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)
2
Q
exertional dyspnea
A
SOB on exertion - hint to possibly cardiac pathology
3
Q
paroxysmal noctural dyspnea
A
must get up out of bed due to SOB
4
Q
orthopnea
A
must sit up - SOB with lying down
5
Q
dyspnea at rest
A
sign of worsening cardiac pathology
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)
7
Q
cough - hints to cardiac origin
A
usually dry or non-productive
seen in HF and ACE-inhibitor medication use
8
Q
blood pressure - orthostatic changes
A
when systolic BP drops >20mm when standing = positive for orthostasis
9
Q
pulse pressure
A
difference b/t systolic and diastolic
- widened = larger stroke volume
- narrow = smaller stroke volume
10
Q
pulse grading
A
1-4; 2 = normal
11
Q
bifed / bisferiens pulse
A
beating 2 x in systole (hypertrophic obstructive cardiomyopathy and aoritc regurgitation)
12
Q
dicrotic pulse
A
exaggerated; early diastolic wave seen in heart failure
13
Q
pulses alternans
A
alternating strong/weak pulse force seen in HF
14
Q
paradoxical pulse
A
> 10mm Hg drop in systolic BP during inspiration in obstructive lung dz and cardiac tamponade
15
Q
jugular venous pulsations
A
provides info about central venous pressures and RIGHT-heart function
16
Q
hepatic jugular reflux (HJR)
A
when press on liver see a >1cm increase in jugular venous pressure
- seen in HF
17
Q
first heart sound - S1
A
“Lub” - results from closing of mitral and tricuspid valves
- loud in mitral stenosis
18
Q
second heart sound - S2
A
“dub” - closure of aortic and pulmonic valves
- split with inspiration - physiologic S2 (normal)
19
Q
third heart sound - S3
A
early, rapid LV filling (normal in young)
associated with LV overload conditions - HF
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)
21
Q
mid-systolic click
A
found in mitral valve prolapse
22
Q
opening snap
A
found in mitral stenosis
23
Q
systolic murmurs
A
most common
Found in normal heart sounds, aortic stenosis, pulmonic stenosis
24
Q
innocent flow murmurs
A
early systolic
80% kids
pregnant females
decreased with sitting up
25
diastolic murmurs
almost always pathology
most common is high-pitched = pulmonic regurg, aortic regurg
HINT: diastolic "rumble" = mitral stenosis
26
continuous murmur
heard through systole and diastole
patent ductus arteriosus = most common ("machinery like")
27
electrocardiogram (ECG)
12-lead ECG - diagnostic study looking for electricity in heart
Holter monitor = 24 hour ECG
28
ECHO - echocardiogram
U/S of heart: good for anatomy and structural problems (any valve issue)
- can see blood flow
29
tilt-table test
often used to R/O vasovagal response as cause of syncope
- test autonomic nervous system functioning
- used before more invasive testing is performed
30
stress testing - types
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
31
chemicals used in pharmacologic stress tests
adenosine
dipyridamole
dobutamine
lexiscan
32
contraindications to stress test
severe aortic stenosis
| fresh MI
33
EP studies - electrophysiologic
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
34
cardiac catheterization (coronary angiography)
best used to evaluate and treat CAD
- coronary angiography (visualize vessels)
- angioplasty (PTCA aka "balloon")
- angioplasty with stent placement
35
hypertension - basics
office BP > or = 140/90
- must have 2 measurments
most common condition in primary care
JNC 8 criteria
36
hypertension - pathophysiology
RAAS mechanism/natriuretic hormone
vasoconstriction at level of arterioles
- leads to electrolyte disturbance
37
hypertension - definition (pre, stage I, stage II)
normal: <120 AND <80
prehypertension: 120-139 OR 80-89
Stage I HTN: 140-159 OR 90-99
Stage II HTN: >160 OR >100
38
hypertension - classification (primary, secondary, resistant)
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
39
primary HTN - exacerbating factors
environmental: salt, obesity
others: tobacco, ETOH, sedentary, polycythemia vera (high HGB, HCT), NSAIDS, low K+, metabolic syndrome (DM)
40
HTN - most common sxs
headache
41
HTN - physical exam
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)
42
red flags for secondary HTN causes
HTN starts early (<25 y/o) w/o FH
HTN first develops >50
previously controlled HTN, now refractory
HTN resistant for 3+ meds
43
secondary HTN - most common cause
chronic renal disease
- screening tests: BUN/Cr, U/A, microalbuminuria
- Dx: renal U/S
- tx: BP control and/or dialysis
44
most common TREATABLE cause of HTN
