Cardio part 2 Flashcards

(49 cards)

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
Tx of MI
``` 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
Definition of hypertensive | emergency
A spectrum of clinical presentations in which uncontrolled blood pressures lead to progressive or impending end-organ dysfunction
27
Presentation of hypertensive emergency
The most common clinical presentations are cerebral infarction, pulmonary edema, hypertensive encephalopathy, and congestive heart failure
28
Evaluation of uncontrolled hypertension
``` CMP UA CBC and peripheral blood smear Tox screen Pregnancy test Endocrine testing as needed Imaging as determined by clinical presentation ```
29
Presentation of malignant HTN
``` Retinal papilledema Encephalopathy Confusion Left ventricular failure Intravascular coagulation Impaired renal function Hematuria Wt loss ```
30
Tx of hypertensive emergency
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
Pathophys of heart failure
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
Etiology of heart failure: underlying causes of systolic heart failure
``` CAD DM HTN Valvular heart disease Arrhythmia Infections and inflammation Peripartum cardiomyopathy Congenital heart disease Drugs Idiopathic cardiomyopathy Rare conditions ```
33
Etiology of heart failure: underlying causes of diastolic heart failure
``` CAD DM HTN Valvular heart disease HCM Restrictive cardiomyopathy Constrictive pericarditis ```
34
Etiology of heart failure: underlying causes of acute heart failure
``` Acute valvular regurgitation MI Myocarditis Arrhythmia Drugs Sepsis ```
35
Hx of heart failure
``` 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
PE of heart failure
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
Workup of heart failure
``` 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
Tx of heart failure
``` 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
Pathophys of cardiogenic shock
A low-cardiac-output state secondary to extensive left ventricular infarction, development of a mechanical defect, or right ventricular infarction
40
Etiology of cardiogenic shock
``` Systolic dysfunction Diastolic dysfunction Valvular dysfunction Cardiac arrhythmias Coronary artery dz Mechanical complications ```
41
Presentation of cardiogenic shock
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
Workup of cardiogenic shock
``` CMP LDH CBC Cardiac enzymes ABG Lactate BNP Echo EKG ```
43
Tx of cardiogenic shock
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
Pathophys of pericardial effusion
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
Etiology of pericardial effusion
Idiopathic Infectious Neoplastic Postoperative/postprocedural
46
Hx of pericardial effusion
``` CP, pressure, discomfort Lightheadedness Syncope Palpitations Cough Dyspnea Hoarseness Anxiety and confusion ```
47
PE of pericardial effusion
``` 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
Workup of pericardial effusion
``` 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
Tx of pericardial effusion
Pts with evidence of hemodynamic compromise- urgent drainage Pericardiocentesis is preferred Treat underlying causes