CARDS Flashcards
Dressler syndrome
- what
- EKG findings
- sx
- autoimmune pericarditis days to weeks after MI
- diffuse J point or ST segement elevation is indicative of pericarditis.
- LG temp, malaise, CP lessened by sitting up
Infective Endocarditis
- sx
- cardiac & dx
- fever, petechiae, splinter hemorrhages, Osler nodes, Janeway lesions, and Roth spots.
- vegetations - TEE
most commonly affected valve in endocarditis in patients with a history of IV drug use
tricuspid valve - first one blood hits after injection
Shock
- definition
- 3 types of shock
Inadequate delivery of oxygen to the tissues
Cardiogenic
Obstructive
Distributive
Shock causes pneumonic
Sepsis Hypovolemia Obstructive Cardiac Kortisal
Causes of Hypovolemic shock x3
- Hemorrhage
- Volume loss (diarrhea)
- Loss of plasma
Causes of Cardiogenic Shock x5
MI Arrhythmia Heart failure Valvular disease Massive PE
Causes of Obstructive Shock x4
Can’t fill your heart
Tension pneumothorax
Cardiac tamponade
Obstructive valvular disease
Massive PE
Distributive Shock Causes x3
Poorly regulated distribution of blood volume
Septic shock
Anaphylactic shock
Neurogenic shock (spinal cord injury)
Syncope definition
brief loss of consciousness & postural tone with spontaneous recovery
Orthostatic Hypotension
> 20 mm drop in SBP or 10 mm DBP from supine to standing
PDA in utero
blood shunted from pulmonary artery to aorta in utero- should close at birth stopping flow from R to L atrium
Functionally closes 15 hours after birth, anatomically by 3 weeks
PDA defect
Risk factors X3
As pulm resistance increase»_space; L to R shunt»_space; CHF ( do become cyanotic b/c L- R shunt)
Prematurity, Hypoxia, Congenital Rubella
Describe Fetal circulation
Mom oxygenates blood > placenta Umbilical vein send blood to placenta Fetus IVC to RA RA to FO to LA to LV to aorto RA to RV to pulm artery From PA some goes to oxygenate lungs From PA, most is shunted thru ductus to aorta to body & back to IVC
PDA murmur
Continuous machinery murmur in left upper chest
Bounding pulses with wide pulse pressure
“Slapping 2nd heart sound”
PDA drug for medical management
Indomethacin - prostaglandin inhibitor to close duct i premature kids
Venous Hum murmur
also continuous murmur (like PDA), but more positional - as you move infants head
Cyantoic Congenital Heart diseases
5 Ts & a P Tetralogy of Fallot (MC) Transposition of the Great Arteries Truncus Arteriosus Tricuspid Atresia Total Anomalous Venous Pulmonary Return Pulmonary Atresia
Tetrology of Fallot
- 4 components
- CXR findings x2
○ RVH
○ Pulmonic Stenosis (PS) causing RV outflow tract obstruction
○ VSD
○ Overriding aorta (sits atop VSD) which causes blood flow from both ventricles
CXR - Boot-shaped heart, decreased pulmonary vascular markings
Presentation if Large VSD with Tetrology of Fallot
If Large VSD
○ Mild PS
○ Presents just like a VSD
○ “Pink tet”
Presentation if Small VSD with Tetrology of Fallot
○ Large PS
○ Presents like a cyanotic congenital heart lesion
○ “Blue tet”
Tetrology of Fallot Murmur
○ Single second heart sound
○ Systolic ejection murmur at left upper sternal border ± radiation to back
diagnosing cyanotic congenital heart disease
Hyperoxia test
○ Give 100% FiO2 for 10 minutes
○ ABG: paO2 <150 mmHg concerning for CCHD
Boot shaped heart
Tet spell
in older infant with tetralogy of fallot
right-to-left shunting through VSD causing blood to bypass lungs unoxygenated
How to temporize/treat TOF in acute setting
reopen ductus with PGE1 @ 0.1 mcg/kg/min
decrease infundibular spasm (beta-blockade)
decrease pulmonary resistance
LT risk of untreated TOF
At risk for subacute bacterial endocarditis (SBE) before and after correction
Untreated, paradoxical emboli → stroke
Coartaction of Aorta
