Complications for Acute MI Flashcards
Electrical or mechanical (relate to dysfunction of heart muscle)
2 broad categories
Relate to electrical system of the heart and initially present as a dysrhythmia
Depend on electrical system deprived of O2 or compensatory mechanism
The type of electrical complication depends on the location of the myocardial infarction (MI).
Atrial dysrhythmias
Atrioventricular (AV) heart block
Ventricular dysrhythmias
Electrical complications of MI
Sinus Bradycardia (HR <60 beats/min)
Sinus Tachycardia (HR >100 beats/min)
The type of electrical complication depends on the location of the myocardial infarction (MI).
Seen early
48 hours after right coronary artery - RCA supplies blood to SA and AV node
Considered comp if symptomatic
Usually occurs early
Inferior wall MI (Right coronary artery)
If symptomatic: Atropine
0.5 to 1.0 mg by intravenous push, repeated every 3 to 5 minutes to a maximum dose of 0.03 mg/kg
Sinus Bradycardia (HR <60 beats/min)
Seen early with LCA MI that supplies blood to LV
Gen compensatory mechanism to maintain CO and compensatory mechanism increases myocardium oxygen demand causing greater ischemic or infarcted area - measures need to be implemented to decrease myocardial O2 consumption
Anterior wall MI (Left coronary artery)
Treat the underlying cause to decrease myocardial oxygen consumption.
Sinus Tachycardia (HR >100 beats/min)
Premature atrial contractions (PAC’s)
Atrial fibrillation
Atrial dysrhythmias
Benign of themself
Frequent PAC’s go into Afib
Premature atrial contractions (PAC’s)
Can decrease cardiac output up to 20%
Develop this after MI greater risk for adverse events - developing pulmonary edema or shock or bleeding or stroke - atria fibrillating - fills with clots rather than pumping blood through and pts can have a stroke
Goal of Treatment is rhythm & rate control
Atrial fibrillation
Usually occurs during an MI
Seen in Inferior wall MI’s - right coronary artery supplies blood to AV node
Developing AV block during or after MI associated with greater mortality rate
Treatment for symptomatic AV blocks: transcutaneous or transvenous pacemaker.
Atrioventricular (AV) heart block
Electrical impulse starts in ventricle
Premature ventricular contractions (PVC’s)
Ventricular fibrillation
Mediations: beta blockers
Ventricular dysrhythmias
Can occur anytime. Most like to occur within the first 24 hours of having a MI
After cardiac cath lab and stent placement, on tele unit to monitor HR and rhythm to watch for this
When LV deprived of O2, irritable - looks like PVCs
Can look diff
2 diff forms
Ectopic beat started in diff part of ventricle
To many of them then all of sudden see couplets then three or four then vfib
Rate controlled with beta blockers
Treatment: Pharmacologically treated if PVC’s are:
More than 6 per minute, Closely coupled, Multiform shapes, Occur in bursts or three or more.
Frequent PVC’s increases the risk of sustained ventricular tachycardia
Treatment: O2 to reduce myocardial hypoxia, correct acid base imbalance, correct electrolyte imbalance.
Premature ventricular contractions (PVC’s)
Ventricular aneurysm
Ventricular septal rupture
Mitral papillary muscle rupture
Cardiac wall rupture
Pericarditis
Acute HF
Mechanical complications of MI
Not seen as often
Pts to hospital faster
LV aneyrism - secondary to big anterior wall MI
Later complication - days/weeks after MI - As body WBC go in to clean up infarcted tissue, weakens that area; LV high pressure side of heart and weakened area thins out and becomes aneurysmol - does not contract
A non-contractile, thinned LV wall that results from an acute transmural infarction.
Most commonly seen with left anterior descending artery (LAD).
Usually a late complication.