aldosteronism - usually caused by an aldosterone-producing adenoma
Presents at age 30-50 with HTN and hypokalemia
45
secondary HTN - renovascular dz
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
46
secondary HTN - Cushing's Syndrome
hypercortisolism
Presents: truncal obesity, striae, acne, hyperpigmented skin, moon facies and buffalo hump
Labs: glucose (hyperglycemia), hypokalemia
Dx: 24 hr free cortisol
47
secondary HTN - pheochromocytoma
rare catecholamine secreting tumor from adrenal medulla
- causes vasoconstriction and inc. cardiac output
Presentation: pulsatile headache, palpitations, diaphoresis
Dx: plasma metanephrine test
48
secondary HTN - coarctation of aorta
narrowing of aorta
Presents: young pt with HTN and delayed femoral pulses
Dx: Echo
CXR: see figure 3 sign of aortic arch
49
secondary HTN - OSA
OSA and HTN are linked
Untreated OSA leads to new HTN
50
secondary HTN - medications
corticosteroids - like Cushings
oral contraceptives
NSAIDS - Na++ retention
ETOH - activates sympathetic system
sympathomimetics: cold and diet meds, cocaine
erythropoietin: increases vascular volume
51
HTN - treatment goals
1. accurate assessment of BP
2. CV risk stratification
3. ID and treat secondary causes
52
HTN - who to treat (JNC 8)
age 30-59: >140/90mmHg
age 60+: 150/90mmHg
Initiate meds if lifestyle interventions failed
53
HTN - prevention / lifestyle changes
Weight loss (BMI 185.-24.9)
Na+ intake (<2.4g/d)
physical activity: 30min/day
ETOH consumption limited
54
HTN - 4 classes of medications
Diuretics (thiazide)
Ca++ channel blockers ("dipines")
ACEI ("prils")
ARBs ("sartans")
Mainstay: thiazide diuretic
NOTE: beta blockers no longer 1st line (2nd line)
55
HTN - medications if non-AA (+/-DM)
Thiazide diuretic
Ca+ channel blocker
ACEI
ARB
56
HTN - medications of AA (+/- DM)
Thiazide diuretic
Ca+ channel blocker
why? AA patients have smaller BP reduction with ACEI and ARB
57
HTN Meds - ACE Inhibitors
"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
HTN Meds - ARB (angiotensin receptor blockers)
"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
HTN med for someone with chronic kidney dz
ACE-I or ARB
60
HTN med - thiazide diuretics
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
HTN treatment - pearls
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
HTN treatment - 2nd line
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
Hypertensive crises
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
hypertensive urgency - definition, sxs, treatment
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
hypertensive emergency - definition, sxs, treatment
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
malignant HTN
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
hypertensive emergency - medications to use
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
hypotension
low BP that can be caused by insufficient peripheral vasoconstriction (orthostatic) or cardiogenic shock
69
orthostatic hypotension - definition, sxs, causes
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
orthostatic hypotension - evaluation and treatment
evaluation:
- tilt-table
- endocrine etiology
- cardiac etiology
treatment:
- discontinue contributing meds
- vasoconstricting agents: midodrine, caffeine
71
cardiogenic shock - definition and causes
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
cardiogenic shock (hypotension) - clinical manifestations
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
cardiogenic shock - diagnosis and parameters
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
cardiogenic shock - management
1st line: norepinephrine and dopamine (vasopressor)
| - if unresponsive: dobutamine (beta-agonist that will inc. CO and myocardial contractility)
75
heart failure - pathophysiology and population most affected
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
heart failure: ejection fraction
Evaluate ejection fraction w/ echo
- reduced: <50%
- preserved: >50%
77
heart failure - stages (A-D)
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
heart failure - classes (NYHA functional classification I-IV)
```
class I: asymptomatic
class II: sympomatic with moderate activity
class III: symptomatic with mild activity
class IV: symptomatic at rest
```
79
heart failure - symptoms
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
heart failure - causes
Leading cause: CAD
- CAD>acute MI>ischemic cardiomyopathy of left ventricle> systolic HF
2nd leading cause: HTN
81
heart failure - findings on PE
