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Clinical Medicine > Cardiology II > Flashcards

Cardiology II Flashcards

1
Q

what is a healthy waist to hip ratio for men? womeN/

A

> 1.0 men; >0.8 women

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2
Q

in addition to diet and exercise, what component is really important in fighting obesity?

A

behavior modification

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3
Q

what level of weight loss is recommended to start?

A

5-7% of body weight

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4
Q

what are the most important things to focus on when helping someone lose weight/

A

portion control, focus on increasing nutrient dense foods (as opposed to “donts”) like veggies fruits and high fiber grains and veggies, decrease added sugars, decrease trans fats

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5
Q

when should a pt be referred to a dietician?

A

pretty much all of them: with obesity, DM, HTN,

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6
Q

what are the recommendations for blood sugar before and after meals?

A

before: 80-130; after

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7
Q

what meal times are important for someone with diabetes and what carb choices/meal are recommended for men and women?

A

consistent meals. men: 4-5 carb choices/meal; women: 3-4 carb choices /meal snacks

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8
Q

grains, starches, peas, corn, milk, yogurt, fruit, fruit juice, sweets and sugary bevs, are all examples of what?

A

carbohydrate foods

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9
Q

what are carb free foods?

A

unbreaded proteins, non starchy vegetables (green beans, peppers), most condiments in appropriate servings

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10
Q

what are some examples of a carb choice? carb choice=15 g of carb

A

1 slice bread, 1/4 bagel, 1 small apple, 1/3 cup rice or pasta, 1/2 cup pasta casserole, 1 cup milk, 1/2 cup juice,

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11
Q

what is a good resource for healthy eating?

A

my plate

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12
Q

what are the recommended dietary changes for metabolic syndrome?

A

diets that promote weight loss and improvement in insulin sensitivity: mediterranean, DASH, low glycemic index, high fiber >30 mg

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13
Q

what are the recommend dietary changes for HTN?

A

DASH diet:

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14
Q

what conditions are associated with an increased risk of CVD and can benefit from dietary changes?

A

dyslipidemia, DM, HTn, metabolic syndrome, obesity

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15
Q

what restriction is going to be lifted in the new dietary guidelines for americans 2015?

A

cholesterol

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16
Q

what is the recommended Na intake? and recommendations per AHA?

A
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17
Q

where do saturated fats come from? how many calories in 1 g of fat?

A

animals and tropical plants: red meat, dairy, eggs, coconut oil, palm oil; 9 calories in 1 g of fat

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18
Q

what is the current dietary guidelines for americans for saturated fat? NCEP? DASH?

A

DGA

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19
Q

what do each of these mean? fat free, low fat, reduced/less fat, low in sat fat, lean, extra lean, light

A

fat free:

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20
Q

is there any research to support that coconut oil or grass fed fats are healthy alternatives?

A

no

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21
Q

how are trans fats made? why are they bad? what foods are they found in?

A

created by adding hydrogen to liquid regular oils to make them last longer, they are solid at room temp, cheap to make. they increase LDL and lower hDL and can be found in a food label with anything that says “hydrogenated in it’. found in your packaged foods that last a long time: cookies,crackers, butter, margarine, microwave popcorn, salad dressing,

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22
Q

what percent of our diet should fats have?

A

20-35% of calories.

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23
Q

if you are on a 1500 calories diet, how much of your calories should come from fats? saturated fats?

A

fats: 20-35% of 1500 is about 300 to 500 calories, or 150 of saturated fat.

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24
Q

what kinds of fats are omega 3s and omega 6s?

A

PUFAS: polyunsaturated fats: more than one unsaturated carbon bond. liquid at room temp, solid when chilled.

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25
Q

what kinds of health benefits do PUFAs have?

A

lower LDL, can also reduce HDL though

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26
Q

what do omega 3s do? example

A

reduce inflammation, control blood clotting, brain health, protect against heart disease and stroke
i.e. walnuts, flaxseed, salmon, fatty fish (tuna, mackerel, trout, herring), canola and soybean oil.

