FINAL EXAM Heart Flashcards
ANGINA
Angina is chest pain or discomfort caused when your heart muscle doesn’t get enough oxygen-rich blood.
It may feel like pressure or squeezing in your chest. The discomfort also can occur in your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion.
CAUSES:
- Insufficient blood flow is caused by narrowing of the coronary arteries by atherosclerosis.
- Angina is a result of ischemia caused by reversible cell injury
MANIFESTATIONS:
- Chest pain or discomfort.
- Constrictive feeling, squeezing, choking, heavy, or suffocating sensation, not sharp.
- Pain does not change with position or breathing.
- Associated symptoms may include shortness of breath, sweating, weakness, numbness and tingling in one or both arms.
- occurs infrequently
- same pattern of onset, duration, and intensity.
- Usually lasts for 3-5 minutes
- lack of oxygen supply is temporary and reversible.
- Subsides when precipitating factor is relieved. (usually exertion)
- ECG usually shows ST-segment depression indicating subendocardial ischemia.
- Stable angina pain can be controlled with medications
*
ANGINA
MEDICAL MANAGEMENT
- Cardiac monitoring
- Cardiac serum enzymes
- Oxygen
- Nitrates, Morphine for pain
- Aspirin, Plavix
- Beta blockers, Calcium channel blockers
- Lipid lowering drugs: (statins)
- Management of risk factors for CAD
- Percutaneous Coronary Intervention/ possible stent placement
- Coronary Artery Bypass Grafting
ANGINA
NURSING MANAGEMENT
- Assessment of precipitating factors and changes in patterns
- Monitor VS carefully including pain.
- Monitor cardiac telemetry for changes or ischemic patterns
- Provide calm, quiet, environment.
- Provide medications as ordered
MYOCARDIAL INFARCTION
Coronary artery occlusion with myocardial death and necrosis.
Myocytes becomes cyanotic within the first 10 seconds of coronary occlusion. ECG changes (S-T elevation) appear.
With total occlusion, contractility stops after a few minutes.
Myocardial cells are deprived of glucose needed for aerobic metabolism. Anaerobic metabolism begins and lactic acid accumulates.
CLINICAL MANIFESTAIONS:
- Coronary artery occlusion with myocardial death and necrosis.
- Myocytes becomes cyanotic within the first 10 seconds of coronary occlusion. ECG changes (S-T elevation) appear.
- With total occlusion, contractility stops after a few minutes.
- Myocardial cells are deprived of glucose needed for aerobic metabolism. Anaerobic metabolism begins and lactic acid accumulates.
- Patient’s skin may be ashen, clammy, with “cold sweat” due to increased catecholamine release of NE and Epi. Increased SNS stimulation results in diaphoresis and peripheral vasoconstriction.
Fever due to inflammatory response from myocardial necrosis.
Pharmacologic management:
Angina/MI
- Nitrates- Intravenous Nitroglycerin
- Narcotics- Morphine usually IV push
- Beta adrenergic blockers- Metoprolol
- Calcium channel blockers- Amlodipine
- Antiplatelet drugs: Plavix
- Aspirin- 325 mg non-coated
- Oxygen by nasal cannula or face mask to keep SpO2> 90%
ER Management/Diagnosis of an Acute MI
- Oxygen therapy: keep 02 sat > 95%.
- Aspirin: 325 mg chewable
- Metoprolol: 5 mg IV push
- Morphine: 2-10 mg IV push
- Nitroglycerin IV titrate to pain and BP
- 12 lead ECG: monitor for S-T elevation, depression.
- Cardiac enzymes- CPK-MB, LDH, Troponin T/I,
- electrolytes, CBC. Transfer to Cath Lab.
Management of Patients Acute MI
Patient’s with an acute Myocardial infarct will either go to the Cardiac catheterization lab for reperfusion of blocked coronaries
OR
Receive intravenous fibrinolytic therapy (Streptokinase, Urokinase) to dissolve the clot.
Current standard of care is to reperfuse heart via Percutaneous Coronary Intervention or PCI with/without stents.
Current standard of care for a patient having an MI
reperfuse heart via Percutaneous Coronary Intervention or PCI with/without stents
HEART FAILURE
HF is not a disease, but an abnormal condition that involves impaired cardiac pumping.
Associated with different forms of heart disease.
Most commonly a result of long term hypertension and coronary artery disease.
