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)

Glucose problems made EZ

Another common subject on the NCLEX and USMLE examinations is the complications associated with elevated glucose. As most of you reading this blog know, glucose levels in the blood typically fluctuate only minor amounts between 80 and 110. This tight control is met through the balanced work of two pancreatic secretions named Insulin and Glucagon. Insulin picks up glucose from the blood and delivers it to cells in need of energy, or to the liver for storage. Glucagon senses when the level is low and frees stored glucose from its glycogen framework, into the bloodstream. However, for some this control malfunctions, and signs and symptoms begin to be seen. This imbalance is a life threatening emergency, and its recognition is vital to helping save our patients. What follows is a brief synopsis of a few glucose imbalance issues, and what we as practitioners must do about it.


Diabetic KetoAcidosis (DKA): (5-10% mortality)
– Almost exclusively in Type 1 diabetics
– S/S: Polyuria, dehydration, ab pain, fruity breath, AMS, ↓ Na/Mg/Phos, ↑K (↓ total body), + following:
• Hyperglycemia (above 250)
• Metabolic acidosis (pH below 7.3, HCO3 below 15, AG above 20)
• Ketonuria/Ketonemia
– TX:
• IV insulin bolus (0.1 unit/kg) then IV infusion with same amount per hr AFTER making sure pt is not ↓ K
– Continue until acidosis corrects then taper
• NS immediately upon diagnosis
– Switch to D5NS when glucose below 250; Why in the world would I give D5NS when a patient still has high glucose levels? The most important problem is the acidosis that is occurring. To reverse this we give insulin to drive glucose into the cell. Remember that K rushes into the cell along with the glucose, and wherever K can go, H+ can go. Since high levels of H+ in the blood is the cause of the acidosis, we give insulin to drive this H+ intercellularly, thereby reversing acidosis. We can't give insulin if the level of glucose is too low, so we give D5NS to keep levels around 250 so we can give insulin until the acidosis is gone.
• Add KCl to IV fluids once K below 5; replenish other electrolytes as necessary


Hyperosmolar Hyperglycemic nonketotic syndrome (HHNS):
– Severe ↑ Glucose, almost exclusively in Type 2 diabetics
– Similar to DKA but usually have much higher glucose (above 600) and NO acidosis or ketonuria/ketonemia
– Treat with fluids and low dose Insulin infusion
– An important distinction is that DKA usually occurs in Type 1 Diabetics, while HHNS most often occurs in Type 2 Diabetics. Remember this as it is a common question in the NCLEX world.

Hypoglycemia:
– Patho: When glucose drops to 80 = insulin levels ↓ ; 70 = Glucagon ↑; 50 = epinephrine ↑ along with s/s such as sweaty, ↑BP, ↑HR, tremors; Also around 50 CNS s/s (drowsy, h/a, confused) begin
– Note: S/S from epinephrine release are absent if pt is on a BB
– TX: If pt is alcoholic give Thiamine before any other treatment to prevent encephalopathy
• Can eat = ↑ sugar food;
• Can Not eat = ½ - 2 amps D50 IV push; (Glucagon alternative option if no IV access is available, however is of no use in prolonged hypoglycemia because stores of glycogen are depleted)

Points to remember:
– For high sugar (DKA, HHNS) most of the signs and symptoms are from polyuria, so look for dehydration and electrolyte imbalances...remember High and Dry
– For low sugar most of the signs and symptoms are from the release of epinephrine, so look for things that would happen when someone was high on adrenaline, such as hypertension, sweating, tachycardia and tremors.
– Imperative that you can recognize the difference between these two, as you are almost guaranteed to see a question relating to this difference!

Antibiotics made EZ...Part 2

If you have been studying for your NCLEX or USMLE examination for a while, you may have noticed there is some confusion about antibiotics. OK, hopefully you had a chance to read through the Antibiotics made EZ, Part 1. If you havn't, it may be better for you to jump down and read about the bugs, before we dive into the drugs. One of our worst mistakes in the vietnam war, was going into a country completely ignorant of our enemy. We took the wrong guns, and the wrong equipment, and paid for it. Same thing goes here. If you don't know the bugs, reading about the drugs listed below, will make little sense.

