Complications of MI Flashcards
What is the list of the most important complications of MI (9)?
- Cardiogenic Shock
- Severe Heart Failure
- RV Infarction
- Mechanical Complications
- MR, Ventricular septal rupture, LV free-wall rupture, LV aneurysm
- Electrical complications
- ventricular arrhythmias, AF, SFTs, Bradycardia, AV Block, interventricular conduction defects
- Pericarditis
- Thromboembolic adn bleeding complications
- Acute Kidney Injury
- Hyperglycemia
What is one of the most common chronic complications from a MI?
Heart Failure with reduced ejection fraction
What are the three reasons for recurrent ischemia and infarction?
What procedure has reduced incidence of this?
- Occlusion of an initially patent vessel
- Reocclusion of an initially recanalized vessel
- Coronary Spasm
Reduced incidence: PTCA (percutaneous transluminal coronary angioplasty)
What complication is the single most important predictor of mortality after a MI?
Left Ventricular Failure
Left Ventricular Failure is characterized by what factors?
What are predictors for the development of symptomatic LV failure?
What is the management strategy?
- LV Failure: Congestive Heart Failure
- systolic dysfunction alone or both systolic & diastolic dysfunction
- hypoxemia (pulmonary vasculature engorgement)
- increased clinical manifestations as the extent of the injury to the LV increases
- systolic dysfunction alone or both systolic & diastolic dysfunction
- Predictors: advanced age & diabetes
- Managed: reduction of ventricular preload (B-blockers) & if possible lowering afterload (ACE-inhibitors)
What drugs are used to treat Left Ventricular Failure?
Describe the physiologic reasoning for each type of drug.
- Treatment
- diuretics
- b/c retaining fluid due to HF – trying to get them to euvolemia
- nitroglycerin
- for pain & decrease afterload
- vasodilators
- decrease afterload
- digitalis
- increase contraction strength
- beta-adrenoceptor agonists
- positive inotropic agents
- other positive inotropic agents
- diuretics
Describe cycle that can occur w/ acute severe heart failure
- Myocardial dysfunction bc heart just took a hit
-
causes pulmonary congestion hypoxemia
- worsens ischemia
-
CO & SV are decreased
- hypotension
- decreases coronary perfusion pressure
- worsens ischemia
- decreases coronary perfusion pressure
- decrease systemic perfusion
- compensatory vasoconstriction; fluid retention
- hypotension
-
causes pulmonary congestion hypoxemia
- All of the above lead to progressive myocardial dysfunction & death
What is the most severe clinical expression of left ventricular heart failure?
cardiogenic shock
Cardiogenic shock is characterized by what features?
- elevated ventricular filling pressures
- low cardiac output
- systemic hypotension (systolic less than 90mmHg)
- evidence of organ hypoperfusion (cool & clammy hands)
- hemodynamic criteria (cardiac index <2.2)
- severly elevated lactate levels (>4)
At autopsy, 2/3 of patients with cardiogenic shock demonstrat what common factors?
- stenosis of 75% or more of lumina diameter of all 3 major coronary vessels
- loss of 40% left ventricular mass
What symptoms suggest Right Heart Failure?
What symptoms suggest Left Heart Failure?
What symptoms are shared by both types of heart failure?
- Right Heart Failure
- lower limb edema
- sacral edema
- hepatomegaly
- increased jugular venous distention
- regurgitant murmur in the tricuspid area
- Left Heart Failure
- Lung crackles
- Respiratory wheeze
- Displaced cardiac apex
- Left-sided murmurs
- Both
- Cool peripheries
- Cyanosis
- Orthopnea
- Delayed capillary refill
What is a major concern with developing cardiogenic shock
Can easly go into caridac arrest
Once a patient in cardiac arrest is taken to a cardiac shock center, what treatments/assessments occur?
- Intra-aortic balloon pump
- similar to impella/tandem heart
- Right heart cath to evaluate shock indices
- if bi-ventricular failure or refractory hypoxemia, start veno-arterial extracorporeal membrane oxygenation
What are the shock indices?
- Cardiac index <2.2
- increased pulmonary capillary wedge pressure
- increased left ventricular end diastolic pressure
- cardiac power output <0.6 watts
- calculated pulmonary artery pulsatility index <0.9
What is the medical management techniques for cardiogenic shock?
- Same as for LV failure
- reduction of ventricular preload (B-blockers) & if possible lowering afterload (ACE-inhibitors)
- Intraaortic balloon counterpulsation
- to decrease afterload
- pump in descending aorta that stops right before renal arteries- at every diastole, the pump will rapidly pump up, which stops back flow of blood & pumps a little of the blood inferiorly to the systemic system
- revascularization
Interventricular Septal Rupture is characterized by features?
Best treatment?
- new, harsh, loud holosystolic murmur
- heard at the lower left sternal border
- usually accompanied by a thrill
- can be recognized by 2-D echocardiography
- surgical intervention still best results
What are the clinical features that are associated with risk of interventricular septal rupture?