```
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
heart failure: EKG findings
LVH
prior MI
Q-waves (indicate past CAD)
BBB
83
heart failure - CXR
cardiomegaly
pulmonary venous
HTN (enlarged veins in upper lobe)
pulmonary edema: perihilar or patchy peripheral infiltrates
- KERLEY B lines
84
heart failure - labs
BNP (brain natriuretic peptide) - released by ventricles when under stress
- not specific (also increases with age, obesity, renal dysfunction)
85
heart failure - best test
echo - helps to determine valve fx and ventricular fx
86
heart failure - non pharmacological treatment
diary of wt and BP daily
| exercise, calorie and Na+ restriction, treat OSA
87
heart failure - pharmacological treatment (stages A and B)
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
heart failure - pharmacological treatment (stages C and D) - patient is having sxs
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
Loop diuretics - key side effect
ototoxicity
90
cardiomyopathy - categories
dilated - MOST COMMON (95%)
restrictive
hypertrophic
91
dilated cardiomyopathy - definition and causes
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
dilated cardiomyopathy -- sxs, imaging, tx
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
atrial fibrillation - what medication is a must
anticoagulation - can throw a clot
| - Ex. Warfarin
94
hypertrophic cardiomyopathy (HCM) - definition and 2 types
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
hypertrophic cardiomyopathy (HCM) - sxs
```
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
hypertrophic cardiomyopathy (HCM) - dx and tx
Echo is diagnostic
tx:
- beta-blcoker: initial for symptomatic pt
- Verapamil: improve diastolic fx
97
restrictive cardiomyopathy - definition and causes
impaired diastolic filling w/ preserved contractility (rare)
causes:
- amyloidosis (rare dz where protein deposits on organs)
- auto-immune dz: sarcoidosis, hemochromatosis, scleraderma
98
restrictive cardiomyopathy - sxs, imaging and EKG results, screening test
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
restrictive cardiomyopathy - tx
diuretics
beta-blockers
corticosteroids (dec. inflammation)
cardiac transpant
100
infective endocarditis (IE)
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
bacterial endocarditis in IV drug users - what bacterial and what valve?
```
staph aureus (60%)
tricuspid valve (90%)
```
102
bacterial endocarditis - findings on PE
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
bacterial endocarditis - dx (general)
echo: vegetations and valve assessment
blood cultures: x 3 one hour apart b/f ABX
104
bacterial endocarditis - dx (Duke Criteria)
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
bacterial endocarditis - prevention (who and when)
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
bacterial endocarditis - prevention (drug of choice)
amoxicillin (PO)
ampicillin (IV)
if PEN allergy: clindamycin, cephalexin
azithromycin
107
acute pericarditis
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
Dressler Syndrome
pericarditis following acute MI
109
acute pericarditis - findings on PE
sharp, retrosternal pleuritic chest pain
- better leaning forward
pericardial friction rub
fever > 100.4 - consider bacterial
110
acute pericarditis - EKG and Echo findings
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
acute pericarditis - tx
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
acute pericarditis - progression to cardiac tamponade
pericarditis increases fluid around heart = heart is compressed = impaired cardiac filling
113
pericardial effusion and cardiac tamponade - history
painful chest pain: acute inflammatory process
painless chest pain: neoplastic, uremia (CKD)
dyspnea
cough
114
pericardial effusion and cardiac tamponade - findings on PE
```
anxious
HR inc.
BP dec. (hypotensive)
CV: muffled heart sounds, pericardial friction rub
pulsus paradoxus
```
115
pulsus paradoxus
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
pericardial effusion and cardiac tamponade - imaging and EKG findings
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
pericardial effusion and cardiac tamponade - treatment
effusion w/o tamponade: treat pericarditis etiology
effusion w/ tamponade: urgent drainage via pericardiocentesis
118
Becks Triad
indicative for cardiac tamponade
- hypotension
- distended neck veins
- muffled heart sounds
119
inotropic
effect force of cardiac contraction
120
chronotropic
effect heart rate