narrowing of proximal aorta
Coarctation Associations
Bicuspid aortic valve VSD Aortic dissection CHF SBE Hypertension Turner syndrome (15-20%) Cerebral aneurysms → can cause intracerebral hemorrhage
Coarctation
- sx (early vs. late)
- findings on CXR
Murmur
Immediate rx
early - shock & CHF
late
- hypertension (esp UE)
- UE/LE pulse difference > 20 mm
- rib notching on CXR
Murmur - systolic L infraclavicular & sub scapular
PGE1 to open ductus
MC type of ASD
Shunt type
Ostium secundum: arises from an enlarged foramen ovale (90% of all ASDs)
L to R initially»_space; pulmonary over circulation +/- CHF
ASD murmur
ASD on EKG
FIXED widely split S2 (no vary with respiration) 2/2 delayed pulmonary valve closure
RBBB
ASD late presentation
Diagnosis often delayed until 5th decade
● Sx: DOE, CP, fatigue, palpitations
● Signs: atrial arrhythmias, right heart failure, ischemic stroke, pulmonary HTN
● Murmur: Fixed split S2, RVOT PS
● Precipitating factors: volume (pregnancy, Mitral Regurgitation), poor left heart compliance
CHF pathophys - initially then over time?
CO vs. Preload vs afterload
Low Cardiac Output (CO) → compensatory increased preload, increased afterload, and increased contractility → over time…
○ Low CO + increased afterload decreased renal perfusion → stimulation of RAAS and ADH
system → fluid and sodium retention → fluid overload peripherally and centrally
○ Low CO + increased preload (volume overload) → ventricular dilatation
Left heart failure sx
○ Dyspnea, orthopnea, PND ○ Weakness/fatigue
○ Tachy, S3, rales
Right heart failure sx
○ JVD (rales if left heart failure also)
○ Peripheral edema
○ RUQ pain, hepatojugular reflex, hepatomegaly
○ Ascites
○ Most common cause is severe Left heart failure
CHF lab abnormalities
Anemia
renal insufficiency, elevated LFTs, hyponatremia secondary to excess free fluid, hypo/hyperkalemia
BNP (>500 if acutely decompensated)
What causes mild elevations in BNP
100-500
Chronic CHF
severe COPD or RHF,
PE (→ RV dysfunction)
Elderly women, a-fib (→ LV dilatation)
CHF CXR findings in order of progression
Cardiomegaly → Cephalization (fluid going to upper lung fields)→ Kerley B lines → Alveolar fluid → Pleural effusion
test of choice for teasing out CHF
Echo
2 drugs to improve survival in CHF
2 decrease sx
ACEI (reduce after load, Inc renal perfusion)
BB (decrease catecholamine levels & afterload)
nitrates & diuretics
how to treat decompensated HF & cardiogenic pumonary edema (lung = buckets - faucet, pump, emptying hose)
dec preload (nitro & loop diuretic/lasix) dec afterload (nitro, ACEI)
inc contractility of pump (LV) - inotrope (dopamine, dopamine), only for HoTN/shocky pt:
best therapy for decompensated HF
Non-invasive ventilation (improves O2 & gas exchange and dec preload and afterload
Prinzmetal angina
- Phys
- Rx
- caused by coronary artery spasm, not occlusion
- CCB, such as diltiazem or verapamil are mainstay (nitrates also effective)
who to Screen for AAA
- size
- MC site
- US Preventative Services Task Force:
1x screening for AAA by US in men ages 65 to 75 years who have ever smoked - > 3cm
- infrarenal
most common drugs that can cause SA node dysfunction or sick sinus syndrome
CCB, BB, antiarrythmics, ACh inhibitors
Sources of cholesterol
All animal based foods contain cholesterol in varying amounts. Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, fish, and shrimp.
phytosterols
- examples
- why important
cholesterol-like compounds called maufactured by plant-based products
- avocado, flax seeds, peanuts
- compete with cholesterol for absorption in the intestines, reducing the absorption of both dietary and bile cholesterol.
electrocardiographic findings is classically associated with acute pericarditis?
