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Clin med 2 > Cardio exam 1 > Flashcards

Cardio exam 1 Flashcards

1
Q

whats the dx for acute pericarditis? 2 things

A

EKG - ST elevation + PR depression
- ST returns normal
- T wave inverts
- T returns normal

ECHO: only use this if you see effusion happening

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2
Q

what is the tx for acute pericarditis?

A
  • Most are self-limiting
  • NSAIDS = mainstay of therapy (ex; ibuprofen/aspirin not Tylenol)
  • Next line: Glucocorticoids if NSAIDS don’t work
  • If Dressler syndrome: Aspirin or colchicine
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3
Q

what are the presentation for acute pericarditis?

A
  • Chest pain (pleuritic (sharp, worse w inspiration radiating to left shoulder/arm), persistent, postural (pain relived by sitting up/leaning forward
  • Pain with lying supine, coughing, swallowing, deep breathing
  • Fever + cough maybe
  • Pericardial friction rub = sound caused by friction between visceral + parietal pericardial surfaces
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4
Q

what are the 5Ps to acute pericarditis?

A

pain, pleuritic, persistent, postural, pericardial friction rub

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5
Q

whats the etiology for acute pericarditis?

A
  • Idiopathic & post viral (echovirus, cox virus)
  • Dressler syndrome (post MI)
  • Acute MI, uremia (ESRD), collagen vascular disease (SLE, scleroderma, RA, sarcoidosis)
  • Majority PT recover 1-3 weeks
  • pericardial space: between parietal + visceral (on organ) pericardium
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6
Q

whats the etiology for pericardial effusion?

A
  • Accumulation of fluid in pericardial space
  • same causes of acute pericarditis that can lead to fluid buildup
  • AXS
  • ass with ascites, pleural effu, CHR, cirrhosis, nephrotic syndrome due to H2O/Na retentions
  • Normal fluid: 50ml (shot glass)
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7
Q

whats the sx for pericardial effusion?

A
  • Muffled heart sounds, dullness at left lung base
  • pericardial friction rub may or may not be there
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8
Q

whats the dx for pericardial effusion? 3 things

A
  • ECHO: most sensitive imaging of choice (confirms effusion)
  • CXR: show enlargement of cardiac silhouette w > 250ml of fluid (heart will stretch to make space for fluid)
  • ECG: low QRS voltage (start of ventricular contraction), T-wave flattering (electrical alternans: alternating amplitudes of QRS complexes)
  • you will see a swinging heart due to the fluid surrounding the heart
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9
Q

whats the tx for pericardial effusion?

A

Tx:
- depends on PT hemodynamic stability!!
- Tx underlying cause
- Pericardiocentesis if there’s a cardiac tamponade for large effusion

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10
Q

whats the etiology for cardiac tamponade?

A
  • When pericardial effusion causes sig pressure on the heart, impeding cardiac filling  decrease CO and shock!
  • buildup of pericardial fluid ~200ml rapidly or 2L slowly
  • Due to trauma to thorax, central line placement, pacemaker insertion, pericardiocentesis, pericarditis, post MI with wall rupture
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11
Q

whats the sx for tamponade?

A
  • Elevated jugular venous pressure M/C (distended neck veins)
  • Narrowed pulse pressure
  • Pulsus paradoxus (pulse getting strong during expiration and weak during inspiration
  • Distant (muffled heart sounds)
  • Tachypnea, tachycardia, hypotension with onset shock
  • BECK’s Triad: HYPOtension, muffled heart sound, JVD
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12
Q

which dx has becks triad?

A

cardiac tamponadeic

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13
Q

which dx shows ST elevation and PT depression?

A

acute pericarditis

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14
Q

whats the dx for tamponade?

A
  • ECHO – most sensitive + noninvasive test!! (Will see effusion and collapsed cardiac chambers)
  • CXR: enlargement of cardiac silhouette + clear lungs
  • ECG: electrical alternans (but should not be used to dx this)
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15
Q

which dx shows low QRS voltage and T wave flattering?

A

pericardial effusion

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16
Q

whats the tx for cardiac tamponade?

A
  • Non-hemorrhagic tamponade: if pt is hemodynamically stable, then monitor closely w CXR, ECG but if not stable, then pericardiocentesis (remove fluid)
  • Hemorrhagic tamponade due to trauma: emergency surgery to repair!
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17
Q

whats the etiology for chronic pericarditis?

