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PANCE Review > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Cardiomegaly - how does heart enlarge in CHF

A

first laterally and then inferiorly - get PMI at 5th ICS , lt anterior axillary line (instead of typical mid-clavicular line)

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2
Q

exertional dyspnea

A

SOB on exertion - hint to possibly cardiac pathology

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3
Q

paroxysmal noctural dyspnea

A

must get up out of bed due to SOB

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4
Q

orthopnea

A

must sit up - SOB with lying down

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5
Q

dyspnea at rest

A

sign of worsening cardiac pathology

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6
Q

syncope/pre-syncope/dizzy

A

results from decreased cerebral blood flow

  • may be due to arrhythmia, low BP, low cardiac output
  • test with BP, EKG, holter monitor, tilt-table test (r/o vasovagal response)
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7
Q

cough - hints to cardiac origin

A

usually dry or non-productive

seen in HF and ACE-inhibitor medication use

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8
Q

blood pressure - orthostatic changes

A

when systolic BP drops >20mm when standing = positive for orthostasis

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9
Q

pulse pressure

A

difference b/t systolic and diastolic

  • widened = larger stroke volume
  • narrow = smaller stroke volume
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10
Q

pulse grading

A

1-4; 2 = normal

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11
Q

bifed / bisferiens pulse

A

beating 2 x in systole (hypertrophic obstructive cardiomyopathy and aoritc regurgitation)

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12
Q

dicrotic pulse

A

exaggerated; early diastolic wave seen in heart failure

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13
Q

pulses alternans

A

alternating strong/weak pulse force seen in HF

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14
Q

paradoxical pulse

A

> 10mm Hg drop in systolic BP during inspiration in obstructive lung dz and cardiac tamponade

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15
Q

jugular venous pulsations

A

provides info about central venous pressures and RIGHT-heart function

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16
Q

hepatic jugular reflux (HJR)

A

when press on liver see a >1cm increase in jugular venous pressure
- seen in HF

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17
Q

first heart sound - S1

A

“Lub” - results from closing of mitral and tricuspid valves

- loud in mitral stenosis

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18
Q

second heart sound - S2

A

“dub” - closure of aortic and pulmonic valves

- split with inspiration - physiologic S2 (normal)

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19
Q

third heart sound - S3

A

early, rapid LV filling (normal in young)

associated with LV overload conditions - HF

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20
Q

fourth heart sound - S4

A

results from vigorous atrial contraction into a resistant/still LV

  • heard with lt ventricular hypertrophy 9HF) or MI
  • NEVER hear in atrial fibrillation (b/c no contraction of atria)
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21
Q

mid-systolic click

A

found in mitral valve prolapse

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22
Q

opening snap

A

found in mitral stenosis

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23
Q

systolic murmurs

A

most common

Found in normal heart sounds, aortic stenosis, pulmonic stenosis

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24
Q

innocent flow murmurs

A

early systolic
80% kids
pregnant females
decreased with sitting up

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25
Q

diastolic murmurs

A

almost always pathology
most common is high-pitched = pulmonic regurg, aortic regurg

HINT: diastolic “rumble” = mitral stenosis

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26
Q

continuous murmur

A

heard through systole and diastole

patent ductus arteriosus = most common (“machinery like”)

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27
Q

electrocardiogram (ECG)

A

12-lead ECG - diagnostic study looking for electricity in heart

Holter monitor = 24 hour ECG

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28
Q

ECHO - echocardiogram

A

U/S of heart: good for anatomy and structural problems (any valve issue)
- can see blood flow

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29
Q

tilt-table test

A

often used to R/O vasovagal response as cause of syncope

  • test autonomic nervous system functioning
  • used before more invasive testing is performed
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30
Q

stress testing - types

A

exercise stress test: detects ischemia, CAD, cardiac response to exercise

nuclear stress test: if need to see more detail of what is going on in heart - use w/ LBBB or ? results from XST
- thallium

pharmacologic/ chemical: is someone cannot exercise

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31
Q

chemicals used in pharmacologic stress tests

A

adenosine
dipyridamole
dobutamine
lexiscan

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32
Q

contraindications to stress test

A

severe aortic stenosis

fresh MI

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33
Q

EP studies - electrophysiologic

A

used to detect and treat rhythm disorders (looks at electrical flow of heart)