Diffuse ST segment elevations
Causes of ST elevation x4
ST elevation MI (STEMI),
early repolarization
pericarditis
left bundle branch block.
Pericardial friction rub
- indicative of?
- describe
- enhaced by?
- pericarditis
- superficial grating or squeaking sound, best heard at the left sternal border, caused by the two layers of the inflammed pericardium rubbing together
- when the patient is leaning forward.
most common immediate complication following surgical repair of an abdominal aortic aneurysm?
MI (10%)
hypertensive emergency
- why only lower BP slowly
blood pressure is >180/>120 mmHg + signs of acute organ damage
- leave certain areas of the brain without sufficient bloodflow, resulting in watershed infarcts.
Atherosclerotic plaque buildup phys
plaques develop in the intima layer of the arteries. The process of plaque formation starts with intimal thickening, then proceeds to intimal xanthoma or fatty streak formation as macrophages accumulate. Building up of extracellular lipids within the intima then occurs, with progression to a fibrous cap atheroma with a lipid-rich necrotic core. When this lesion ruptures, it leads to thrombosis and possible obstruction of blood flow. The lesion can then heal with smooth muscle cells and a collagen-rich matrix.
I See All Leads
Inferior - II, III, aVf
Septal - V1 V2
Anterior - V3, V4
Lateral - V5, V6, I, aVL, aVR
Na restriction in CHF
limit their sodium intake to 2-3 grams
PE for HTN
PE: ○ Funduscopic exam ○ Presence of S4 ○ Presence of carotid or renal bruits ○ Eval of peripheral pulses
LVH by EKG
- why important?
deepest R in V1, 2 or 3 + Tallest S in V4, 5 or 6… if 35 or > = LVH
- indicative of prolonged HTN
Secondary HTN
- when to think about it?
- causes?
- MC cause
Abrupt onset
○ Age <30
○ Uncontrolled HTN on ≥ 3 meds
○ Excessive end organ damage
Common etiologies: ○ Renal artery stenosis ○ Cushing syndrome ○ Hyperaldosteronism ○ Aortic coarctation ○ Pheochromocytoma ○ Obstructive sleep apnea ○ Drug induced (chronic NSAID use, OCP)
MC renal artery stenosis (2/2 atherosclerosis in older pots)
ACEI to treat RAS?
Ultimate Rx
yes to unliateral disease
no for BIL
stenting and angio
CABG indications
> 50% of left main
>70% stenosis LAD, RCA
INR recs for mechanical valves
aortic 2-3
mitral 2.5-3.5
Aortic & mitral 2.5-3.5
indications for AAA repair
symptomatic despite size
> 5.5 cm
expansion > 0.5 in 6 mo
Aortic dissection Rx
- Stanford Type A
- Stanford Type B
- ascending = surgical emergency
- descending: if HD stable q 6 mo CT
- both benefit from IV BB & nitroprusside
Cor Pulmonale
- sx
- on EKG
- murmur
pulmonary HTN & RHF
- often 2/2 COPD
- DOE, LE edema, S3 gallop, RUQ tenderness & hepatomegaly
- RAD, RVH
- tricuspid reg: holosystolic on L sternal border
STEMI
STE > 1 mm in 2 continuous leads
Venous insufficiency
- sx
brawny skin, pitting edema, itching, pain worse with standing, tibial or medial ulcers
Claudication
- sx
2/2 arterial insufficiency
- dec pulses, hair loss, pallor, thick nails
thromoangiitis oblierans
(Beurger’s disease)
- what
- who
non- atherosclerotic inflammatory disease in small A & V in extremities
- pts < 40 with smoking hx
EKG changes 2/2 hyperkalemia
- Mild hyperkalemia
- K > 7
- peaked T
- prolonged PR, QRS, AV conduction delays and loss of P
EKG changes 2/2 hypokalemia x3
- prominent U waves
- ST depression
- T wave flattening
Best way to dx valvular vegetation
- TEE
Murmurs:
- MVP
- AS
- AR
- MS
- PDA
- ASD
- MR
- mid- late systolic click
- LATE SEM radiates to carotids & apex
