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Emergency Med rotation > Cardio part 2 > Flashcards

Cardio part 2 Flashcards

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1
Q

Pathophys of VFib

A

Most often associated with CAD
Can result from AMI or ischemia or from myocardial scarring from an old infarct
VTach can aslo degenerated into VFib
Reentrant patterns break up into multiple smaller wavelets and the level of disorganization increases, with reentrant circuits producing high-frequency activation of cardiac muscle fibers

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2
Q

Etiology of VFib

A 
Acute and chronic ischemic heart disease
Valvular disease
Congenital structural heart disease
Paroxysmal VFib or short-coupled torsades
Idiopathic VFib and VTach
PE
Aortic dissection
Electronic control devices
Nonstructural abnormalities
Catecholaminergic polymorphic VTach
WPW syndrome
Brugada syndrome
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3
Q

Presentation of VFib

A

Pts at risk may have prodromes of CP, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic

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4
Q

What is the single greatest RF for sudden death from VF?

A

Hx of left ventricular dysfunction

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5
Q

Considerations when thinking about VFib?

A 
CAD
Previous cardiac arrest
Syncope or near-syncope
Prior MI, esp within 6 mos
LVEF <30-35%
H/o frequent ventricular ectopy
Drop in SBP or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia
Dilated cardiomyopathy from any cause
HCM
Use of inotropic meds
Valvular heart disease
Myocarditis
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6
Q

Triggers of VFib

A

Antiarrhythmic drug administration
Hypoxia
Ischemia
Atrial fibrillation with very rapid ventricular rates in the presence of preexcitation
Electric shock administered during cardioversion
Electric shock caused by accidental contact with improperly ground equipment
Competitive ventricular pacing to terminate VTach

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7
Q

Cardiac arrest score

A

ED SBP: >90 = 1 pt <90 = 0 pts
Time to ROSC: <25 mins = 1 pt >25 mins = 0 points
Neurologically responsive = 1 pt, comatose= 0 pts

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8
Q

Workup for VFib

A 
Confirm only with EKG
Echo
Nuclear imaging for assessment of pts at risk
Labs:
'lytes, including calcium and magnesium
Cardiac enzymes
CBC
ABG
Quantitative drug levels
Tox screens and levels
TSH
BNP
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9
Q

Tx of VFib

A

Defibrillation
Postresuscitation:
Admit to ICU with close monitoring
Assess for complications and establish the need for emergent interventions
Mild therapeutic hypothermia
BBs
Thorough diagnostic testing to establish underlying etiology

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10
Q

When is radiofrequency ablation indicated for the prevention of VFib?

A

AV bypass tracts
Bundle branch block ventricular tachycardia
Right ventricular outflow tract tachycardia
Idiopathic left ventricular tachycardia
Idiopathic VFib
Rare forms of automatic focal VTach
Scar-related VTach due to ischemic or nonischemic myopathy

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11
Q

Pathophys of premature ventricular contractions

A

Suggested mechanisms are reentry, triggered activity, and enhanced automaticity

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12
Q

Etiology of premature ventricular contractions

A 
Cardiac:
Acute MI or myocardial ischemia
Myocarditis
Cardiomyopathy
Myocardial contusion
Mitral valve prolapse
Other causes:
Hypoxia and/or hypercapnia
Medications
Illicit substances
Hypomagnesemia, hypokalemia, hypercalcemia
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13
Q

Hx of PVCs

A

Pts are usually asymptomatic
Paplpitations and neck and/or chest discomfort
Pt may report feeling that his or her heart stops after a PVC
Pts with frequent PVS or bigeminy may report syncope
Long runs of PVCs can result in hypotension
Exercise can increase or decrease the PVC rate

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14
Q

PE of PVCs

A

BP- frequent PVCs may result in hemodynamic compromise
Pulse- ectopic beat may produced a diminished or absent pulse
Hypoxia may precipitate PVCs- check pulse oximetry
Cardiac findings- Cannon A waves may be observed in the jugular venous pulse
Cardiopulmonary- Elevated BP and S4 or S3 and rales are important clues to the cause and clinical significance of PVCs
Neuro- Agitation and findings of sympathetic activation suggest that catecholamines may be the cause of the ectopy

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15
Q

PVCs workup

A 
In young, healthy pts without concerning concomitant sx, labs are not typically necessary
Otherwise:
Serum electrolyte levels
Drug screen
Drug levels
Echo
EKG
Holter monitor
Exercise stress testing used complementary to Holter monitoring
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16
Q

Tx of PVCs

A

In absence of cardiac disease, no tx needed
Otherwise:
Establish telemetry and IV access, initiate oxygen, and obtain 12-lead
Treat the underlying cause of hypoxia
Treat any drug toxicity
Correct electrolyte imbalances
BBs with those who have sustained an MI
Amiodarone
In PVCs from the right or left ventricular outflow tract that occur in structurally nl hearts, catheter ablation

