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S2B6: MEDI > Complications of MI > Flashcards

Complications of MI Flashcards

1
Q

What is the list of the most important complications of MI (9)?

A
  1. Cardiogenic Shock
  2. Severe Heart Failure
  3. RV Infarction
  4. Mechanical Complications
    • MR, Ventricular septal rupture, LV free-wall rupture, LV aneurysm
  5. Electrical complications
    • ventricular arrhythmias, AF, SFTs, Bradycardia, AV Block, interventricular conduction defects
  6. Pericarditis
  7. Thromboembolic adn bleeding complications
  8. Acute Kidney Injury
  9. Hyperglycemia
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2
Q

What is one of the most common chronic complications from a MI?

A

Heart Failure with reduced ejection fraction

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3
Q

What are the three reasons for recurrent ischemia and infarction?

What procedure has reduced incidence of this?

A
  1. Occlusion of an initially patent vessel
  2. Reocclusion of an initially recanalized vessel
  3. Coronary Spasm

Reduced incidence: PTCA (percutaneous transluminal coronary angioplasty)

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4
Q

What complication is the single most important predictor of mortality after a MI?

A

Left Ventricular Failure

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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
  • Predictors: advanced age & diabetes
  • Managed: reduction of ventricular preload (B-blockers) & if possible lowering afterload (ACE-inhibitors)
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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
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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
      • decrease systemic perfusion
        • compensatory vasoconstriction; fluid retention
  • All of the above lead to progressive myocardial dysfunction & death
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8
Q

What is the most severe clinical expression of left ventricular heart failure?

A

cardiogenic shock

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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)
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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
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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
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12
Q

What is a major concern with developing cardiogenic shock

A

Can easly go into caridac arrest

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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
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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
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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
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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
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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
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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%)

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19
Q

Interventricular Septal Rupture develops most often in patients with what anatomical feature?

A

lack collateral network

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20
Q

The size of the interventricular septal rupture determines what 3 variables?

A
  1. The magnitude of the left-to-right shunt
  2. extent of hemodynamic deterioation
  3. likelihood of survival
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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
Q

What is a pseudoaneurysm and how is it diagnosed?

A
  • 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
Q

What causes acute mitral regurgitation & and what levels can it present?

A
  • 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
Q

Acute mitral regurgitation is characterized by what clinical features?

How is it diagnosed?

A
  • 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
Q

What complication frequently accompaines inferior LV infarction?

A

Right Ventricular Infarction

29
Q

What are the clinical features of right ventricular infarction & in what situations can it occur?

A
  • 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
Q

What ECG change accompanies a right ventricular infarcion?

How does it show up on a 2-D echocardiography?

A
  • 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
Q

If a right ventricular infarctoin is not identified & only the left ventricular infarction is treated, what complication can occur? How do you respond?

A
  • May produce profound hypotension (NTG, ACEI, diuretics)
  • initial treatment of hypotension in patients with RV infarction include volume expansion
32
Q

What types of arrhythmias commonly occur after a MI?

A
  • Ventricular arrhythmias
    • ventricular premature beats
    • accelerated idioventricular rhythm
    • ventricular tachycardia
    • ventricular fibrillation
  • Brady arrhythmias
    • sinus bradycardia
33
Q

What atrioventricula & Intraventricular blocks commonly occur after a MI?

A
  • 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
Q

What supraventricular tachyarrhythmias commonly occur after a MI?

A
  • sinus tachycardia
  • atrial premature contractions
  • atrial flutter
  • atrial fibrillation
  • paroxysmal supraventricular tachycardia
35
Q

How are Ventricular Premature Beats identified on an ECG?

Treatment?

A
  • 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
Q

What are Accelerated Idioventricular Rhythms & how are they identified on an ECG?

When do they most commonly occur?

A
  • 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
Q

What physiological states can increase risk of developing ventricular tachycardia?

How often does this occur to patients post-MI?

Treatment?

A
  • 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
Q

Ventricular fibrillation in association with what other complication can lead to a poor prognosis?

Treatment & management?

A
  • marked LV failure or cardiogenic shock
  • Treatment
    • ACLS with prompt defibrillation
      • to organize rhythm before it stops quivering
  • Management
    • amiodarone
    • revascularization by PCI
39
Q

When does Sinus Bradycardia most commonly occur in the even of an acute MI?

Treatment?

A
  • 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
Q

How common is a first degree AV delay?

Treatment?

What medications can increase risk of delay?

A
  • less than 15% of patients with acute MI
  • Treatment
    • generally does not require specific treatment
  • Increased Risk
    • digitalis, B-blockers, Calcium antagonists
41
Q

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?

A
  • 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
Q

What are the associated complications of a Mobitz Type II that occur after a MI?

How is it treated?

A
  • 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
Q

How does Complete (third degree) AV block occur?

How is it treated?

A
  • often develops gradually, progressing from first-degree or type II second-degree block
  • Treament:
    • temporary external or transvenous demand pacemaker
44
Q

What intraventricular blocks can occur after a MI?

A
  • 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
Q

Sinus Tachycardia is often accompanied by what other symptoms?

Treatment?

A
  • 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
Q

What is the specific concern associated with Paroxysmal Supraventricular Tachycardia?

Treatment?

A
  • 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
Q

Atrial fibrillation in patients with acute Mi is often associated with what factor?

Why?

Treatment?

A
  • 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
Q

What impact does atrial flutter have on patients post-MI?

A

usually transient

49
Q

How are pericardial effusions detected?

They are more common in patients with what types of MI?

Additional complications?

A
  • Generally detected by 2-D echocardiography
  • Common
    • anterior MI
    • larger infarcts
    • congestive heart failure
  • Complications
    • majority do not cause hemodynamic compromise
50
Q

Cardiac tamponade is most commonly caused by what conditions?

A

ventricular rupture or hemorrhagic pericarditis

51
Q

Pericarditis can produce pain during what time periods post-MI?

Treatment?

A
  • 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
Q

What is Dressler Syndrome?

How does it present?

Treatment?

A
  • 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

S2B6: MEDI (15 decks)

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