Cardiovascular Emergencies Flashcards
1. Explain concept related to the care of an ED patient experiencing a cardiovascular emergency. 2. Describe various patient presentations related to cardiovascular emergencies. 3. List interventions necessary for a patient presenting with a cardiovascular emergency.
cardiac output
SV x HR
SNS r/t HR
increases HR d/t:
- stress
- anxiety
- acute pain
- release of catecholamines
- hypotension
- drugs w/ + chronotropic effects
PNS r/t HR
decreases HR d/t:
- vagus nerve stimulation
- cardiac conduction abnormalities
- drugs with (-) chronotropic effects
heart rhythm r/t HR
some dysrhythmias can impair adequate filling of heart chambers or result in loss of atrial kick which contributes to 20-40% of ventricular filling in healthy adult
define stroke volume
amount of blood ejected from each ventricle per contraction
stroke volume overview
measured in ml/beat
amount ejected / ventricle is equal in healthy patient
positively influenced by preload and contractility
define contractility
strength of each myocardial contraction
contractility overview
significantly contributes to CO
affected by preload (Frank-Starling law), afterload, electrolyte status, myocardial oxygenation, amount of functional myocardium, and drugs with inotropic effects
define preload
volume of blood that results in pressure or stretch of the ventricles during diastole
affected by amount of venous return to heart
what increases preload?
peripheral venous constriction
alpha adrenergics (epi, norepi, dopamine)
what decreases preload?
decreased intravascular volume 2/2:
- hemorrhage
- diuresis
- v/d
- third spacing
- redistribution of blood flow
also vasodilators
define afterload
resistance to ventricular emptying during systole
negatively influences stroke volume
what increases afterload?
vasoconstriction or mechanical obstruction of ventricular outflow such as:
- aortic or pulmonic stenosis
- HTN
- hypothermia
- compensatory shock mechanisms
what decreases afterload?
- hyperthermia
- distributive shock
- vasodilators
increasing CO: adults vs children
adults: HR and SV
children: tachycardia (cannot increase SV)
define MAP
average pressure over entire cardiac cycle
(DBPx2 + SBP)/3
define pulse pressure
difference between systolic and diastolic BP
calculate via systemic or pulmonary pressure
low systemic pulse pressure
narrowing pulse pressure
decreased LV SV, blood loss, low stroke volume 2/2 shock or cardiac tamponade
high pulse pressure
widening pulse pressure
may be transient and normal effect of activity
caused by chronic or acute conditions
chronic causes of high pulse pressure
atherosclerosis
aortic regurg
acute causes of high pulse pressure
aortic aneurysm aortic dissection PDA endocarditis anxiety fever pregnancy
Cushing Triad
indicative of increased intracranial pressure
widening pulse pressure or HTN
bradycardia
irregular breathing pattern
chronotropes
affect HR (generation of electrical impulse) at SA node
inotropes
affect contractility
dromotropes
affect automaticity (electrical impulse velocity) of heart at AV node
alpha beta receptors
Alpha 1 causes peripheral vascular Constriction
Beta2 causes bronchial smooth muscle Dilation
(AB,CD)
ACE inhibitors pharmacology
-angiotensin-converting enzyme, -pril
-affect RAAS by blocking angiotensin I to angiotensin II
-results in decreased BP (HTN) and afterload (CHF)
decreased preload and -afterload via vasodilation an diuresis
ACE inhibitors adverse effects
dry cough
angioedema, rash
renal impairment
category D in pregnancy
ARBs pharmacology
- angiotensin receptor blockers, -sartan
- inhibit angiotensin II receptors
- results in vasodilation, decreased aldosterone levels, increasing excretion of Na and sparing of K+
- for HTN and CHF
- only oral
ARBs adverse effects
hypotension dizziness HA hyperK rarely dry cough
calcium channel blockers
-dipine
negative inotropic, chronotropic, dromotropic effects
beta blockers
- lol
- negative inotropic, chronotropic, dromotropic effects
- beta receptors
- cardioselective (B1) or non cardioselective (lungs) (B2)
CP risk factors
CAD angina MI stents pacemaker age, sex, genes weight, diet, smoking, exercise, stress
sx of MI
vary by vessel
- pain in chest, jaw, neck, left arm, epigastrum, scapular
- N/V
- hemodynamic instability (hypotension, sx decreased CO or shock, sob, dysrhythmias, anxiety, impending doom)
assessing MI
OPQRST onset provoke, precipitate, palliate quality radiate, region severity, sx timing
atypical MI presentations
women, elderly
- sob, palpitations
- fatigue, syncope
- n/v
- diaphoresis
- pain/discomfort
assessing MI
labs rads (CXR, echo, doppler, stress, catheterization)
phosphodiesterase inhibitors in MI
i.e. sildenafil, etc.
