Part 2: Diseases Flashcards
Coronary Atherosclerosis
Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium.
Cholesterol
HIGH is HAPPY!!
HDL is “good” cholesterol
Keep HDL above 60mg/dl
LOW is LOUSY!!
LDL is “bad” cholesterol
Keep LDL less than 100mg/dl
Total Cholesterol should be less than 200mg/dl
Angina Pectoris
Physical exertion or emotional stress increases myocardial oxygen demand and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand.
There is a deficit between supply and demand-therapy is geared towards correcting this imbalance
Angina pain varies from mild to severe
May be described as tightness, choking, or a heavy sensation “like an elephant sitting on my chest.”
Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left).
Anxiety frequently accompanies the pain.
Other symptoms may occur: dyspnea, dizziness, nausea, and vomiting.
The pain of stable angina subsides with rest or NTG.
Angina Treatment
Beta blockers: lower sympathetic response
Aspirin: clot busting
CCB: diltiazem/cardazem
Patient is to stop all activity and sit or rest in bed.
Assess the patient while performing other necessary interventions. Assessment includes VS, and observation for respiratory distress, and assessment of pain. In the hospital setting, the ECG is assessed or obtained.
Administer oxygen (remember that O2 is a drug and therefore, requires an order)
Angina Pharmacological Treatment cont.d
Nitrates (decrease preload and afterload)
Beta Blockers (negative inotrope, chronotrope and dromotrope—reduces myocardial O2 demands)
Antiplatelet (Aspirin most common)
Antilipemic (statin drugs, HMG inhibitors)
Assess BP/HR for beta blocker
Assess respiratory sounds: wheezing/asthmatic patients bronchospasm
Unstable Angina
Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention!
Myocardial Infarction
An area of the myocardium is permanently destroyed and becomes necrotic. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.
In unstable angina, the plaque ruptures but the artery is not completely occluded. Unstable angina and acute myocardial infarction are considered the same process but at different points on the continuum.
The term acute coronary syndrome (ACS) includes unstable angina and myocardial infarction.
MI Clinical Manifestations and Indications
Chest pain, central (retrosternal), crushing, feels like a band around the chest, often radiates down left arm, up to jaw. Nausea, vomiting Diaphoresis Pallor Feeling of impending doom ECG changes
Laboratory tests—biomarkers CK-MB Troponin T or I---Troponin is the most specific cardiac marker for INJURY. If MI is being ruled out, Cardiac Enzymes (CK, CK-MB, and Troponin) will be ordered Q6 hours x 3, then daily if necessary. Normal Troponin T < 0.1ng/ml Normal Troponin I < 0.4ng/ml
MI Clinical Manifestations and Indications cont.d
Women and diabetics have non-specific symptoms of MI and this often delays treatment:
Backache
Dyspepsia
Sleep disturbances
MAN Acronym
Everyone with chest pain gets a MAN!!!
Morphine
Aspirin
Nitroglycerin
Two types of MI
Injury/infarct may reduce pump function or changes in electrical conductivity in affected cells
Injured cells do not depolarize completely, remaining more positive than the uninjured cells in the surrounding area
This is seen as ST-Segment Elevation in the lead facing the area of injury. The leads facing away from the area of injury may show ST depression (reciprocal changes).
Two types of MI:
ST Elevation MI or STEMI
Non-ST Elevation MI or NSTEMI
STEMI vs. NSTEMI
STEMI worse than NSTEMI.
STEMI-coronary artery completely occluded, tissue dying quickly. Needs immediate intervention to prevent further loss of functional tissue.
NSTEMI-coronary artery partially occluded. Treatment determined by severity of symptoms. Often managed with medication but may require Percutaneous Coronary Intervention later.
Lead II, III, aVF
Inferior wall
Right coronary artery
Lead V1-V4
Anterior or Antero-Septal
Left Anterior Decending
Lead V5-6, I , aVL
Lateral wall
Left Circumflex
Lead V1-V2 ST depression
Posterior wall
Left circumflex or Right coronary artery
Complications of MI
Dysrhythmias: Most common complication
Most common cause of death in the pre-hospital period (usually V-Fib or V-Tach)
Life-threatening dysrhythmias seen most often with anterior MI (Left Anterior Descending artery known as the “widow maker”)
Bradycardias and heart blocks seen most often with Inferior wall MI
Heart failure
Occurs when the pumping power of the heart has diminished—dead tissue does not move
Thromboemboli
DVT, PE, Stroke
Complications of MI cont.d
Cardiogenic shock
Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure
The left ventricle is severely impaired and unable to pump effectively
Requires aggressive management or death will result.
Ventricular aneurysm
Results when the infarcted myocardial wall becomes thinned and bulges out during contraction (can rupture)
Myocardial rupture after transmural MI, usually occurs (24 hrs highest risk) 5-10 days post-MI.
Complications of MI cont.d 3rd
Papillary muscle dysfunction
Causes mitral valve regurgitation
Condition aggravates an already compromised LV
Acute pericarditis
An inflammation of visceral and/or parietal pericardium
May result in cardiac compression, ↓ LV filling and emptying, heart failure
Pericardial friction rub may be heard on auscultation
Chest pain different from MI pain
Sitting up feels better
NSAIDS/sterioids for pericarditis. High dose ibuprofen/steroids
Dressler syndrome
Characterized by pericarditis with effusion and fever that develop 4 to 6 weeks after MI
Pericardial (chest) pain
Pericardial friction rub may be heard on auscultation
Treatment of Acute MI
Obtain diagnostic tests including ECG within 10 minutes of admission to the ED
Morphine, Oxygen, Nitroglycerin, Aspirin (MONA)
Beta-blockers to reduce workload of heart
Angiotensin-converting enzyme inhibitor(ACEI) within 24 hours(slow heart rate, reduce workload)
Evaluate for Percutaneous Coronary Intervention (GOLD STANDARD). Not all hospitals equipped for this. Also should have cardiac surgery facility in case of arterial rupture.
