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Cardiology Unit I
Clinical medicine I Final Review
| Question | Answer |
|---|---|
| Vector same direction as the axis | + deflection |
| Vector and Axis perpendicular to each other | Straight line or equal deflections up and down |
| Vector and axis is opposite direction | - deflection |
| Length of the PR interval, QRS width, | .12-.20s, <.12 |
| SA, AV, Ventricle node conduction rates | SA: 60-100, AV: 40-60, Ventricles: 20-40 |
| Time from the SA node to the AV node | PR interval |
| How do we determine the axis? | look at lead I and lead aVF, |
| Determination BPM on EKG sheet | 300 150 100 75 60 52 45 |
| Rhythm that is no NSR but is irregular | Sinus arrhythmia |
| Another name for Paroxysmal atrial tachycardia (PAT) | Supraventricular tachycardia (SVT) |
| Atrial rate in atrial flutter | 250-350bpm sawtooth pattern |
| MC cause of Atrial flutter | Underlying Heart dz, 30% find no cause, seen w/ dig tox, and PE |
| MC cause of Afib | Rheumatic ht dz, HTN, Ischemic ht dz, thyrotoxicosis ->predisposes for thrombus in atria |
| If SVT stimulus is near SA node, how can we tell the diff b/w SVT and sinus tach? | Rate, Sinus tach |
| Tx of SVT | vagal maneuvers, Adenosine, verapamil, break conduction through re-entry circuit |
| Three or more ectopic beats in a row w/ wide QRS | V-tach –usually underlying ht dz |
| Tx Vtach | Immediate electrical defibrillation, CPR, amiodarone, lidocaine |
| PR interval >,20 sec, in nl hearts, no tx | 1st degree heart block |
| Preogressive prolongation of PR interval until blocked non-conducted P wave | 2nd degree ht block type I (wenckebach) |
| Do distance b/w P waves change with type I 2nd degree ht block? | No, PR gets longer to no QRS complex |
| Causes of 2nd degree block type II | Acute anteroseptal MI, Cardiomyopathy |
| Nl PR interval with sudden dropped QRS complexs | 2nd degree AV block: mobitz II, (non-wenkebach) |
| Atrial and ventricular depolarizations are independent of each other | 3rd degree AV block |
| Causes of 3rd degree AV block | Acute MI, drugs (dig, BB) |
| Are premature atrial contractions problematic | no happen in all ages all ppl, frequent |
| MC cause of PVC’s | hypoxia (uncommon in absence of ht dz): stress, alcohol, caffeine |
| 3 or more PVC’s in a row | considered Vtach , problematic w/ >10/min |
| Dz orientated, ability of a test to correctly identifiy those w/ the dz (true +) | sensitivity True +/True + + false - |
| Healthy orientated, refers to true negatives | specificity |
| Main components of CBC | Hgb, Hct, WBC, MCV, platelets (also get MCH, MCHC, RBC) |
| Nl value of Hgb and Hct | 12-18gm/dl, 21-48% |
| Causes of elevated hgb | dehydration, ^altitude, smokers, Congential ht dz, polycythemia vera |
| Cuases of low hgb | ^ destruction RBC, dec production of RBC, blood loss, preggo, Vit def. |
| Nl value of WBC | 4,000-10,000 x 10^9/L |
| WBC w/ diff components | Neutrophils, lymphocytes, eosinophils, basophils, macrophages |
| MC WBC and found when | Neutrophils 50-70%, bacterial infx, inflammatory condistion |
| When do we see lymphocytes and eosinohpils | lymphocytes: viral (25-40%) E: 1-3%, allergic or fungal infx |
| When do we see basophils and monocytes | B: inflammatory states/parasitic infx, M: phagocytosis bacterial infx |
| Reasons for low WBC | Viral, overwhelming bact. Infx, hypersplenism, meds that suppress bone marrow, |
| Left shift | ^ ration of band cells (immature neutrophils): healthy immune response to infx |
| Increase and decreased of MCV | I: Vit b12, folic acid def. D: iron def. nl: 90-100femoliters |
| Nl platelet count | 150,000-400,000 |
| What is found in with a urinalysis dipstick? | Specific gravity, pH, protein, glucose, ketone, leukocyte esterase, bilirubin, blood, urobilinogen, nitrates |
| Bence Jones Proteins is associated with | Multiple myeloma |
| What do RB casts and WB casts signify | R: glomerulonephritis, W: pyelonephritis |
| Nl values of AST and ALT | AST: 10-40IU/L: elevated w/ liver, muscle, cardiac injury ALT: 5-35IU/L ^w/ liver injury (more sensitive) |