That being said, lets take a look at some of the most common medications used to treat Bacterial infections. NOTE that this is empiric therapy only...meaning these are the best options for treatment, BEFORE, our culture and sensitivity comes back. Once those results are ready, they should guide what we use. Also, the spectrum of resistance may be different wherever you live, so these are general recommendations on the most popular drugs. Ok that being said, lets take a look at the first and largest group...the Beta Lactams

Beta Lactams: the Penicillins

Penicillins (PCNs)

MOA: All Beta Lactams are Bactericidal, inhibiting cell wall synthesis; Preg Cat B

Natural Penicillins
Spectrum: G(+): Strep, Bacillus, Clostridium; G(-): Neisseria
Facts: Relatively few side effects; Allergic reactions relatively common; 98% of Staph are resistant to PCN due to enzyme able to destroy medication (PCNase)
PCN G: IV, IM (often only 1 injection need, i.e. Syphillis)
PCN V: PO, poorly absorbed so only for minor infections

Penicillinase (PCNase) Resistant PCNs
Spectrum: G(+): Staph (only indication though spectrum similar to PCN)
Facts: Original Drug was Methicillin but caused too much Interstitial Nephritis and was withdrawn; Despite this, Staph resistant to this class was termed Methicillin resistant (MRSA or MRSE)Oxacillin (PO, IV); Cloxacillin & Dicloxacillin (PO); Nafcillin (IV)

Aminopenicillins
Spectrum: G(+): Same as PCN plus Enterococcus plus G(-): Moraxella, E.Coli, Salmonella, H.influenzae, H.Pylori;Facts: NH3 group makes enhanced activity against G(-); 2nd most common cause of C.Dif Colitis Amoxicillin: PO; ENT infections, Cellulitis, Gonorrhea, C.A.Pneumonia (Strep)
Ampicillin: IV; Listeria, Enterococcus

Extended Spectrum PCNs
Spectrum: Same as AminoPCNs plus G(-): Pseudomonas, Proteus, Bacteroides
Facts: Broad Spectrum, usually reserved for serious infections with susceptible bacteria; No PCNase resistance when given alone; Often combo w/Aminoglycoside for Pseudomonas
Ticarcillin (IV); Piperacillin alone withdrawn (Combination drug Zosyn still available)

PCN/Beta Lactamase Inhibitor Combinations
Facts: PCNase inhibitor added to a Beta Lactam to extend coverage, mainly against S.aureus
Unasyn: Ampicillin + PCNase inhibitor
Augmentin: Amoxicillin + PCNase inhibitor
Zosyn: Piperacillin + PCNase inhibitor (Very Broad Spectrum)

Beta Lactams: the Cephalosporins

Class Facts:
Similar to PCN in most ways, but only 5-10% of PCN allergic will be allergic to Cephs
Generally avoided only if history of Anaphylaxis with PCN
Generally do not cover Anaerobes, Pseudomonas or cross BBB unless indicated
Do not cover MRSA (except Ceftaroline) or Enterococcus
Preg Cat B; Do not take with Alcohol; Consume at least 3 L water daily; Take w/food (avoid GI probs)
All Cephs can cause ↑PT/INR (give Vit K) and C.Dif Colitis

1st GenerationSpectrum: Broad G (+) i/c PCNases; limited G (-): E.Coli, Proteus, Klebsiella
Cephalexin (Keflex): PO; Cellulitis, Cystitis
Cefazolin (Ancef, Kefzol): IV; Surgical prophylaxis (protect against skin bugs)

2nd GenerationSpectrum: G (+): Same as 1st Gen plus G (-): H.Influenzae, Neisseria
Cefuroxime (Zinacef): PO, IV; Limited anaerobes; Cross BBB
Cefoxitin (Mefoxin): IV; Abdominal surgery prophylaxis; Excellent against Anaerobes (i.e. DM foot infections, Peritonitis, etc)