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27
Q

what do omega 6s do? example

A

help brain function, growth and development; examples: safflower/sunflower oil, nuts and seeds, egg yolks, animal based products

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28
Q

what should the correct ratio of omega 6 to omega 3s be?

A

4:1 - 2:1

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29
Q

what are the health benefits of MUFAS/ examples?

A

reduce ldl and maintain HDL, examples: olive, canola, sunflower, sesame, peanut oil (do not cook with at temps over 325), almonds, hazelnuts, pecans, avocados

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30
Q

what are the kinds of fiber? recommended daily amount/ why is it good?

A

soluble=attracts water and promotes fullness, satiety. insoluble doesn’t attract water and passes through GI tract quickly and adds bulk to stool. soluble examples: oatmeal, oat bran, nuts, seeds, most fruits, dry beans and peas. it lowers cholesterol by binding the bile acids and excreting them. recommended DV 20-35 gm

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31
Q

what are some tips to get more fiber? what are some cautions?

A

choose fruit over fruit juice (unnecessary sugar), try eating 2 veggies at dinner, keep a bowl of veggies cut and washed in fridge so they are easier to eat, always choose whole grains, eat fiber at breakfast to stay fuller longer and lose weight because you don’t overeat later; caution: gradually increase to avoid GI sx, can cause gas, bloating, cramps, don’t forget to include more water! good suggestion is adding 5g/wk

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32
Q

what is a serving of vegetables/fruits/ what is recommended DV?

A

get more veggies than fruits. veggies=1 cup raw or 1/2 cup cooked. fruits=1 medium size fresh or 1/2 cup canned. 3 veggies, 2 fruits per day is rec.

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33
Q

light or moderate alcohol consumption (1-2 per day) can decrease risk of CHD by how much? how does it work?

A

40-70% but binge drinking can increase your risk; it increased HDL, insulin sensitive, thrombotic activity, and inflammation reduction

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34
Q

is there evidence to prove that supplemental folic acid, b6, b12 or folic acid can prevent cvd?

A

no, but elevated homocysteine levels are assoc with higher risk for CVD, folic acid can reduce risk only when consumed via diet >1000 mcg/day

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35
Q

what is the evidence regarding antioxidants?

A

no strong evidence to support that these give a reduced risk of CVD, may be linked to just eating more fruits and vegetables

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36
Q

what are some potassium rich foods? serum K above 4.0 meg/L is rec for MI pts

A

bananas, avocados, orange, mango, raisins, potatoes and sweeet potatoes, cooked spinach, chocolate, milk, pb, yogurt

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37
Q

what increased risk of death from heart issues do people have who increase

A

38% higher risk

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38
Q

what is the rec daily limit for added sugars?

A

75g

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39
Q

what are the four categories of exercise we should get?

A

aerobic, muscle strengthening, flexibility, balance

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40
Q

what are the 3 rec options for exercise?

A

moderate intensity aerobic for >30 min for 5d/wk; vigorous for >20 min 3 d/wk, combo of mod and vig. can do 30 minutes in 10 min intervals!

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41
Q

what is the rec for resistance training?

A

2 days per week to increase muscle strength and endurance

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42
Q

what is the rec exercise for wt loss and to reduce risk of chronic disease and improve overall health and fitness?

A

150 min of mod to vig exercise per week, or >300 of mod intensity for overweight adults

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43
Q

what are the 5 as of AHAs recs for physical activity and public health?

A

assess current level of physical activity, advise on health benefits of physical activity, agree with pts degree of readiness and counsel based on this , assist in developing an action plan, arrange a method for follow up

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44
Q

what are some ways we can ask about pts eating habits at home to help them?

A

ask about where their food comes from: homemade? eating out? food security: live near a grocery store? assess nutrient comp of foods based on dietary recall and suggest alternatives and suggest adding MFA and omega 3s, address portion control (half of plate should be veggies, limit all added sugars, meat and grains to 1/4 of plate, eating out, choices, consider plant sterol esters–give specific recs in writing. acknowledge the strengths of their current diet and focus on those. highlight potential problem areas from diet hx. identity foods they consume that are major sources of unhealthy fats, sugar, sodium. be ready to assess barriers. negotiate. set only a few goals and start small and practical. let the patient decide what to do from your recommendtions. give written and verbal instructions. patient must be motivated.