- high pitched descrecendo in early diastole
- low-pitched, mid systolic with opening snap
- continuous, rough, machinery over L pulmonary artery
- wide, fixed split S2
- apical holosystolic, radiates to axilla
S1
S2
S3
S4
- closing of mitral & tricuspid
- closing of atrial & pulmonic
- ventricular gallop (during LV filling, compliant LV), may be seen with SHF
- atrial gallop (during LV filling in non-compliant LV), may be seen with DHF
CAD & Chronic HF med recs X6
statin BB ASA ACEI diuretic nitro
Splitting of S2
- physiologic
- Paradoxical (and MC cause)
- fixed split
- occurs on inspiration
- occurs on expiration ( LBBB)
- ASD and RV failure
3 drugs for diabetetic (high risk of CAD)
ASA, statin, ACEI
3 drugs for secondary prevention of STEMI (had prior MI)
ASA, BB, ACEI
diastolic dysfunction
decreased ventricular COMPLIANCE leads to inabilitiy to draw blood from LA to LV
often in setting of LVH
(normal EF)
Beck’s triad
2/2
HoTN
Distant heart sounds
JVD
-Cardiac tamponade
MC cause of cardiomyopathy worldwide
Chagas disease
- 2/2 protozoan parasite Trypanosoma cruzi
coxackie B virus
RNA enterovirus associated with acute mycoarditis & pericarditis
HF Classification I to IV
I - no limitation of physical activity
II - mild symptoms with ordinary exertion
III - Marked limitation with activity
IV - Symptomatic at rest
drugs x2 to prevent monomorphic VT in pt with cardiac disease (if QT normal)
Amiodarone
Sotalol
Most toxic SE of Amiodarone
- less serious SE
puomary toxicity
- corneal deposits, photodermatitis, peripheral neuropathy
minimum target INR & duration before cardioversion
> 1.8 for 3 weeks
First degree Heart Block
fixed & prologed PR interval (> .2 sec)
Second Degree Heart Block
Type I
Type II
- Wenckebach long, long, drop
- fixed PR and occosainal dropped beat
Criteria to dx Metabolic Syndrome in men
Must have Atleast 3 of 5:
BP > 130/85 waist > 40 HDL < 40 Fasting BS > 100 TG > 150
Cilostazol
Phosphodiasterase inhibitor used to manage claudication
indications for Holter monitoring
Suspected tachy inducuced cardiomypathy
Dec systolic function after MI (to determine risk of death)
asymptomatic afib to see about anticoagulant
non- life threatening arrythmias if symptomatic
ACLs Rx for symptomatic bradycardia
Atropine
Pacing if ineffective
Cardiac Syndrome X
classic angina CP, treadmill test with ischemia & normal coronaries by cath
3 electrolyte abnormalities that increase risk of Dig toxicity
hypomag
hypoK
hypercalcemia
Dig increase intracellular Na»_space; drives Calcium into heart»_space; inc contractility
Delta wave on EKG
slurring of QRS upstroke
Seen in Wolf Parkinson White
Most common cause of restrictive cardiomyopathy
Amyloidosis
Dromotropy
Conduction velocity of AV node
ACLS for SVT
- carotid massage or vagal
- then Adensoine
- then CCB or BB
- cardiovert if HD unstable
symptoms of Dig toxicity
PVS, lifethreatening arrhythmia, symptomatic bradycardia
GI - anorexia, N/V, diarrhea
Neuro - lethargy, confusion, dizziness, changes in visual acuity
Patients with Congenital Bcuspid aortic valven have increased risk for
- risk for offspring to have disease
- thoractic aortic aneurysms
- 30%
Explain QT interval
beginning of QRS (V depol) to end of T (V repol)
Torsades
Polynmorphic WIDE complex tachycardia with a twisting of the pointes
Venous Hum
systolic murmur over BIL upper sternal borders that disppears when jugulars compressed (benign condition)
Takotsubo cardiomyopathy
stress induced - presents like MI but w/o coronary stenosis
- apical ballooning
- treat same as MI 2/2 CAD