Prevention
Early reperfusion
Complications
Symptoms – correlate with the complication
Ventricular aneurysm
Acute heart failure
Have HF sx
Systemic emboli
Outpouching - area not pump; blood stagnats and coags; high risk for systemic emboli and stroke
Angina
Aneurysmol segment not beat - affects CO causing angina and ventricular dysrhythmias - VT
VT
Complications - Ventricular aneurysm
An abnormal communication between the right & left ventricle. - result of having ventricular septal wall MI
Rare complication of ventricular septal wall MI
Usually a late complication - days/weeks after MI - As body WBC go in to clean up infarcted tissue, weakens that area; LV high pressure side of heart and weakened area thins out and becomes aneurysmol - does not contract
Prevention
Early reperfusion
Complications/Symptoms
Treatment
Ventricular septal rupture
Sudden severe sx - go from fine to not fine
Severe chest pain
Crushing chest pain suddenly
Syncope
Fine to passing out; no warning
Hypotension
Sudden hemodynamic deterioration
Hemodynamically unstable
New communication between RV and LV = shunt; everytime LV pumping - pumping blood out to systemic vasculature and into RV - suddenly decreased CO
New holosystolic murmur at the left sternal boarder
Because of new communication
Complications/Symptoms - Ventricular septal rupture
Decrease afterload
New shunt have to make it easier for LV to make it easier to get the blood out
IABP
Nitroprusside given - decrease SVR; have to get interventional cardiology and get intraaortic balloon pump or impella device to decrease the afterload
Vasodilators
Does cause hypotension
Every time LV - least amount resistance to get blood out into systemic sys
Surgery
Only way fix this; open heart surgery
Have surgeon fix abnormal communication
Treatment - Ventricular septal rupture
Result of MI in area of heart where mitral valve leaflets anchored into the myocardium
Results in one or all leaflets not functioning properly - not synchronous; flapping in the wind; not doing anything
The valve does not fully close.
One or all mitral valve leaflets can be involved.
Complications/Symptoms
Treatment
Mitral papillary muscle rupture
Everytime LV beats - blood ejected through aortic valve into systemic circ and back through mitral valve - causes sudden onset of severe HF sx
Sx
Cardiogenic shock
Mitral valve regurgitation
Heart failure - Mitral papillary muscle rupture
LV
Tachypnea
Tachycardia
Cough
Bibasilar crackles
Gallop rhythms (S3 and S4)
Increased PA pressure
Hemoptysis
Cyanosis
Pulmonary edema
Fatigue
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Nocturia
RV
Peripheral edema
Hepatomegaly
Splenomegaly
Hepatojugular reflex
Ascites
JVD
Increased central venous pressure
Pulmonary HTN
Weakness
Anorexia
Indigestion
Weight gain
Mental changes
Sx
Rapidly fine to symptomatic cardiogenic shock
Cardiogenic shock
Everytime blood pumps, have regurgitation
New murmur: High-pitched, holosystolic, blowing murmur at the cardiac apex heralds mitral valve regurgitation resulting from papillary muscle dysfunction.
Mitral valve regurgitation
Vasodilators
IABP
Definitive treatment: surgery to fix the valve
Treatment - Mitral papillary muscle rupture
Decrease SVR - more blood ejected into systemic vasculature - goal perfusing organs/end organ perfusion
Vasodilators
Interventional cardiology - intraaortic balloon pump/impella device
IABP
Occurs later
Usually a late complication - days/weeks after MI - As body WBC go in to clean up infarcted tissue, weakens that area; LV high pressure side of heart and weakened area thins out and becomes aneurysmol - does not contract
Occurs either within the first 24 hours or at 3 to 5 days.
Sudden onset
Complications/Symptoms:
Cardiac wall rupture
Sx sudden and severe
Cardiac tamponade
Cardiogenic shock
PEA - pulseless electrical activity - nothing wrong with electrical activity at first; all mechanical; LV cannot expand to pump blood out; blood in pericardial sac - preventing it from expanding
True emergency and most pts not make to treatment
Death - imminent within mins
Blood ejected from LV into pericardial sac with each pump - each pump - squishing LV so no longer expand to fill with blood to eject into systemic vasculature causing CO of 0 - not pumping blood out into systemic sys (brain and other end organs) - death
Complications/Symptoms: - Cardiac wall rupture
Inflammation of the pericardial sac - surrounds the heart
Occurs during or after acute MI - can last days to weeks
Caused by MI - result of inflamed myocardium irritating pericardial sac
Treatment
Complications/Symptoms
Pericarditis
Nonsteroidal anti-inflammatory drugs
Aspirin
Rest
Treatment - Pericarditis
Most common
Chest pain - Pain
Pericardial friction rub - new
Auscultated at the sternal border
Grating, scraping, or leathery scratching
Progress to Pericardial effusion - irritation and whole inflammation process causes more albumin type fluid to collect around the heart
On a 12-lead ECG, global ST elevation - may affect global conduct of heart and show as global ST elevation on 12-lead
Complications/Symptoms - Pericarditis
One comps of acute MI
s&s
Treatment
Nursing interventions
Initial Signs & symptoms
Acute HF
LV
Tachypnea
Tachycardia
Cough
Bibasilar crackles
Gallop rhythms (S3 and S4)
Increased PA pressure
Hemoptysis
Cyanosis
Pulmonary edema
Fatigue
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Nocturia
RV
Peripheral edema
Hepatomegaly
Splenomegaly
Hepatojugular reflex
Ascites
JVD
Increased central venous pressure
Pulmonary HTN
Weakness
Anorexia
Indigestion
Weight gain
Mental changes
s&s - Acute HF
Relief of Symptoms and Enhancement of Cardiac Performance
Correction of Precipitating Causes
Palliative Care for End-Stage Heart Failure
Treatment - Acute HF
In the acute phase of advanced heart failure, the patient may have a pulmonary artery catheter in place so that left ventricular function can be monitored closely.