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45
Q

what are the 4 functional classes of HF?

A

determineNew York Fcnl Classes: 1) no sx with ordinary activity 2)slgiht limitation of physical activity. Comfortable at rest but ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain 3)marked limitation of physical activity. comfortable at rest but less than ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain 4) unable to carry out any physical activity without discomfort. sx at rest.

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46
Q

What are the 4 stages of heart failure?

A

stages A)at risk for development of HF (HTN, valvular disease, hx of MI) B) asx LVD (NYHA class I) C: mild to moderate (NYHA II-III) D: severe HF sx not responsive to med therapy

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47
Q

what is a cardiomyopathy? why is it good to use this term with pts?

A

aka HF: an abnormality of heart muscle. it can be dilated, hypertrophic, conduction abnormality, ischemic, valvular, metabolic. pts listen to this term better and what it means, if they hear heart failure they stop listening and freak out!

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48
Q

what’s a good working definition of heart failure?

A

a clinical syndrome in which heart disesae reduces CO, increases venous pressures, and is accompanied by molecular abnormalities that cause progressive deterioration of the failing heart and premature myocardial cell death (heart failure begets more heart failure)

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49
Q

how do you describe the path phys behind heart failure?

A

myocardial cell damage (HTN, MI pregnancy, etc) causes myocardial dysfunction. Myocardial dysfunction causes decreased cardiac output and increased filling pressures. This causes the body to have compensatory responses like activated the sympathetic nervous system (vasoconstriction) and RAAS leading to increased sodium and water retention (increasing BP and preload) and increased stroke volume (increasing afterload). the sympathetic response can also lead to increased demand and ischemia/energy depletion and remodeling leading to necrosis or apoptosis and cell death, continuing the cycle. when RAAS is activated thus leading to angiotensin II, upon reaching the receptor for angiotensin II it starts vasoconstriction, oxidative stress, cell growth, proteinuria, LV remodeling, and vascular remodeling

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50
Q

what are some of the causes of heart failure?

A

etioloyg: ishcemia/CAD, HTN, valvular heart disease, congential abnormalities, myocarditis, toxins (alchohol, chemo), metabolic abnormalities (uremia, hyper/hypothyroidism, hypocalcemia) infiltrative diseases (amyloidosis, hemochromatosis) tachy/bradycardia, high output failure (anemia, AV fistulas)pathophysiology: myocardial cell damage (HTN, MI pregnancy, etc) causes myocardial dysfunction

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51
Q

what are some of the RFs for CHF?

A

HTN, advanced age, CAD (60-75%), renal dysfunction, Male, black, LVH, DM, obesity

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52
Q

what are some of the sx of HF?

A

orthopnea, PND, DOE, ascites, 2-3+ pitting edema.assess for NYHA functional class: sx of fatigue, weakness, dyspnea, orthopnea, edema, abdominal distention, and chest discomfort, postural lightheadedness, decreased mental acuity, bloating/nausea, weight gain, anorexia/weight loss, palpitation

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53
Q

how does the severity of the disease (HF) affect mode of death?

A

the less severe the disease, the greater the chances they will die of sudden death. late stage CHF pts usually die of CHF slowly.

54
Q

what are the signs/physical findings you may see in someone with HF?

A

pink, frothy sputum. BP, HR, RR can be high or low. Distended neck veins. Enlarged heart with possible murmurs, diminished tones, gallop sounds. Crackles, wheezes, rhonci dullness to percussion in lungs. Distended abdomen and enlarged liver, ascites. peripheral edema and diminished pulses or pulses alternans (varied tones). pallor, tired appearing.

55
Q

what are some of the ways they test/dx HF?