A
  • loss of pericardial elasticity
  • inflammation of pericardium which begins gradually, long lasting (> 6months) + results in fluid accumulation in space or thickening of muscle
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18
Q

what are two ex of chronic pericarditis and what are they and their causes?

A
  1. Chronic effusive pericarditis: fluid slowly accumulates in space
    Causes: unknown, cancer, TB, chronic kidney disease, hypothyroidism
  2. Chronic constrictive pericarditis: rare, scar like fibrous tissue forms throughout pericardium fibrous tissue contracts over yrs, compressing heart  prevents filling  HR
    Causes: viral, radiation therapy, surgery, or any condition that causes acute pericarditis (RA, lupus, injury, bacterial infection)
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19
Q

whats the sxs for chronic pericarditis?

A
  • shortness of breath, coughing, fatigue
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20
Q

whats the dx for chronic pericarditis?

A
  • ECHO: pericardial thickening+ + calcification(severe)
  • sometimes cardiac catheterization or MRI + CT
  • BX or samples of blood/fluid to determine cause of chronic pericarditis
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21
Q

whats the tx for chronic pericarditis? think of both types

A
  • Tx underlying cause
  • Salt restriction + diuretics to relieve sxs
  • Cure for constrictive pericarditis: pericardiectomy (cures 85% of pt but risk of death from surgery is 5-15%)
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22
Q

whats the etiology for cardiac myxoma? where does m/c occur?

A
  • noncancerous primary heart tumor, irregular shape, and jellylike consistency - M/C cardiac neoplasm
  • 50% of cardiac tumors are myxomas + RARE
  • Metastases from other tumors are more common (75% of cardiac neoplasm)
  • ¾ of myxomas = left atrium
  • usually in women - ages 40-60
  • uncommon are hereditary, in young males 20s, occur in 1+ chambers
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23
Q

whats the presentation for myxoma?

A
  • fatigue, fever, syncope (fainting), palpitation, malaise, low pitched diastolic murmur that changes w body positions
  • ass with mitral stenosis findings (ex; prominent S1 low pitched diastolic murmur)

M = M (myxoma = mitral stenosis)

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24
Q

which dx is associated with mitral stenosis with having S1 low pithced diastolic murmur?

A

cardiac myoxma

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25
Q

whats the dx for myxoma?

A
  • clinical evaluation
  • murmur heard “LOW PITCHED diastolic murmur” during physical exam
  • ECHO
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26
Q

whats the tx for myxoma?

A

surgery bro

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27
Q

whats the etiology of fibroelastoma?

A
  • 2nd M/C primary cardiac tumors in adults, incidence is <0.1%
  • normally known: Papillary fibroelastomas (PFE)
  • M/C in aortic valve (35-63%) but can be in other valves
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28
Q

whats the M/C cardiac neoplasm and m/c cardiac tumors ?

A

myxoma and fibroelastoma

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29
Q

whats the presentation for fibroElastomas?

A
  • mostly AXS
  • can manifest with features of embolization like stroke, TIA, MI

fibroElastoma = E = emobilization related

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30
Q

whats the dx for fibroelastoma?

A
  • TEE
  • observations for AXS PT if tumor is small and immobile, we good
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31
Q

whats the tx for fibroelastoma?

A
  • surgery for pt who have prior embolic events
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32
Q

whats the defintion of cardiomyopathies?

A
  • Heterogenous group of diseases involving structural dysfunction of heart muscle not related to CAD, hypertension, valvular disease or CHD
  • ALL the cardiomyopathies can lead to HR with time
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33
Q

what is dilated cardiomyopathy

A

Systolic/contraction dysfunction
- ventricular cavity dilation, thin walled ventriculus and impaired ventricular contraction

  • ALL leads to sig systolic dysfunction with dilated + thin-walled ventricles
  • Systolic dysfunction: decreases myocardial contractility results in decrease CO
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34
Q

whats the etiology for DCM

A
  • damage to myocardial tissues via autoimmune destruction, viral destruction, drug + alcohol, genetic abnormalities
  • idiopathic #1, inflammation from infection, peri-partum, B1, thiamine deficiency (beriberi)
  • 5/100,000 cases, M/C younger pt (20-60yrs)
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35
Q

whats the presentation for DCM?