| Marker of liver fxn | albumin |
| Coagulation studies | Prothrobin time PT, Partial thromboplastin time aPTT |
| Pancrease studies | Amylase 12-60 U/L, elevates first. Lipase: 20-200U/L remains elevated longer |
| Na+ elevation causes | V/D endocrine K+ dec w/ V/D |
| Nl blood fasting glucose, A1C | 60-126, <5% |
| Nl BUN, creatinine | 6-20 mg/dL C: .6-1.3 (elevated: impaired renal fxn) |
| Increases w/ congestive heart failure | BNP brain natriuretic peptide: produces by ventricles |
| Grades of Heart murmurs | 1-6, 1 hard to hear w/ stethoscope, 4-6loud with palpable thrills |
| Where are most murmurs located? | 95% L sided 50%mitral 45% aortic |
| Sxs frequently seen w/ murmurs | Decreased exercise tolerance, fatigue, syncope, CP, dyspnea, BP^ delayed upstroke or bounding |
| Crescendo-decrescendo murmurs | Systolic, Aortic& Pulmonic stenosis, hypertrophic cardiomyopathy |
| Holosystolic murmurs | Systolic: Mitral & tricuspid regurg, VSD |
| Decrescendo, pistol shot sound murmur | Aortic regurgitation (diastolic) |
| Mid-diastolic murmur | Pulmonic regurg, (diastolic) |
| Low pitched ruble, opening snap murmur | Mitral stenosis (diastolic) |
| Low pitched ruble w/ RV heave | Tricuspid stenosis (diastolic) |
| MC of all valvular ht dz | Aortic stenosis: d/t athreloclerosis, bicuspid valve in the young, Rheumatic ht dz |
| Aortic Stenosis Complications | Angina, Syncope, CHF |
| Palpable S4 heard with heave | aortic stenosis, ECG makes dx |
| Mitral stenosis is a complication of? Sxs? | Rheumatic fever, sxs: exercise intolerance, CHF, Horseness, Afib |
| Crisp systolic click and late systolic murmur | MVP |
| Causes of MVP | Congenital, Autosomal dominant, Connective tissue disorders |
| What increases/decreases the length of a MVP murmur | Standing: valsalva, brings the click closer to S1, squatting: relax, click closer to s2 |
| Primary and secondary causes of Mitral regurg | 1: MVP, leaflet defects, 2: LV dilation, Endocardial cushions d/t ischemic ht dz |
| When are prophylactic Abx recommended? | With prosthetic ht valve, hx endocarditis, Cong HD, |
| Types of prosthetic heart valves and uses | Bioprosthetic: mitral, reoperation common, Mecahnical: bleeding common: aortic valve Tissue: recommended w/ life expectancy <15 yrs |
| RF of PVD | age, smoking, obesity, sedentary, hyperlipidemia, HTN, DM |
| PVD Chart | Refer to it :D |
| Significant about sxs of PAD | reproducible pain w/ cramping and tightness |
| Gold std for Temporal arteritis | temporal artery bx: shows giant cells infiltrating the tissue |
| Ankle brachial test | assessing for PAD, take the systolic pressure in legs/ SP in arms Nl: .9-1.2 if > than that: hardening of arteries, .8-.9mild, .5-.8 mod <.5 severe |
| Diff b/w raynauds dz and phenomenon | D: young, no other factors, both hands, -Allen’s P: secondary to HTN, unilateral, + Allen’s |
| Inflammatory changes in sm/med sized arteries and veins in extremities | Buerger’s Dz (Thromoangitis Obliterans) |
| Sxs Buerger’s dz | Male, 20-40 smokers, severe pain w/o physical findings, Clinically dx, w/ angiogram for integrity of arteries |
| Tx Buerger’s dz | Avoid vasoconstriction, proper fitting shoes, elevate foot of bed |
| Etiology of thrombus formation | Virchow’s Triad: Stasis, Intimal Injury, Hypercoagulability |
| Prolonged venous thrombosis | Chronic Venous Insufficiency or Venous Stasis |
| Diagnostic test for DVT, | Homan’s test, Wells Score |
| Wells score results | >3 75% DVT, 1-2, 17%, <1 3% |
| Tx for Superficial venous thrombosis, DVT | SVT: warm compression, NSAIDs for pain and inflammation, DVT, anticoag, compression socks, may need surgery |
| Leading cause of death for men and women of all races and ethnicities | Coronary Heart Disease |
| Types of cholesterol | LDL: bad HDL: good, removes excejss cholesterol from tissues, Chylomicrons and VLDL: transport exogenous lipids, TG’s Main storage for fat |
| Patho of Atherogenisis | ^LDL->oxidized, Macrophages ingest ox. LDL—Foam cells, collegen over it:fibroud plaque: ruptures:platelet aggregation:thrombus |