A

TTE is gold std to look at EF, chamber sizes,and ventricular wall thickness, systolic fcn, and diastolic fcn, valvular stenosis, regurgitation, estimate atrial pressures and quantify stroke volume and cardiac output .ECG only shows prior MI, conduction disease or hypertrophy. Cxray can show cardiomegaly, infiltrates, effusions, and signs of pulmonary congestion. CBC for anemia and electrolyte abnormalities. TSH to r/u hyper/hypothyroidism and for hemochromatosis. HIV infection test. Fasting lipids and glucose for modifiable RFs. BNP if normal can tell you that its not heart failure. can do a heart catherization/angiography to look at intracardiac pressures and stenosis but its risky. rarely they do a biposy but this can put a hole in the heart.

56
Q

how accurate is the BNP test for dx of HF

A

83% accurate and a BNP of

57
Q

which is more important: sodium or fluid restriction?

A

sodium

58
Q

what are the JCAHO core measurements for HF?

A

aimed to improve quality of care, outcomes, and decreased hospitalizations. 1. assess EF q yr 2. ACEI, ARB unless CI. 3. smoking cessation counseling documented. 4. comprehensive discharge instruction

59
Q

what are the some of the exacerbating factors of HF?

A

exacerbating factors: non compiance with meds or diet, NSAIDS (worsen renal function and counteract effect of ACE, negative inotrpic drugs (antiarrythmics: BBs, CCBs, antifungals cardiotoxic: chemos like daunorubicin/daunomycin, imatinib, ethanol, amphetamines; Na and h20 retention: NSAIDS, COX2, glucocorticoids, androgens, estrogens, salicylates (high doses), other illnesses, ongoing myocardial ischemia, progression of valvular lesions, htn, heat and humidity, cold

60
Q

how does aldosterone help IN HF?

A

aldosterone antagonist. IN HF: prevents or slows ventricular remodeling. Decreases preload by inhibiting aldosterone. Reduces morbidity and mortality and hospitalizations. Indicated for pts with NYHA class II-IV with LVEF

61
Q

which diuretic is rec’d for mild overload in hF? moderate? severe?

A

mild=thiazide, moderate=loop; severe=IV loop

62
Q

how can furosemide (loop diuretic) be used in diuretic resistance management?

A

May be increased to 480 mg/day; bid is more effective than tid. Reemphaszie sodium restriction

63
Q

what is the typical presentation o stable angina?

A

episodic lasting 5-15 min,provoked by exertion/stress, relieved by rest/NTG. EKG may be normal or show ST depression and T wave flattening or inversion. Normal cardiac enymes.

64
Q

what is prinzmetal angina and how does it present?

A

Prinzmetals (rare) occurs at rest at same time of day from coronary artery spasm, 2/3 have ASCVD 1/3 normal arteries. Relieved by nitro. Shows STE during attacksame time of day, relieved by nitro.

65
Q

what is the typical presentation of unstable angina?

A

Unstable angina: may see ST depression or T wave changes for several hours to go back to normal or progress to MI. possible minor elevations in cardiac enzymes.change in prior angina pattern either in amount of exertion req’d or time of day or increased duration or severity, more nitro req’d to relieve the pain, pain may come on at rest.

66
Q

what is the typical presentation of an acute mI?

A

acute MI: CP, assoc sx, risk factors. substernal or left sided pain that radiates to jaw, shoulders, left or both arms, heaviness, pressure, tightness, squeezing, unaffected by body position or change or deep breaths. often brought on by physical exertion or emotional stress, relieved by rest or nitro. assoc sx: SOB, diaphoresis, nausea, palpitations, dizzy/light headed. may be sweaty, anxious, pale, may have increased HR or decreased if pacemaker affected, may have increased BP or decreased if it can’t pump, may have new murmur from mitral regurgitation, papillary muscle rupture, ventricular septal rupture, may have signs of CHF, STE and Q wave formation, may have reciprocal changes in distant leads (usually ST depressions), elevated cardiac enzymes. may have a new bundle branch block. . usually begins as hyperacute T waves, then giant R waves, then STE and Q waves

67
Q

what are some of the atypical presentations of

A

up to 25% of MIs are “silent”. women may have different sx: pain in back, neck, jaw, SOB, nausea, diaphoresis, exhaustion.

68
Q

what does BNP help find?