CHARACTERIZED BY:
- Ventricular dysfunction
- Markedly reduced activity/exercise tolerance
- Diminished quality of life
- Shortened life expectancy
Compensated vs. Decompensated Heart Failure
Compensated heart failure- when compensatory mechanisms are successful at maintaining cardiac output, meeting metabolic demands and maintaining adequate tissue perfusion.
Decompensated heart failure- when compensatory mechanisms fail to maintain cardiac output, do not meet metabolic demands, and can’t maintain adequate tissue perfusion.
Pharmacology for Chronic HF
GOAL- improve symptoms and quality of life, prevent morbidity, prolong survival.
MEDICAL MANAGEMENT:
- ACE inhibitors-1st line therapy in all stages of HF for both systolic and diastolic HF.
- Diuretics- Lasix, HCTZ
- Inotropes- Digoxin
- B-Adrenergic Blockers- Metoprolol
- Calcium channel Blockers- Amlodipine
- Vasodilators- Imdur
- Antiarrhythmics- Amiodarone
- Blood thinners, platelet inhibitors- ASA, Plavix,
- Nitrates/ vasodilators
ACUTE HEART FAILURE:
Clinical Manifestations
- Heart Failure that occurs acutely- no matter what the etiology- presents as PULMONARY EDEMA.
- This is LIFE THREATENING!!!
- The alveoli become filled with serosanguinous fluid.
- Most common cause is acute left ventricular failure secondary to CAD or acute MI.
PULMONARY EDEMA:
- Abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs
- A life threatening medical emergency
- A complication of various heart and lung diseases
- Common causes- HF, over hydration with IVF, hypoalbuminemia secondary to nephrotic syndrome, hepatic disease, nutritional disorders, severe hypoxia, acute resp distress syndrome, O2 toxicity,etc.
Cardiac Markers (labs) for a patient having an MI
Cardiac markers: Proteins are released into blood in large quantities from necrotic heart muscle.
- Myoglobin
- CK(creatine kinase) – MB-bands
- Troponin T-myocardial muscle protein
- Troponin I-myocardial muscle protein
Normal Heart Rhythms
- There is a P-wave in front of every QRS.
- Distance between P wave and QRS complex is the same in each complex.
- Distance between R-R waves is the same.
- Rate is between 60-100 beats per minute.
- Rate increases as metabolic demand increases with activity- ex: exercise
Atrial Fibrillation
Atrial Fibrillation (AF): most common arrhythmia and a significant public health problem in the U.S.
ATRIAL FIBRILLATION: no visible P-waves, irregular R-R intervals, irregular ventricular rate.
Ventricular rate is 110-180 beats per minute.
Cardiac output is decreased as ventricular rate increases.
With quivering atria, atrial systole is incomplete.
- Right and left Atria fibrillate or quiver in chaotic and disorganized firing of many cells.
- Abnormal arrhythmia- not life threatening but can make patient feel very tired, SOB, fatigued.
- All impulses do not conduct to the ventricles- they are stopped at the AV node (gatekeeper). Atrial rate is 400-600 beats per minute.
- Patients may experience a variety of clinical manifestations, including embolism and/or stroke and a 1.5- to 1.9-fold higher risk of death.
Both classic anticoagulants: Heparin (IV), and Coumadin (po) and newer anticoagulants (Pradaxa) (Enoxaparin) can decrease the risk/incidence of strokes.
It is critical to diagnose and treat AF to prevent serious and potentially life-threatening thromboembolic complications.
Ventricular Tachycardia
- Ventricular tachycardia (VT) is a rapid, regular heartbeat originating from a site in one of the ventricles (note wide QRS).
- Frequently, the site is an area of scar tissue caused by damage from a heart attack.
- VT significantly impairs the heart’s ability to pump blood.
- May degenerate to ventricular fib.
- During VT, heart rate is much faster than usual, ranging from 100 to 280 bpm. Minimal cardiac output!!
- VT may cause symptoms: palpitations, chest tightness, dizziness, shortness of breath, and/or loss of consciousness.
- When a patient loses consciousness it is a life-threatening emergency and requires immediate cardioversion/defibrillation.
Ventricular Fibrillation:
CODE BLUE
Ventricular fibrillation: Chaotic quivering of the ventricles. Patient has no blood pressure or respirations or heart rate.
- Heart is unable to pump blood throughout the body. Cardio-pulmonary arrest!!
- Heart can’t deliver blood to the lungs, brain, and other vital organs. No perfusion anywhere.
- For the patient to be saved without brain damage, circulation must usually be restored to the vital organs within 6 minutes.
