Tables Flashcards
Table 1
9 Modifiable risk factors for heart disease
Hypertension, cholesterol, smoking, diet, obesity, sedentary, oral contraceptives, hormone replacement therapy, stress
Table 2
4 nonmodifiable risk factors for heart disease
Age, Family history, carbohydrate intolerance, type A personality traits
Table 3
Sodiums role in cardiac function
Flows into the cell to initiate depolarization
Table 3
Potassium’s role in cardiac function
Flows out of the cell to initiate repolarization
Hypokalemia increases myocardial your ability
Hyperkalemia decreases automaticity conduction
Table 3
Calcium’s role in cardiac function
Maintains pacemaker cell depolarization and involved in contraction of heart muscle tissue
Hypocalcemia leads to decreased contractility and increased myocardial irritability
Hypercalcemia leads to increased contractility
Table 3
Magnesium’s role in cardiac function
Stabilizes the cell membrane acts with potassium and against calcium
Hypomagnesemia leads to decreased conduction
Hypermagnesemia leads to increased myocardial your debility
Table 5
P wave represents
Depolarization of the atria
Table 5
PR interval represents
Depolarization of the atria and delay at the AV node
Table 5
QRS complex represents
Depolarization of the ventricles
Table 5
ST segment represents
Time between ventricular depolarization and beginning of repolarization
Table 5
T-wave represents
Repolarization of the ventricles
Table 5
R-R interval represents
Time between two ventricular depolarization’s
Table 6
Primary chemical mediator of the…
1. parasympathetic
2. sympathetic nervous system
- acetylcholine
2. norepinephrine, epinephrine
Table 6
Primary nerves regulating cardiac function of the…
1. sympathetic
2. parasympathetic
- Vagus
2. Nerves of the thoracic and lumbar ganglia
Table 6
Primary effects of stimulation
1. Sympathetic
2. Parasympathetic
- positive inotropic, positive dromotropic, positive chronotropic, dilates pupils, constricts blood vessels, slows digestion, dilates the bronchi
- negative inotropic, negative dromotropic, negative chronotropic, constricts pupils, increases salivation, increases gut motility
Table 6
Prime agonists of the…
1. Sympathetic
2. Parasympathetic
- alpha: phenylephrine, beta: isoproterenol, beta-2: albuterol, alpha + Beta: norepinephrine, epinephrine, dopamine
- Neostigmine, Reserpine
Table 6
Prime antagonists of the…
1. sympathetic
2. Parasympathetic
- alpha: chlorpromazine, phentolamine, Beta: propranolol, metoprolol, labetalol, atenolol
- atropine
Table 9
Physiologic effects of dopamine at a dose of 1 to 2 µg per kilogram per minute
Increased renal perfusion
Dopaminergic receptor site
Table 9
Physiologic effects of dopamine at a dose of 2 to 10 micrograms per kilogram per minute
Positive chronotropic and inotropic effects
Beta-1 receptor site
Table 9 physiologic effects of dopamine at A dose of 10 to 20 µg per kilogram per minute
Vasoconstriction
Alpha receptor sites
Common beta-1 blockers
Atenolol
Bisoprolol
Metoprolol
Common nonselective beta blockers
Propranolol
Carvedilol
Labetalol
Common calcium channel blockers
Amlodipine
Felodipine
Diltiazem
Verapamil
Commonly used antidysrhythmic to drugs
Amiodarone
Digoxin
Lidocaine
Procainamide
Commonly prescribed diuretics
Furosemide Torsemide Hydrochlorothiazide Metolazone Triamterene
Commonly prescribed antihypertensive agents
Labetalol
Propranolol
Clonidine
Reserpine
Commonly prescribed anticoagulant and antiplatelet drugs
Plavix
Aspirin
Warfarin
What occurs during the S1 “lub” sound
Closure of mitral and tricuspid valves at the start of systole
What occurs at S2 “dub” sounds
Closure of aortic and pulmonic valves at the end of systole
What causes the S3 sound
Vibrations of the ventricular waltz into rapid filling.