Control of symptoms involves management of fluid overload and improvement of cardiac output by decreasing SVR and increasing contractility.
Contractility is initially increased by continuous infusion of positive inotropic medications (dopamine) or by combination inodilators such as dobutamine or milrinone, which have both inotropic and vasodilatory effects.
After the acute exacerbation is resolved, the patient is transitioned to oral agents and weaned off the intravenous medications.
Relief of Symptoms and Enhancement of Cardiac Performance
After symptoms of heart failure are controlled, diagnostic studies such as cardiac catheterization, echocardiography, and diagnostic imaging tests to determine myocardial perfusion are undertaken to uncover the cause of the heart failure and tailor long-term management to treat the cause.
Correction of Precipitating Causes
Heart failure is a progressive disease, and patients do not recover.
The primary aim of palliative care is symptom management and relief of suffering. Fundamental to all symptom management strategies for heart failure is the optimization of medications according to current guidelines. The most common symptoms of advanced heart failure are dyspnea, pain, and fatigue.
Palliative Care for End-Stage Heart Failure
Optimizing Cardiopulmonary Function
Promoting Comfort and Emotional Support
Monitoring Effects of Pharmacologic Therapy
Nutritional Intake
Educate the Patient and Family
Nursing interventions - Acute HF
The patient’s ECG is evaluated for dysrhythmias that may be present as a result of medication toxicity or electrolyte imbalance.
Oxygen is administered through a nasal cannula to relieve dyspnea.
Diuretics or vasodilators are used to decrease excessive preload and afterload.
Generally, the daily weight is used in fluid management, and a weekly weight is optimally used for tracking body weight
Optimizing Cardiopulmonary Function
Activity must be restricted during periods of breathlessness.
Frequent position changes and mobilization can help provide comfort and prevent this complication.
Promoting Comfort and Emotional Support
Patients experiencing acute heart failure require aggressive pharmacologic therapy.
The patient’s hemodynamic response to these agents is closely monitored. Fluid intake and output balances are tabulated daily or hourly in the critical care unit.
Monitoring Effects of Pharmacologic Therapy
Patients experiencing heart failure often have decreased appetite and nausea, so small, frequent meals may be more appropriate than the standard three large meals.
Not all patients with heart failure have the same nutritional needs.
Nutritional Intake
The nurse assesses the patient’s and family’s understanding of the pathophysiology and individual risk factor profile for heart failure. Primary topics of education include (1) the importance of a daily weight, (2) fluid restrictions, (3) written information about the multiple medications used to control the symptoms of heart failure, (4) physical activity, and (5) when to call a health care provider
Achieving the optimal outcomes for a patient with heart failure requires contributions from a team of educated health care clinicians
Educate the Patient and Family
↓ exercise tolerance
Fluid overload– most reliable clinical sign: jugular venous distention (JVD)
Initial Signs & symptoms - Acute HF
Two broad categories: Balance myocardial oxygen supply and demand and prevent comps
Balance myocardial oxygen supply and demand
Prevent complications
Complication of MI - nursing management
If pt has↓ Cardiac Output
Coronary artery vasodilators
Early β blockers (in the absence of cardiogenic shock)
Limit activity
Balance myocardial oxygen supply and demand
admin meds to increase cardiac contractility
Increase cardiac contractility
If pt has↓ Cardiac Output - Balance myocardial oxygen supply and demand
Positive inotropic medications
Phosphodiestrase inhibitor
Increase cardiac contractility
Dobutamine
Dopamine
Optimizes contractility
The nurse considers the effect of these pharmacologic agents on contractility when following the trend of the patient’s hemodynamic profile. No single hemodynamic number reflects contractility. However, if LV contractility is increased in response to treatment, this effect is frequently reflected by changes in PAOP (wedge pressure) and by an increase in CO.
