Cardiovascular Flashcards
Causes of Takotsubo Cardiomyopathy
disordered response of the myocardium d/t enormous amount of catecholamine being produced (i.e. stress, grief)
Takotsubo cardiomypoathy
Stress-induced cardiomyopathy
Mimics a STEMI
Typically follows severe emotional or physiologic stress
May be due to an anatomic predisposition to ischemia in states of extreme catecholaminergic tone
Takotsubo cardiomyopathy: Labs/Dx
ST-elevations or pronounced T-wave inversions
Cardiac Cath is required to make the diagnosis through an absence of significant coronary disease on angiography
- kinesis of the LV apex (apical ballooning)
Wolff-Parkinson-White syndrome: EKG changes
delta waves
wide QRS
shortened PR
ST-T wave repolarization abnormalities
pseudo-inferior MI pattern suggesting accessory AV conduction
Wolff-Parkinson-White syndrome: complications
tachyarrhythmias that can lead to VF and death
Wolff-Parkinson-White syndrome: what meds are contraindicated?
nodal blocking agents: digoxin, beta blockers, CCBs
Wolff-Parkinson-White syndrome: treatment
ablation
Grade I murmur
barely audible
Grade II murmur
audible but faint
Grade III murmur
moderately loud; easily heard
Grade IV murmur
loud; associated with a thrill
Grade V murmur
very loud; heard w/one corner of stethoscope lifted off the chest
Grade VI murmur
loudest
A murmur heard at the 5th ICS is associated with…
the apex of the heart
mitral valve
A murmur heard at the 2nd or 3rd ICS is associated with…
base of the heart
aortic valve
A murmur heard during systole is associated with…
mitral regurgitation
aortic stenosis
Ms. ArD & Mr. AsS
A murmur heard during diastole is associated with…
mitral stenosis
aortic regurgitation
Ms. ArD & Mr. AsS
arterial ulcers: presentation
Punched out or stellate appearance
Painful
Surrounding red, tight skin
May be pale or have eschar
Often associated with trauma and occur over pressure points
most common cause of lower extremity ulcers
chronic venous stasis disease
venous stasis ulcers: presentation
Typically appear on the lower legs above the ankle
Tender, shallow
Exudative with granulation tissue at the base
Irregular borders
AHA recommendation for daily sodium intake for hypertension
<1.5g/day
S1
mitral/tricuspid (AV) valves close
aortic/pulmonic (semilunar) valves open
S2
mitral/tricuspid (AV) valves open
aortic/pulmonic (semilunar) valves close
period between S1 and S2
systole
period between S2 and S1
diastole
S3
increased fluid states (e.g. heart failure, pregnancy)
S4
stiff ventricular wall (e.g. MI, LVH, chronic hypertension)
HFrEF
systolic failure
inability to contract
results in decreased cardiac output
HFpEF
diastolic failure
inability to relax and fill
results in decreased cardiac ouptut
acute heart failure
L sided failure
abrupt onset
usually follows MI or valve rupture
can result in LVH d/t L ventricular failure 2/2 chronic hypertension
chronic heart failure
R sided failure
develops as a result of inadequate compensatory mechanisms that have been employed over time to improve cardiac output
result of L sided failure
L heart failure: S/Sx
dyspnea at rest
coarse rales all over lung fields
wheezy frothy cough
appears generally healthy except for the acute event
S3 gallop
murmur of mitral regurgitation (systolic murmur loudest at apex)
R heart failure: S/Sx
Appears chronically ill
JVD
Diffuse chest wall heaves
Displaced PMI
S3 and/or S4
hepatomegaly
splenomegaly
Abdominal fullness
dependent edema d/t increased capillary hydrostatic pressure
paroxysmal nocturnal dyspnea
fatigue on exertion
NYHA Functional Classification of Heart Failure: Class I
no limitations on physical activity
