Cardiology Flashcards
Cardiomegaly - how does heart enlarge in CHF
first laterally and then inferiorly - get PMI at 5th ICS , lt anterior axillary line (instead of typical mid-clavicular line)
exertional dyspnea
SOB on exertion - hint to possibly cardiac pathology
paroxysmal noctural dyspnea
must get up out of bed due to SOB
orthopnea
must sit up - SOB with lying down
dyspnea at rest
sign of worsening cardiac pathology
syncope/pre-syncope/dizzy
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)
cough - hints to cardiac origin
usually dry or non-productive
seen in HF and ACE-inhibitor medication use
blood pressure - orthostatic changes
when systolic BP drops >20mm when standing = positive for orthostasis
pulse pressure
difference b/t systolic and diastolic
- widened = larger stroke volume
- narrow = smaller stroke volume
pulse grading
1-4; 2 = normal
bifed / bisferiens pulse
beating 2 x in systole (hypertrophic obstructive cardiomyopathy and aoritc regurgitation)
dicrotic pulse
exaggerated; early diastolic wave seen in heart failure
pulses alternans
alternating strong/weak pulse force seen in HF
paradoxical pulse
> 10mm Hg drop in systolic BP during inspiration in obstructive lung dz and cardiac tamponade
jugular venous pulsations
provides info about central venous pressures and RIGHT-heart function
hepatic jugular reflux (HJR)
when press on liver see a >1cm increase in jugular venous pressure
- seen in HF
first heart sound - S1
“Lub” - results from closing of mitral and tricuspid valves
- loud in mitral stenosis
second heart sound - S2
“dub” - closure of aortic and pulmonic valves
- split with inspiration - physiologic S2 (normal)
third heart sound - S3
early, rapid LV filling (normal in young)
associated with LV overload conditions - HF
fourth heart sound - S4
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)
mid-systolic click
found in mitral valve prolapse
opening snap
found in mitral stenosis
systolic murmurs
most common
Found in normal heart sounds, aortic stenosis, pulmonic stenosis
innocent flow murmurs
early systolic
80% kids
pregnant females
decreased with sitting up
diastolic murmurs
almost always pathology
most common is high-pitched = pulmonic regurg, aortic regurg
HINT: diastolic “rumble” = mitral stenosis
continuous murmur
heard through systole and diastole
patent ductus arteriosus = most common (“machinery like”)
electrocardiogram (ECG)
12-lead ECG - diagnostic study looking for electricity in heart
Holter monitor = 24 hour ECG
ECHO - echocardiogram
U/S of heart: good for anatomy and structural problems (any valve issue)
- can see blood flow
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
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
chemicals used in pharmacologic stress tests
adenosine
dipyridamole
dobutamine
lexiscan
contraindications to stress test
severe aortic stenosis
fresh MI
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
cardiac catheterization (coronary angiography)
best used to evaluate and treat CAD
- coronary angiography (visualize vessels)
- angioplasty (PTCA aka “balloon”)
- angioplasty with stent placement
hypertension - basics
office BP > or = 140/90
- must have 2 measurments
most common condition in primary care
JNC 8 criteria
hypertension - pathophysiology
RAAS mechanism/natriuretic hormone
vasoconstriction at level of arterioles
- leads to electrolyte disturbance
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
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
primary HTN - exacerbating factors
environmental: salt, obesity
others: tobacco, ETOH, sedentary, polycythemia vera (high HGB, HCT), NSAIDS, low K+, metabolic syndrome (DM)
HTN - most common sxs
headache
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)
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
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
most common TREATABLE cause of HTN
aldosteronism - usually caused by an aldosterone-producing adenoma
Presents at age 30-50 with HTN and hypokalemia
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
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
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
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
secondary HTN - OSA
OSA and HTN are linked
Untreated OSA leads to new HTN
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
HTN - treatment goals
- accurate assessment of BP
- CV risk stratification
- ID and treat secondary causes
HTN - who to treat (JNC 8)
age 30-59: >140/90mmHg
age 60+: 150/90mmHg
Initiate meds if lifestyle interventions failed
HTN - prevention / lifestyle changes
Weight loss (BMI 185.-24.9)
Na+ intake (<2.4g/d)
physical activity: 30min/day
ETOH consumption limited
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)
HTN - medications if non-AA (+/-DM)
Thiazide diuretic
Ca+ channel blocker
ACEI
ARB
HTN - medications of AA (+/- DM)
Thiazide diuretic
Ca+ channel blocker
why? AA patients have smaller BP reduction with ACEI and ARB
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
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
