EKG's made EZ

The NCLEX exam doesn't expect you to be a highly trained cardiologist, and the USMLE on average only asks 2 questions about EKGs, but recognition of important pathological rhythms is a requirement for all future nurses and physicians. One of the most important, yet daunting tasks in the nursing and medical fields is to learn to recognize, both accurately and rapidly, Electrocardiograms (ECGs). Variations from the normal p, QRS, and T waves can be completely harmless to fatal in minutes, and it is up to us in the healthcare field to be able to tell the difference, and act accordingly.

Lets take a look at these variations and see if there is a way to make this a bit easier to understand. We will divide these variations up into three groups: Bradyarrhythmias (abnormal rhythms with rate usually below 60),Tachyarrhythmias (abnormal rhythms with rate usually above 100 bpm), and Dysrhythmias (alterations to the normal sinus rhythm pattern).


Bradyarrhythmias

1.Sinus Bradycardia
–HR less than 60 requires treatment with Atropine only if symptomatic

2.AV Block
A.1st Degree•Key: PR interval above 0.2 seconds; Delay is in AV node
•Usually benign but low HR responds to Atropine


B.2nd Degree type I•Key: Progressive prolongation of PR until a P wave fails to conduct and no QRS follows a P wave; Delay is in AV node
•Usually benign condition seen with normal aging not requiring treatment, but if symptomatic with bradycardia, will respond to Atropine


C.2nd Degree type II
• Key: Normal EKG with a sudden drop of a QRS; Block usually in the His-Purkinje system usually as a result of ischemia
•Can turn into the deadly 3rd degree so temporary transcutaneous pacer may be needed until an implantable pacemaker can be inserted


D.3rd Degree
• AV dissociation often from irreversible damage to the AV node following a MI
• Key: P-P length does not equal R-R length
•Ventricles do not pump fast enough to maintain CO and requires pacemaker



Tachyarrhythmias
•Atrial impulse

A.Sinus Tachycardia•HR 100-140, may occur with exercise or anxiety, but also may be earliest indication of hypovolemia
•Usually not symptomatic until above 140 when diastolic filling time is impaired
•Count the large boxes from top of a QRS to another: 1 box = 300bpm, 2 box = 150bpm, 3 box = 100bpm, 4 box = 75bpm, 5 box = 60bpm
•TX: Eliminate cause (i.e. anemia, stimulant; fluid bolus)



B.SupraVentricular Tachycardia•A conduction signal loops and reenters the atrium causing rapid, atrial driven HR usually above 140bpm
•Atrial tachycardia results in narrow QRS complexes
•TX: Adenosine given rapid IV push



D.Atrial Flutter•One foci in atrium fires rapidly, leading to sawtooth P waves and regular QRS with HR between 75-175
•Occurs most often in COPD, but may be seen with CAD and Atrial septal defects (ASD)
•TX: Identical to AFib



•Atrial Fibrillation•Multiple atrial foci cause lack of P waves and very irregular QRS waves with widely varied HR from 75-175 bpm

•Caused by CAD, MI, HT, PE, Pericarditis, Hyperthyroidism
•Major risk for thrombotic events (CVA) so treat according to protocol
•Treatment Protocol; Determine length/onset of AFib:
• Acute: less than 48hrs
Unstable: (Hypotensive, AMS) Immediate cardioversion
Stable:
»Tachycardic: Control Rate w/ Beta Blocker (Atenolol) then electrical cardioversion
»NSR: Proceed directly to cardioversion (electrical preferred to pharmacologic; If electrical fails or is unfeasible use Amiodarone to convert)
•Acute: greater than 48 hrs or unknown duration
–Before cardioversion: If longer than 2 days must use Warfarin to anticoagulate for 3 weeks before and 4 weeks after
–Avoid the wait: Can obtain an echo to r/o thrombus and load pt with Heparin and proceed to cardioversion; Still require the 4 week Warfarin anticoagulation after
•Chronic: Under 60 with no heart disease or risk factors require no treatment; All others get Warfarin for good


