Arrhythmias/Perfusion

transesophageal echocardiogram

detailed view via the esophagus for posterior structures

VFIB

this patient will never have a pulse; first intervention is call for help and initiate CPR, DFIB as quickly as possible

flash pulmonary edema

acute complication of heart failure characterized by: rapid accumulation of fluid in the lungs; person will be short of breath with pink, frothy sputum

QRS

part of heart rhythm that depicts the contraction of the ventricles

PVC

the ventricles fire earlier than expected; makes wide QRS; can come from multiple pacemakers

atropine

treatment for bradycardia

3rd degree

heart block where atria and ventricles are not correlated

PEA

looks normal on screen, but patient is found with no pulse

angina

choking in the chest

inotropes

drugs that increase myocardial contraction force and improve cardiac output

AFIB

irregularly, irregular rhythm; atria quiver

atrial flutter

atrial shark teeth

wenckebach

randomly drops a beat, QRS interval gets longer with each contraction

clots

high risk for this when in AFIB

VTACH

regularly, irregular rhythm; rate is 150 - 250 BPM and treated with antiarrhythmic amiodarone, but you need to find the underlying cause (H’s and T’s); can be pulseless

bradycardia

rate below 60 BPM

asystole

absolutely no heart contraction at all

sinus tachycardia

regular rhythm @ 100 - 160 BPM

PR interval

contraction of the atria and AV node transmission

atherosclerosis

plaque accumulation within the arterial lumen

P wave

SA node firing and atrial depolarization

intermittent claudication

pain with exercise and alleviated with rest

torsades de pointes

polymorphic VT; this is due to a low magnesium level

epinephrine

opens airways, reduces swelling, and constricts blood vessels; 1 mg every 3-5 minutes with no max dose

digoxin

well known inotrope; check apical pulse for 60 seconds before administration; check toxicity levels with AM labs

SVT

6 mg adenosine and then 12 mg if no change; cardiovert with no change

cardioversion

synch to R wave

QRS complex

ventricle depolarization; normal is <0.12

PRI

amount of time it takes for the electrical signal to go from the atria to the AV node; normal is <0.20

P wave

atrial depolarization; SA node firing

SA node

normal pacemaker of the heart (60 - 100 BPM)

AV node

gatekeeper; kicks in if SA node fails rate about 40 BPM

depolarization

contraction

repolarization

relaxation

normal sinus rhythm

60 - 100 BPM; PR interval <0.20; QRS <0.12

bradycardia

rate below 60 BPM; treat with atropine or pacing if pt. is symptomatic

atropine

raise HR; 1 mg every 3 min with max dose of 3 mg

sinus tachycardia

100 - 160 BPM; treat underlying cause, beta blockers, or calcium channel blockers

cardizem

common calcium channel blocker

afib with RVR

atrial fibrillation with rate > 100 BPM

AFIB

irregularly irregular rhythm; p waves are fibrillation of aorta; high risk for clots due to small ejection fraction

paroxysmal AFIB

pt. goes in and out of AFIB when they get sick

permanent AFIB

pt. always has AFIB

anticoagulants

heparin, enoxaparin, eliquis

antiarrhythmics

amiodarone and flecanide

cardiac ablation

stimulates heart out of AFIB by getting rid of faulty tissue

atrial flutter

P waves sawtooth; can be regular or irregular; same treatment as AFIB

supraventricular tachycardia

150 - 250 rate; regular; absent or hidden P waves

vagal maneuvers

blow into straw, bear down; treatment for SVT

adenosine

slow HR; use for SVT - 6 mg IVP, then 12 mg IVP, then cardioversion protocol

premature atrial contractions

irregular rhythm; normal P waves in underlying rhythm and different in early beat; treat underlying cause, beta blocker

premature ventricular contractions

irregular rhythm; p waves absent in ectopic beat; QRS wide during ectopic beat; beta blockers

multifactorial PVC

dangerous PVCs; overlapping triggers instead of root cause

bigeminy PVCs

PVC every other beat

couplet PVCs

two PVCs back to back

ventricular tachycardia

100 - 250 BPM; QRS complex is wide; no P waves; determine if stable or unstable

stable VTACH

no signs of poor perfusion; vagal maneuver

pulseless VTACH

start CPR; defib as soon as possible; epi 1 mg every 3 min IVP; amiodarone 300 mg IVP

amiodarone

antiarrhythmic; medically cardiovert

torsades de pointes

polymorphic VTACH; no p waves; irregular rhythm; wide QRS; caused by magnesium deficiency, ETOH, and malnourished

magnesium sulfate

treatment for torsades de pointes

ventricular fibrillation

never has a pulse; CPR and meds until restored or TOD; early defib is key

hypovolemia, hypoxia, hyper/hypo kalemia, hypoglycemia, hypothermia, hydrogen ions

H’s - identify underlying treatable causes of cardiac arrest

trauma, toxin, tamponade, thrombus, tension pneumo

T’s - identify underlying treatable causes of cardiac arrest

asystole

check in 2 leads and check pads to confirm cardiac death; no electrical activity; CPR with epi: 1 mg every 3 min with NO MAX dose; cannot be shocked

pulseless electrical activity

shows on telemetry but pt has no pulse; treat same as asystole

1st degree HB

PRI >0.20

2nd degree HB type 1

PRI gets longer until P wave with no QRS complex

second degree HB type 2

PRI is always the same but QRS will randomly drop; treat with pacemaker

3rd degree HB

P waves and QRS have no correlation; treatment with pacemaker

2, 3, aVF

inferior leads

1, aVL, V5, V6

lateral leads

V3, V4

anterior leads

V1, V2

septal leads

right coronary artery

supplies right atrium and ventricles

left coronary artery

branches into circumflex and LAD

circumflex artery

supplies left atrium and posterior left ventricle

S1

mitral and tricuspid (AV) valves close and ventricular systole starts

S2

aortic and pulmonary valves close; beginning of diastole

S3

after S2; fluid overload, HF, cardiomyopathy; can be normal in young adults, children, and pregnancy

S4

before S1; result of stiff ventricles, aortic stenosis, and ischemic disease; ALWAYS abnormal in adults

murmur

turbulent blood flow; valves don’t close properly; narrowing of valves or valve regurgitation

rub

caused by pericardial inflammation; pericarditis; pt. lean forward

atherosclerosis

plaque accumulation within the arterial lumen leads to significant physiological changes

angina

chest pain

stable angina

chronic; paroxysmal with exertion; relieved with rest and nitroglycerin

unstable angina

periinfarction; needs immediate treatment and can be new onset; occurs at rest and does not go away with rest

variant angina

vasospastic; occurs at rest but during stress

silent angina

no symptoms of chest pain; pt does not seek treatment

precipitating events, quality, radiation, severity, and timing

assessment of angina; PQRST

20 to 40 min

amount of time is takes for ischemia of MI to cause permanent damage

acute coronary syndrome

o2 therapy, and IV access needed; 12 lead EKG and telemetry needed; pain relief with nitroglycerin and morphine

morphine

pain relief and vasodilator

aspirin, heparin, beta blockers/ACE inhibitors

medication regimen for acute coronary syndrome

atherectomy

surgery to remove a clot

CABG

open heart surgery where a healthy vessel is taken out of another area of the body to bypass a blocked vessel in the heart; bypass

papillary muscle dysfunction

valves don’t close fully

inotropes

drugs used to increase myocardial contraction force and cardiac output; enhance hemodynamic stability

HFpEF

EF > 50%; diastolic HF; ventricular stiffness - cannot fully expand

HFmrEF

EF 40 - 49%