can lead to profoundly decreased CO with inferior wall infarct or nitroglycerins
indications of pacemaker
refractory bradycardia
heart block
idioventricular dysrhythmias
transvenous pacing
catheter electrode threaded into the right atrium or ventricle via the subclavian, internal jugular, brachial, or femoral vein
transcutaneous pacing
pad on mid-thoracic back and front of chest at lead V3
fixed or demand, 60-80 bmp, 60-80 mA, increasing 5-10 mA until capture
electrical component of pacing
pacer spike precedes each:
QRS complex (ventricular pacing) P wave (atrial pacing) both (atrioventricular pacing)
mechanical component of pacing
palpable pulse that correlates to each paced beat
lack of capture on pacemaker
acidosis
hypoxemia
wires not connected
wet/diaphoretic skin/electrodes
define cardioversion
synchronized defibrillation
cardioversion overview
with spontaneous circulation, usually hemodynamically unstable
V.tach with pulse
SVT
refractory a.fib/flutter
cardioversion procedure
sync
marker above R waves
hold defib button until shock delivered
rest sync mode for every delivery
12 lead before, during, after
why defibrillate?
lack of spontaneous circulation
most types of defibrillators
biphasic
joules for adult defibrillation
biphasic 120-200
monophasic 200-300
joules for ped defibrillation
2/kg then 4/kg
max of 10/kg
define dysrhythmias
abnormal cardiac electrical activity resulting in aberrant rhythms
asymptomatic or sx r/t altered CO
types of dysrhythmias
bradycardia tachycardia supraventricular arrhythmias ventricular arrhythmias heart block
define bradycardia
impaired/delayed electrical impulse
SA node or CNS activation of heart is affected
adults below 60 bpm
peds is age specific
causes of bradycardia
CAD aging respiratory (peds) cardiac defects drugs
sx bradycardia
hypotension ams shock cp acute HF
interventions for stable bradycardia
correct cause
atropine, IV crystalloids
if asymptomatic, observation
interventions for unstable bradycardia
correct cause
dopamine, epi infusion
transcutaneous pacing
define tachycardia
adults > 100 bpm (unstable > 150)
peds age specific
causes of tachycardia
acute pain, fever, activity CAD cardiac defects electrolytes excessive drug use/OD
sx tachycardia
anxiety, diaphoresis palpitations, chest discomfort sob dizziness, syncope hypotension, shock loss of VS MS change
interventions for stable tachycardia
correct cause
amiodarone IVPB
interventions for unstable tachycardia
cardioversion w/ sedation
regular, narrow complex: 50-100 joules, biphasic
irregular, narrow complex: 120-200 joules, biphasic
interventions for pulseless tachycardia
defib and CPR
epi q 3-5 min
amiodarone VI
interventions for tachycardia in general
cardiac work up, EP consult
cath, surgery
labs
AICD/pacemaker
where do supraventricular dysrhythmias originate?