A
  • gradual onset of HR symptoms:

SOB, orthopnea, cough, pleural effusion (decrease breath sounds), pulmonary edema (crackles), inadequate organ perfusion (cool extremities, kidney diseases)

  • (+) S3 gallop: early diastolic extra heart sound indicative of blood splashing around dilated filled ventricle as it is filled by atria
  • Right HR: JVD, peripheral edema, hepatic congestion
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36
Q

whats the dx for DCM?

A
  • ECHO #1: systolic (contraction) dysfunction w decreased myocardial contractility/ED  decrease CO
    • LV enlargement/dilation
    • Thin ventricular walls

-CXR: cardiomegaly

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37
Q

which dx would u hear a S3 gallop sound?

A

DCM + peripartum CM

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38
Q

whats the tx for DCM?

A
  • similar to HR management
  • Triple therapy: ACE-1/ARB + Beta blockers + diuretics
  • Cardiac Transplantation: definitive management
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39
Q

whats the etiology for RCM?

A

Fucked up diastolic/filling dysfunction pressure (cant stretch)

  • caused by infiltration of ventricular wall (amyloidosis, sarcoidosis, hemochromatosis)
  • damaged leads to diastolic noncompliance w elevated filling pressure + impaired filling  leads to pulmonary congestion
  • diastolic dysfunction in non-dilated ventricle which impedes ventricular filling
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40
Q

whats the presentation for RCM?

A
  • PT presents with exercise intolerance
    -Exertion intolerance + fluid retention
    -Right HR w JVD, edema + congestion
    • S3,S4, mitral, tricuspid valve regurgitation
  • Kussmaul’s sign: lack of inspiratory decline or increase in JD pressure w inspiration (normally inspiration should suck blood into RA and OUT of jugular veins but it doesn’t so leads to RA dysfunction, impaired RA filling and RA pressure increases)
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41
Q

which dx would you see a kussmaul sign?

A

restrictive CM

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42
Q

if you have right side heart failure what sxs do u get ?

A

JVD, peripheral edema and hepatic congestions

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43
Q

what dx would u do for RCM?

A
  • ECHO (TOC): decrease in EF (25-50%), normal LV thickness, increase atrial size (high pressure of stiff ventricle cause atrial enlargement)

-Endomyocardial BX: definitive dx

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44
Q

what tx for RCM?

A
  • tx underlying cause
  • Diuretic for CHF
  • ACEi and B-blockers
  • transplant
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45
Q

whats the etilogy for HOCM?

A

Diastolic dysfunction

  • M/C in sudden death in young athletes
  • inherited disorder (autosomal dominant), HTN, aortic stenosis
  • unexplained hypertrophy  LV outflow obstruction + impaired diastolic filling (cant stretch) pulmonary congestion
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46
Q

whats the sxs for HOCM?

A
  • Most AXS
  • dyspnea on exertion, syncope, palpitations, angina
  • can lead to sudden cardiac arrest 
  • mitral regurgitation murmur  increases with Valsalva maneuver + exercise / decreases with handgrip + leg elevation ??

-may have loud S4 sound

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47
Q

which dx would you hear a loud S4 sound with increase valsalva maneuver?

A

HOCM

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48
Q

whats the dx for HOCM?

A
  • EKG: abnormal Q waves, ST-T wave changes

-ECHO: septal wall thickness

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49
Q

which dx would you see abnormal Q waves and S-T wave changes?

A

HOCM

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50
Q

what the tx for HOCM?

A
  • no competitive sports or exercise
  • Beta blockers (decreases HR and improve filling)
  • Ca+ channel blockers (improve ventricle - compliance)
  • diuretics for fluid overloads
  • surgery
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51
Q

whats the etiology for takotsubo CM?

A
  • stress cardiomyopathy or “broken heart syndrome”
  • Takotsubo = octopus trap in Japanese
  • MI in absence of atherosclerotic etiology
    • 1-2% of ST- elevated myocardial infarctions
  • M/C in post-menopausal women
  • unknown RF
  • happens when emotional stress causes catecholamine surge  leads to coronary artery vasospasm + myocardial stunning (akinesia)
  • Apical akinesia = “apical ballooning”
  • Coronary artery vasospasm  myocardial infarction without acute coronary artery obstruction
    NO coronary artery atherosclerosis
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52
Q

which dx would you see apical balloning=apical akinesia?

