Cardio part 2 Flashcards
Pathophys of VFib
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
Etiology of VFib
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
Presentation of VFib
Pts at risk may have prodromes of CP, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic
What is the single greatest RF for sudden death from VF?
Hx of left ventricular dysfunction
Considerations when thinking about VFib?
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
Triggers of VFib
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
Cardiac arrest score
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
Workup for VFib
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
Tx of VFib
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
When is radiofrequency ablation indicated for the prevention of VFib?
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
Pathophys of premature ventricular contractions
Suggested mechanisms are reentry, triggered activity, and enhanced automaticity
Etiology of premature ventricular contractions
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
Hx of PVCs
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
PE of PVCs
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
PVCs workup
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
Tx of PVCs
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
Pathophys of MI
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
Etiology of MI
Atherosclerosis is primarily responsible for most ACS cases
Nonatherosclerotic causes of MI
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
Hx of MI
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
Other sx of MI
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
PE of MI
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
Workup of MI
EKG Troponins I and T CK-MB Myoglobin BNP CBC CMP Lipid profile Angiography
Trajectory of troponins
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
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
Definition of hypertensive
emergency
A spectrum of clinical presentations in which uncontrolled blood pressures lead to progressive or impending end-organ dysfunction
Presentation of hypertensive emergency
The most common clinical presentations are cerebral infarction, pulmonary edema, hypertensive encephalopathy, and congestive heart failure
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
Presentation of malignant HTN
Retinal papilledema Encephalopathy Confusion Left ventricular failure Intravascular coagulation Impaired renal function Hematuria Wt loss
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
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
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
Etiology of heart failure: underlying causes of diastolic heart failure
CAD DM HTN Valvular heart disease HCM Restrictive cardiomyopathy Constrictive pericarditis
Etiology of heart failure: underlying causes of acute heart failure
Acute valvular regurgitation MI Myocarditis Arrhythmia Drugs Sepsis
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
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
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
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
Pathophys of cardiogenic shock
A low-cardiac-output state secondary to extensive left ventricular infarction, development of a mechanical defect, or right ventricular infarction
Etiology of cardiogenic shock
Systolic dysfunction Diastolic dysfunction Valvular dysfunction Cardiac arrhythmias Coronary artery dz Mechanical complications
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
Workup of cardiogenic shock
CMP LDH CBC Cardiac enzymes ABG Lactate BNP Echo EKG
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
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
Etiology of pericardial effusion
Idiopathic
Infectious
Neoplastic
Postoperative/postprocedural
Hx of pericardial effusion
CP, pressure, discomfort Lightheadedness Syncope Palpitations Cough Dyspnea Hoarseness Anxiety and confusion
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
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
Tx of pericardial effusion
Pts with evidence of hemodynamic compromise- urgent drainage
Pericardiocentesis is preferred
Treat underlying causes