- Lack of development of collateral network
- advanced age
- hypertension
- anterior locatin of infarction
- thrombolysis
Patients with interventricular septal rupture is highly correlated with what additional post-MI complication?
higher 30-day mortality (74%) compared to patients who did not develop this complication (7%)
Interventricular Septal Rupture develops most often in patients with what anatomical feature?
lack collateral network
The size of the interventricular septal rupture determines what 3 variables?
- The magnitude of the left-to-right shunt
- extent of hemodynamic deterioation
- likelihood of survival
Interventricular septal rupture is associated with what situations other than MI?
- complete heart block
- right bundle branch block
- atrial fibrillation
What features characterize a free wall rupture?
- elderly
- Hypertension
- more frequently occurs in left ventricle
- seldom occurs in the atria
- usually involves the anterior or lateral walls
- usually associated with a relatively large transmural infarction involving at least 20% LV
- between 1 day & 3 weeks – usually 1-4 days
- most often in patients without a previous MI
A free wall rupture can lead to what additional complications?
- hemopericardium & death from cardiac tamponade (cardiac sac fills up w/ fluid and compresses the RV/RA & decrease blood that is able to return to the heart, decreasing preload, eventually leading to arrest)
- occasionally, the first clinical manifestation of patients with undetected or silent MI & considered a form of “sudden cardiac death”
What are the possible outcomes from free wall rupture & survival depends on what factor?
- Outcome
- Catastrophic- acute tear leading to immediate death
- subacute- with nausea, hypotension & pericardial discomfort
- Survival
- depends on recognition of the complication, hemodynamic stabilization, & prompt surgical repair
What is a pseudoaneurysm and how is it diagnosed?
- Incomplete rupture of the heart w/ organizing hematoma
- w/ pericardium- seal a rupture of the LV
- with time, this area can become a pseudoaneurysm that maintains communication with the cavity of the LV
- high risk of complete rupture
- Can become as large as the tru LV cavity & communicate via narrow neck
- Diagnosis: 2-D echocardiography & contrast angiography
What causes acute mitral regurgitation & and what levels can it present?
- Due to partial or total rupture of papillary muscle -
- transmural MI
- Levels
- Complete transection of LV papillary muscle leads to sudden, massive mitral regurgitation that develops & cannot be tolerated (death results)
- Rupture of a portion of papillary muscle resutls in severe mitral regurgitation
- occurs more often & is not immediately fatal
Acute mitral regurgitation is characterized by what clinical features?
How is it diagnosed?
- Features
- now holosystolic murmur & increasingly severe HF
- murmur may become softer or disappear as arterial pressure falls
- now holosystolic murmur & increasingly severe HF
- Diagnosed: 2-D echocardiography with color flow Doppler
What complication frequently accompaines inferior LV infarction?
Right Ventricular Infarction
What are the clinical features of right ventricular infarction & in what situations can it occur?
- Clinical Features
- Right-sided filling pressures are elvated
- left ventricular filling pressure is normal or only slightly raised
- CO is often markedly depressed
- esp in response to nitroglycerin
- arterial hypotension out of proportion to size of infarct
- Occurs
- frequently acompanies inferior LV
- rarely occurs in isolated form
- may occur in association with “saddle” PE
What ECG change accompanies a right ventricular infarcion?
How does it show up on a 2-D echocardiography?
- ECG
- ST segment elecation in lead V4R (right precordial lead in V4 position)
- 2-D echocardiography
- abnormal wall motion of the right ventricle
- right ventricular dilation
- depressed RV ejection fraction
- “d” shaped septum
If a right ventricular infarctoin is not identified & only the left ventricular infarction is treated, what complication can occur? How do you respond?
- May produce profound hypotension (NTG, ACEI, diuretics)
- initial treatment of hypotension in patients with RV infarction include volume expansion
What types of arrhythmias commonly occur after a MI?
- Ventricular arrhythmias
- ventricular premature beats
- accelerated idioventricular rhythm
- ventricular tachycardia
- ventricular fibrillation
- Brady arrhythmias
- sinus bradycardia
What atrioventricula & Intraventricular blocks commonly occur after a MI?
- first-degree AV nodal-delay
- by definition, block indicated a drop of a QRS complex
- second-degree AV block (Mobitz I / II)
- Third degree (complete) AV block
- Intraventricular block
- asystole
What supraventricular tachyarrhythmias commonly occur after a MI?
- sinus tachycardia
- atrial premature contractions
- atrial flutter
- atrial fibrillation
- paroxysmal supraventricular tachycardia
How are Ventricular Premature Beats identified on an ECG?
Treatment?
- Ventricular Arrhythmias
- Ventricular Premature Beats (PVCs)
- wide QRS with compensatory pause afterward & no associated P wave
- commonly seen in patients with acute MI
- Treatment
- usually conservative approach
- determine whethere recurrent ischemia or electrolyte/metabolic disturbances are present
- Ventricular Premature Beats (PVCs)
What are Accelerated Idioventricular Rhythms & how are they identified on an ECG?
When do they most commonly occur?