NYHA Functional Classification of Heart Failure: Class II
slight limitations of physical activity but comfortable at rest (physical activity results in fatigue, palpitations, dyspnea, angina)
NYHA Functional Classification of Heart Failure: Class III
marked limitations of physical activity but comfortable at rest
3 pillows to sleep but able to sleep
- ACEI indicated
NYHA Functional Classification of Heart Failure: Class IV
severe; inability to carry out any physical activity without discomfort (symptomatic at rest
-continuous IV inotropic support indicated
Heart failure: labs/Dx
ABG: hypoxemia, hypocapnia
BMP normal unless chronic heart failure is present
Obtain baseline BNP or NT-proBNP
UA
CXR: pulmonary edema, Kerley B lines, effusions
TTE to assess L ventricular function
EKG may show deviation or underlying problem: acute MI, dysrhythmia
PFTs for wheezing
Heart failure: non pharmacologic management
sodium restriction
rest/activity balance
weight reduction
Heart failure: pharmacologic management
1st line: diuretics
ACEI or ARB
beta blocker
Sacubitril/valsartan (Entresto) - useful for HFrEF
Digoxin
ACs for AFib
dilated cardiomyopathy
dilation of the heart muscle
most common type of cardiomyopathy
hypertrophic cardiomyopathy
hypertrophy of the left, and occasionally the right, ventricle
restrictive cardiomyopathy
scarring/stiffening of the heart muscle
the least common type of cardiomyopathy
arrhythmogenic right ventricular dysplasia
irregular heart rhythms caused by the dying of muscle tissue in the right ventricle that is replaced by scar or fat tissue
transthyretin amyloid cardiomyopathy (ATTR-CM)
abnormal protein buildup (deposits of amyloid protein fibrils) in the walls of the left ventricle
cardiomyopathy: routine management
Three drug combination for most patients with HF: diuretic, ACEI/ARB, beta blocker
- Beta blockers once euvolemia is achieved
cardiomyopathy: long-term management
Lifestyle changes: diet, exercise, sleep patterns, stress reduction, avoidance of alcohol and other drugs
Maintaining treatment of comorbidities
cardiomyopathy: acute management
Symptomatic relief: vasodilators to reduce preload and afterload (nitrates, hydralazine, nitride, nesiritide, ACEIs/ARBs, diuretics)
Inhibition of neurohormonal activation: ACEIs/ARBs, beta blockers, aldosterone antagonists
inpatient management of acute pulmonary edema
supplemental O2 while awaiting ABGs
sitting or semi-fowler position
Morphine 2-4mg IVP, repeat 20-30 min PRN, stop if hypercapnia occurs
Furosemide 40mg IVP; repeat in 10 min if no response
Severe bronchospasm: inhaled sympathomimetics
Severe pulmonary edema: nitroprusside, hydralazine for afterload and preload reduction
If cardiac index remains low: dobutamine
hypertension: S/Sx
elevated BP
epistaxis in the late afternoon
dizziness/lightheadedness
S4 r/t LVH
AV nicking (chronic sign)
severe: suboccipital pulsating headache, occurring early in the morning and resolving throughout the day
tearing chest pain may indicate aortic dissection
hypertension: labs/Dx
rule out secondary causes
- renovascular disease studies
- CXR if cardiomegaly suspected
- plasma aldosterone level to rule out aldosteronism
- AM/PM cortisol levels to rule out Cushing’s syndrome
CBC, BMP, ca, phos
cholesterol, triglycerides
UA, uric acid
EKG
JNC Normal BP
SBP <120 and DBP <80
JNC elevated BP
SBP 120-129 and DBP >80
JNC stage 1 hypertension
SBP 130-139 or DBP 80-89
JNC stage 2 hypertension
SBP >140 or DBP >90
hypertension: pharmacologic management for non-African American
thiazide diuretic
ACEI
ARB
CCB
hypertension: pharmacologic management for African American
thiazide diuretics
CCB?