A

distinguish CHF from other causes of dyspnea

69
Q

who would get cardiac catheterization?

A

pts being considered for angioplasty/stent or coronary artery bypass grafting because of anginal sx not responding ot meds, unstable angina, non invasive tests demonstrating high risk disease, recurrent sx in pts with prior angioplasy or CABG, pts surviving sudden death from life threatening arrythmia in which CAD may be the cauase, chest pain or cardiomyopathy of unknown cause, acute STEMI

70
Q

how long does it take to know with enzymes if someone has had an MI?

A

need serial enzymes. myoglobin rises 1-2 hrs after, peaks 4-6 hours, normalizes after 1 day. Troponin rises 3-6 hrs, peaks 12-24 hours, normalizes 7 days.

71
Q

what is a coronary angiogram? what are some downsides?

A

noninvasive imaging of coronary arteries. sx pts at intdmt risk for CAD or if there was a nondx stress test. downside=radiation, can’t do anything about a blockage if you find one.

72
Q

how is an echocardiography procedure done?

A

two dimensional cross section of cardiac structures. Can also use it with a color flow doppler to assess for direction and speed of blood flow or regurgitation, ASD/VSD. TEE is where a transducer is actually passed into the esophagus to enable clearer visualization of cardiac structures.

73
Q

what can an echocardiography show?

A

segmental wall motion abrnomaltiies (especially with concomitant stress test) signify ischemia or prior mI.–this is a prognostic indicator of CHF because if lots of the muscle is gone they will likely develop CHF.

74
Q

what is the indicator for a positive ischemic stress EKG?

A

positive ischemic test if >1 mm ST depression: signifies underlying CAD.

75
Q

what can an MRI look at in the heart?

A

provides excellent anatomic definition of heart thickness, size, congenital defects, can show LV fcn and wall motion if rapid sequence of pics taken. Use if echo is suboptimal. Can image coronary arteries for CAD (still investigational).

76
Q

what is MUGA? (multiple gated blood pool imaging)

A

RBCs labeled with technetium 99. heart is imaged through 100s of cardiac cycles to provide a clear image/movie of the heart. Calculates LVEF and can look for “wall motion abnormalities” after MI. can look for temporary wall motion abnormalities with exercise.

77
Q

how does a PET scan evaluate ischemia or past Mis?

A

distinguishes those areas of heart that are still metabolically active as they use the substrae

78
Q

how does a radionuclide study work?

A

radionuclide uptake is proportional to myocardial blood flow. Areas of diminished uptake signify hypoperfusion and ischemia, or cell death like past MI

79
Q

what is the difference between a subendocardial ischemia and a transmural ischemia

A

a subendocardial ischemia is just the innermost part of the heart–there is not enough blood to get into those perforating arteries. a transmural one is where the entire vessel is occluded and no blood gets down artery to even get to the perforating vessels.

80
Q

what do large Q waves mean on an ECG?

A

dead muscle

81
Q

what are some typical signs of an impending MI?

A

hyperacute T waves within minutes, giant R waves with increased voltage that occurs before STE–bascially an intermediate between hyper acute T waves and STE

82
Q

what artery corresponds with an anterior MI?

A

lad

83
Q

which artery corresponds with a posterior MI?

A

right coronary (posterior descending)

84
Q

what artery corresponds with an inferior MI?

A

RCA

85
Q

what artery corresponds with an lateral MI?

A

usually left circ

86
Q

how do you distinguish a posterior Mi>

A

reciprocal changes in anterior leads like ST depressions and tall wide R waves in leads v1-v3 (R/s ratio>1 and doesn’t follow the normal pattern of R waves starting small and getting bigger).

87
Q

what are some of the complications that can result from an acute MI?

A

acute MI has 30% mortality rate. Electrocardiac disturbances can occur resulting in sudden death. LV pump failure/cardiogenic shock, papillary muscle insufficiency, ventricular septal rupture, cardiac rupture, thromboembolism, pericarditis, ventirclar aneurysm, right ventricular infarcation

88
Q

what are some of the signs of cariogenic shock?