3rd GenerationSpectrum: Excellent G (-) coverage; limited G (+)
Ceftriaxone (Rocephin): IV; qd dosing; Crosses BBB; Meningitis, Encephalitis, Gonorrhea
Ceftazidime (Fortaz): IV; Pseudomonas, Neutropenic Sepsis, Serious infx only; Cross BBB

4th GenerationSpectrum: Excellent G (+), Excellent G (-) coverage i/c Pseudomonas; Cross BBBSE: Psuedomembranous Colitis (C.Dif) most frequent in class
Cefipime: IV; Cross BBB; Complicated UTI, Severe Sepsis
Cefdinir: PO

5th Generation
Spectrum: Excellent G (+), Excellent G (-) coverage i/c MRSA
Ceftaroline: IV/IM; Pneumonia and Skin infections including MRSA
Ceftobiprole (proposed): Not yet available, but on FDA Fast-track; Claims more extensive coverage with less susceptibility though FDA states studies not conclusive



Beta Lactams: The Carbapenems

Carbapenems
Spectrum: Broadest Spectrum of any Antibiotic; Indicated for severe bone, skin, tissue infections, as well as Endocarditis, Abdominal infx, Pneumonia, UTIs, Sepsis, Acinetobacter
Used as last resort in hospitalized patientOnly obvious omission is lack of coverage against C.Difficile, Atypicals, and MRSA
Restricted use by ICU IV infusion for significant infections, to keep resistance low
SE: Nephrotoxicity and Seizures (usually with preexisting Renal or CNS disease) Preg Cat C
Imipenem (Primaxin): IV; Combined with Cilastatin to block enzyme that breaks down drug
SE: Sz in 1.5% of pts on typical dose, 10% if above 500 mg q6h (So not for Meningitis)
Meropenem: IV; May kill G (+) a bit slower than Imipenem, but less Sz, no need for Cilastatin

Beta Lactams: The Monobactams

Monobactams
Spectrum: Limited to aerobic G (-) i/c Pseudomonas; Severe systemic infections and UTIsThis powerful GNR drug is usually combo with Vanco or Clinda for Powerful Broad spectrum
Preg Cat B
Safe to administer to pt w/PCN allergy
Crosses BBB
SE: Severe nephrotoxicity if given with aminoglycosides; Monitor renal function even if given alone; Eosinophilia rarely
Aztreonam: IV, Advantage of preserving all normal G (+) and anaerobic flora

Macrolides

Class Facts:
Broad Spectrum: Similar coverage to PCN plus Atypicals (Chlamydia and Mycloplasma), plus Spirochetes (Syphillis and Lyme) plus additional G (-) i/c H.influenzae
As a rule, Clarithromycin has most and Azithromycin the least G (+) coverage
Bacteriostatic, inhibiting protein synthesis
Do NOT cross BBB, so not for meningitis
Except Azithromycin, CP450 inhibited, increasing drug levels of Theophylline, Digoxin, Coumadin, etcFood decreases absorption of Macrolides
Often used as alternative when pt is PCN allergic
Can cause QT prolongation and Rhabdomyolysis (especially with Statins)
Exhibits Enterohepatic recycling (excreted in bile, then reaborbed; cx for buildup to toxic levels)
Since excreted in bile, not kidneys, no need for adjustment in renal failure
Azithromycin: IV, PO; qd dosing; No effect on CP450 so fewer drug interactions, and no enterohepatic recycling; Atypical Pneumonia, Chlamydia
Clarithromycin: PO; H.Pylori, Pneumonia, M.Avium Complex
Erythromycin: PO, IV, Topical, Opthalmic; Acne, Skin Infx, Eye infx, Diabetic Gastroparesis
SE: Cholestatic jaundice, GI distress (overall a very safe drug)