Indication of heart failure in the elderly
What causes S4 sounds
Turbulent filling of a stiff ventricle usually occurring in hypertrophy and possibly MI.
Heard just prior to S1
13 common causes of cardiac dysrhythmias
MI Ischemia Hypoxemia Autonomic nervous system imbalance Increased vagal tone Increased sympathetic output Heart failure (distention of cardiac chambers) Electrolyte disturbances Drug toxicity Hypothermia Metabolic imbalances CNS damage Trauma
Leads II, III, and aVF “see” what part of the heart?
LV Inferior wall
RCA; Posterior Descending
Leads V1, V2 “see” what part of the heart?
Septum
LCA; LAD, Septal
Leads V3 and V4 “see” what part of the heart?
LV anterior wall
LCA; LAD, diagonal
Leads V5 V6 and aVL “see” what part of the heart?
LV lateral wall
LCA; circumflex
Lead V4R “sees” what part of the heart?
RV
RCA; proximal
Possible complications found in leads II, III and aVF
Hypotension, LV dysfunction
Possible complications found in V1 and V2
Infranodal blocks and BBB’s
Possible complications found in V3 and V4
LV dysfunction, CHF, BBB’s, complete heart block, PVCs
Possible complications found in V5 and V6, I and aVL
LV dysfunction, AV node block
Possible complications found in V4R
Hypotension, Infranodal and AV Noble blocks, A-fib, PACs
Looking at leads I and aVF, how can you tell axis deviation?
Right (axis deviation) together, left (axis deviation) apart
Normal = both upward
Extreme right = both downward
The EKG changes commonly seen in ischemia
T-wave inversion
ST depression
Occurs at onset
EKG changes commonly seen in injury
ST elevation
Occurs within minutes to hours
EKG changes commonly seen in infarct
Q waves may appear, usually wide and deep
Occurs within several hours to days
Step 1 of the bradycardia algorithm
HR >50
If yes go to step 2
Step 2 of the bradycardia algorithm
ABC's O2 > 94% Monitor BP 12 lead IV
Step 3 of the bradycardia algorithm
If persistent bradycardia are the following present; AMS Acute heart failure Ischemic chest pain Hypotension Shock If no, continue to monitor vitals If yes go to step 4
Step 4 of the bradycardia algorithm
Administer atropine
.5mg every 3 to 5 min not to exceed total dose of .4mg/kg
If ineffective go to step 5
Step 5 of the bradycardia algorithm
Perform TCP, or dopamine infusion, or FB infusion
2-10mcg/kg/min
If ineffective go to step 6
Step 6 of the bradycardia algorithm
Consider transvenous pacing
Possible causes of PEA to consider during cardiac arrest
Hypovolemia, hypoxemia, hypoglycemia, hypothermia, hyperkalemia, hypokalemia, hydrogen ions
Tension pneumo, cardiac Tamponade, toxins
Clues to causes and treatment of hypovolemia
Patient history
Volume infusion
Clues to causes and treatment of hypoxemia
Cyanosis, airway problem
Intubation and ventilation with O2
Clues to causes and treatment of hypoglycemia
BG<60
D50 25g
Clues to causes and treatment of hypothermia
History of cold exposure
Hypothermia algorithm
Clues to causes and treatment of hyperkalemia, hypokalemia, hydrogen ions
Renal history, ECG changes
Immediate transport, consider sodium bicarb if certain of acidosis
Clues to causes and treatment of tension pneumo
History, no pulse with CPR, unequal breath sounds with hyper resonance to percussion unaffected side
Needle decompression
Clues to causes and treatment of cardiac tamponade
History, no pulse with CPR, JVD
Pericardiocentesis
Clues to causes and treatment of toxicities
History
Narcan