hypertension: pharmacologic management for diabetics
ACEI (or ARB)
hypertension: pharmacologic management for adults with CKD
ACEI - slow the progression of CDK and decrease proteinuria
hypertension: treatment algorithm for initial treatment
1 month
then increase the dose
then add a second drug
continue to assess monthly until goal is reached
Using an ACEI and ARB together is a risk for
hyperkalemia
first line treatment for hypertension
thiazide diuretics
hypertensive urgency
> 180/110
May or may not be associated with severe headache, SOB, epistaxis, severe anxiety
hypertensive urgency: treatment
oral therapies such as clonidine
hypertensive emergency
> 180/120
Requires immediate (within 1 hour) BP reduction to prevent or limit target organ damage
or
<180/120 with any of the following:
-malignant hypertension
-hypertensive encephalopathy
-ICH
-unstable angina
-acute MI
-acute heart failure
-dissecting aortic aneurysm
-eclampsia
hypertensive emergency: management
ICU
nicardipine, sodium nitroprusside (Nitride)
For compelling conditions (e.g. aortic dissection, severe preeclampsia, eclampsia, pheochromocytoma crisis): SBP should be reduced to <140 in the first hour
- <120 in aortic dissection
For adults without a compelling condition: SBP should be reduced by no more than 25% within the first hour
- if stable, to 160/100 within the next 2-6 hours
- cautiously to normal during the next 24-48 hours
Lowering BP too quickly can damage blood flow to organs accustomed to functioning at high levels and cause ischemia or infarction
stable angina
exertional
most common
Prinzmetal’s angina
occurs at various times, including rest
d/t sudden influx of intracellular calcium
- treat w/CCBs
ST elevations on EKGs rather than depressions
Dx of exclusion often in Cath lab
unstable angina
pre-infarction, rest or crescendo, coronary syndromes
microvascular angina
metabolic syndrome
angina: labs/Dx
EKG: normal with ST depressions
Exercise EKG
Serum lipid levels
definitive diagnostic procedure: coronary angiography
Normal lipid panel
total cholesterol <200
triglycerides <150
VLDL <150
LDL <100
HDL 40-60
angina: management
Diet
Low dose aspirin
Nitrates
Beta blockers
CCBs
Optimize lipid panel values
Identify patients who would benefit from statin therapy
-ASCVD
-elevated LDL
-DM
Bile acid sequestrates
lower LDL
may increase triglycerides
Examples:
-cholestyramine (Questran)
-Colesevelam
-colestipol
Fibrates
lower triglycerides
slightly lower LDL
possibly elevate HDL
Examples:
-gemfibrozil
-fenofibrate
-fenofibric acid
Cholesterol absorption inhibitor
used w/statin to lower LDL
Example:
-ezetimibe (Zetia)
Niacin
lowers LDL and triglycerides
elevates HDL
high doses may cause “flushing” sensation which will pass
How are ACEIs helpful after MI
prevent ventricular remodeling
MI/ACS management
ASA 325 to chew
NTG SL Q5 min x3
O2
12 lead EKG
Morphine
Furosemide if pulmonary edema present
Metoprolol IV x3 if not contraindicated
ACEIs
Heparin vs Lovenox
Monitor therapeutic coagulation values
Normal INR
0.8-1.2 s
Normal aPTT
28-38 sec
normal PT
11-16 sec
normal PTT
60-90 sec
MI/ACS: indications for pharmacologic revascularization
Unrelieved chest pain (>30 min and <6 hrs) with ST elevations >0.1 mV in two or more contiguous leads
MI/ACS: contraindications for pharmacologic revascularization (tPA)
Prior ICH
Ischemic stroke within 3 months
Intracranial or intraspinal surgery within 2 months
Significant closed head trauma or facial trauma within 3 months
Structural cerebral vascular lesion or malignant intracranial neoplasm
Suspected aortic dissection
Severe uncontrolled hypertension (>185/110)
Active bleeding or risk thereof, including abnormal coagulation values
PVD: pathology
arteriosclerotic narrowing of the lumen of arteries resulting in decreased blood supply to the extremities
PVD: Causes/Risk factors
atherosclerosis
HLD
smoking
DM
PVD: S/Sx
Common first symptom: intermittent claudication, calf pain
