MedSurg I Unit 3 - Down & Dirty

olanjones's version from 2016-12-12 06:03

ECG Basics

Question Answer
P wave descriptiontime for the passage of electrical impulse through the atrium causing atrial contraction (should be upright)
P wave normal duration0.06-0.12
P wave source of possible variationdisturbance in conduction within the atria
PR interval descriptionmeasured from beginning of P wave to beg. of QRS complex; represents the time taken for impulse to spread through the atria, AV node & bundle of His, Purkinje fibers to a point immediately preceding ventricular contraction
PR interval normal duration0.12-0.20
PR interval source of possible variationdisturbance in conduction usually in AV node, bundle of His or bundle branches, but can be in atria as well
QRS interval descriptionmeasured from beg. to end of QRS complex; represents time taken for depolarization of both ventricles
QRS normal duration0.12 seconds
QRS source of possible variationdisturbance in conduction in bundle branches or in ventricles
ST segment descriptionmeasured from S wave of QRS complex to the beg. of the T wave; represents the time b/t ventricular depolarization & re-polarization; should be isoelectric (flat)
ST segment normal duration0.12
ST segment source of possible variationdisturbances usually caused by ischemia, injury or infarction
T wave descriptionrepresents time for ventricular repolarization; should be upright
T wave normal duration0.16
T wave source of possible variationdisturbances usu caused by electrolyte imbalances, ischemia, or infarction
QT interval descriptionmeasured from beg. of QRS complex to end of T wave; represents time taken for entire electrical depolarization & repolarization of ventricles
Normal Sinus Rhythm you want a 1:1 ratio of which waveforms?P:QRS should be "married"
Time interval for large box0.2 seconds (300 boxes = 1 minute)
Time interval for small box0.04 seconds (1500 boxes = 1 minute)

Heart Failure

Question Answer
HF characterized by:vent. dysfunction; ↓exercise intolerance; diminished QOL; shortened life expectancy
HF is a good ex of where the feedback & defense mechs start to work against us, how?They increase the workload of the increasingly weaker and weaker heart (interventions work to stop the compensatory mechanisms)
Systolic failure hallmark finding↓ in LV ejection fraction (EF is % of blood that leaves LV compared to what enters – normal = 55%)
Diagnosis of diastolic failure is based on the presence of what manis?pulm congestion, pulm HTN, ventricular hypertrophy (L&R), normal EF
Left-sided HF back up of blood into left atrium & pulm vein s= pulm congestion & edema
R sided HF from LHF, what happens with blood if LV failure?backed up into R atrium & venous circulation→pulm congestion→pulm HTN→↑RVafterload→RV hypertrophy→RV failure
ADHF physical findings **SATA ??*** *(Think SNS response)orthopnea, dyspnea, tachypnea, use of accessory muscles, cyanosis, cool & clammy skin, frothy/blood-tinged sputum, breath sounds: crackles, wheezes, rhonchi, tachy, hypoTN/hyperTN
NYHA Functional Classification of Heart DiseaseClass I: no limitation of physical activity
II: slight limit of physical actv. no sx at rest
III: marked limitation of physical activity but usu comfortable at rest
IV: can't do physical activity w/o discomfort
AHA stages of HFA: pts. at high risk with HTN, DM, etc.
B: structural HD pts.
C: pts. with prior or current sx of HF
D: pt's with refractory HF (severe sx)
CORE MEASURES in acute mgmt of HF (Joint Commission)D/C: activity, diet, meds, follow up appt., how to take & record daily wt., sx mgmt; LV functioning before/after; If EF <40% then ACE inhibitors; smoking cessation
CC Reduce preload↓ intravascular volume (preload) & ↓ venous return (preload)-reduces amount of volume returned to LV during diastole (high fowler's, IV nitro for vasodilation)
CC reduce afterloadarterial dilation to improve CO & ↓ pulm congestion: IV Na nitroprusside-reduces pre/afterload
Chronic HF collaborative mgmtO2 administration, physical and emot'l rest, non-pharm therapies (Intra aortic balloon pump, VADs, CRT, cardiac transplant is best)
Chronic HF drug therapy-DIURETICS do what??REDUCE PRELOAD auscultate to determine effectiveness; mobilize edema & get it out which will ↓ fluid demand returning & ↑ cardiac function **watch apical pulses
Chronic HF drug therapy-VASODILATORS MOA??reduce afterload & preload: ↑ venous capacity, easier/better contraction, thus reduces dysfunction, ↓ cardiac size: ACE inhibitors *1st line; ARBs; nitrates; BB's
Chronic HF drug therapy-DIGITALISpositive intropic agents increase strength of push; apical pulse; toxicity can kill you; WATCH K!!
Why so important to watch K with digitalis?likelihood of dig toxicity is ↑ in an env't of needs to have K in it.