Tachyarrhythmias
•Ventricular impulse

A.Ventricular Tachycardia
•Ventricular foci initiate rapid HR with wide QRS complexes
•Caused by prior MI (most common), active ischemia, hypotension, cardiomyopathy, Drugs, Electrolyte abnormalities•May initially have a pulse, but can rapidly evolve into a deadly pulseless VTach
•TX: VTach with a pulse treated with 150mg Amiodarone
•TX: Pulseless VTach treated identical to VFib with Code being called: CPR, Defibrillation, Epinephrine, Amiodarone, and Lidocaine (Alternate drugs w/ Epi being only drug you can not max out on)



B.Ventricular Fibrillation
•Ventricular foci initiates rapid rhythm which causes heart to fatigue and quiver
•Typically evolves from VTach
•Ischemic heart disease most common cause
•Always pulseless, so initiate a code as above



C.Torsades de Pointe•A polymorphic VTach with varying direction of QRS amplitude (points alternate down to up)
•Often caused by electrolyte problems and long QT, so give a trial of Mag and Calcium



D.Asystole
•Loss of electrical signal initiation so it doesn’t respond to Defibrillation (basically resets rhythm to asystole)
•Epinephrine and Atropine are only hopes



Arrhythmias
•Dysrhythmias

A.Premature Ventricular Contraction (PVC)•Abnormal Foci causes random, wide QRS contractions
•May not progress to any other rhythm and have no symptoms
•Can progress to VTach and VFib, so treat more than 6/min or if symptoms present with BBs



B.ST Elevation
•Usually an ominous sign of actual myocardial infarction
•Treat with ACS protocol including ECG and Enzymes
•If present in all 12 leads may suggest Pericarditis

C.T wave Inversion
•An ominous sign of cardiac ischemia, can precede B
D.Q wave
•If deeper than ½ of QRS, suggests a prior infarction, Follows B

E.U wave
•Suggestive of hypokalemia
F.ST Depression
•Often a sign of ischemia, use MONA, ECG, Enzymes

G.Peaked T wave•Suggestive of hyperkalemia

H.Prolonged QT
•QT width is more than ½ the width of QRS-QRS
•Often caused by low Mg or Ca, as well as many drugs that effect these electrolytes
•TX: Withdrawal medication that caused and check/treat electrolyte abnormalities

Cardiovascular Drugs made EZ: Part 2

One subject that often confuses nursing students preparing for the NCLEX exam and practitioners alike, is that of clotting and anticoagulants. The problem with this, is these medications are extremely common in both inpatient and outpatient populations, so this knowledge is imperative for those in the healthcare industry to have. Lets take a look together and see if we can make it a bit more simple, in case your NCLEX exam decides to drill you on this point. We will go step by step through the clotting process, taking small sidetracks to look at specific medications.

Hemostasis

• When vascular injury occurs, various mechanisms are available to stop the loss of blood
• The mechanism employed depends upon the extent of injury, but the end result of all is to produce strands of Fibrin to patch the hole; The difference in the various mechanisms is the speed and amount of Fibrin produced
1.Platelet Plug
2.Intrinsic Coagulation
3.Extrinsic Coagulation


Platelet Plug

When vascular endothelial tissue is damaged, a platelet plug can form, sealing the hole. If no deeper tissues are exposed, this may be the extent of the healing process. If damage is more extensive, platelets, as well as tissue exposure can initiate further coagulation. Platelet plug formation occurs in 4 steps (use pic to right of text as visual guide):



1) Adhesion: When subendothelial tissue is exposed, sticky proteins (Von Willebrand factor) are exposed to passing blood and act as magnets to passing platelets.

2) Aggregation: ADP, a breakdown product of ATP released from damaged cells, stimulates the production of receptors (GPIIb) on the platelets that bind a free floating soluble protein Fibrinogen.

Pharm Note: Plavix and Ticlid inhibit ADP, so platelets are not stimulated to produce fibrinogen receptors and clots are more difficult to produce
Pharm Note: Abciximab (Reopro) binds to the platelet GPIIb receptor and blocks fibrinogen from binding, and clots are more difficult to make





3) Secretion: Stimulated platelets release chemicals like Thromboxane, that attracts other platelets. Fibrinogen can bind two platelets, thus platelets begin to collect in mass.