increased pain with elevation of lower extremities
progresses to pain at rest
cold/numbness to extremities
shiny/hairless skin
dependent rubor
pallor
cyanosis
ulcerations
reduced pulses
PVD: labs/Dx
1st line: ankle-brachial index (ABI) <0.9 (least invasive)
doppler US to evaluate flow
X-rays may show calcification
Arteriography: most definitive test, but invasive
PVD: management
Lifestyle changes:
-Stop smoking/tobacco
-Exercise, stop during pain and resume when pain subsides to develop collateral circulation
-weight reduction as needed
Cilostazol (Pletal)
manage DM, HLD
angioplasty
bypass surgery
amputation
chronic venous insufficiency: pathology
impaired venous return d/t either destruction of valves, changes d/t DVT, leg trauma, or sustained elevation of venous pressure
chronic venous insufficiency: causes/risk factors
more common in women
may have genetic predisposition
Hx of leg trauma
may be associated with varicose veins
chronic venous insufficiency: S/Sx
BLE heaviness and pain relieved with elevation of the legs or with walking
edema after prolonged standing
skin discoloration
numbness
tingling
pruritis
telangiectasis and varicosities are frequently seen
stasis leg ulcers
dermatitis
cool to touch
chronic venous insufficiency: labs/Dx
r/o edema d/t HF and other causes
chronic venous insufficiency: management
bed rest with legs elevated to diminish edema
compression stockings
weight reduction, exercise
aspirin may accelerate healing
treat dermatitis/ulcers
acute weeping dermatitis
- tap water compresses
- hydrocolloid dressings
- hydrocortisone cream
pericarditis
inflammation of the pericardium
pericarditis: causes
viruses: most common cause
post MI
renal failure
neoplastic, TB, septicemia
endocarditis
collagen diseases (e.g. scleroderma, RA, SLE, etc)
drug/trauma induced
pericarditis: S/Sx
very localized retrosternal/precordial chest pain, pleuritic in nature
pain increased by deep inspiration, coughing, swallowing, or recumbent
pain relieved by sitting forward
SOB 2/2 pain w/inspiration
malaise
headache
pericarditis: physical findings
pericardial friction rub - best heard w/patient leaning forward; high pitched
pleural friction rub may also be present (creaking/scratching sound/sandpaper)
fever may be present depending on underlying cause
endocarditis
infection of the endothelial surface of the heart
usually affects the valves
Dx of infective endocarditis must be considered and excluded in all patients with a heart murmur and FUO
endocarditis: causes
usually caused by bacteria
known valvular heart disease; esp in rheumatic, bicuspid aortic valve/mitral valve prolapse with significant regurgitation
recent dental/oropharyngeal surgery
GU instrumentation
surgery of the respiratory tract
congenital heart disease
prolonged use of IV catheters or TPN
patients with burns
hemodialysis
endocarditis: S/Sx
fever and malaise
night sweats
weight loss
general “sick” feeling
endocarditis: physical findings
murmur often present
fever
Osler’s nodes
petechiae
purpura
pallor
splinter hemorrhages
splenomegaly
Janeway lesions
Roth spots
Osler’s nodes
painful red nodules in the distal phalanges
seen in endocarditis
Splinter hemorrhages
linear, subungal splinter-appearing
seen in endocarditis
Janeway lesions
small painless macules on the palms and soles
Seen in endocarditis
Roth spots
small retinal infarcts, white in color, encircled by areas of hemorrhage
seen in endocarditis
endocarditis: labs/Dx
WBC normal or elevated, but always a left shift
TEE for valvular damage
BC for causative organism
- three separate cultures at three separate sites in 1 hour
ESR always elevated
endocarditis: management
Subacute endocarditis (delayed): empiric therapy is generally not started until BC results
Acute endocarditis (rapidly progressive): usually due to staphylococcus aureus (both MRSA and MSSA), streptococci, and enterococci
-empiric therapy: vancomycin until BC results