A

(tachy, low BP, confused, cold extremties, no urine, high mortality 65%)

89
Q

what is the indication for lyrics?

A

for those with acute massive embolism who are hemodynamically unstable, plus lower risk of bleeding, and without risk of right ventricular injury. If STE in 2+ continuous ECG leads and new LBBB with typical MI sx.

90
Q

what do cardiomyopathies result in?

A

HF, arrythmias, conduction abnormalities and thromboembolic strokes

91
Q

what is the most important thing to control with HF?

A

blood pressure

92
Q

what are some of the physiological reasons for HF?

A

pump dysfunction, increased resistance, activation of RAAS

93
Q

what are the 3 clinical forms of cardiomyopathy?

A

dilated, hypertrophic, restrictive

94
Q

what are the most common causes of dilated cardiomyoapthy/

A

often cause can’t be identified=idiopathic. MC: idiopathic. Others: inflammtory (post viral, myocarditis), toxins (alcohol, chemo, heavy metals, occupational like arsenics, catecholemines like amphetamines/cocaine), metabolic (nutritional deficiencies, elecrolyte deficiencies, thyroid, DM, pheochromocytoma, obesity), familial (dominant or abnormality in sarcomere proteins), sustained rapid afib, post partum, stress induced (takostubo), hemochromatosis, amyloidosis, sarcoidosis.

95
Q

what will be some of the history and physical exam findings in someone with dilated cardiomyopathy?

A

HX: intolerance to exertion. Non specific non ischemic chest pain (may not be brough on by exertion or relieved by rest). Syncope (from arrythmias or emboli), sx of HF: DOE or at rest, pND, orthopnea, peripheral edemaPE:

96
Q

what are the causes of sudden death in young athletes?

A

hypertrophic cardiopmyopathy, commotio cordis, coronary artery abnormalities, dysrythmias

97
Q

what are the causes of hypertrophic cardiomyopathy?

A

genetic,

98
Q

what are some of the RFs of hypertrophic cardiomyopathy?

A

ventricular arrythmias, afib, sudden death in athletes

99
Q

what is the cause of hypertrophic cardiomyopathy?

A

genetic heterogenous autosomal dominant muation in genes for sarcomeres. Left ventricle and septum thickened. presents between ages 20-40.

100
Q

what are some of the signs and sx of hypertrophic cardiomyopathy?

A

exertional dyspnea, CP, syncope, palpitations, esp during exercise (warning sign of HD, if in young athletes it needs a cardio exam and EKG, echo and exercise stress test) EF>60% but left volume decreased. Prominent left ventricular impulse. S4 gallop. Murmur along left sternal border that’s heard best with less volume like on inspiration and when standing/valsalva.

101
Q

what does the tx for hypertrophic cardiomyopathy involve?

A

DON’T MISS THIS IN YOUNG ATHLETES GETTING PHYSICALS!!! Meds: beta blockers or CCBs (allow better ventricular filling), treat HF, rate control and anticoag if afib occurs, anti arrythmics or ICD b/c of risk for sudden death, endocarditis prophylaxis, septal myomectomy. AVOID vasodilators, digitalis, alcohol–these can cause increase in HR?

102
Q

what are some of the causes of restrictive cardiomyopathy?

A

infiltrative diseases: amyloidosis, sarcoidosis, storage disases (like glycogen), metabolic diseases, radition, restrictive pericarditis, chemotherapy, endomyocardial fibrosis(africans, children, young adults), idiopathic

103
Q

what findings may you see in someone with restrictive cardiomyopathy?

A

may be normal. May be signs of Left sided HF. May have afib. decreased diastolic and systolic dysfnction. Ef

104
Q

which cardiomypathy is assoc with systolic dysfunction? which with diastolic dysfunction/

A

dilated cardiomyopathy is assoc with systolic dysfunction (can’t pump adequately bc so dilated); restrictive and hypertrophic cardiomyopathies are assoc with diastolic dysfcn b/c they can’t relax/fill normallly so you get weird sounds diastole

105
Q

what are the different ways HF is categorized?