  • performed in cath lab
  • certain identified arrhythmias (WPW, SVT, A-fib, VT) are treated pharmacologically or with radio-frequency ablation or cryotherapy
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34
Q

cardiac catheterization (coronary angiography)

A

best used to evaluate and treat CAD

  • coronary angiography (visualize vessels)
  • angioplasty (PTCA aka “balloon”)
  • angioplasty with stent placement
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35
Q

hypertension - basics

A

office BP > or = 140/90
- must have 2 measurments

most common condition in primary care

JNC 8 criteria

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36
Q

hypertension - pathophysiology

A

RAAS mechanism/natriuretic hormone
vasoconstriction at level of arterioles
- leads to electrolyte disturbance

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37
Q

hypertension - definition (pre, stage I, stage II)

A

normal: <120 AND <80
prehypertension: 120-139 OR 80-89
Stage I HTN: 140-159 OR 90-99
Stage II HTN: >160 OR >100

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38
Q

hypertension - classification (primary, secondary, resistant)

A

essential/primary

  • most common (90%)
  • cause unknown
  • incurable (controlled w/ lifestyle mod and meds)

secondary/identifiable

  • less common (<10%)
  • most common cause: chronic renal dz
  • other cases: pheochromocytoma, coarctation of aorta, OSA, meds

resistant/pseudoresistant

  • uncontrolled on 3 meds
  • controlled on 4 meds
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39
Q

primary HTN - exacerbating factors

A

environmental: salt, obesity
others: tobacco, ETOH, sedentary, polycythemia vera (high HGB, HCT), NSAIDS, low K+, metabolic syndrome (DM)

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40
Q

HTN - most common sxs

A

headache

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41
Q

HTN - physical exam

A

retinopathy: hemorrhages, cotton wool spots, AV nicking
neck: bruits, JVD, thyroid enlarge

CV exam: lt vent heave, aortic regurg, presystolic S4 gallop

ABD exam: abd bruits, aortic pulsations

PV exam: loss of peripheral pulses (atherosclerosis), radial-femoral delay (coarctation)

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42
Q

red flags for secondary HTN causes

A

HTN starts early (<25 y/o) w/o FH
HTN first develops >50
previously controlled HTN, now refractory
HTN resistant for 3+ meds

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43
Q

secondary HTN - most common cause

A

chronic renal disease

  • screening tests: BUN/Cr, U/A, microalbuminuria
  • Dx: renal U/S
  • tx: BP control and/or dialysis
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44
Q

most common TREATABLE cause of HTN

A

aldosteronism - usually caused by an aldosterone-producing adenoma

Presents at age 30-50 with HTN and hypokalemia

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45
Q

secondary HTN - renovascular dz

A

1-2% HTN causes

  • artherosclerosis (85%)
  • fibromuscular dysplasia (25% - F)

Presents:

  • b/f age 20 and after age 50
  • HTN resistent to 3+ drugs
  • bruits, peripheral artherosclerosis
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46
Q

secondary HTN - Cushing’s Syndrome

A

hypercortisolism

Presents: truncal obesity, striae, acne, hyperpigmented skin, moon facies and buffalo hump

Labs: glucose (hyperglycemia), hypokalemia

Dx: 24 hr free cortisol

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47
Q

secondary HTN - pheochromocytoma

A

rare catecholamine secreting tumor from adrenal medulla
- causes vasoconstriction and inc. cardiac output

Presentation: pulsatile headache, palpitations, diaphoresis

Dx: plasma metanephrine test

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48
Q

secondary HTN - coarctation of aorta

A

narrowing of aorta

Presents: young pt with HTN and delayed femoral pulses

Dx: Echo

CXR: see figure 3 sign of aortic arch

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49
Q

secondary HTN - OSA

A

OSA and HTN are linked

Untreated OSA leads to new HTN

50
Q

secondary HTN - medications

A

corticosteroids - like Cushings
oral contraceptives
NSAIDS - Na++ retention
ETOH - activates sympathetic system
sympathomimetics: cold and diet meds, cocaine
erythropoietin: increases vascular volume

51
Q

HTN - treatment goals

A
  1. accurate assessment of BP
  2. CV risk stratification
  3. ID and treat secondary causes
52
Q

HTN - who to treat (JNC 8)

A

age 30-59: >140/90mmHg

age 60+: 150/90mmHg

Initiate meds if lifestyle interventions failed

53
Q

HTN - prevention / lifestyle changes

A

Weight loss (BMI 185.-24.9)
Na+ intake (<2.4g/d)
physical activity: 30min/day
ETOH consumption limited