Fluoroquinolones

Class Facts:
Spectrum: Broad coverage of G (-), variable G (+), broad coverage of Atypicals
As a rule, increasing Generations have better G (+) and anaerobic coverage, but less Pseudomonas
Bactericidal, inhibiting bacterial DNA production
Precautions
Cx w/arrhythmias, CI if pt on antiarrhythmic meds
As a rule, any abx that targets bacterial flora (G -), effects coagulation by inhibiting Vitamin K
Preg Cat C
Binds Ca, Al, Zn, Mg so do not administer with Milk, Vitamins, or Antacids
Electrolyte interference may cause arrhythmias (QT prolongation), Seizures, Neuropathy, and this is increased when taking with NSAIDs
May cause weakness in M.Gravis
May cause Pseudomembranous colitis, Rhabdomyolysis
Spontaneous tendon rupture can occur when taken with Corticosteroids
Do not administer with Milk, Vitamins, or AntacidsHigh % of unmetabolized drug is excreted in urine, making it excellent for UTI
1st Gen: Did not contain Fl, and were just Quinolones; Much less effective, not used today
2nd Gen: Best antipseudomonal and G (-) in class; weakest G (+) and anaerobe
Ciprofloxacin: PO, IV, Opthalmic; Nosocomial Pneumonia, UTI, Infx Diarrhea (not C.Dif); Not for children below 18

3rd Gen: Levofloxacin (Levaquin): IV, PO; qd dosing; UTI, Community (CAP) or Legionella Pneumonia

4th Gen: Best G (+) and anaerobe in class; weakest G (-) and antipseudomonal in class Moxifloxacin: Pneumonia (CAP); Only Quinolone not renally excreted

Aminoglycosides

•Class Facts:
–Spectrum: Primarily aerobic G (-) coverage i/c Pseudomonas, some G (+) staph
–Often used in combination with G (+) drugs for Broad Spectrum coverage; Rarely used alone
–Quinolones are often used initially instead, due to high resistance to this class, unless high suspicion of Pseudomonas
–Bactericidal, blocking protein synthesis
–Allergies are very uncommon with this class
–Precautions:•Nephrotoxicity (renal failure) and Ototoxicity (hearing loss) fairly common, so not for long term –Nephrotoxicity risk increased when taking with Vanco, Cyclosporine, or IV contrast–Ototoxicity risk increased when taking with Loop Diuretics
•Measure Trough concentrations to assure efficacy, at least every 5d (30m before next dose)
•Most Preg Cat D (exception is Streptomycin which is a B)
•Decrease intestinal Vitamin K synthesis (anticoagulant quality)
•Can bind Ca, causing neuromuscular weakness and neuropathy
–Not absorbed well, so no PO
•Streptomycin: Eye infx, Tuberculosis; Limited use due to high resistance
•Tobramycin: Best antipseudomonal in class; MRSA (w/Ampicillin)
•Gentamicin: Excellent antipseudomonal; Endocarditis (w/PCN)
•Neomycin: Hepatic Encephalopathy (kills Ammonia producing GI flora); Only drug in class given PO as it is used to clean GI tract and is not absorbed; Very toxic if given IV
•Amikacin: Synthetic derivative of Neomycin; Often still effective when bugs are resistant to all other Aminoglycosides

Tetracyclines

•Class Facts:
–Spectrum: Very broad coverage of G (-), G (+), Atypicals, Protozoa; i/c Chlamydia, Mycoplasma, and Acinetobacter–Broad spectrum limited only by significant resistance, and indications now i/c: Acne, Rosacea, Anthrax, Bubonic Plague, Elephantitis, Malaria, Cholera, Syphillis, Rickettsia (Q fever)–Also inhibits ADH, and is used for SIADH–Bacteriostatic, inhibiting protein synthesis
–Precautions
•With odd strength comes odd SE; These i/c: Candida superinfections, Pseudomembranous Colitis (C.Dif), Thrombocytopenia, Coagulation irregularities, Hemolytic anemia, Lupus exacerbations, Nephrotoxicity•Bind Ca, Mg, Al, so do not give with milk, antacids, or iron salts; Also cause tooth discoloration in growing teeth (young pts); Cause weakness in M.Gravis
•Preg Cat D–Cause fibrosis in pleura, so used for direct administration to resolve pleural effusions
•Doxycycline (Vibramycin): PO, IV; You name it this will treat it, but use less harmful drugs, if effective, first
•Demeclocycline (Declomycin): PO; Reserved for the treatment of SIADH