A

dilated, hypertrophic, restrictive; high vs low output; acute vs. chronic; systolic vs. diastolic

106
Q

how do you tx acute decompensated HF?

A

decompensation: o2 mask/CPAP, lower BP, nitro, IV diuretics (usual daily dose of loop)

107
Q

what is the tx for HF?

A

HFrEF: pharm:quadruple tx is std. 1st line: ACEI, BB, AA, diuretics. 2nd line: ARB, hydraizaine/isosorbide, digoxin, sacubitril/valsartan, B type natriuretic peptide. For pulmonary sx: O2 and diuretics (relieve fluid, increase exercise tolerance). Nitro to reduce preload. Other tx if arrythmias. nonpharm: Restrict sodium to 2g/day. daily weights and when to call. smoking cessation. exercise. Weight reduction to reduce workload of failing heart. avoid alcohol and other cardiotoxic substances like gingko. HFpEF: control the known physiological facotrs like BP, HR, blood volume, and ischemia: HTN meds (BB, ACEI, ARB), diuretics for sx, coronary revascularization for CAD, manage AF. ICD if arrythmias (to prevent sudden death from vfib). last resort of heart transplant. conditioning. tx specifically for acute decompensation: o2 mask/CPAP, lower BP, nitro, IV diuretics (usual daily dose of loop)

108
Q

what are the various labs/tests you can do to assess HF?

A

TTE is gold std to look at EF, chamber sizes,and ventricular wall thickness, systolic fcn, and diastolic fcn, valvular stenosis, regurgitation, estimate atrial pressures and quantify stroke volume and cardiac output .ECG only shows prior MI, conduction disease or hypertrophy. Cxray can show cardiomegaly, infiltrates, effusions, and signs of pulmonary congestion. CBC for anemia and electrolyte abnormalities. TSH to r/u hyper/hypothyroidism and for hemochromatosis. HIV infection test. Fasting lipids and glucose for modifiable RFs. BNP if normal can tell you that its not heart failure (if >100 correlates with HF). can do a heart catherization/angiography to look at intracardiac pressures and stenosis but its risky. rarely they do a biposy but this can put a hole in the heart. can look for genetic causes. can do drug screen or viral titers. can do blood alcohol/liver fcn. serological tests for AI diseases. iron levels to rule out hemochromatosis.

109
Q

What are the various findings in HF?

A

pink, frothy sputum. BP, HR, RR can be high or low. Enlarged heart with possible murmurs (in hypertrophic or valvular insufficiency or stenosis), diminished tones, gallop sounds or s3 or s4. Crackles, wheezes/rales, rhonci dullness to percussion in lungs. signs of congestion: Distended abdomen and enlarged liver, ascite,. peripheral edema, Distended neck veins, rales, orthopnea, PND. signs of low perfusion at rest:diminished pulses or pulses alternans (varied tones). pallor, tired appearing, obtunded, cool extremities, hypotension with ACEI, renal dysfunciton. enlarged liver, stasis in lower extremities. stigmata of liver disease: swollen carotids, ruddy skin, no need to shave, ascites, foot drop, spider angiomas, palmar erythema. 3 different CLINICAL FORMS: dilated (most common), hypertrophic, restrictive. signs of thyroid issues: reflexes, tremor, lid lag. orthopnea, PND, DOE, ascites, 2-3+ pitting edema.assess for NYHA functional class: sx of fatigue, weakness, dyspnea, orthopnea, edema, abdominal distention, and chest discomfort, postural lightheadedness, decreased mental acuity, bloating/nausea, weight gain, anorexia/weight loss, palpitation. Assess for comorbidites like HTN, DM, dyslipidemia, obesity and sleep disordered breathing. Ask about hw of exposue to cardiotoxic agents like chemo. ask about social hx of alcohol, tobacco, illicit durgs. FH for hx of sudden cardiac death, CAD, cardiomyopathy. get a three generation hx for those with familial cardiomyopathy

110
Q

cessation of breathing or hypopnea (shallow breathing) while sleeping associated with excessive daytime sleepiness

A

obstructive sleep apnea

111
Q

what are some of the sx of osa?