54
Q

HTN - 4 classes of medications

A

Diuretics (thiazide)
Ca++ channel blockers (“dipines”)
ACEI (“prils”)
ARBs (“sartans”)

Mainstay: thiazide diuretic

NOTE: beta blockers no longer 1st line (2nd line)

55
Q

HTN - medications if non-AA (+/-DM)

A

Thiazide diuretic
Ca+ channel blocker
ACEI
ARB

56
Q

HTN - medications of AA (+/- DM)

A

Thiazide diuretic
Ca+ channel blocker

why? AA patients have smaller BP reduction with ACEI and ARB

57
Q

HTN Meds - ACE Inhibitors

A

“prils”
- inhibit ACE from converting angiotensin I to angiotensin II
- angiotensin II likes to vasoconstrictor and stimulates aldosterone
- aldosterone: keep Na+ in, keep H2O in, inc. BP
HINT: prevents death from HF following acute MI
- SEs: cough
- DO NOT use in pregnency

58
Q

HTN Meds - ARB (angiotensin receptor blockers)

A

“sartans”

  • blocks angiotensin II binding to receptor; thus, prevents aldosterone
  • aldosterone: keep Na+ in, keep H2O in, inc. BP
  • SEs: less than w/ ACE (only use if pt not tolerating ACE)
  • DO NOT use in pregnancy
59
Q

HTN med for someone with chronic kidney dz

A

ACE-I or ARB

60
Q

HTN med - thiazide diuretics

A

mainstay of treatment
Inhibit Na+ reabsorption (and water follows Na)

common ones: hydrochlorothiazide, chlorthalidone

SEs: thirst, inc. urination, hypo-mag, hypokalemia

Take in AM so not peeing a lot overnight

NOTE: caution for use in gout

61
Q

HTN treatment - pearls

A

if BP goal not achieved in 1 mo, increase dose of initial drug or add 2nd drug

after 3 drugs, search for secondary causes and refer to HTN specialist

DO NOT use ACE-I and ARB together

62
Q

HTN treatment - 2nd line

A

beta blockers (“olols”)

  • AVOID in asthmatics and patients with heart block
  • NOTE: 1st lin tx if compelling indication (MI/CVA)

aldosterone antagonist
- spironolactone

alpha blockers
- high incidence of CV and heart failure events

direct renin inhibitors

  • aliskerin
  • inhibit renin and therefore formation of ATII
  • avoid in pregnency
63
Q

Hypertensive crises

A

hypertension urgency / emergency due to dysregulation

  • end organ damage (encephalopathy, renal failure, pulmonary edema)
  • treatment: parenteral (IV med)

Note: cannot lower BP too quickly since it may hypo perfuse the brain

64
Q

hypertensive urgency - definition, sxs, treatment

A

BP must be reduced within a few hours

SBP>220 or DBP>130

Sxs: HA, malaise, anxiety
- do not see target organ damage yet

Tx: goal is partial reduction of BP w/ sxs relief
- parenteral drug therapy NOT required

65
Q

hypertensive emergency - definition, sxs, treatment

A

BP must be reduced within an HOUR
- elevated BP + target organ damage (MI, cerebral ischemia, renal failure, aortic dissection)

SBP>220 or DBP>130

Sxs: HA/confusion, blurred vision, vomit, seizures, oliguria, retinopathy

Tx: reduce BP slowly (no more than 25% w/in 1-2 hrs; then to 160/100 w/in 2-6hrs)

  • parenteral drug therapy
  • AVOID sublingual or oral fast acting agents (nitroglycerin, nifedipine)
66
Q

malignant HTN

A

SUSTAINED elevated arterial BP

  • SBP>200 or DBP>130
  • once patient has developed hypertensive encephalopathy, hypertensive nephropathy w/ papilledema

Tx: identical to all HTN emergencies

67
Q

hypertensive emergency - medications to use

A

beta- and alpha-blockers, calcium channel blockers

  • labetalol (IV): comboned beta and alpha blocker
  • esmol: less potent beta blocker
  • nicardipine (IV): ca++ channel blocker (vasodilator so may cause reflex tachycardia)
  • clevidipine: CCB (no vasodilation or reflex tachycardia)

AVOID: sublingual or oral fast acting agents (nitroglycerin, nifedipine)