HTN med for someone with chronic kidney dz
ACE-I or ARB
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
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
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
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
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
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)
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
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)
hypotension
low BP that can be caused by insufficient peripheral vasoconstriction (orthostatic) or cardiogenic shock
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)
orthostatic hypotension - evaluation and treatment
evaluation:
- tilt-table
- endocrine etiology
- cardiac etiology
treatment:
- discontinue contributing meds
- vasoconstricting agents: midodrine, caffeine
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
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
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)
cardiogenic shock - management
1st line: norepinephrine and dopamine (vasopressor)
- if unresponsive: dobutamine (beta-agonist that will inc. CO and myocardial contractility)
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
heart failure: ejection fraction
Evaluate ejection fraction w/ echo
- reduced: <50%
- preserved: >50%
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
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
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
heart failure - causes
Leading cause: CAD
- CAD>acute MI>ischemic cardiomyopathy of left ventricle> systolic HF
2nd leading cause: HTN
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
heart failure: EKG findings
LVH
prior MI
Q-waves (indicate past CAD)
BBB
heart failure - CXR
cardiomegaly
pulmonary venous
HTN (enlarged veins in upper lobe)
pulmonary edema: perihilar or patchy peripheral infiltrates
- KERLEY B lines
heart failure - labs
BNP (brain natriuretic peptide) - released by ventricles when under stress
- not specific (also increases with age, obesity, renal dysfunction)
heart failure - best test
echo - helps to determine valve fx and ventricular fx
heart failure - non pharmacological treatment
diary of wt and BP daily
exercise, calorie and Na+ restriction, treat OSA
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)
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
Loop diuretics - key side effect
ototoxicity
cardiomyopathy - categories
dilated - MOST COMMON (95%)
restrictive
hypertrophic
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
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
atrial fibrillation - what medication is a must
anticoagulation - can throw a clot
- Ex. Warfarin
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
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
hypertrophic cardiomyopathy (HCM) - dx and tx
Echo is diagnostic
tx:
- beta-blcoker: initial for symptomatic pt
- Verapamil: improve diastolic fx
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
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
restrictive cardiomyopathy - tx
diuretics
beta-blockers
corticosteroids (dec. inflammation)
cardiac transpant
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
bacterial endocarditis in IV drug users - what bacterial and what valve?
staph aureus (60%) tricuspid valve (90%)
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
bacterial endocarditis - dx (general)
echo: vegetations and valve assessment
blood cultures: x 3 one hour apart b/f ABX
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
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
bacterial endocarditis - prevention (drug of choice)
amoxicillin (PO)
ampicillin (IV)
if PEN allergy: clindamycin, cephalexin
azithromycin
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
Dressler Syndrome
pericarditis following acute MI
acute pericarditis - findings on PE
sharp, retrosternal pleuritic chest pain
- better leaning forward
pericardial friction rub
fever > 100.4 - consider bacterial
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
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
acute pericarditis - progression to cardiac tamponade
pericarditis increases fluid around heart = heart is compressed = impaired cardiac filling
pericardial effusion and cardiac tamponade - history
painful chest pain: acute inflammatory process
painless chest pain: neoplastic, uremia (CKD)
dyspnea
cough
pericardial effusion and cardiac tamponade - findings on PE
anxious HR inc. BP dec. (hypotensive) CV: muffled heart sounds, pericardial friction rub pulsus paradoxus
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
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
pericardial effusion and cardiac tamponade - treatment
effusion w/o tamponade: treat pericarditis etiology
effusion w/ tamponade: urgent drainage via pericardiocentesis
Becks Triad
indicative for cardiac tamponade
- hypotension
- distended neck veins
- muffled heart sounds
inotropic
effect force of cardiac contraction
chronotropic
effect heart rate