A

takotsubo cardiomyopahty

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53
Q

whats the sx for takotsubo CM?

A
  • Acute substernal chest pain, shortness of breath after intense emotional stress
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54
Q

whats the dx for takotsubo CM?

A

few things
- EKG: ST elevation myocardial infraction (~50%)

  • Labs: troponin elevation
  • Coronary angiography: done after EKG/labs show signs of MI, absence of atherosclerotic coronary disease/plaque rupture
  • ECHO #1:apical akinesia  apical ballooning
55
Q

if you see a pt with elevated troponin levels and EKG ischemia changes with NO atherosclerosis what dx is it ?

A

takotsubo CM

56
Q

tx for takotsubo CM?

A
  • NOT ENOGUH RESEARCH!
  • supportive and conservative care! (beta blockers, ACE inhibitors)
  • resolve emotional stress 
  • inotropic agents (help w contractility) + diuretics
57
Q

what is the etiology for peripartum CM? and RFs and when do you see it?

A
  • RARE cause of HF in late pregnancy or early puerperium *period of 6 weeks after birth)

RF: age greater than 30yrs, African descent, pregnancy w multiple gestation, prior preeclampsia, cocaine abuse, long term oral tocolytic therapy with beta adrenergic agonist (terbutaline)

  • less commonly seen between 36 weeks of gestation, happens during first month of post-partum
58
Q

whats the sx for peripartum CM?

A
  • dyspnea, cough, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, hemoptysis
  • elevated JV pressure, displaced apical impulse, S3 sound, murmur of mitral regurgitation
59
Q

whats the dx for peripartum CM?

A
  • EKG: nonspecific
  • ECHO: reduction in LV systolic function (only other systolic dysfunction like DM)
  • plasma brain natriuretic peptide (BNP) or N- terminal pro-BNP (NT-proBNP) elevations
60
Q

which dx would you see high levels of BNP and NT-proBNP?

A

peripartum CM

61
Q

whats the M/C for transplation?

A

CLASS IV HR SX

62
Q

what is blood pressure?

A
  • BLOOD PRESSUE = CARIDAC OUTPUT (CO) X SYSTEMIC VASCUALR RESISTANCE (SVR)
    • INCREASE IN SVR AND INCREASE CO WILL INCREASE BP
    • Vascular resistance can be due to narrowing of the vascular lumen or vasoconstriction
63
Q

what is primary HTN and its RF

A

-UNKNOWN, M/C 95%
- gradual onset
- happens in ages 30-50 and AXS for 10-20 years
- RF:
Age, obesity, lack of exercise, family hx/genetics, increase alc/Na+ intake, race (African Americans M/C)

64
Q

what is 2nd HTN and its multiple RF?

A

Severe or resistant HTN – persistence of HTN despite usage of three antihypertensive agents from diff classes
- ACUTE RISE of BP in a PT with stable values
- AGE less than 30, non-obese pt with no family hx
- Malignant/accelerated HTN – signs of end organ damage such as retinal hemorrhage, papilledema, HF, neuro issues, acute kidney injury
- HTN ass with electrolyte disorders = hypocalcemia and metabolic alkalosis

65
Q

whats the M/C of 2nd HTN?

A

kidney dieaseas

66
Q

what is primary aldosteronism?

A

excess mineralcorticoids - TRIAD: HTN, hypokalemia and metabolic alkalosis!

67
Q

explain the renin system

A

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS):
- Kidney’s baroceptors senses a decrease in blood flow so renin is released by the juxtaglomerular cells  increases NA conc in renal tubules or sympathetic stimulate of juxtaglomerular cells
- Angiotensin II causes vasoconstriction of systemic arteries  increases CO, resistances, high BP
- Aldosterone  increases NA retention  increases blood volume w the help of ADH

68
Q

whats the M/C of 2nd HTN ? specific

A

Renal Atherosclerosis

69
Q

whats the eitology for both renal atherosclerossi and fibromuscular dysplasia?

