses given off by your heart. Impulses are recorded as waves displayed on a monitor or printed on paper. An ECG can provide clues about whether the left ventricle is enlarged, a problem which can occur with aortic valve regurgitation.

Transesophageal echocardiogram. This type of echocardiogram allows an even closer look at your aortic valve. The esophagus, the tube that runs from your throat to your stomach, lies close to your heart. In a traditional echocardiogram, a device called a transducer is moved across your chest to produce the sound waves necessary to create the image of your beating heart. In a transesophageal echocardiogram, a small transducer attached to the end of a tube is inserted down the esophagus. Because the esophagus lies close to your heart, having the transducer there provides a clearer picture of your aortic valve and blood flow through it.

Exercise tests. Different types of exercise tests help measure your tolerance for activity and check your heart's response to exertion (exercise).

Cardiac catheterization. Your doctor may order this procedure if noninvasive tests haven't provided enough information to firmly diagnosis the type or severity of your heart condition. Your doctor threads a thin tube (catheter) through a blood vessel in your arm or groin, into your heart. Dye is injected through the catheter into your heart, making details visible on an X-ray. Cardiac catheterization can show if blood is leaking back from the aorta into the heart's left ventricle. Some catheters with special sensors also can measure pressure within heart chambers, such as the left ventricle. Pressure may be increased in the left ventricle with aortic valve regurgitation.
Cardiomyopathy affects the structure and function of the heart muscle. Causes is often known, but can be related to chronic alcohol abuse, myocardial ischemia, or a viral infection.

Dilated cardiomyopathy - Microscopic examination of the muscle tissue shows dimin- ished contractile elements of the muscle fibers and diffuse necrosis of myocardial cells. The result is poor systolic function. These structural changes decrease the amount of blood ejected from the ventricle with systole, increasing the amount of blood remaining in the ventricle after contraction. Less blood is then able to enter the ventricle during diastole, increasing end-diastolic pressure and eventually increasing pulmonary pressures. Altered valve function can result from the enlarged stretched ventricle, usually resulting in regurgitation. Embolic events caused by ventricular and atrial thrombi as a result of the poor blood flow through the ventricle may also occur. Most people die within 2 years of symptoms but can last for years asymptomatically. Dysrhythmias

Hypertrophic cardiomyopathy - The increased thickness of the heart muscle reduces the size of the ventricular cavities and causes the ventricles to take a longer time to relax, making it more difficult for the ventricles to fill with blood during the first part of di- astole and making them more dependent on atrial contraction for filling. The increased septal size may misalign the papillary mus- cles so that the septum and mitral valve obstruct the flow of blood from the left ventricle into the aorta during ventricular contraction. Hence, HCM may be obstructive or nonobstructive. It is a hereditary disorder, and can be treated. Angina, dyspnea, syncope (loss of oxygen to the brain which causes brains). May be surgically treated by reseceting excess muscle away from aortic valve outflow tract.

Restrictive cardiomyopathy - Restrictive cardiomyopathy is characterized by diastolic dysfunction caused by rigid ventricular walls that impair ventric- ular stretch and diastolic filling. Systolic function is usually normal. It is a hereditary disorder (cannot be treated with a transplant because the body will do the same thing) Poor prognosis. Minimize heart failure, treat dysrhythmias, preventing cardiac death, physical activity restricted.

nursing goals for a client with cardiomyopathies ar to prevent complications, assist the client to conserve energy while encouraging self-care, and support coping skills.