Miscellaneous

Bactrim
•PO, IV; Sulfonamide, primarily used for UTI and Pneumocystis Carinii Pneumonia (in HIV pt)
•SE: Renal stones, Stevens Johnson syndrome, Allergic reaction common; Many drug interactions; Blood Dyscrasias (report any s/s of new infx)

Vancomycin•PO, IV; Spectrum i/c all G (+); Used for MRSA and MRSE; PO is useful for C.Dificile Colitis

•SE: Nephro/Ototoxic (Measure Peak/Trough levels); Red Man Syndrome (from rapid infusion; 60m min)

Metronidazole
•PO, IV; Excellent GPR/GNR Anaerobic coverage, used for intrabdominal; C.Dificile Colitis

•SE: Serious reaction if taken within days of Alcohol

Clindamycin
•PO, IV; Excellent Anaerobic coverage (rule is Clinda above diaphragm, Metro for below) as well as G (+)
•Often used for serious G (+) sepsis w/possible anaerobic component (i.e. postop abdomen surgery)
•Does not cross BBB; Esophagitis common if not administered with water
•SE: Pseudomembranous Colitis (C.Dif) common post treatment (10%)

Linezolid (Zyvox)
•PO, IV; Spectrum similar to Vanco plus most anaerobes; Used for VRSA, VRE
•SE: May decrease platelet count (3%); MAOI w/high risk of Serotonin Syndrome with SSRIs

Synercid
•IV; Alternative to Zyvox for VRSA, VRE
•SE: Serious arthralgia, myalgias; Central line only as thrombophlebitis in up to 75% of pts via Peripheral

Colistin
•IV; Mainly used for treatment of Acinetobacter and severe Pseudomonal infx; Spectrum i/c GNR
•Was actually first G (-) drug on market, gradually replaced by Aminoglycosides, then brought back into use by developing resistance to those drugs
•Developed so long ago, no actual recommended dosages have been studied (nightmare to prescribe)
•SE: Nephrotoxicity, Neurotoxicity (less common than with Aminoglycosides)

Antibiotics made EZ

Whether you are studying for your NCLEX or USMLE examination, or you are a practicing nurse or physician, the first step in understanding antibiotic drugs, is to know about the bugs you are trying to kill. We will take a two blog look at this subject, first by summarizing the bacteria that we frequently encounter in the hospital.

First lets take a broad look at bacteria:

•Gram Positive Cocci–STAPHYLOCOCCUS sp.
•STAPH. AUREUS
•STAPH. EPIDERMITIS
–STREPTOCOCCUS sp.
•STREP. PNEUMONIAE
•STREP. VIRIDANS
•STREP. PYOGENES (GAS)
•STREP. AGALACTIAE (GBS)
–ENTEROCOCCUS sp.

•Gram Positive Rods
–LISTERIA
–CORNYBACTERIUM DIPTHERIAE–BACILLUS ANTHRACIS (anaerobe)
–CLOSTRIDIUM (anaerobes)
•c. DIFFICILE
•c. TETANI
•c. BOTULINUM
•c. PERFRINGES

•Gram Negative Cocci
–NEISSERIA MENINGITIS
–NEISSERIA GONORRHEA
–MORAXELLA CATARRHALIS
•Gram Negative Rods–ENTERIC BUGS•ESCHERICHIA COLI
•PROTEUS sp.
•ENTEROBACTER sp.
•HELICOBACTER sp.
•SALMONELLA sp.
•SHIGELLA sp.
•KLEBSIELLA sp.
–HAEMOPHILUS INFLUENZAE
–LEGIONELLA sp.
–PSEUDOMONAS AERUGINOSA
–ACINETOBACTER sp.
–BACTEROIDES (anaerobes)
•B. FRAGILIS