Thrombolytic (Fibrinolytic) therapy (TPA , Retevase)
As indicated; IV heparin or LMWH, clopidogrel or ticlopidine
Bed rest
Thrombolytic Therapy aka Fibrinolytic Therapy for Acute MI
Treatment of MI with fibrinolytic agents is aimed at stopping the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium.
Best result when given within one hour of symptom onset. Can be given up to six hours after onset of symptoms. Not usually effective after this—the damage has been done.
REMEMBER—-MINUTES COST MUSCLE
Contraindications to Acute MI treatment
Active bleeding (not including menstruation)
Recent stroke (within 3 months)
Known cerebral neoplasm or AV malformation
Suspected aortic dissection
History of cerebral aneurysm
Significant closed head or facial fracture in last 3 months
Acute MI Nursing Considerations
Continuous ECG monitoring
Specialized setting preferred (CCU/ICU)
Place two or preferably three large-bore (18fr) peripheral IVs PRIOR to starting infusion of fibrinolytic drug.
Be careful when using an automatic BP cuff once infusion has started—nurses forget that they have set it to go off every 5 minutes and sometimes it pumps up too high—pt will end up with massive hematoma on arm.
Sometimes clot in coronary artery dissolves but the ruptured plaque is unstable and another clot forms—re-occlusion. HCP may order heparin drip to run concurrently to help prevent this.
Often see dysrhythmias as clot dissolves (reperfusion) and sometimes when it re-occludes.
If treatment successful-ischemic changes on ECG disappear, chest pain resolves, cardiac enzymes begin to fall.
Induced Hypothermia Treatment
Therapeutic hypothermia, which lowers the patient’s body temperature to levels between 32–34 °C (90–93°F), is used to help reduce the risk of ischemic injury to the brain following a period of insufficient blood flow.
Cold IV fluids given rapidly and hypothermia pads wrapped around patient.
Patient is intubated, sedated, and sometimes chemically paralyzed to prevent shivering.
Kept like this for 24-36 hours, then re-warmed SLOWLY.
Drugs do not work as effectively in a hypothermic patient (need more).
Electrolyte imbalances common, especially potassium.
Interventional Cardiology Treatments: Nursing Care Pre-procedure
NPO at least 4 hours if possible (patient may require emergency intervention if having MI)
Labs (check electrolytes, PT, PTT-INR, CBC)
12-lead ECG
CXR
Insert at least one PIV (20 fr or larger)
Hair at insertion site should be removed with clippers, not razor.
Patient education regarding procedure and after-care.
Warn patient that they will feel an uncomfortable “flush” when dye is injected.
Nursing Care Post PCI
Patient must stay flat with leg/arm straight to prevent bleeding or hematoma at insertion site.
For traditional femoral artery approach, maintain bedrest for at least 6 hours, sometimes up to 12 hours
Position is flat then HOB elevated after several hours to 30 degrees if femoral approach utilized
Check insertion site for bleeding or hematoma. May have “Femostop” or similar in situ
Keep affected extremity straight
CHECK PULSES!!!!!!!!
Nursing Care Post PCI cont.d
Fluids IV or po to flush contrast out (can be nephrotoxic). Patients with impaired renal function may need immediate dialysis.
Monitor urine output (male pts have difficulty urinating lying flat but they CANNOT sit up—teach them about this pre-procedure)
Frequent vital signs per protocol
Continuous EKG monitoring
Post-op care for open heart patient
Usually intubated for first few hours.
Will have between 1 and 4 chest tubes, at least one will be mediastinal
Epicardial pacing wires in case of dysrhythmias
*May require combination of vasoactive drips to stabilize condition (Dopamine, Primacor, Levophed, NTG)
Specialized monitoring lines—PA catheter, arterial line
Pulmonary Artery catheters
PA catheter also gives us a continuous cardiac output reading. Very useful when titrating inotropic drips in patients with compromised cardiac function.
Also measures pressures in the right atrium (CVP, or preload) and pulmonary artery.
Calculates other values such as Systemic Vascular Resistance (SVR). The SVR is the patient’s AFTERLOAD. Normal SVR is approx. 900-1300.
PA Catheters cont.d
PA pressures are expressed as a systolic and diastolic, just like systemic BP. Normal PAS is between 20-30mmHg, normal PAD is between 8-15mmHg.
PAWP between 8-12mmHg.
Right atrial pressure (or CVP) is between 0-8mmHg.
Cardiac output 4-8 liters/min
Cardiac index takes patient’s BSA into account. More accurate than cardiac output. Normal cardiac index is between 2.5-4 liters/min/m2
HF Management
Decreased Intravascular volume (Diuretics, fluid restriction: 1000 mL or 1500 mL, depending on renal function)
Decreased Venous return-preload (vasodilators, nitrates)
Decreased Afterload (normotension, vasodilators)
Increased Gas exchange
Increased Cardiac function (positive inotropes-e.g Digoxin, assess apical pulse, potassium levels)