A

snroing, nocturnal arousals, excessive daytime sleepiness, personality changes, intellectual deterioration, morning HA, automatic behaviors, loss of libido, chronic fatigue.

112
Q

what are some of the RISK FACTORS or causes of OSA?

A

obesity, nasal obstruction, adenoidal or tonsillar hypertrophy, micrognathia, macroglossia, acromegaly, hypothyroidism, vocal cord paralysis, neuromuscular diseases

113
Q

what are some of the comorbidites of OSA?

A

systemic hTN, HF, stroke, DM, metabolic syndrome

114
Q

when and where is an aortic stenosis heard best?

A

heard best downstream of aortic valve at aortic area in systole

115
Q

when and where is mitral regurgitation heard best?

A

heard best downstream of mitral valve at apex. it occurs throughout=pansystolic

116
Q

when and where is mitral valve prolapse heard best?

A

heard best at apex like mitral regurgitation, occurs in mid systole with a click of the prolapse and a possible late crescendo murmur as well

117
Q

when and where is tricuspid regurgitation heard best/

A

heard best at left sternal border, pansystolic

118
Q

when and where are signs of hypertrophic obstructive cardiomyopathy heard best?

A

at aortic area

119
Q

what signs point to a murmur being innocent/

A

in systole in aortic area, pt looks and feels well, normal pulse, grade

120
Q

which murmurs are always pathologgic/

A

diastolic

121
Q

when and where are aortic regurgitation murmurs heard best?

A

best heard at left sternal border in diastole (quiet blowing decrescendo murmur)

122
Q

when is mitral stenosis heard best?

A

in diastole, at apex. sounds like an opening snap.

123
Q

what are the causes of murmurs/valvular disease/

A

can be pathologic or innocent. Rhematic heart disease, endocarditis (vegetation), calcification, chordae tendonae rupture, CT dissease, congenital malformation.

124
Q

what are the different causes of murmurs in valves?

A

can be pathologic or innocent. Rhematic heart disease, endocarditis (vegetation), calcification or congenital bicuspid valve or atherosclerosis (aortic stenosis), chordae tendonae rupture, CT dissease, congenital malformation, dilation of aortic root (aneurysm, dissection), syphilis rarely (aortic regurg), marfan’s syndrome (aortic regurg), leaflet/annulus/papillary muscle abnormalities (mitral regrug), left ventricular dilation (mitral regurg), mitral valve prolapse (mitral regurg), congenital problems with mitral valve=mitral valve prolpase. pulmonary HTN (tricupsid regurg), infective endocarditis (IV drug users–in tricuspid regurg)

125
Q

what are some of the sx you can have with aortic stenosis?

A

chest pain, syncope, CHF

126
Q

how is mortality influenced by symptoms in valvular disease?

A

symptoms means a much decreased life expectancy

127
Q

what are some of the sx often experienced in someone with aortic regurgitation?

A

exercise intolerance, dyspnea, orthopnea, CHF, angina, bounding water hammer pulses (literally getting sucked back up in left ventricle

128
Q

what are some of the sx often experienced by someone with mitral stenosis?

A

subtle, exercise intolerance, palpitations with increasing severity, CHF, hoarseness (enlarged left atria pushes on left recurrent laryngeal nerve, afib

129
Q

what are some of the sx experienced by someone with mitral regurg?

A

asymptomatic usually, some exercise intolerance, palpitations, angina, severe regurg can cause dyspnea, afib

130
Q

what positions/hand grips accentuate which murmurs?

A

standing/valsalva to decrease LV volume and hear hypertrophic obstructive cardiomyopathy. Squatting or release increases aortic and mitral stenosis. Hand grips increase LV volume/increased returna nd increased peripheral tone/afterload make it easier to hear mitral and aortic regurg (blood will go back through valve instead of through next valve). mitral valve prolpase click will be heard sooner with standing/valsalva (less blood to keep it open).

131
Q

at what points do you refer a pt for valvular disease?

A

yes, if moderate disease of aortic stenosis: 1-1.5 cm or

Clinical Medicine (19 decks)

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