| Unmodifiable RF for atherosclerosis | Fhx, Dm, Age, also maybe CRP, impaired fasting glucose |
| Modifiable RF for atherosclerosis | Smoking, HTN, low HDL, lifestyle: obesity, physical inactivity, atherogenic diet |
| What cause secondary hyperlipidemia | DM, Hypothroidism, obstructive liver dz, chronic renal failure, drugs ^LDL and dec. HDL |
| Metabolic Syndrome sxs | >3 of following TG’s >150, HDL <40, BP: >130/85, Fasting BGC>110, Waiste obesity |
| When do we check for lipoprotein disorders | parts of cholesterol are way high for the pt’s habitus, age, wt, etc |
| Routine lipid screening recommendations | 20yo every 5 years, FLP |
| CHD Risk equivalents | DM, PAD, AAA, symptomatic carotid A. dz, Multple RF’s confer a 10-yr risk of CHD >20% |
| Major CHD RF’s | Current cigarette smoking, HTN or on antiHTN med, Low HDL <40, FMhx CHD death/MI M<55 F<65, pt age M>45, F>55, Subtrat one RF for HDL >60 |
| CHD risk or equivalents LDL goal | <100, Drug therapy of >100 or considered <100 |
| Moderate high risk, 10-yr 10-20%(>2RF’s) | LDL <130, consider drugs 100-130 |
| Miderate Risk , 10 yr <10% | LDL: <130, Drugs >160 |
| 0-1RF Lower risk | LDL < 160, Consider Drug >190 |
| TLC’s | Healthy diet, wt reduction, increased Physical activity |
| Complications of untreated hyperlipidemia | cardiovascular, cerebrovascular, peripheral vascular dz |
| Comorbitities to HTN | CAD, L ventricular hypertrophy, Ischemic stroke, chronic kidney dz, DM, PAD |
| Phase of cardiac cycle in which venctricles contract | systole |
| Phase of cardiac cycle in which ventricles relax | diastole |
| Understand wiggers diagram | wiggers diagram |
| Maximuc atrial pressure during ventricle contraction | systolic pressure |
| Point of lowest arterial pressure, pressure which L ventricle must overcome to open aortic valve | Diastolic pressure |
| Cardiac output | HR x SV |
| Nl BP | systolic < 120, Diastolic < 80 |
| Prehypertension | systolic 120-139, Diastolic, 80-89 |
| HTN stage 1 and 2 | 1: S: 140-159 D: 90-99 2: S: >160 D: >100 |
| Measurement needed to classify HTN | two or more readings at 2 or more visits after initial screen |
| Uncomplicated and Comorbities HTN goal | U: 140/90,C: 130/80 |
| Some secondary causes of HTN | Pheochromcytoma, Cushing’s, 1 aldosteronism, congenital adrenal hyperplasia, Hyperparathyroidism, Hyper,Hypothyroidism |
| Causes of 2 HTN: Renal, Mechanical, Medication-induced, “white-coat” | |
| Malignant HTN classifications | SBP ≥ 180, DBP ≥ 120 |
| Longstanding HTN can lead to what? | encephalopathy, seizures/ and or coma if not treated |
| Modifiable RF’s for HTN | smoking, ETOH intake, physical inactivity, Renal Dz, Obesity, Dyslidemia, DM |
| Unmodifiable RF’s for HTN | age, genetics, race |
| Metabolic syndrome | THBFW, TG’s ≥150, HDL < 40 B: BP ≥ 130/85 F: Fasting BG: >110 Waist: >40M >35F |
| Sxs of HTN | usually asymptomatic, but Neuro: occipital HA early morning, Dizzi, palpitations, fatigue, impotence, Vascular: Epistaxis, hematuria, metorrhagia, blurred vision, CP |
| Labs for HTN workup | find underlying causes, CBC, K+ BUN/Creatinint, Ca+, phosphate, FBG, Lipid profile, TSH, UA, CXR, EKG |
| What are end organ damage evidence of HTN | Brain: stroke, TIA, Eye: Retinopathy |
| Papilledema, A/V nicking, Heemorrhage, Exudates, Cotton Wool spots | Signs of retinopathy of HTN |
| When can S4, cardiomegaly on CXR, and EKG changes all be seen together | longstanding HTN |
| Lifestyle modifications for HTN | Lower BP, Wt reduction, Diet, Exercise, Reduce ETOH to 1-2/day |
| Causes of orthostatic BP drop | MS, Parkinson’s, peripheral neuropath (DM), Gullain-barre’ syndrome, raynaud’s, Reflux sympathetic dystrophy, Drugs, Physical deconditioning, Dec. BV, |
| Dx of Orthostatic testing | Measure BP and HR from supine to standing; Sustained drop of SBP >20mg or DBP >10, HR ^ of 15 BPM: neurogenic Upright Tilt table testing |
Created by:
becker15
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