atria
types of supraventricular dysrhythmias
- premature atrial contractions (PACs)
- paroxysmal supraventricular tachycardia (PSVT)
- Wolff-Parkinson-White
- AV node re-entry tachy
- a.fib
- a.flutter
Wolff-Parkinson-White syndrome
fast HR d/t extra/abnormal pathway between atria and ventricles
impulse travels via normal and extra route, causing impulse to travel rapidly
presence of delta wave
AV node re-entry tachycardia
more than one pathway through AV node
a.fib
common irregular pattern
many impulses in atria with complete travel thru AV node w/o coordinated electrical activity
fibrillating/quivering atria
RVR: > 100 bpm
a.flutter
1+ rapid circuits in atrium that result in organized, reg rhythm
sawtooth waves
AV conduction fixed or variable
causes of supraventricular tachycardias
conduction abnormalities CAD cardiac defects aging excessive drug use
sx supraventricular tachycardias
100-150 bpm any bp sob, dypsnea palpitations, chest tightness MS change
interventions for stable supraventricular tachycardia
vagal maneuvers
pharm cardioversion as appropriate
interventions for unstable supraventricular tachycardia
synchronized cardioversion
interventions for supraventricular tachycardia with HR > 150 bpm
cardioversion at 50-200 joules (biphasic)
amiodarone IVPB
define PVCs
originate in ventricles
failure of SA node or overriding of ventricle-generated impulses
PVC overview
“skipped’ HB sensation
usually benign but may be caused by specific condition and produce specific sx
may be bigeminal or trigeminal
3+ PVCs = tachycardia
ventricular tachycardia
w/ or w/o pulse
torsades
- polymorphic VT
- rhythm twists
- QRS variable amplitude
v.fib
quivering ventricles
no coordination for filling or ejecting of blood in chambers
causes of PVCs
blunt trauma underlying conditions (prolonged QT) heart disease hypoxic myocardium electrolytes
sx PVCs
HR 150-300 palpitations, chest discomfort syncope dyspnea hypotension loss of VS
interventions of PVCs with pulse
cardioversion (VT)
magnesium (torsades)
interventions for PVCs w/o pulse
defib, CPR, epi
correct cause
1st heart block
usually benign
prolonged PR interval
2nd degree heart block, type I
aka Wenckebach (most common)
gradual increase in PR interval until dropped QRS
2nd degree heart block, type II
consistently long PR interval until dropped QRS
3rd degree heart block
no electrical coordination between atrium and ventricles
P-wave intervals consistent
QRS intervals consistent
causes of heart block
aging
CAD
drug OD
interventions for heartblock
atropine for low grade (ineffective for high grade or heart transplant)
transcutaneous pacing for high degree, or heart transplant
identify cause (H and Ts)
H and Ts in cardiac dysrhythmias
hypovolemia hypoxia hydrogen ion (acidosis0 hyper/hypokalemia hyper/hypoglycemia hypothermia toxins tamponade tension pneumo thrombosis (coronary, pulm) trauma
define sudden cardiac arrest
failure of cardiac electrical system
NOT and MI
risk factors for sudden cardiac arrest
CAD, MI syncopal episodes exertional cp, dyspnea, syncope HF, hx MI EF < 40% modifiable CAD risk factors
interventions for sudden cardiac arrest
defib, cpr
implanted defib for future
causes of cardiopulmonary arrest
trauma
chronic, acute illness
sudden cardiac arrest
bls interventions
recognize activate response high quality CPR rescue breaths rapid defib
interventions for cardiopulmonary arrest
CPR airway breathing defib meds
compressions in cardiopulmonary arrest
most important to have effective, continuous compressions for cardiac perfusion and CO
100-120 bpm
adequate depth and recoil
minimize interruptions
airway in cardiopulmonary arrest
advanced airway can delay cpr or defib
use bls maneuvers to ensure airway patency
breathing in cardiopulmonary arrest
rise and fall of chest bag-mask unless ineffective prevent hyperventilation 30:2 ventilate q 5-6 sec with advanced airway
hyperventilation in cardiopulmonary arrest
prevent!