68
Q

hypotension

A

low BP that can be caused by insufficient peripheral vasoconstriction (orthostatic) or cardiogenic shock

69
Q

orthostatic hypotension - definition, sxs, causes

A

caused by insufficient peripheral vasoconstriction when under orthostatic stress (e.g. stand up)

orthostatic drop of:

  • SBP>20
  • DBP>10

can result in positional syncope or near-syncope

Sxs: lightheaded, weak, visual disturbance

Causes: elderly, BP, BP meds, Parkinson’s, volume loss (blood loss, diuretic, vomiting, diarrhea)

70
Q

orthostatic hypotension - evaluation and treatment

A

evaluation:

  • tilt-table
  • endocrine etiology
  • cardiac etiology

treatment:

  • discontinue contributing meds
  • vasoconstricting agents: midodrine, caffeine
71
Q

cardiogenic shock - definition and causes

A

tissue hypoxia due to decreased cardiac output (with adequate intravascular volume)
- cardiac index < 2.2 L/min/m2

causes:

  • LV failure 2nd to acute MI (main)
  • other cardiac pathology, sepsis, massive PE w/ RV failure
72
Q

cardiogenic shock (hypotension) - clinical manifestations

A

determine if “wet” or “dry” AND “cold” or “warm”

signs of congestion (wet): JVD, pulmonary congestion, ascites, edema

signs of cold (lack of systemic perfusion): cyanotic, m bottled, cool skin

MOST common: cold and wet

73
Q

cardiogenic shock - diagnosis and parameters

A

diagnosis is clinical: low urine output (oliguria), cool extremities, in setting of myocardial dysfunction

hemodynamic parameters: sustained systemic hypotension

  • SBP<90 or dec. of 30 form baseline
  • cardiac index < 2.2 L/m/m2
  • echo: decreased LV contractility (helps to distinguish b/t cardiogenic shock and hypovolemic shock)
74
Q

cardiogenic shock - management

A

1st line: norepinephrine and dopamine (vasopressor)

- if unresponsive: dobutamine (beta-agonist that will inc. CO and myocardial contractility)

75
Q

heart failure - pathophysiology and population most affected

A

pathophysiology:
- CO dec
- neurohormonal mechanisms attempt to inc. renal perfusion
- renin is released: BP inc. and fluid is retained (required inc. work of heart)
- low CO causes catecholamine release (causes heart to pump harder - bad for failing heart)

dz of aging: leading cause of hospitalization for >65 y/o

76
Q

heart failure: ejection fraction

A

Evaluate ejection fraction w/ echo

  • reduced: <50%
  • preserved: >50%
77
Q

heart failure - stages (A-D)

A

A: no structural heart dz, just at risk
B: structural heart dz w/ NO signs or sxs of HF
C: structural heart dz w/ signs or sxs of HF
D: HF refractory to tx requiring special intervention

78
Q

heart failure - classes (NYHA functional classification I-IV)

A 
class I: asymptomatic
class II: sympomatic with moderate activity
class III: symptomatic with mild activity
class IV: symptomatic at rest
79
Q

heart failure - symptoms

A

dyspnea - most common
- PND: postural noctural dyspnea (waking from sleep short of breath)

Others: fatigue, fluid retention, edema, non-productuve cough, impaired exercise performance

Left-Sided: dyspnea is most common due to pulmonary edema

Right-Sided: LE edema, hepatic congestion, nocturia

80
Q

heart failure - causes

A

Leading cause: CAD
- CAD>acute MI>ischemic cardiomyopathy of left ventricle> systolic HF

2nd leading cause: HTN

81
Q

heart failure - findings on PE

A 
JVD
lungs: rales or crackles
cardiac: PMI displaced to left due to LV dilation; pulsus alternans (left-sided failure)
ABD: hepatic congestion
MSK: LE edema
82
Q

heart failure: EKG findings

A

LVH
prior MI
Q-waves (indicate past CAD)
BBB

83
Q

heart failure - CXR

A

cardiomegaly
pulmonary venous
HTN (enlarged veins in upper lobe)

pulmonary edema: perihilar or patchy peripheral infiltrates
- KERLEY B lines

84
Q

heart failure - labs

A

BNP (brain natriuretic peptide) - released by ventricles when under stress
- not specific (also increases with age, obesity, renal dysfunction)