pericarditis: labs/Dx
ST elevations in all leads
-return of ST segment to normal in a few days followed by temporary T wave inversion
Depression of PR segment
ESR elevated
BC if bacterial cause suspected
CBC to r/o infx
baseline BMP
echo to confirm presence of pericardial fluid or other abnormalities
pericarditis: Management
1st line: colchicine
NSAIDs
-indomethacin
-ketorolac
-ibuprofen
Corticosteroids only for refractory pericarditis or very severe symptoms
-can increase viral replication
ABX if bacterial infx
Monitor for tamponade (hypotension, JVD, muffled/distant heart sounds, pulsus paradoxus)
Adverse effects of amiodarone
hypo/hyperthyroidism
interstitial lung disease
elevated LFTs
skin photosensitivity
corneal deposits
optic neuropathy
Before starting amiodarone, what should you check
thyroid levels
LFTs
baseline PFTs
referral to ophthalmology for monitoring may be needed
metabolic syndrome
large waistline: men >40 in, women >35 in
hypertension
hyperglycemia
high triglycerides, low HDL
Indications for urgent referral to a vascular surgeon or vascular laboratory in patients with ischemic arterial ulcers
Cellulitis
Gangrene
Visible tendon or bone at the ulcer base
Severe infection
ABI <0.5
Wolff-Parkinson-White Syndrome: S/Sx
during episodes of tachyarrhythmia:
-diaphoresis
-cool skin
-hypotension
-crackles d/t pulmonary vascular congestion
aortic stenosis: symptoms
dyspnea
heart failure
angina
syncope on exertion
systolic murmur over the 2nd R ICS radiates to carotid arteries
S4 gallop
1st line therapy for hyperlipidemia
statin
2nd line: niacin
digoxin toxicity
GI upset
visual disturbances with yellow-green halos
palpitations, dyspnea, syncope
bradycardia, PVCs, LBBB
diltiazem potentiates the effects of digoxin
Indications for statin therapy
Clinical evidence of ASCVD
Elevated LDL >190
Age 40-75 with diabetes and LDL 70-189 but no ASCVD
LDL 70-189 with no diabetes or ASCVD, but estimated 10-year risk of ASCVD >7.5
Statins potentiate the effects of what medications?
anticoagulants
TEE or TTE for endocarditis?
TEE is more specific
Patients with a history of ventriculostomies such as tetralogy of Fallot have an increased risk of…
ventricular tachycardia
Diagnostic test for POTS
tilt table test
S4 gallop is most commonly associated with…
aortic stenosis
Holosystolic murmurs are most often associated with…
mitral valve regurgitation
An opening snap can be heard in patients with…
mitral valve prolapse
mitral valve regurgitation
cardiac tamponade: S/Sx
Beck’s Triad:
-hypotension
-JVD
-muffled/distant heart sounds
pulsus paradoxus
decreased cardiac output
tachycardia
increased RR
weak peripheral pulses
cool skin
dark yellow urine
EKG: low voltage, no ST or T wave changes
cardiac tamponade: labs/Dx
echo
cardiac tamponade: management
pericardiocentesis
diuretics are contraindicated - may cause intravascular volume depletion and worsen hypotension
1st medication to give for suspected or confirmed cardiac ischemia
aspirin due to anti platelet effect
1st choice for management of ischemic cardiac pain due to vasodilatory effects
nitroglycerin
1st medication to give for acute heart failure
IV diuretic
pericardial effusion: S/Sx
dyspnea
fatigue
weight loss
occasional fever
dry cough
constant chest pain
pericardial friction rub
pericardial effusion: management
Assess cardiac function with TTE
Pericardiocentesis
PE: management
anticoagulant therapy for 3 months after initial therapy
Goal BP for patients with CKD
<130/80 if proteinuria is also present
ACE Inhibitors: mechanism
reduce afterload, preload, systolic wall stress
increase cardiac output without increasing heart rate
Cushing’s triad
increased SBP, decreased DBP (widening pulse pressure)
decreased RR
decreased HR
When do you see Cushing’s triad?
acute elevations of ICP
STEMI: management
Priority: PCI
fibrinolytic therapy within 30 mins of admission to the hospital
HFpEF or HFrEF: which has better outcomes?