increases intrathoracic pressure which decreases venous return to heart
defib in cardiopulmonary arrest
early defib has better outcomes
CPR while charging
resume immediately after shock
no pulse checks w/o organized rhythm
meds in cardiopulmonary arrest
circulate with CPR
epi q3-5 min
amiodarone or lidocaine
benefits of family presence during cardiopulmonary arrest
more likely to understand
grieving process
medical hx
reduce fear/anxiety/isolation
concerns for family presence during cardiopulmonary arrest
interference
misinterpret efforts, litigation
traumatic
grief response may be violent
procedure for family presence during cardiopulmonary arrest
one staff member to remain with family and explain procedure in clear, simple terms
allow for interaction with patient if possible
trauma considerations for cardiopulmonary arrest
poor survival rates (0-3.7%), especially with hypovolemia
thoracotamy in trauma cardiopulmonary arrest
high mortality rate
maybe for penetrating injury with quick transport and objective signs of life upon arrival
also for massive intrathoracic hemorrhage, tamponade, internal cardiac massage
causes of pediatric cardipulmonary arrest
usually resp failure or shock
apparent life threatening event
SIDS
pediatric apparent life threatening event
ALTE
cause of cardiopulm arrest
color change, marked change in muscle tone, choking, gagging
SIDS
cause of cardiopulm arrest
unknown cause
accidental suffocation
<1 year, most 2-3 mo
interventions for pediatric cardiopulm arrest
high quality BLS
PALS
family presence
causes of maternal cardiac arrest
BEAU-CHOPS
bleeding/DIC embolism anesthesia uterine atony cardiac disease HTN/preeclampsia Others: H/Ts placentae abruptio/previa sepsis
interventions for maternal cardiopulm arrest
- ACLS
- higher chest compressions
- displace uterus to left to prevent vena cava syndrome
- PIV above diaphragm
- remove fetal monitoring device prior to defib
- remove cause
- emergency C section if no ROSC within 4 min
PCI in cardiopulm arrest
early PCI is gold standard
thrombolytics if no PCI
transfer to PCI hospital
therapeutic hypothermia in cardiopulm arrest
only therapy shown to improve neuro recovery after ROSC with persisting neuro deficits
initiate immediately after ROSC when pt comatose
procedure for therapeutic hypothermia
32-34 C for 12-24 hrs continuous core temp control shivering sedation, analgesia, neurmusc block baseline electrolytes hourly glucose IUC with temp monitor
consistent findings in at least two contiguous EKG leads indicates what?
ischemia, injury, or infarct
opposite changes from contiguous EKG leads that may be found in reciprocal leads indicates what?
confirm interpretation
EKG alteration for ischemia
tall or inverted T waves
ST depression
EKG alteration for heart injury
elevated ST with reciprocal changes
T-wave may invert in some leads
EKG alteration for infarction (acute)
ST elevation
T-wave may be inerted
EKG alteration for infarction (old)
abnormal Q wave
normalized baseline
indications for Right Sided EKG
acute MI of R ventricle or posterior wall
adult and geriatric
ACS
s/sx of MI
caused by imbalance of myocardial oxygen supply and demand
four stages of MI
stable angina
unstable angina
NSTEMI
STEMI
stable angina overview
cp with exertion, short duration
relieved by rest or meds
unstable angina overview
cp with no exertion/at rest, lasts longer than stable
indicates unstable atherosclerotic plaque, may lead to acute MI
NSTEMI overview
MI with ischemic cp
rupture of unstable plaque that resulting in intermittent coronary occlusion
STEMI overview
MI with complete obstruction of 1+ coronary arteries with thrombosis
anterior left ventricle infarct
sx LV failure
crackles, S3, resp distress d/t pulm edema
right ventricle infarct
sx RV failure
hypotension, increased CVP, jugular venous distention, no crackles
pain, EKG, trop in stable angina
relieved by rest or nitro
transient ST depression
normal
pain, EKG, trop in unstable angina
> 20 min, unrelieved by rest, nitro
transient ST depression
T wave inversion
normal
pain, EKG, trop in NSTEMI
continuous cp
ST segment depression
T wave abnormal
elevated
pain, EKG, trop in STEMI
pain worse than angina
ST elevation > 2mm in V1-3 and > 1 mm in other leads
elevated
trop and CK-MB trends during infarct
trop:
3-12 hours
peak 10-24 hrs
CK-MB:
4-12 hrs
peak 10-24 hrs
moNA
morphine
oxygen
nitro