A

renal atherosclerossi can lead to renal arterial stenosis
- effective blood flow within the renal arteries is decreased so RAAS is activated and will increase systemic BP

fibromuscular dysplascia is -NON atherosclerotic disorder that leads to arterial stenosis due to excessive arterial wall thickening (due to renal arterial stenosis 80%)

70
Q

where do you see renal atherosclerossi and fibromuscular dysplsia?

A

renal - elderlies with hypokalcemia
fibro - young females 30years

71
Q

whats the tx for renal atheroscleorsis and fibromuscular dysplaia?what will u see for fribomuscular?

A
  • Renal arteriography – GOLD STANDARD
    in fibro you will see string of beans
  • Initial testing: DUPLEX UNTRASOUND, CTA and MRA

-LABS: increased renin, increased aldosterone, decrease K serum

72
Q

whats the tx for atheroscleorsis and fibromuscular dysplaia?

A

angioplasty !!!
and ACEi

73
Q

what is primiary hyperaldesteronism and what sxs do they have?

A

uncontrolled secretion of aldosterone
- M/C due to bilateral adrenal hyperplasia or unilateral adrenal adenoma

they have hypokalcemia and HTN

74
Q

whats the labs and dx for primiary hyperaldesteronism ?

A
  • LABS: decreased renin, increases aldosterone, decreases K+ serum

-CT adrenal: to differentiate hyperplasia from adenoma

75
Q

whats the tx for primary hyperaldosteronism?

A

bilateral: spiro
unilateral: surgery adrealectomy

76
Q

how does NSAIDS casue HTN

A
  • NSAID use  prostaglandin inhibitors  renal artery vasoconstriction  decrease renal blood flow  RAAS activation  hypertension
77
Q

what do prostaglandins normally do ?

A

Prostaglandins: normally cause renal artery vasodilation  increased renal blood flow

78
Q

what is asprin effect on prostaglandins?

A

Low does’ aspirin (81mg) has minimal effect on prostaglandin formation in kidney

79
Q

what is aortic coarctation?

A

congenital abnormal narrowing of the descending aorta, leading to increased vascular resistance  HTN

80
Q

what presentation would you see for aortic coarctation?

A
  • absent or delayed LOWER EXTREMITY pulses
  • Claudication pain w ambulation due to poor perfusion of lower extremities
  • headache, epistaxis
81
Q

whats the dxf or aortic coarctation?

A

ECHO: discrete area of narrowing within lumen of descending aorta

82
Q

what is pheochromocytoma?

A
  • catecholamine-secreting TUMOR of the chromaffin cell of the adrenal medulla
83
Q

whats the sxs for pheochromocytoma? think PHE

A
  • P.H.E
    Palpitation (tachycardia): beta 1-receptor on heart innervated by catecholamines

Headaches/HTN: beta 1 receptors on heart innervated by catecholamines

Excessive sweating (diaphoresis) and episodic anxiety: sweat glands are innervated by catecholamines

84
Q

whats the dx for pheochromocytoma?

A

24 hour urine fractioned metanephrine analysis

-serum metanephrine has high false + rates

metanephrine are made when your body breaks down catecholalime

85
Q

whats the tx for HTN emergency?

A

IV VASODILATERS AGENTS #1 (nitroprusside, nitroglyercine, labetalol)

supportaitve measures, intensive care unit admission

86
Q

whaat is HTN emergency “malignant HTN”?

A

elevated blood pressure (typically >180mmHg systolic and/or >120mmHg diastolic) AND signs of ACUTE end-organ damage/failure

Rare: 1 case per million per year; not everyone with high blood pressures has
a hypertensive emergency!

87
Q

which is worse: value of BP or degree of change in BP from baseline?

A

degree of change in BP from baseline

88
Q

what do end organ damage include for HTN emergency?

A

Neurologic: Hypertensive Encephalopathy, CVA (ischemic or hemorrhagic)

Cardiovascular: Myocardial infarction, Acute Heart Failure
(and/or pulmonary edema), Aortic dissection

Renal: acute kidney injury

89
Q

what are the many dx testing for htn emergency?

A

EKG: identify STEMI or ischemic changes

CXR: identify pulmonary edema from Heart failure

Echocardiogram: low ejection fraction in Heart failure

CT Head: identify hemorrhagic stroke (ischemic stroke and hypertensive encephalopathy difficult to see early on)

90
Q

what are the lab testing for hypertensive emergecny?