85
Q

heart failure - best test

A

echo - helps to determine valve fx and ventricular fx

86
Q

heart failure - non pharmacological treatment

A

diary of wt and BP daily

exercise, calorie and Na+ restriction, treat OSA

87
Q

heart failure - pharmacological treatment (stages A and B)

A

ACE-I / ARB (prils and sartans): inhibits remodeling

Beta-Blockers: counters effect of SNS
• Must if post MI (inhibits remodeling)
• Atenolol / Metoprolol (Beta-1 selective) are best
• General: start low and go slow

Note: avoid these drugs (exacerbate HR)
• Antiarrhythmic agents, CCB’s, NSAID’s (Na retention, peripheral vasoconstriction)

88
Q

heart failure - pharmacological treatment (stages C and D) - patient is having sxs

A

Optimize ACEI / ARB

Consider beta-blocker: esp. if hx of previous MI
- lifesaving benefits

Diuretics: loop (moderate to severe HF), HCTZ (thiazide) (mild HF)
- MOST effective for treating sxs of HF

Aldosterone blockers: spironolactone

Digoxin (inhibit Na/K ATPase pump): must monitor closely; allow cardiologist to Rx
• Positive inotropic effect (use in Afib)
• Neurohormonal effects (dec. renin and NE at low doses) – PNS effect

89
Q

Loop diuretics - key side effect

A

ototoxicity

90
Q

cardiomyopathy - categories

A

dilated - MOST COMMON (95%)

restrictive

hypertrophic

91
Q

dilated cardiomyopathy - definition and causes

A

decreased myocardial contractility –> impaired systolic fx

  • reduced EF (<40%)
  • more common AA
  • 50% mortality in 5 yrs

causes: inherited, ETOH use, thyroid dz, postpartum state

92
Q

dilated cardiomyopathy – sxs, imaging, tx

A

sxs of HF: rales, inc. JVP, S3 gallop, edema, ascites

echo: LV dilation

tx: same as for HF
- ALL should get beta-blockers and ACEIs

93
Q

atrial fibrillation - what medication is a must

A

anticoagulation - can throw a clot

- Ex. Warfarin

94
Q

hypertrophic cardiomyopathy (HCM) - definition and 2 types

A

left ventricular hypertrophy caused by a gene mutation (rare)

  • MOST COMMON CAUSE: sudden death < 35 y/o
  • M>F, family hx
  • Echo: LV wall thickness > 1.5 cm

2 types: non-obstructive and obstructive (intraventricular septum can obstruct)

NOTE: valsalva can make obstruction more apparent during auscultation

95
Q

hypertrophic cardiomyopathy (HCM) - sxs

A 
dyspnea and chest pain: most common
syncope (post-exertion)
atrial fibrillation
JVP w/ "a" wave
S4 gallop
Loud systolic murmur 
 - inc. w/ valsalva
Mitral regurgitation
96
Q

hypertrophic cardiomyopathy (HCM) - dx and tx

A

Echo is diagnostic

tx:

  • beta-blcoker: initial for symptomatic pt
  • Verapamil: improve diastolic fx
97
Q

restrictive cardiomyopathy - definition and causes

A

impaired diastolic filling w/ preserved contractility (rare)

causes:

  • amyloidosis (rare dz where protein deposits on organs)
  • auto-immune dz: sarcoidosis, hemochromatosis, scleraderma
98
Q

restrictive cardiomyopathy - sxs, imaging and EKG results, screening test

A

sxs:

  • dec. exercise tolerance
  • amyloidosis: periorbital purpura, thickened tongue, hepatomegaly

Echo: small but thickened LV w/ dec. EF

EKG: low voltage

Screening test: cardiac MRI

99
Q

restrictive cardiomyopathy - tx

A

diuretics
beta-blockers
corticosteroids (dec. inflammation)

cardiac transpant

100
Q

infective endocarditis (IE)

A

typically bacterial (staph aureus = leading cause)

can effect valves or endocardial surface of heart

  • embolization
  • acute valvular regurgitation
  • myocardial abscess

pre-disposing valvular abnormalities / risk factors:

  • rheumatic involvement
  • mitral valve prolapse
  • congenital cardiac conditions: teratology of fallot and PDA
  • dental, URI, and lower GI procedures
  • IVDU
101
Q

bacterial endocarditis in IV drug users - what bacterial and what valve?