4) Platelet Coagulation: Stimulated platelets now produce factor V, which leads to fibrinogen being transformed into Fibrin threads to incase the aggregated platelets

Pharm Note: Aspirin blocks the release of Thromboxane for the life of the platelet, so cell aggregation is made difficult. This is why aspirin is known to make platelets less sticky, and is so frequently given as prophylaxis against clot formation. Since platelets are still allowed to bind Von Willebrand, there is still some platelet plug action, meaning some bleeding is stopped. This is why Aspirin is not as powerful an antiplatelet drug as prescription drugs like Plavix and Reopro.


(platelet aggregation)

(fibrin threads creating plug)

Intrinsic Coagulation

When the insult is deeper, collagen may be exposed, initiating the intrinsic coagulation cascade. Collagen activates factor 12 then 11 then 8 + 9 then 10. 10 converts Prothrombin into Thrombin, which then converts Fibrinogen to Fibrin. This process is faster than a platelet plug as you don’t need to wait for platelets to collect, and it forms more extensive Fibrin patches.

Pharm Note: Heparin inhibits the Intrinsic Factors, making them slower to respond, which makes clotting more difficult and less extensive
Lab Note: Partial Thromboplastin Time (PTT) measures the speed of collection of these factors, thereby measuring the effectiveness of Heparin. PTT, usually 30-40 seconds is the amount of time it takes all of the necessary factors to gather at site of need. Heparin binds these factors, slowing their collection, and lengthening PTT.

Extrinsic Coagulation

When deep injury occurs, tissue is exposed to blood, initiating the extrinsic coagulation cascade. Tissue factor activates factor 7 then 10. 10 then follows same route as above. With fewer steps this cascade is faster than the intrinsic and develops more extensive Fibrin patch. Of importance to note is just as Ca makes muscle contract stronger, its presence also makes clots stronger.

Pharm Note: Factor 7 is made in the liver from Vitamin K. Warfarin (Coumadin) blocks Vitamin K and thereby reduces the amount of Factor 7 made. Now it takes longer to collect enough Factor 7 to initiate this extrinsic clotting, and you have slower clotting that is less extensive. Since the medication effects future Factor 7 production and not that currently present in the blood, it takes a few days to see its effects.
Lab Note: Prothrombin Time (PT) measures the speed of collection of Factor 7, thereby measuring the effectiveness of Coumadin therapy. This value is converted to the INR. Think of this value as a stopwatch that starts timing as soon as injury occurs. PT, usually 10-12 seconds is the amount of time it takes factor 7 to reach the area of need.

(extensive fibrin patch)

Regulation of Coagulation

To assure coagulation does not go too far, 2 specific mechanisms inhibit or reverse the process:

1) Antithrombin III (AT III): AT III inhibits the production of Thrombin by blocking Prothrombin, thereby reducing the amount of Fibrin formed. Healthy endothelial cells produce this, thereby quarantining off the damaged area so clotting does not extend beyond where it is needed.

Pharm Note: Lovenox (Enoxaparin) enhances the activity of AT III, thereby slowing clot formation. The low molecular portion of heparin is the active part here, so regular Heparin partially works here in addition to Intrinsic factor inhibition.
Lab Note: Partial Thromboplastin Time (PTT) is not effected by Low Molecular weight heparins (Lovenox) because no Intrinsic factors are inhibited.

2) Tissue Plasminogen Activator (TPA): Injured cells also release TPA, which converts free floating Plasminogen to Plasmin. Plasmin degrades Fibrin, so clots are constantly broken down, even as they are built. The more active system wins, depending upon how much clotting is actually needed.

Pharm Note: TPA (Alteplase) can be synthetically injected to actively break down clots, such as in the case of a Stroke or Myocardial Infarction. Great caution should be used when administering this as massive, even fatal bleeds are possible. (Streptokinase and Urokinase are alternatives that work by same method)

Cardiovascular Drugs Made EZ: Part 1

Pharmacology is a key subject when studying for any healthcare board exam, such as the NCLEX or USMLE. This word can be a simple stimulus for nightmares in many in nursing or medical school studying for their boards. We are going to take a multi-part look at this subject by looking at one of the biggest classes of drugs that you will need to know: Drugs effecting the heart and vasculature.


