Tables Flashcards by Jeff Krekling

Table 1

9 Modifiable risk factors for heart disease

Hypertension, cholesterol, smoking, diet, obesity, sedentary, oral contraceptives, hormone replacement therapy, stress

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Table 2

4 nonmodifiable risk factors for heart disease

Age, Family history, carbohydrate intolerance, type A personality traits

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Table 3

Sodiums role in cardiac function

Flows into the cell to initiate depolarization

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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

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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

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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

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Table 5

P wave represents

Depolarization of the atria

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Table 5

PR interval represents

Depolarization of the atria and delay at the AV node

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Table 5

QRS complex represents

Depolarization of the ventricles

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Table 5

ST segment represents

Time between ventricular depolarization and beginning of repolarization

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Table 5

T-wave represents

Repolarization of the ventricles

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Table 5

R-R interval represents

Time between two ventricular depolarization’s

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Table 6
Primary chemical mediator of the…
1. parasympathetic
2. sympathetic nervous system

acetylcholine

2. norepinephrine, epinephrine

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Table 6
Primary nerves regulating cardiac function of the…
1. sympathetic
2. parasympathetic

Vagus

2. Nerves of the thoracic and lumbar ganglia

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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

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Table 6
Prime agonists of the…
1. Sympathetic
2. Parasympathetic

alpha: phenylephrine, beta: isoproterenol, beta-2: albuterol, alpha + Beta: norepinephrine, epinephrine, dopamine
Neostigmine, Reserpine

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Table 6
Prime antagonists of the…
1. sympathetic
2. Parasympathetic

alpha: chlorpromazine, phentolamine, Beta: propranolol, metoprolol, labetalol, atenolol
atropine

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Table 9

Physiologic effects of dopamine at a dose of 1 to 2 µg per kilogram per minute

Increased renal perfusion

Dopaminergic receptor site

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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

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Table 9 physiologic effects of dopamine at A dose of 10 to 20 µg per kilogram per minute

Vasoconstriction

Alpha receptor sites

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Common beta-1 blockers

Atenolol
Bisoprolol
Metoprolol

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Common nonselective beta blockers

Propranolol
Carvedilol
Labetalol

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Common calcium channel blockers

Amlodipine
Felodipine
Diltiazem
Verapamil

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Commonly used antidysrhythmic to drugs

Amiodarone
Digoxin
Lidocaine
Procainamide

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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