A

CMP (e.g. creatinine!!!) and UA (blood/proteins in kidney injury): identify acute kidney injury

Troponin: elevated in STEMI/NSTEMI

91
Q

whats the mangement for HTN emergency “malignant HTN”? what are the three topics we talked about?

A

mangement depends on the type of organ injury.

ischemic stroke
arotic dissection
acute heart failure

92
Q

for ishemic stroke for HTN emergency, what is the mangement?

A
  • typically keep BP <185/110 (permissive
  • hypertension to allow for continued perfusion of brain); or MAP 60
  • IV Nitroprusside(#1) or IV labetalol
93
Q

for aortic dissection for HTN emergency, what is the mangement?

A
  • goal is to reduce aortic shearing forces
  • RAPID BP lowering to 120mmHg systolic and RAPID HR lowering
  • IV Labetalol: decreases heart rate and blood pressure
  • IV Nitroprusside usually added to rapidly decrease systemic vascular resistance
94
Q

for acute HF for HTN emergency, what is the mangement?

A
  • the goal is the decrese preload and afterload
  • IV nitroprussie (#1) - will decrease in preload and afterload VIA vascular dilation
  • IV furosemide which will decrease blood volume VIA diuresis –> decreased preload and pulmonary edema
95
Q

what TX you want to avoid for acute HR due to hypertensive emegrengy?

A
  • AVOID BB/CCB bc they will decrease cardiac contracility and casue flash pulmonary edema (which is massive backup of fluid into the lungs due to poor contractile heart)
96
Q

when should u decrease MAP and by how much?

A

you should decrease MAP for hypertensive emergency (except aortic dissection) gradually approx 10-20% in the first house

97
Q

KNOW THIS NOTE:
It is generally unwise to lower the blood pressure too quickly or too much as it may result in ischemic damage to vascular beds that have become habituated with the higher level of blood pressure (ie, autoregulation)

A
98
Q

what is htn urgency and htn emergecny?

A

Hypertensive Urgency – NO signs of end organ damage
BP: more than 180/ more than 120

Hypertensive Emergency –signs of organ damage
Kidney diease, eye problems

99
Q

what happens if HTN is left untreated what % die?

A

50% of pt die from coronary heart disease or CHF

33% die from stroke

5-15% die from renal failure

100
Q

what BP levels would a pt with hypertensive urgeny/emergecny have?

A

grater than or equal to 180/ greater than equal to 120

101
Q

when do u use ABPM? ambulatory BP monitoring?

A

if pt has high in office reading you would use this devide for them to take out of office reading

102
Q

how would u evaluate HTN?

A

funduscopic examination to evaluate for hypertensive retinopathy ( Hemorrhage, Papilledema, Cotton wool spots, anterior narrowing and arteriovenous nicking)

Evaluate for goiters that may be associated with hyperthyroidism

Carotid auscultation: bruits (venturi effect) indicate carotid atherosclerosis, increasing risk of ischemic stroke

Heart auscultation: left shift of PMI (apex shifting) may indicate cardiomegaly from LVH or heart failure

Lung auscultation: decreased breath sounds may indicate pleural effusion 2/2 heart failure

Abdomen: palpate for abdominal aortic aneurysm (widened diameter of abdominal aortic pulsation); auscultate for renal bruits, indicative of renal arterial stenosis

Extremities: palpate peripheral pulses, which may be diminished in peripheral arterial atherosclerosis

103
Q

what would u do first for HTN magnement?

A

lifestyle changes - weight loss, exercise, DASH dieet, mediterrna deit, furits veggie, low fat low sodium, low alc, no cigs

104
Q

whats the goal for HTN management

A
  • to lower the incidence of complication
  • those with stage 2 140-149/90-99 should be started on BP meds
  • TARGET: 120-130 systolic

high risk pt should be around 120
low risk pt is ok to be around 130+

105
Q

whats the four classes of drugs for HTN

A

M/C Thiazide-like or thiazide-type diuretics

Long-acting calcium channel blockers (most often a dihydropyridine such asamlodipine)

Angiotensin-converting enzyme (ACE) inhibitors

Angiotensin II receptor blockers (ARBs)

106
Q

whats the best to use for intial monotherpy?