This is a huge class of drugs, accounting for a huge chunk of the drugs that we actually need to know well, and is one that the NCLEX and USMLE are going to ask you about. Lets break this class down into smaller, more manageable chunks. We will start with drugs used to treat Hypertension, as this class is very large and very important. First of all, take a look at the picture below for a summary of the drugs we will discuss.

ACE Inhibitors

Names:
• “Prils” Think an ACE is a Pro (kinda like a pril)
• Examples: Enalapril (Vasotec), Captopril, Lisinopril
Uses:
• Hypertension, Heart Failure, Protection for diabetics vs nephropathy, Decrease Mortality in post-MI patients due to afterload reduction
Action:
• blocks the enzyme that converts angio I to angio II in the lungs. Angio II leads to vasoconstriction, aldosterone release, and sodium retention: this is blocked, which decreases blood pressure and puts less strain on heart
Common Side Effects:
• Dry hacking cough; Angioedema; Hyperkalemia
• Taste disturbance; Rash; Insomnia, Orthostasis
Nursing Implications:
• CI: Pregnancy Category D; Bilateral Renal Stenosis
• Use K supplements carefully due to hyperkalemia concerns
• Stop drug if cough, angioedema
• Taste of food may be diminished during first month of therapy

Angiotensin Receptor Blockers (ARBs)

Names:
• “Sartans”
• Examples: Losartan (Cozaar), Irbesartan, Valsartan (Diovan)
Uses:
• Hypertension, Heart Failure
Action:
• Blocks the receptor for Angiotensin II, blocking the effects of this potent vasoconstrictor
Common Side Effects:
• Hyperkalemia, Angioedema, Orthostatic hypotension
Nursing Implications:
• CI: Pregnancy Category D in 2nd/3rd trimesters; Bilateral Renal Stenosis
• Safer side effect profile than ACE inhibitors but less studied

To understand ACE and ARB it is vital that you have an idea of what the Renin-Angiotensin-Aldosterone System (RAAS) is. Remember the purpose of RAAS is to increase blood pressure in response to decreased renal blood flow or pressure, and the purpose of the drugs that work here is to block this system and lower blood pressure. Check out the pick below for a summary of the RAAS and where certain drugs work.

Beta Blockers (or beta antagonists)

Names:
• “OlOls: Remember Beta video tapes? They are OLdOLd
• Ex: Selective B1: Metoprolol, Atenolol (I MET A TEN last night)
• Ex: B1B2: Propanolol (Inderal), Labetalol, Carvedilol (Coreg) (ilol, alol-also alpha blocker)
Uses:
• Hypertension, Angina, Arrhythmias, Glaucoma, MI prophy, Migraines
Action:
• Block adrenergic Beta receptors (1 heart, 2 lungs), leading to lower sympathetic activity = decrease in cardiac output, blood pressure and renin activity. Also some drugs lower aqueous humor production
Common Side Effects:
• Bradycardia, fatigue, insomnia, bizzare dreams, sex dysfunction, lipid dysfunction; Respiratory distress (wheezing), Agranulocytosis, depression
Nursing Implications:
• C/I in asthma, bradycardia, severe renal/hepatic disease, hyperthyroid, CVA
• Signs of hypoglycemia (DM), tachycardia (hyperthyroid) may be masked
• Glucagon may reverse overdose

Calcium Channel Blockers (Antagonists)

Names:
• Dihydropyridines: “Pines”: Amlodipine (Norvasc), Nifedipine (Procardia)
• Non-Dihydropines: Diltiazem (Cardizem), Verapamil
Uses:
• Angina, Arrhythmias (Non-D’s have more AV node effect)
• Hypertension (Dihydro’s have more vasodilation effect)
• HT (Pines), Dysrhythmias (Verapamil), HT/Dys (Diltiazem)
Action:
• Blockade of Ca channels causes arteries to relax (vasodilate) and cardiac conduction to slow through the AV node
Common Side Effects:
• All: H/A, hypotension, dizziness, peripheral edema, Renal/Hepatic dysfunction
• Dihydros: Ankle edema, flushing, tachycardia, gingival hyperplasia
• Non-D’s: AV block, bradycardia, worsened systolic dysfunction
Nursing Implications:
• Use very cautiously with heart failure/left ventricle inpairment, AV block
• Don’t abruptly stop medication; Warn patient to contact MD if irregular HR, SOB, swelling, pronounced dizziness, constipation, nausea, hypotension