aspirin
morphine during ACS
decrease pain, anxiety
for persistent cardiac pain unrelieved by nitro
oxygen during ACS
if SpO2 below 94% or severe resp sx or shock
initial nitro during ACS
sublingual
- reduce myocardial oxygen demand
- coronary artery dilation
- improve collateral blood flow to ischemic myocardial tissue
- dilate peripheral vasculature
- reduce preload
additional nitro during ACS
transdermal or IV if necessary
contraindications for nitro during ACS
hypotension
bradycardia
phosphodiesterase inhibitors
inferior wall infarcts
aspirin during ACS
greatest benefit if taken asap
160-324 mg
few contraindications class D pregnancy
stemi interventions
early reperfusion
PCI gold standard (less than 90 min)
fibrinolytic therapy if PCI unavailable
pharm interventions post-infarct
beta blockers (for all ACS)
ACE inhibitors or ARBs to reduce infarct size and improve ventricular remodeling
define heart failure
inadequate CO and oxygen delivery to tissues
LV EF < 40%
types of HF
systolic: inability to pump effectively
diastolic: inability to fill adequately
sx R side HF
peripheral edema JVD ascites hepatomegaly increased CVP
sx L side HF
SOB dyspnea crackles S3 pulm edema
interventions for HF
ABCs cardiac monitor oxygen > 90% BiPap IV fluids with caution loop diuretics, vasodilators
+ inotropes if cardiogenic shock
define aortic dissection
tear in intimal layer of aorta that exposes medial layer to forces of blood pressure
results in dissection of two layers of arterial wall
risk factors for aortic dissection
HTN atherosclerosis 60 + years cardiovascular surgery connective tissue disease cocaine trauma
sx aortic dissection in general
sudden pain to chest, back, flank, shoulders
tearing, ripping, sharp, stabbing
not relieved by analgesia
20 mmHg BP difference
sx ascending aortic dissection
MS change
sx stroke, MI, cardiac tamponade, aortic valve insufficiency
sx descending aortic dissection
renal failure
paraplegia
loss of distal pulses
interventions for aortic dissection
ABCs
O2
two large bore IVs
SBP > 100-120
IV nitroprusside, nitroglycerin, beta blockers
analgesics prn
surgical repair
define hypertensive urgency
substantial elevation in bp that should be treated w.in 24 hours
define hypertensive emergency/crisis
SBP > 180
DBP > 120
evidence of end organ damage
sx hypertensive emergency/ crisis
AMS cp, dizziness epistaxis, HA HF hematura, oliguria S3, S4 SZs, visual disturbance
interventions for hypertensive emergency/crisis
O2 IV continuous BP (art line) nitro/nitroprusside IV labetalol if other meds contradinicated
ICU
define endocarditis
inflammation of endocardium, including valves
sx endocarditis
sx infection
pleuritic cp
abd or back pain
signs of embolization
- stroke like sx
- hemoptysis
- conjunctival petechiae
complications of endocarditis
MI pericarditis cardiac arrhythmias valvular insufficiency CHF stroke arthritis aneurysm abscesses
define pericarditis
acute or chronic inflammation of pericardial sac
causes of pericarditis
virus, bacterial infection acute MI aortic dissection cancer, radiation renal failure mediastinal injury connective tissue disorder
sx pericarditis
sudden onset cp worse with inspiration, activity, supine and relieved by leaning forward
pericardial friction rub
tachycardia
sx infection
EKG changes in pericarditis
-ST elevation
-absent reciprocal changes
tall, peaked T waves in all leads except aVR, V2
-PR segment depression in lead II
pharm management of pericarditis
anti-inflammatory meds
corticosteroids if refractory to tx
if with HF:
- high dose NSAIDs
- colchicine
- abx/antifungals
- corticosteroids or diuretics
define blunt cardiac injury
blunt force to chest that may result in damage to myocardium, coronary arteries, or other heart structures
causes of blunt cardiac injury
MVCs with thorax on steering wheel
falls, crush injuries, violence, sports
mechanism of injury for blunt cardiac injury
rapid deceleration
shearing forces
compression
areas of injury during blunt cardiac trauma
RV and RA
coronary arteries
pericardium
thoracic aorta
sx blunt cardiac trauma
varies, maybe asymptomatic
cp
dysrhythmias and ectopy
sx of:
- cardiac tamponade
- great vessel rupture
- shock
- thorax, thoracic spine fx
- pulse changes
- cardiac failure
define pericardial tamponade
potentially life threatening condition in which pericardial sac, which normally holds 20-50ml fluid, accumulates additional fluid, resulting in pericardial or cardiac effusion
