Complications of MI Flashcards
1
Q
What is the list of the most important complications of MI (9)?
A
- 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
2
Q
What is one of the most common chronic complications from a MI?
A
Heart Failure with reduced ejection fraction
3
Q
What are the three reasons for recurrent ischemia and infarction?
What procedure has reduced incidence of this?
A
- Occlusion of an initially patent vessel
- Reocclusion of an initially recanalized vessel
- Coronary Spasm
Reduced incidence: PTCA (percutaneous transluminal coronary angioplasty)
4
Q
What complication is the single most important predictor of mortality after a MI?
A
Left Ventricular Failure
5
Q
Left Ventricular Failure is characterized by what factors?
What are predictors for the development of symptomatic LV failure?
What is the management strategy?
A
- 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)
6
Q
What drugs are used to treat Left Ventricular Failure?
Describe the physiologic reasoning for each type of drug.
A
- 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
7
Q
Describe cycle that can occur w/ acute severe heart failure
A
- 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
8
Q
What is the most severe clinical expression of left ventricular heart failure?
A
cardiogenic shock
9
Q
Cardiogenic shock is characterized by what features?
A
- 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)
10
Q
At autopsy, 2/3 of patients with cardiogenic shock demonstrat what common factors?
A
- stenosis of 75% or more of lumina diameter of all 3 major coronary vessels
- loss of 40% left ventricular mass
11
Q
What symptoms suggest Right Heart Failure?
What symptoms suggest Left Heart Failure?
What symptoms are shared by both types of heart failure?
A
- 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
12
Q
What is a major concern with developing cardiogenic shock
A
Can easly go into caridac arrest
13
Q
Once a patient in cardiac arrest is taken to a cardiac shock center, what treatments/assessments occur?
A
- 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
14
Q
What are the shock indices?
A
- 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
15
Q
What is the medical management techniques for cardiogenic shock?
A
- 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
16
Q
Interventricular Septal Rupture is characterized by features?
Best treatment?
A
- 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
17
Q
What are the clinical features that are associated with risk of interventricular septal rupture?
A
- Lack of development of collateral network
- advanced age
- hypertension
- anterior locatin of infarction
- thrombolysis
18
Q
Patients with interventricular septal rupture is highly correlated with what additional post-MI complication?
A
higher 30-day mortality (74%) compared to patients who did not develop this complication (7%)
19
Q
Interventricular Septal Rupture develops most often in patients with what anatomical feature?
A
lack collateral network
20
Q
The size of the interventricular septal rupture determines what 3 variables?
A
- The magnitude of the left-to-right shunt
- extent of hemodynamic deterioation
- likelihood of survival
21
Q
Interventricular septal rupture is associated with what situations other than MI?
A
- complete heart block
- right bundle branch block
- atrial fibrillation
22
Q
What features characterize a free wall rupture?
A
- 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
23
Q
A free wall rupture can lead to what additional complications?
A
- 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”
24
Q
What are the possible outcomes from free wall rupture & survival depends on what factor?
A
- 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
25
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
26
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
27
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
* _Diagnosed_: 2-D echocardiography with color flow Doppler
28
What complication frequently accompaines inferior LV infarction?
Right Ventricular Infarction
29
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
30
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
31
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_
32
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
33
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
34
What supraventricular tachyarrhythmias commonly occur after a MI?
* sinus tachycardia
* atrial premature contractions
* atrial flutter
* atrial fibrillation
* paroxysmal supraventricular tachycardia
35
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
36
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
37
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)
38
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
* Management
* amiodarone
* revascularization by PCI
39
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)
40
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
41
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
42
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
43
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
44
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
45
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)
46
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
47
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
48
What impact does atrial flutter have on patients post-MI?
usually transient
49
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
50
Cardiac tamponade is most commonly caused by what conditions?
ventricular rupture or hemorrhagic pericarditis
51
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
52
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