•Atypical Bacteria: Think Doxy!
–CHLAMYDIA (intracellular)
–MYCOPLASMA (no cell wall)
–SPIROCHETES (curves: Syphillis)
–BORRELA (Corkscrews: Lyme)
Think INH/Rifampin/Azithro
–MYCOBACTER (Acid fast: TB, Leprosy, M.Avium Complex)

Gram Positive Cocci

•Staphylococcus
–Staph aureus (coagulase positive)
•Most pathogenic of the staphs; toxins cause Toxic Shock, Scalded Skin, Gastroenteritis
•Cause skin infections, Pneumonia (nosocomial), Endocarditis, Osteomyelitis•Abscess formation common; Can initiate clotting (think DIC)
•Tx: Oxacillin family; (Vancomycin if MRSA; Zyvox if VRSA; Bactrim or Doxy if Community MRSA)
–Also susceptible to: 1/2/4 Gen Cephs, Carbapenems, Macrolides
•MRSA: Staph resistant to Oxacillins and most other drugs; Use Vanco, Zyvox, or Synercid

–Staph epidermidis (coagulase negative)
•Normal flora of human skin
•Causes infection in immuno-compromised or depressed patients often via Central lines
•Tx: Similar to Staph Aureus (Vanco if MRSE, Zyvox if VRSE)

•Streptococcus
–Alpha Hemolytic•Strep pneumoniae (Pneumococcus): Leading cause of Pneumonia, Otitis Media, and Meningitis
•Strep viridans: Normal flora of mouth, can cause Dental abscess and Endocarditis

–Beta Hemolytic
•Group A (Strep pyogenes): Strep throat, Rheumatic fever, Scarlet fever, Glomulerulonephritis, Necrotizing fasciitis•Group B (Strep agalactiae): Can colonize vagina and cause Meningitis or Pneumonia in newborn
–Tx: PCN G; (Quinolone if PCN resistant; Ceftriaxone if in brain)
•Also susceptible to: 1/2/4 Cephs, Macrolides, AminoPCNs, Vancomycin, Quinolones

•Enterococcus
–Facts
•Common nosocomial infection with multi-drug resistance
•Cause Sepsis, Cellulitis, Intraabdominal infx, Endocarditis, UTI
•Tx: Ampicillin (or Vancomycin) + Gentamycin; (Zyvox or Synercid if VRE)
–Only other effective drugs: Zosyn, Imipenem, and Quinolones

Gram Positive Rods

•Listeria
–Commonly reside in soil, sewage, and stream water but rarely cause disease; If the immune response is slow, however, they move into cells and then are missed by immune cells
–Cause of Listeriosis, a lethal food bourne illness with mortality rate of 25%; Can invade CNS
–Tx: Ampicillin (often with Gentamicin)

•Cornybacterium diptheriae
–Toxin producing (2nd most lethal toxin to humans) causes Pharyngitis w/heart/CNS damage
–Tx: Antitoxin + PCN (Erythromycin if PCN allergic)

•Bacillus anthracis
–This anaerobic bacteria is the cause of Anthrax (meaning Coal = large black lesions)
–Lives in soil, and can be ingested by grazing animals where it causes rapid death (is then possible to inhale or ingest the bacteria from dead animals)
–Tx: PCN; (Cipro or Doxycycline if PCN allergic)

•Clostridium (anaerobic species)
–C. difficile
•Overgrowth in gut after Antibiotic treatment (Clindamycin, 3/4 Gen Cephs, Amp/Amox), causes Pseudomembranous Colitis•Tx: PO Metronidazole (or PO Vancomycin if relapse after taking Metro)
–C. tetani
•Toxin producing (3rd most lethal toxin to humans) causes PNS blockade (Tetany, Seizure, Death)
•Tx: Toxin irreversible once bound, so rapid treatment with PCN or Metronidazole imperative
–C. botulinum
•Toxin producing (Most lethal toxin to humans; 500 g could kill the entire world) that causes Botulism (a nerve blockade disease that leads to rapid paralysis and death)
•Bacteria can not survive in high oxygen or acidic environment, so usually ingesting bacteria not fatal as they are killed rapidly in GI tract; Must ingest toxins to have effects
•Infants (pre solid food) have a less acidic GI tract, so things harboring this bacteria (honey) can deliver the organism, which is then allowed to grow in more basic pH GI tract
•Tx: Hardy bacteria are not killed by antibiotics; Antitoxin very hard to find so Mechanical Ventilation and removal of cause (i.e. vomiting or debridement of wound) usually only thing possible