- Ventricular Arrhythmia
- ventricular rhythm witha rate of 60-100 beats/min
- “slow v. tach”
- probaly results from enhanced automaticity of purkinje fibers
- Occurs
- frequently durign first 2 days from acute MI
- shortely after successful repurfusion
What physiological states can increase risk of developing ventricular tachycardia?
How often does this occur to patients post-MI?
Treatment?
- Hypokalemia & hypomagnesemia may increase risk
- nonsustaind paroxysms of VT may be seen in up to 67% patients in the first 12 hours
- less than 30s
- Treatment
- amiodarone, magnesium, beta blockers (? lidocaine)
Ventricular fibrillation in association with what other complication can lead to a poor prognosis?
Treatment & management?
- marked LV failure or cardiogenic shock
- Treatment
- ACLS with prompt defibrillation
- to organize rhythm before it stops quivering
- ACLS with prompt defibrillation
- Management
- amiodarone
- revascularization by PCI
When does Sinus Bradycardia most commonly occur in the even of an acute MI?
Treatment?
- Occurrence
- early phases of acute MI
- patietns with inferior & posterior infarction
- Treatment
- Isolated sinus bradycardia: observed
- Sinus bradycardia w/ hypotension or ventricular ectopy
- atropine (increase SA nodal rate)
How common is a first degree AV delay?
Treatment?
What medications can increase risk of delay?
- less than 15% of patients with acute MI
- Treatment
- generally does not require specific treatment
- Increased Risk
- digitalis, B-blockers, Calcium antagonists
At what point after an MI does second-degree AV block most commonly occur?
What does it look like on an ECG?
What is it caused by & what are the associated complications?
Treatment?
- Second-degree AV block (Mobitz Type 1 or Wenckebach)
- usually transient & does not persist more than 72 hrs after MI
- rarely progress to complete AV block
- ECG: prolonging PR interval with every beat & then drop a beat
-
Caused: ischemia of AV node
- does not affect survival
- Treatment: no specific thearpy required
- usually transient & does not persist more than 72 hrs after MI
What are the associated complications of a Mobitz Type II that occur after a MI?
How is it treated?
- Often progresses suddenly to complete AV block
- Treatment:
- temporary external or transvenous deman pacemaker
- set at a base rate & if patient’s heart ever drops below this rate, it will start pacing them
- temporary external or transvenous deman pacemaker
How does Complete (third degree) AV block occur?
How is it treated?
- often develops gradually, progressing from first-degree or type II second-degree block
- Treament:
- temporary external or transvenous demand pacemaker
What intraventricular blocks can occur after a MI?
- Intraventricular Block
- isolated fasicular blocks
- Left Anteiror Fasicular Block (LAFB)
- Left Posterior Fasicular Block (LPFB)
- both = left bundle branch block
- right bundle branch block
- Bifasicular block
- and isolated fasicular block + right bundle branch block
- Third degree block
- left bundle branch block & right bundle branch block
- isolated fasicular blocks
Sinus Tachycardia is often accompanied by what other symptoms?
Treatment?
- Supraventricular Tachyarrhythmias
- Typically associated with augmented sympathetic activity
- anxiety, persistent pain, LV failure, hypovolemia, epinephrine, atropine
- Treatment: b-adrenoceptor blocking agents (to decrease heart rate)
- Typically associated with augmented sympathetic activity
What is the specific concern associated with Paroxysmal Supraventricular Tachycardia?
Treatment?
- Supraventricular Tachyarrhythmias
- Requires aggressive management b/c rapid ventricular rate
- Treatment
- augmentation of vagal tone: manual carotid massage
-
drug: adenosine (in non-AMI patients) - AV nodal blocking agent, to “reset” heart
- IV verapamil, diltiazem, metroprolol
Atrial fibrillation in patients with acute Mi is often associated with what factor?
Why?
Treatment?
- Increased mortality
- the increased ventricular rate & loss of atrial contribution to LV filling results in a significant reduction in cardaic output
- Treatment: focus on rhythm control
What impact does atrial flutter have on patients post-MI?
usually transient
How are pericardial effusions detected?
They are more common in patients with what types of MI?
Additional complications?
- Generally detected by 2-D echocardiography
- Common
- anterior MI
- larger infarcts
- congestive heart failure
- Complications
- majority do not cause hemodynamic compromise
Cardiac tamponade is most commonly caused by what conditions?
ventricular rupture or hemorrhagic pericarditis
Pericarditis can produce pain during what time periods post-MI?
Treatment?
- Pain
- as early as first day & late as 6 weeks post MI
- Treatment:
- aspirin - as high as 650mg every 4-6 hurs
- AVOID corticosteroids b/c may interfere w/ myocardial scar formation
What is Dressler Syndrome?
How does it present?
Treatment?
- Type of post-MI pericarditis
- immune response after damage to heart
- 1-8 weeks after MI
- Presentation:
- malaise, fever, pericardial discomfort, leukocytosis, elevated ESR, pericardial effusion
- Treatment: NSAIDs, Colchicine