A

ACEi or ARBS for those with diabetic nephropahty or nondiabetic chrocnic kidney diease

107
Q

KNOW: combintation drugs is the best for greater effect low risk

NEVER use ACE and ARB tg

A

KNOW: awlays use ACE or ARB w CCB or dirueitcs

108
Q

what happens to the heart in chronic HTN?

A

when theres HTN, the left ventricule will hypertrophy in order to overcome BP.

high BP can also lead to coronary artery atheroscleorsisi.

so hypertropic muscuels needs enegery and blood work well but without good perfusion it wont work and muscles will atropy and die –> HF

109
Q

what happens to peripheral vessels in chronic HTN

A

high BP can leave to shear stress on peripheral vessels –> leading ot peripheral vascular disease

it can lead to impotence in men, claudication (pain w walking), arotic dissection (when aortic tears and it bleeds into pericaridum)
or abdominal aoritc aneurysm (ballooning of aorta due to weak walls can rupture)

110
Q

what happens to the brain in chronic HTN

A

high BP can casue shearing on ceberal vessels –> Cerebrovascular atherosclerosis —> low perfusion –> ishcemic stroke

high BP can also rupture the vessels –> hemmoragic stroke :(

S/S: ACUTE onset of neurolgoic deficits

111
Q

what else can chronic HTN do to the brain?

A

HTN encephalopathy!! prolong HNT can lead to leakage of neuronal fluid and protein and lead to cerebral edema.

112
Q

whats the clinical manifestation, dx and management, tXfor Hypertensive Encephalopathy?

A

clinical manifestation: insidious onset of headache, nasuease, vomitting, confusion–> seizuresm coma and YOU WILL SEE PAILLADEMA IN FUDOSCOPY

DX: exclusion (exclude stroke) confirmed when pt symstoms improve with lowering BP

mangement: rapid lowering of MAP by 10-20% within first hour. lowering TOO much can cuase acute decrease in blood supply to major organs –> organ ischemia

tx: IV nitroprusside (good vasodilator)
IV nicardipine (CCB, very rapid)

113
Q

how does chronic HTN affect eyes? MILD CASE

A

mild case can affect arterole changes
- AV nicking: when the aterioles nick the venules
- arteriolar narrowing: when arteriles vasoconstrict to prevent blood to retina
- coppor/silvar wiring: when u see light shining from copper and silver wires = thickened arterioles

114
Q

how does chronic HTN affect eyes? MODERATE CASE

A

moderate cases can lead to leaking from the reitnal vessels.

  • Dot-blot hemmorage: bleeding within deep retinal layer (D for DEEP)
  • flame hemmorage: bleeding within superficial reinal layer (flame is always superficial)
  • hard excudate (lipid deposits in retina)
  • soft excudates (cottwon wool) : ischemai of nerve fibers
115
Q

how does chronic HTN affect eyes? SEVERE CASE

A

Severely elevated blood pressures leads to papilledema
(optic disc edema due to optic nerve ischemia)

  • to leakage of fluid/proteins around the optic disc as well as ischemia of the optic disc–> optic disc edema
116
Q

how does chronic HTN affect KIDNEY?

A

high BP can casue shearing stress on renal –> arterioles –> renal artery atheroclerosis –> decreased renal purfusion –> ischemia –> CKD

NOTE THAT RENAL DIEASE CAN LEAD TO HTN AND HTN CAN LEAD TO RENAL DIEASE - WOW!!

M/C/C of chornic kidney diease is DM
- 2nd M/C/C is HTN

117
Q

what is the definition of HF?

A

inability of myocardium to pump blood to meet metabolic requirements or at high diastolic pressure/volume

118
Q

whats the epidemiology of CHF? causes?

A

6.5millions in US have CHF. Typically 65 older
its an aging disease. those with no hx of MI will have 10% risk and with MI 20% risk

CAUSES:
Valvular Heart Disease
Ischemic Heart Disease (Most common, especially post MI)
Arrhythmias
HTN
Cardiomyopathy
Myocarditis
Medications (e.g. doxorubicin)

119
Q

what is HF with reduced and preserved EJ?