Gram Negative Cocci

•Neisseria meningitidis (aka Meningococcus)
–Common cause of meningitis; Also Meningococcemia (a rapidly fatal sepsis that kills over 50% of effected infants) and DIC
–Tx: PCN G (Ceftriaxone if PCN allergic) ; Best treatment is prevention with vaccine

•Neisseria gonorrhea–Cause of the STD Gonorrhea, as well as Conjunctivitis in newborn of infected mom
–Tx: Ceftriaxone (or Ciprofloxacin) and Azithromycin for possible concurrent Chlamydia

•Moraxella catarrhalis
–Causes URI and Otitis Media, as well as Pneumonia in smokers; Also COPD exacerbations
–Tx: Augmentin and Erythromycin
•Also susceptible to 2/3 Gen Cephs, Quinolones, Bactrim

Gram Negative Rods

A very common bug to recognize during your NCLEX or USMLE studying. It is useful to divide this class into the usual medical pathologies caused by each

•Urinary pathogens

–E. coli•Normal intestinal flora cause 90% of UTI; Also Pyelonephritis
•Pathogenic varieties are not normal flora and can cause Infectious diarrhea, Hemolytic Anemia
•Tx: Ciprofloxacin or Bactrim (Zosyn also effective)

–Proteus
•Causes UTI, in addition to renal calculi (struvite, CaCO3)
•Tx: Levaquin or Bactrim (Often treated without knowing you are treating Proteus)

•Respiratory pathogens

–Haemophilus influenzae
•Cause: Pneumonia, AOM; Also Sepsis, Meningitis, Cellulitis
•Tx: Azithromycin
–Also susceptible to po 3/4 Gen Cephs, Augmentin, Doxycycline, Quinolones, Carbapenems
–Klebsiella pneumoniae
•Usually only pathogenic in hospitalized immunocompromised causing Pneumonia and/or Sepsis
•Rapid resitance develops, especially against Cephalosporins and Quinolones
•S/S: Profuse, Jelly-like, Bloody sputum and high mortality rate
•Tx: Carbapenems or Zosyn

–Legionella•Pneumonia, derived airborn from water ducts, air conditioning units, water towers
•Tx: Macrolide (or Quinolone or Doxycycline)

–Pseudomonas aeruginosa
•Opportunistic infection causes Pneumonia, Sepsis, UTI, Right side Endocarditis, Osteomyelitis in Diabetic foot ulcers•First s/s often overwhelming Gram negative sepsis; 2nd most common cause of infection in ICU
•Extremely resistant to many drugs; All effective drugs IV, except Cipro and Levaquin so their use is severely restricted to avoid development of resistant strains
•Tx: Ceftazidime and Gentamycin (or Imipenem or Zosyn- varies widely between hospitals)
–Also susceptible to the following: Tobramycin, Cefipime, Colistin, Aztreonam

–Acinetobacter
•Pneumonia, Sepsis, Shock common, Up to 70% mortality; Can live 3 weeks on dry surface
•Tx: Imipenem
–Colistin or Doxycycline is alternative

•Gastrointestinal pathogens

–Helicobacter Pylori
•Common cause of Peptic Ulcer Disease
•Tx: (CAP) Clarithromycin, Amoxicillin, PPI (proton pump inhibitor)

–Salmonella
•Common cause of Diarrhea; Some forms also cause Typhoid or Sepsis
•Ciprofloxacin (rule out C.Dif with any infectious diarrhea)