Coronary Artery Disease - Part 1

Question Answer
Non-modifiable risk factorsage 65+, gender M>F, ethnicity (A.A. at higher risk), family hx,
Modifiable MAJOR risk factors -TEACH elevated serum lipids, HTN, tobacco use, physical inactivity, obesity
Modifiable RF – Serum lipids-Total cholesterol >200 mg/dL
-Triglycerides ≥150 mg/dL
-LDL cholesterol >160 mg/dL
-HDL cholesterol <40 mg/dL in men or <50 mg/dL in women
Modifiable CONTRIBUTING risk factorsDM (even if well-controlled); metabolic syndrome (r/t insulin resistance); psychologic states (type-A, depression, anxiety); homocysteine (byprod. of a.a. breakdown)
Guaranteed test question from?Begins bottom right pg. 737
Drugs that restrict lipoprotein productionHMG-CoA Reductase Inhibitors (Statins), Niacin (nicotinic acid), Fibric Acid Derivatives (finofibrate, gemfibrozil), Omega-3 Fatty Acid – inhibit synthesis
Drugs that increase lipoprotein removalBile-Acid Sequestrants (cholestyramine)- binds wtih bile acids in intestine & excreted in feces
Drugs that decrease cholesterol absorptionCholesterol Absorption Inhibitor (ezetimibe) – inhibits intestinal absorption
Anti-platelet therapyASA, works for men better than women
Angina vs. infarctionangina-from ischemia caused by reversible cell injury (no damage) vs. infarction from sustained ischemia=cell death (damage)
PQRST?Precipitating event (exertion of exercise causes ↑pain?); Quality of pain; Radiation (yes or no?); Severity (0-10) get a # to compare for next time); Timing (when, changed, ever had it before?)
Angina types*silent ischemia: absence of objective symptoms (esp. DM neuropathies)
*nocturnal angina: only at night, but not necessarily asleep
*angina decubitus: only when lying down & relieved by getting up
*Prinzmetal's angina: at rest, usually a spasm, associated with migraines & raynauds; associated with ↑Ca++; CCB and/or nitrates

Coronary Artery Disease - Part 2

Question Answer
Drug therapy focuses on vasodilationshort-acting nitrates (nitroglycerin); long-acting nitrates (isordil, nitro ointment, transdermal controlled release nitrates)
Other drugs for management of chronic stable anginaBB's (propranolol to ↓ sympathetic activity); CCB's (amdolipine works in heart for less contraction & in vessels to reduce afterload); ACE inhibitors to ↓vascular resistance/↓afterload; Ranolazine (do not use in conjunction with others)
Suspected CAD – common diagnostic studiesdetailed H&P, CXR (look for cardiac enlargement, aortic calcifications, & pulmonary congestion), 12-lead ECG (compare w/ previous tracing when possible), Lipid profile, Diagnostic studies (e.g., echocardiogram)
Measurement useful for predicting adverse cardiac eventsCalcium-score screening heart scan (CT)) locates calcium deposits in atherosclerotic plaque in the coronary arteries - additional testing (e.g., stress testing) is needed to know the impact of the lesion on coronary blood flow.
Known CAD & chronic stable angina - common diagnostic studies12-lead ECG, echocardiogram, exercise stress testing, and pharmacologic nuclear imaging.
ACS acute coronary syndromeprolonged unstable ischemia that is not immediately reversible (could be ST elevation→MI sign; non ST elevation does not R/O MI
Clinical Manis of MIPain, SNS stimulation (shunting blood to vital organs), N/V, fever
Where is the "widow maker"Left anterior descending artery
Healing Process MI - why are the first three days so important?cardiac markers are diagnostic d/t inflammation process in effect
Why is day 10-14 so tricky?scar tissue is still weak and vulnerable to ↑ stress. this is when pt. starts to ↑ exercise too. About six weeks is "healed"
CK-MB marker time it begins to rise, peak and return to normal post MI? rise: 3-12 peak: 24 normal: 2-3 days
Troponin marker time it begins to rise, peak and return to normal post MI? 3-12; 1-2 days; 5-14 days;
Myoglobin marker time it begins to rise, peak and return to normal post MI? 1-2 hours; 3-5 hours; 12-18 hours
CC: emergent PCIopen coronary arteries w/in 90 minutes of arrival; cardiac cath, maybe stent, maybe intraaortic balloon or CABG
CC: thrombolytic therapyclot busters; goal is to dissolve thrombus (best w/in 1 hours)
Distinguish Non-cardiac from Cardiac chest painNon-cardiac = no ECG changes, no cardiac enzyme changes (e.g. pneumothorax, pleurisy, peptic ulcer, GERD, psychosomatic)
Distinguish PE from Cardiac chest painMay have ECG changes, may have CPK changes, D-dimer elevated (a fibrin degradation product, small protein fragment in blood after clot is broken down by fibrinolysis)

Normal Lab Values

Question Answer
Sodium135 – 145 mEq/L, Chief electrolyte of ECF (extracellular fluid)
Potassium3.5 – 5.0 mEq/L, Chief electrolyte of ICF (intracellular fluid)
Calcium8.5 – 10.5 mg/dL
Magnesium1.3 – 2.1 mEq/L
Phosphorus2.5 – 4.5 mg/dL
Fasting glucose60 – 100 mg/d
BUN8 – 20 mg/dL
Serum Creatinine0.6 – 1.2 mg/dl
Albumin3.5 – 5.5 g/dL
Creatinine Clearance59-137 mL/min/1.73 m2
PT11.0 – 13.5 seconds, Coumadin Therapy will be Prolonged
PTT 25 – 35 seconds, Heparin Therapy will be Prolonged (up to 2.5 times longer)
INR (International Normalized Ratio) ≤ 1.1, Coumadin Therapy will be Prolonged (btwn 2-2.5 and 3.0-3.5 depending on goal)
pH7.35 – 7.45