increase pressure compresses heart and affects ability to pump
precipitating factors for pericardial tamponade
dissecting aortic aneurysm end stage lung CA and other CA MI cardiac surgery pericarditis trauma
complications of pericardial tamponade
pulm edema
shock
rapidly fatal w/o tx
sx pericardial tamponade
beck triad
kussmaul sign
obstructive shock
Beck triad
3 D’s
distant (muffled) heart sounds
distended jugular veins (JVD)
decreased BP
Kussmaul sign
paradoxical increase in JVD and jugular venous pressure on inspiration
interventions for pericardial tamponade
pericardiocentesis or pericardial window
fluids with caution (consider vasopressors)
advanced airway with caution
define peripheral vascular disease
slow and progressive circulation disorder that may affect arteries, veins, or lymphatic system
2ndary affects on organs
primary cause of peripheral vascular disease
atherosclerosis
types of peripheral vascular disease
artrial
venous
lymphatic
define atherosclerosis
“hardening” of arteries that results from plaque accumulation on arterial wall
atherosclerosis overview
arterial wall becomes narrow and stiff
leg muscles work harder to get oxygenated blood since they are most distal and most commonly affected
define peripheral artery disease
narrowing or hardening of arteries outside of heart in which blood flow is compromised d/t compromised vessels
complications of peripheral artery disease
organs supplied by these arteries damaged d/t decreased blood flow, oxygenation, nutrients
sx peripheral artery disease
might be asymptomatic weakness/numbness sores w/ delayed healing shiny skin decreased pedal pulses hair loss intermittent claudication
define peripheral venous disease
chronic venous insufficiency where one or more veins do not adequately return blood flow from lower extremities to heart d/t damaged venous valves
complications and sx of peripheral venous disease
PE dilated veins, varicose veins edema leg pain skin fibrosis, venous ulcers venous claudication cellulitis, hair loss, redness, bruising delayed wound healing
define DVT
thromboembolic disease where blood clots develop in deep peripheral veins
risk factors for DVT
injuries to LE veins slow blood flow 2/2 decreased mobility increased estrogen chronic conditions genetics, age obesity
complications and sx of DVT
venous stasis ulcers delayed healing clot traveling, PE skin color changes edema
define thrombophlebitis
blood clot in superficial or deep vein that is inflamed, usually in legs
risk factors for thrombophlebitis
varicose veins
recent surgery or trauma
prolonged inactivity
complications of thrombophlebitis
limb ischemia
PE
varicose veins
sx thrombophlebitis
edema
erythema
persistent pain, heaviness
define lymphedema
most common peripheral lymphatic disease
edema 2/2 blockage to normal drinage pattern of lymph nodes
causes of lymphedema
surgery CA radiation lymph node infection inherited conditions
sx lymphedema
asymmetry of affected extremity
progressive, painless swelling
leg heaviness
define thromboembolic disease
blood clots that travel through blood stream and lodge in end organs, causing significant damage
thromboembolic disease overview
typically in legs, but also arms
DVT type of thromboembolic disease
improve/worsen pain in PVD
arterial:
-constant, worse with movement
venous:
-w. standing, better with elevation, rest
quality of pain in PVD
arterial: burning
venous: aching, throbbing
region of pain in PVD
arterial: distal to occlusion
venous: local to occlusion
severity of pain in PVD
arterial: excruciating
venous: aching, throbbing
timing of pain in PVD
arterial: as occlusion develops, not easily relieved
venous: pain evolves
objective findings of PVD
arterial: cold extremity, decreased pulses progressing to paralysis
venous: extremity swelling with deep muscle tenderness, darkened skin, fever
interventions for PVD
arterial: elevate HOB, not extremity
venous: elevate extremity
activitity for PVD
arterial: encourage activity
venous: absolute bed rest
complications of PVD
arterial: emboli, CAD, MI, stroke, ulcers, gangrene, limb ischemia
venous: emboli, PE, stroke
tx of PVD
arterial: thrombolytics, embolectomy, balloon catheter extraction or bypass graft, surgery for ischemia
venous: anticoags or thrombolytics, vena cava filter, compression socks