–Shigella
•Causes bloody, purulent diarrhea in nursing homes and preschools
•Tx: Ciprofloxacin

–Vibrio Cholera
•Causes rice water diarrhea, with death from dehydration
•Tx: Doxycycline, fluids and electrolytes

–Yersenia•One form causes diarrhea; Another form causes Bubonic Plague
•Tx: Gentamicin

•GNR and Sepsis: Notes of Interest
–Many GNR have endotoxins, which are actually components of their cell wall
•When antibiotics begin their destruction, these toxins are released into the bloodstream in massive quantities, leading to Sepsis (Massive immune response) and eventually Septic Shock (Low BP and organ dysfunction)
•For this reason, Bacteremia (bugs in blood) with GNR is among the most serious of diseases, and should be treated aggresively in an ICU
•With Shock and 2 organs dysfunctioning the mortality rate is over 40%; With each additional organ dysfunction add 15%
•Sepsis is the #1 killer in the ICU, but is more preventable than you would think; The dirty source, is more often than not, indwelling catheters, so take extreme care with hygiene if you are ICU bound!!!

The Portal System...made EZ

The Portal system? I was asked that during my NCLEX review class last week by some Jr students, and figured there may be more that are more than confused by this term. So what follows is a simple description of this system that is involved in some of the more common pathologies in the hospital.

The liver is a selfish organ. It demands first access to blood that is bringing anything new into the system, kind of like a checkpoint at the border. At this checkpoint, the liver removes anything toxic by metabolism or excretion, converts nutrients into useable or stored forms, as well as a host of other responsibilites. There are four main areas that drain their blood to the liver, before it is dumped into the system. Check out the picture below, to get an idea before we discuss this.


The easiest to picture, is blood coming from the intestines, where new food was just absorbed. The liver wants first access to this blood, and gets it via the portal system. The problem is, what if the liver is congested or scarred and little blood can get through the liver. Well anyone who has ever been on the interstate understands, that there is backup, when something is blocking the road. The blood trying to get to the liver now backs up and dilates these portal veins. In the intestines, this blood can leak out into the tissue, becoming Ascites.

The next drainage, comes from the rectum. That is a port of entry into your body, right? Well the liver wants to analyze blood coming from this area of your body (that is good when there is a medication jammed in there) and gets that blood through the portal system. If this blood backs up, you will get big dilated veins in the rectum, called Hemorrhoids.

The Spleen also drains into the Liver before its blood has access to the main system. That is good, since broken down RBCs (bilirubin) get processed there. If this part of the portal system backs up you would see Splenomegaly.

The final system that drains via the portal system, is the other port of entry into your body, the esophagus. Veins partially drain this area in case there are invaders or new toxins to metabolize. If this backs up you would see big, dilated veins in the esophagus, called Esophageal Varices (Varicose veins in the throat). This is a significant issue...imagine our patient is eating a Dorito, and an edge of that cool ranch chip nicks the dilated vein. You would get bleeding into the esophagus. Remember that the liver also makes important clotting factors, and if the liver is damaged and congested we are not going to clot well. (Remember that PT measures one of the key clotting factors? It is also the fastest lab value to change with liver damage so check that PT/INR!)

So Esophageal Varices are a very important pathology to notice in any liver patient as we must stop that bleeding. Luckily, blood is very irritating and is usually thrown at you with very violent, bloody vomiting, so you shouldn't miss that sign. One you may miss is if you forget that the Liver also makes Albumin, which, because it is so attractive to water, is what keeps volume in your blood. If you lose this albumin from a diseased liver, you are already looking at a patient that has falling blood pressure. Now take some blood away via these Esophageal varices, and you may see significant Hypotension. So make sure you are measuring those vital signs frequently!

Here is a picture that hopefully summarizes what we just covered. Now you should at least be able to recognize what the portal system is, and why we see certain signs in Liver patients, like Splenomegaly, Ascites, Hemorrhoids, Esophageal Varices, and Hypotension.