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17
Q

Pathophys of MI

A

Ischemia occurs when blood supply to the myocardium does not meet the demand
If it persists, it triggers a cascade of cellular, inflammatory and biochemical events, leading to irreversible death of heart muscle cells

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18
Q

Etiology of MI

A

Atherosclerosis is primarily responsible for most ACS cases

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19
Q

Nonatherosclerotic causes of MI

A 
Coronary occlusion secondary to vasculitis
Ventricular hypertrophy
Coronary artery emboli
Coronary trauma
Primary coronary vasospasm
Drug use
Arteritis
Coronary anomalies
Factors that increase oxygen requirement
Factors that decrease oxygen delivery
Aortic dissection
Respiratory infections
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20
Q

Hx of MI

A

Typical:
CP, usually intense and unremitting for 30-60 mins, retrosternal and often radiates up to neck, shoulder, and jaws, and down to the left arm
Prodromal sx of fatigue, chest discomfort, or malaise in the days preceding the event
Typical STEMI may occur suddenly without warning
In some pts, the symptom is epigastric, with a feeling of indigestion or of fullness and gas
In some cases, pts do not recognize the chest pain
Occurs most often in the early morning hours

21
Q

Other sx of MI

A 
Anxiety
Pain or discomfort in areas of the body, including arms, left shoulder, back, neck, jaw, or stomach
Lightheadedness
Cough
Nausea, with or without vomiting
Profuse sweating
SOB
Wheezing
Rapid or irregular heart rate
Fullness, indigestion, or choking feeling
22
Q

PE of MI

A

Tachycardia or depressed heart rate
Possible irregular pulse
BP initially elevated or there could be hypotension
RR could be increased
Fever usually present within 24-48 hrs
With RV involvement, distention of neck veins
Depending on the cause, murmurs and other heart abnormalities
May auscultate wheezes or rales
Could elicit hepatojugular reflux
May find peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill

23
Q

Workup of MI

A 
EKG
Troponins I and T
CK-MB
Myoglobin
BNP
CBC
CMP
Lipid profile
Angiography
24
Q

Trajectory of troponins

A

Serum levels increase within 3-12 hrs from the onset of CP, peak at 24-48 hrs, and return to baseline over 5-14 days

25
Q

Tx of MI

A 
Oxygen
ASA
Nitrates
Morphine
STEMI- PCI
If PCI can't be performed, fibrinolytics
Anticoagulation as adjunct, no matter the strategy
May use antiplatelet agents
NSTEMI- BBs, CCBs only if contraindications to BBs, antiplatelet agents
Anticoagulants
26
Q

Definition of hypertensive

emergency

A

A spectrum of clinical presentations in which uncontrolled blood pressures lead to progressive or impending end-organ dysfunction

27
Q

Presentation of hypertensive emergency

A

The most common clinical presentations are cerebral infarction, pulmonary edema, hypertensive encephalopathy, and congestive heart failure

28
Q

Evaluation of uncontrolled hypertension

A 
CMP
UA
CBC and peripheral blood smear
Tox screen
Pregnancy test
Endocrine testing as needed
Imaging as determined by clinical presentation
29
Q

Presentation of malignant HTN

A 
Retinal papilledema
Encephalopathy
Confusion
Left ventricular failure
Intravascular coagulation
Impaired renal function
Hematuria 
Wt loss
30
Q

Tx of hypertensive emergency

A

Sodium nitroprusside, with constant monitoring in ICU
-Avoid with hypertensive encephalopathy
-Preferred in perioperative HTN
Labetalol preferred in pts with acute dissection and end-stage renal dz as well as acute ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, preeclampsia, and ACS
Use diazepam, phentolamine, and nitro/nitroprusside for cocaine toxicity or pheochromocytoma
Admit to ICU
For adults with a compelling condition, lower SBP to <140 during the first hour and <120 in aortic dissection
Without a compelling condition, reduce SBP to a max of 25% within the first hour

31
Q

Pathophys of heart failure

A

Adaptations:
-Frank-Starling mechanism, where an increased preload helps to sustain cardiac performance
-Alterations in myocyte regeneration and death
-Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented
-Activation of neurohumoral systems, such as RAAS, sympathetic nervous system
Angiotensin II
Myocytes and myocardial remodeling
Activation of atrial natriuretic peptide and B-type natriuretic peptide
LV chamber stiffness

32
Q

Etiology of heart failure: underlying causes of systolic heart failure

A 
CAD
DM
HTN
Valvular heart disease
Arrhythmia
Infections and inflammation
Peripartum cardiomyopathy
Congenital heart disease
Drugs
Idiopathic cardiomyopathy
Rare conditions
33
Q