A 
staph aureus (60%)
tricuspid valve (90%)
102
Q

bacterial endocarditis - findings on PE

A

fever - almost always

Skin and nail exam (25% of patients get these):

  • petechiae: conjunctivae, palate, extremities
  • Osler nodes: PAINFUL lesions on fingers and toes
  • Janeway lesions: PAINLESS erythematous lesions on palms/soles
  • splinter hemorrhage: under nailplate
  • roth spots: exudates in retina
103
Q

bacterial endocarditis - dx (general)

A

echo: vegetations and valve assessment

blood cultures: x 3 one hour apart b/f ABX

104
Q

bacterial endocarditis - dx (Duke Criteria)

A

Major:

  • 2+ blood cultures of typical causative organism
  • evidence of endocardial involvement by echo
  • development of new murmur

Minor:

  • presence of pre-disposing condition
  • fever (100.4)
  • vascular phenomena
  • immunologic phenomena
    • blood cultures not meeting major criteria

For dx:

  • 2 major
  • 1 major + 3 minor
  • 5 minor
105
Q

bacterial endocarditis - prevention (who and when)

A

prophylaxis recommended for:

  • prosthetic valves
  • previous bacterial endocarditis
  • transplant
  • congenital heart defect

prophylaxis recommended when:

  • dental procedures (gingival manipulation or perforation of mucosa)
  • respiratory tract procedures (requiring incision of mucosa)
  • infected skin/MSS tissue
106
Q

bacterial endocarditis - prevention (drug of choice)

A

amoxicillin (PO)
ampicillin (IV)

if PEN allergy: clindamycin, cephalexin
azithromycin

107
Q

acute pericarditis

A

infection of pericardium (avascular but well-innervated (painful); has 2 layers: visceral and parietal)

causes:

  • viral: MOST COMMON
  • bacterial: from lung infection (pneumococcus): have fever, toxic appearing
  • uremic: CKD: no fever
  • neoplastic: most common are Hodgkin and lymphoma: no pain
  • post MI = Dressler Syndrome
  • radiation
  • connective tissue: SLE, RA
108
Q

Dressler Syndrome

A

pericarditis following acute MI

109
Q

acute pericarditis - findings on PE

A

sharp, retrosternal pleuritic chest pain
- better leaning forward

pericardial friction rub

fever > 100.4 - consider bacterial

110
Q

acute pericarditis - EKG and Echo findings

A

EKG: diffuse ST elevation across all leads (except aVR)

Echo: done to exclude tamponade

when to do pericardiocentesis:

  • tamponade
  • malignant pericarditis
  • purulent TB expected
111
Q

acute pericarditis - tx

A

avoid activity until resolves (up to 3 months)

aspirin or ibuprophen x 2 weeks (with taper)

add Colchicine (anti-inflammatory) x 3 months to prevent reoccurance

  • avoid if kidney or liver issues
  • avoid if on macrolide

severe: add corticosteroid

112
Q

acute pericarditis - progression to cardiac tamponade

A

pericarditis increases fluid around heart = heart is compressed = impaired cardiac filling

113
Q

pericardial effusion and cardiac tamponade - history

A

painful chest pain: acute inflammatory process

painless chest pain: neoplastic, uremia (CKD)

dyspnea

cough

114
Q

pericardial effusion and cardiac tamponade - findings on PE

A 
anxious
HR inc.
BP dec. (hypotensive)
CV: muffled heart sounds, pericardial friction rub
pulsus paradoxus
115
Q

pulsus paradoxus

A

hallmark of cardiac tamponade

during inspiration, >10mmHg drop in systolic BP

during inspiration, absent brachial or radial pulse (severe)

Note: need peroicardiocentesis if have this

116
Q

pericardial effusion and cardiac tamponade - imaging and EKG findings

A

CXR/CT/Echo: globular heart (fluid surrounding)

EKG:

  • low voltage
  • electrical alternans: alternation of QRS complex amplitude or axis b/t beats

Note: echo is key diagnostic test

117
Q

pericardial effusion and cardiac tamponade - treatment

A

effusion w/o tamponade: treat pericarditis etiology

effusion w/ tamponade: urgent drainage via pericardiocentesis

118
Q

Becks Triad

A

indicative for cardiac tamponade

  • hypotension
  • distended neck veins
  • muffled heart sounds
119
Q

inotropic

A

effect force of cardiac contraction

120
Q

chronotropic

A

effect heart rate

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