Positive inotropic medications
Milrinone
Optimizes contractility
The nurse considers the effect of these pharmacologic agents on contractility when following the trend of the patient’s hemodynamic profile. No single hemodynamic number reflects contractility. However, if LV contractility is increased in response to treatment, this effect is frequently reflected by changes in PAOP (wedge pressure) and by an increase in CO.
Phosphodiestrase inhibitor
When the SVR is elevated
Nitroglycerin
Promotes O2 supply to myocardium
Coronary artery vasodilators - Balance myocardial oxygen supply and demand
Make LV slow down
Decreasing O2 demand of heart
Early β blockers (in the absence of cardiogenic shock) - Balance myocardial oxygen supply and demand
Recovering from acute MI, esp first couple days, decrease activity; most O2 supply going to heart to help fix/recover that ischemic rather than infarcted
Limit activity - Balance myocardial oxygen supply and demand
Cardiac Monitoring
Assess for s/s continued ischemic pain
Diet
DVT suppression
Avoid increasing intraabdominal pressure (Valsalva maneuver)
Risk factor reduction
Prevent complications - Complication of MI - nursing management
24-72 hours
Highest risk in first 24 hours for ventricular dysrhythmias - PVCs and vtach
Cardiac Monitoring - Prevent complications
Pain free or still having issues
Assess for s/s continued ischemic pain - Prevent complications
Low fat and low sodium
Diet - Prevent complications
Encouraging more rest
Leg squeezers
DVT suppression - Prevent complications
Colace to prevent increase - bowel movement - vagal self out - bearing down
Avoid increasing intraabdominal pressure (Valsalva maneuver) - Prevent complications
Educate on this
Risk factor reduction - Prevent complications
Yes - s&s of HF; see baseline or new - complication of MI
The nurse is assessing a patient who is recovering from a myocardial infarction. The patient states he feels exhausted and feels short of air.
Should the nurse be concerned?
Check pulses - weak
Looking at comps - lower CO and classic s&s of CHF
Skin - concerning - s&s of increased SVR - arteries constricting to get BP up
Pulmonary - lower CO/CHF sx - blood backing up to lungs with left sided HF sx
General - HF sx
VS - BP low, HR low, RR high, Sats on low side of normal - classic s&s of HF
All of it - whole assessment
The nurse decides the symptoms are concerning. He completes a focused assessment & obtains a set of vital signs.
Which assessment finding are concerning?
Recovering from MI - can have arrhythmias - afib - can irregular HR and lower BP
Could have frequent PVCs - early heartbeat not perfusing as well
Get 12-lead EKG - see what irregular arrhythmia present
What could be causing the irregular heart rate?
Balance myocardial-oxygen supply and demand; see what causing sx; acute sx; figure out why have profound, new HF sx
Priority: relax, lay down, give O2 - bump O2 sat up
Check BP - see if need increase that somehow
What is the priority intervention?
The heart needs time to recover from an acute MI even if the coronary artery is opened.
Patients who survive an acute coronary syndrome are at risk for many complications. Know the causes, signs and symptoms, assessment, medical and nursing management of the following.
s&s different for each of them - what makes each dysfunc unique
Complications from electrical dysfunction
Complications from mechanical dysfunction (pump)
Summary
The areas of the heart that were ischemic can cause reperfusion arrhythmias.
The areas of the heart that are infarcted are not contracting.
The areas of the heart that are ischemic are not contracting as well as normally perfused cardiac tissue.
The heart needs time to recover from an acute MI even if the coronary artery is opened.
Bradycardia/tachycardia
Heart blocks
Ventricular dysrhythmias: PAC’s, PVC’s
Complications from electrical dysfunction
Heart failure
Pulmonary edema
Cardiogenic shock
Pericarditis
New murmur
Ventricular septal rupture
Papillary muscle rupture
Complications from mechanical dysfunction (pump)
Know have CO issue - acute CHF sx - BP low so output low
Murmur is new = not good sign
pale/ashen and diaphoretic - low CO - skin not perfused; need adequate CO to have normal for ethnicity skin tone
Ventricular septal rupture
Sats low because blood from RV and LV as output - venous with arterial
HR high to try compensate; RR high - try compensate - get more O2; BP low - have bidirectional flow through septal defect and into vasculature
The nurse is going over dismissal instructions with a patient who is 11 days post massive anterior wall MI. The patient is getting dressed and suddenly develops 10/10 chest pain and passes out. A rapid response is called. Immediately start assessing
BP low, HR high, RR high, SpO2 low
Bad assessment
Which complication does this patient have?
Decrease afterload - very short term - vasodilators
Cardiac cath lab - IABP, impella
Surgery ASAP
How is this complication treated?