A

Heart Failure with Reduced Ejection Fraction (HFrEF): x >55% of cases
“Systolic Heart Failure” due to impaired cardiac contractility

Heart Failure with Preserved Ejection Fraction (HFpEF): <45% of cases
“Diastolic Heart Failure” due to impaired cardiac filling

120
Q

where would you see diastolic HF in women or man? what age?

A

women older age

121
Q

what is Left side HF cuased by and what is Right side HF casued by ?

A

Left side HF - CAD or CVD
right side HF: m/c right side or pulmonary edeuma, sleep apnea, COPD

122
Q

whats the s/s and examination of CHF?

A

Signs and symptoms:
Dyspnea – most common symptom (due to fluid and congestion)
Orthopnea (Difficulty breathing while laying flat – fluid lays flat too)
PND – nocturnal dyspnea (so they sleep w elevation so fluid can go to the base of the lung)
Cough (pink and frothy due to pleural effusion)
Fatigue
Edema
Exercise intolerance

Physical Examination:
JVD > 8 cm (more common on right side HF, measured the right atria pressure)
Rales and crackles on auscultation (rales = indicate fluid)
Tachycardia( HR >100 bpm)
Displaced PMI
S3 heart sound ( indicator of LV dysfunction) and (+) S4 in diastolic failure
Edema
Ascites

123
Q

whats the dx for CHF?

A

EKG Findings:
Left Ventricular Hypertrophy (check for h/o MI)

Labs
- Elevated B-type natriuretic peptide (BNP)
- BNP: released by ventricles and brain in response to elevated ventricular filling pressures, assist in vasodilation and natriuresis
- Elevated serum creatinine
- Cardiac enzymes

CXR findings:
Cardiomegaly
Increased pulmonary vasculature
Pleural Effusions
Kerley B lines

Echo findings:
Systolic or diastolic dysfunction
Decreased EF – CANT PUMP OUT BLOOD
LV/RV hypertrophy - duh cant pump blood so heart overcompensates
Regional Wall motion – not as severe as swinging of the heart)

124
Q

which dx would u see kerley B lines?

A

congestion heart failure

125
Q

what is the tx for CHF?

A
  • diurectics (enhance NA and water excretion)
    -loop diuretics #1 (furosemide) (lasix)
    • thaizide diuretics (for milkd HF)
  • ACEi - decreases BP
  • ARB - decreases BP
  • beta blockers - slows heart, vasodilation
  • hydralazine - casues vasodilation
  • digoxin (be careful)
126
Q

whats the definite magment fo STAGE 5 HF?

A

cardiac transplantation

127
Q

when should you use AICD (automatic implantable cardiovascualr defribillator?

A

when EF is less than 35%

128
Q

what medication should you avoid for tx for CHF

A

glucocorsteirods, NSAIDS, CCB

129
Q

ACEi Adverse Effects

A

First Dose Hypotension
Cough
Renal Failure
Hyperkalemia
Congenital Defects
Angioedema

CHAR CF

130
Q

Diuretics Side Effects

plus chand

A

Worsening Renal Failure - Fluid Depletion
Hypokalemia
Ca metabolism
Loop diuretics  HYPOcalcemia
Thiazides  HYPERcalcemia
Ototoxicity (loop diuretics)
Sulfa allergy (loop diuretics)
Metabolic alkalosis
Hyperuricemia
Hypertriglyceridemia

131
Q

Digoxin-Adverse Effects

A

Gynecomastia
Toxicity
Anorexia, nausea, vomiting, diarrhea
Confusion, visual impairment (yellow hallo)
Arrhythmias
Avoid in
Elderly
Renal failure
Electrolyte disturbances
Hypothyroidism

132
Q

Beta blockers Side Effects

A

Worsening heart failure
Bradycardia – slows the Heart
Asthma exacerbation
Worsening peripheral vascular disease
Weakness
Depression
Impotence

133
Q

what is it and whats the management for acute decompenstated heart failure?

A
  • (lasix) IV furosemide loop duirectics - decreases blood volume as it improves pulmonary edema and breathing
  • nitrogylecerin (Vasodilator) = decrease preload and HTN
  • nitroprusside (vasodialtor) = decreases afterload and HTN
  • O2 = as needed BIPAP usefull
  • postion upright - releives respiratory symptoms by decreasing preload
  • inotropic agents: only used in hypotension present improves CO, but hurts heart
134
Q
A

Clin med 2 (7 decks)

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