HFrEF
HFpEF is managed with diuresis and BP control, but there is no medical treatment proven to reduce mortality and morbidity
HFpEF or HFrEF: L ventricle is normal in size
HFpEF
HFpEF or HFrEF: associated with exercise intolerance
both
HFpEF or HFrEF: associated with pulmonary hypertension
both
HFpEF or HFrEF: dilated left ventricle
HFrEF
aortic dissection: presentation
severe, sudden onset back pain between shoulder blades
tearing, ripping, stabbing chest pain
BP unequal in both arms
CXR: widened mediastinum
aortic dissection: management
emergent CT angiogram
cardiac surgery consult
Intervention that decreases the final size of the infarcted myocardium in the acute phase of an anterior STEMI
PCI
Intervention for patients who do not stabilize after PCI or fibrinolytic therapy
IABP counterpulsation therapy
Who is IABP counterpulsation therapy indicated for?
patients with mechanical defects such as VSD or mitral regurgitation
In decompensated heart failure, what medications may support cardiac function and cardiac output?
IV inotropic agents (e.g. dobutamine)
-especially useful for patients who can’t tolerate vasodilator therapy
-useful for afterload reduction
acute onset AFib: management
cardiac glycosides (e.g. digoxin) to increase contractility and decrease HR
CCBs to control ventricular response
statins: side effect
elevated CK d/t skeletal muscle breakdown
heart failure r/t dilated cardiomyopathy: management
- Afterload reducing agent (ACEI)
- IV inotropic agent
- LVAD after medical management has been maximized
VTach is most frequently associated with
heart failure
2nd degree AV block Type II is most frequently associated with
anterior wall MI
junctional tachycardia is most frequently associated with
digoxin toxicity
hypertrophic cardiomyopathy: presentation, EKG
syncope
non-radiating systolic murmur
biphasic P wave in leads V1 and V2
Deep narrow Q waves in lateral leads I, aVL, V5, V6
hypertrophic cardiomyopathy: confirmed by?
echo
What medications are contraindicated in systolic heart failure but can be used to treat tachycardia in diastolic heart failure?
CCBs
most likely etiology of aortic valve disease in elderly
calcification
most likely etiology of aortic valve disease in adults (not elderly)
congenital bicuspid aortic valve
Rheumatic fever as a child can cause…
mitral stenosis
hypertension: management
- diuretics
- ACE, ARB, CCB
common complication of CEA
hypoglossal nerve damage
-tongue deviates to ipsilateral side of surgery
-order swallow study
sudden cardiac death following MI is usually caused by..
VF 2/2 myocardial scarring
–ICD
Right coronary artery: EKG leads
Inferior leads: II, III, aVF
Left circumflex artery: EKG leads
Lateral leads: I, aVL, V5, V6
Inferior leads: II, III, aVF
Left anterior descending (or interventricular artery): EKG leads
Septal: V1, V2
Anterior: V3, V4
Diagonal branch: EKG leads
Lateral leads: I, aVL, V5, V6
Lateral leads
I
aVL
V5
V6
Anterior leads
V3
V4
Septal leads
V1
V2
Inferior leads
II
III
aVF
nitroglycerin
ventilator used to increase myocardial blood flow
acute ventriclar septal defect
complication of MI
acute onset SOB and CP
associated with cardiogenic shock
Which valvular disorder is most commonly associated with an aortic aneurysm?
aortic regurgitation
Patients with Marfan syndrome commonly have which valvular disorders?
mitral valve prolapse
mitral regurgitaiton
complications after anterior MI
Post-infarct angina
Ventricular rupture
Septal aneurysms
Arrhythmias
L heart failure
Cardiogenic shock
Acute mitral regurgitation
Valve most often affected by endocarditis
tricuspid
IVDU is associated with what valvular disorder?
mitral valve regurgitation