Question Answer
Primary tx for those not at goal BPLifestyle modifications (<140/90 or <130/80 for DM or CKD)
Stage 1 HTN Initial drug choice w/o compelling indications (after lifestyle mods)SBP 140-159 or DBP 90-99; thiazide-type diuretics for most; may consider ACE inhibitor; ARB; BB; CCB; or combo
Stage 2 HTN initial drug choices w/o compelling indications (after lifestyle mods)for SBP >160 or DBP >100; two-drug combo for most (usu thiazide-type diuretic & ACE inhibitor, or ARB, BB, CCB)
Drug choices for HTN WITH compelling indicationsdiuretics, ACE inhibitors, BB's, CCB's as needed
If person is still not at goal BP after initial drug choices, then what?Optimize dosages or add additional drugs until goal BP is achieved. Consider consultation with HTN specialist
Weight loss of 10kg may decrease SBP by5-20mmHg
Isolated systolic HTNmost common form of HTN in individuals age >50
Auscultatory gapfind the 2nd rhythmic Kortokoff sound, wait 5 minutes and then find the higher one. Do not underestimate the SBP!
What is the baroreceptor reflexOne of the body's homeostatic mechanisms for maintaining BP. Provides a negative feedback loop in which an elevated BP causes BP to ↓; similarly a ↓BP depresses the baroreflex to cause a ↑in BP
Hypertensive ER = evidence of acute target organ damageHypertensive encephalopathy (cerebral hemorrhage); acute renal failure; MI; HF with pulmonary edema
Hypertensive Crisis you need to be hospitalizedIV drug therapy: titrated to reduce the mean arterial pressure (MAP) - no more than 20% to 25% in the first hour, with further gradual reduction over the next 24 hours
MAP (mean arterial pressure) equationSBP + 2(DBP) divided by 3
Hypertensive crisis you should monitorcardiac and renal function; neurologic checks; determine cause; education to avoid future crises

Vascular Disorders

Question Answer
PAD Drug Therapy-Antiplatelet (ASA, adenosine diphosphate receptor inhibitors {ticlopidine, clopidogrel})
-ACE-I (ramipril) used even if no ↑ BP, EBP shows ↓ Mortality & Cardiovascular morbidity, ↑Peripheral blood flow & ABIs, ↑ Walking distance
-Vasodilators to tx Intermittent claudication (pentoxifylline, cilostazol)
Critical Limb Ischemia ManagementProtect from trauma, Reduce vasospasm, Prevent/control infection, Maximize arterial perfusion
PAD Indications for Intervention Radiologic ProceduresIncapacitating Intermittent claudication; Pain at rest; Ulceration/gangrene that threatens limb
(May be candidate tPA if within 3 hours of onset OR may nick skin at femoral artery put tPA directly on clot – then can be 6 hours)
PAD Intervention Radiologic ProceduresAlternative to open surgical approach - usually done in cath lab; Includes PTA, Stents, Atherectomy, Cyroplasty
Percutaneous transluminal balloon angioplasty (PTA)Insertion of a catheter (contains cylindrical balloon) through the femoral artery - Balloon inflates to dilating the vessel (works best in vessels with < 4 inches (10CM) of occlusion, but high rate of recurrence within 1 year)
Common Surgical for PAD-Peripheral arterial bypass operation (autogenous vein or synthetic - synthetic typically for long bypasses)
-Balloon angioplasty with stenting used in combination with bypass surgery
-Endarterectomy (cut artery & remove plaque)
Venous thrombosis - Two main classifications1. Superficial (65% of IV patients get - usually minor & resolves) 2. Deep vein (usually iliac/femoral, can produce emboli which can migrate --> = PE!!!)
RF (Virchow’s Triad)1. Venous stasis (poor blood return to the heart) 2. Damaged endothelium (trauma, IVs, DM, burns) 3. Blood hypercoagulability (clotting problems, anemia, cancer, pregnancy/postpartum, BC)
S/S of Superficial ThrombPalpable/firm/sub-q cord, redness/warmth/edema, Can be in upper or lower extremities (may become septic if undiagnosed)
DVT Prevention/ProphylaxisEarly ambulation (OOB X 3 daily with meals in chair), Position changes (dorsiflexion & rotate ankles Q2), TED hose (measure and apply correctly) & ICDs (NOT IF ALREADY HAS A CLOT)
Purpose of Anticoagulant txIf no clot, it is preventative; If clot, used to stop growth, stop new development, or decrease chance to throw emboli
Warfarin Blood test & AntidotePT/INR (therapeutic INR btwn 2-3); Vitamin K
Heparin Blood test & AntidoteaPTT (therapeutic btwn 46-70 sec); Protamine sulfate

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