Etiology of heart failure: underlying causes of diastolic heart failure

A 
CAD
DM
HTN
Valvular heart disease
HCM
Restrictive cardiomyopathy
Constrictive pericarditis
34
Q

Etiology of heart failure: underlying causes of acute heart failure

A 
Acute valvular regurgitation
MI
Myocarditis
Arrhythmia
Drugs
Sepsis
35
Q

Hx of heart failure

A 
Exertional dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Dyspnea at rest
Acute pulmonary edema
CP/pressure
Palpitations
Anorexia
Nausea
Wt loss
Bloating 
Fatiuge
Weakness
Oliguria
Nocturia
Cerebral sx of varying severity
36
Q

PE of heart failure

A

May be dyspneic when lying flat without elevation of the head for more than a few minutes. Severe heart failure appear anxious and may exhibit signs of air hunger in this position.
Chronic severe heart failure often malnourished and sometimes even cachectic
Can have visible pulsation of the eyes and of the neck veins
Severe heart failure- central cyanosis, icterus, and malar flush
Dusky discoloration of the skin and diminished pulse pressure in severe
Pulse may be weak, rapid, and thready
Tachycardia, diaphoresis, pallor, peripheral cyanosis with pallor and coldness of extremities
Rales
Edema
S3 gallop

37
Q

Workup of heart failure

A 
CBC
CMP, including Ca and Mg
Renal and liver function studies
Consider iron deficiency assessment
BNP or NT-proBNP
EKG
CXR
Echo for initial eval
MUGA and other nuclear imaging
In systolic dysfunction of unexplained cause- angiography
38
Q

Tx of heart failure

A 
Lifestyle modifications, including sodium restriction
Pharmacologic therapy:
-Diuretics
-ACEs/ARBs
-Hydralazine and nitrates to improve sx
-BBs
-Aldosterone antagonists as an adjunct
Acute heart failure:
O2 administration for sat <90% and noninvasive positive pressure ventilation
Initial IV loop diuretic
Consider additional vasodilators
Use inotropes for organ hypoperfusion
Later on:
Electrophysiologic intervention
Revascularization
Valve surgery
ECMO
Ventricular assist devices
Transplant
39
Q

Pathophys of cardiogenic shock

A

A low-cardiac-output state secondary to extensive left ventricular infarction, development of a mechanical defect, or right ventricular infarction

40
Q

Etiology of cardiogenic shock

A 
Systolic dysfunction
Diastolic dysfunction
Valvular dysfunction
Cardiac arrhythmias
Coronary artery dz
Mechanical complications
41
Q

Presentation of cardiogenic shock

A

Can present after an MI
Sinus tachycardia
Low urine output
Cool extremities
Systemic hypotension
Ashen or cyanotic with cool skin and mottled extremities
Rapid and faint peripheral pulses and may be irregular if arrhythmias present
JVD and crackles in lungs
Distant heart sounds with some third and fourth heart sounds
AMS

42
Q

Workup of cardiogenic shock

A 
CMP
LDH
CBC
Cardiac enzymes
ABG
Lactate
BNP
Echo
EKG
43
Q

Tx of cardiogenic shock

A

Admission to ICU
Central venous and arterial lines are often required
Oxygenation and airway protection
MI or ACS- ASA and heparin
Vasopressors- try dopamine first
IABP or other revascularization strategies

44
Q

Pathophys of pericardial effusion

A

Pericardium usually limits the ability of the left-sided chambers to dilate
This contributes to the bowing of the atrial and ventricular septums to the left, which reduces LV filling volumes and leads to a drop in cardiac output
As intrapericardial pressures rise, this effect becomes pronounced

45
Q

Etiology of pericardial effusion

A

Idiopathic
Infectious
Neoplastic
Postoperative/postprocedural

46
Q

Hx of pericardial effusion

A 
CP, pressure, discomfort
Lightheadedness
Syncope
Palpitations
Cough
Dyspnea
Hoarseness
Anxiety and confusion
47
Q

PE of pericardial effusion

A 
Beck's triad
Pulsus paradoxus
Pericardial friction rub
Tachycardia
Hepatojugular reflux
Tachypnea
Decreased breath sounds
Ewart sign-dullness to percussion beneath the angle of left scapula from compression of the left lung by pericardial fluid
48
Q

Workup of pericardial effusion

A 
CMP
CBC with diff
Cardiac biomarkers
ESR and CRP
TSH
BCx in the present of SIRS or fever
RF, ANA, etc for suspected rheum cases
Infectious disease testing
CXR- water bottle heart
Echo- imaging modality of choice
EKG
Pericardiocentesis
49
Q

Tx of pericardial effusion

A

Pts with evidence of hemodynamic compromise- urgent drainage
Pericardiocentesis is preferred
Treat underlying causes

Emergency Med rotation (12 decks)

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