Peripheral Alpha Blockers

Names:
• Mixed names: “Zosins” for BPH, “ilol” for HT;
• Examples: Carvedilol (Coreg), Tamulosin (Flomax), Prazosin (Minipress)
Uses:
• Hypertension, Peripheral Vascular Dz (raynaulds, phlebitis, etc), BPH
Action:
• Blockade of Alpha 1 relaxes smooth muscle in arteries and prostate capsule, leading to lower blood pressure, reduction in BPH, and increased blood in tissues (warm/pink skin) as well as Renal arteries
Common Side Effects:
• Orthostatic Hypotension (especially first dose), Reflex Tachycardia, Ejaculation problems, nasal congestion
Nursing Implications:
• Begin with small dose and give at bedtime to avoid dizziness and syncope
• Change positions slowly to decrease orthostatic hypotension
• Alcohol, Excessive exercise, prolonged standing, heat make S/E worse

Central Alpha Blockers

Names:
• Clonidine (Catapres); Methyldopa (Aldomet)
Uses:
• Hypertension
Action:
• Central acting sympatholytic stimulates pre-synaptic alpha receptors to release NE, which paradoxically reduces peripheral NE release, inhibiting vasoconstriction = vasodilation and lower BP
Common Side Effects:
• Sodium/Water retention, Dry mouth, Bradycardia, Impotence, Depression
Nursing Implications:
• Advise patient not to abruptly withdrawal because significant rebound hypertension can result
• C/I in impaired liver function so monitor liver function tests occasionally
• Do not confuse with the benzo Klonipin (patients have done so and taken a bunch of Clonidine for a high, only to end up with a real low…BP that is.


Diuretics

Types:
• Loop: Furosemide (Lasix), Bumetanide (Bumex), Torsemide (Demadex)
• Thiazide: Hydrochlorothiazide (HCTZ)
• K-sparing: Amiloride, Spironolactone
• Carbonic Anhydrase Inhibitors: Acetazolamide (Diamox)
Uses: Edema associated with heart failure; Ascites with Cirrhosis; Hypertension
Action:
• Loop: Inhibit Na, Cl, and H2O resorption in the loop of henle thus decreasing blood volume; Also increase the excretion of K; Potent diuretics
• Administer IV Lasix slowly because hearing loss can occur if given rapidly
• Thiazide: Inhibit Na resorption and increase Cl, H2O, K, Ca, Bicarb, Mg excretion in the urine; Also cause arterial dilatation; Moderate diuretic
• While K and Na may be excreted, HyperCa is more likely to develop so never administer to patient with hypercalcemia;
• Eat foods rich in potassium, use sunscreen, and change position slowly
• Caution when taking with Lithium, Digoxin, Corts, PO Diabetic meds
• K-sparing: Block Na-K exchange in distal tubule causing loss of Na and water and retention of K; Weak diuretic mostly added to preserve K
• C/I in severe renal/hepatic dysfunction, hyperkalemia, Current ACE-I use
• Carbonic anhydrase inhibitors:
• Used to treat M.Alkalosis, Open Angle Glaucoma, Epilepsy, High altitude sickness
• Inhibits the enzyme carbonic anhydrase which normally is responsible for excreting H to combine with HCO3 for elimination of excess acidity, as well as promoting diuresis. This drug obviously leads to an increase level of H+ in the blood (M.Acidosis) and an increased excretion of Bicarb (HCO3)
• C/I with CLOSED (narrow) angle Glaucoma
• S/E i/c Renal Calculi, Hypercalcemia, and Hemolytic anemia
Common Side Effects:
• Loop/Thiazides: Hypokalemia, Hyperuricemia, Glucose intolerance, sexual dysfunction, increase cholesterol/triglyceride levels
• K-Sparing: Hyperkalemia especially when used with ACE inhibitors
Nursing Implications:
• Caution for electrolyte disturbances; Watch for cramping, paresthesia
• Administer in morning to avoid diuresis during night, Supplements (PhosLo)