Cardio Flashcards
sinus brady
<50 and symptoms
1) initial resus - id and treat underlying causes IV, monitor, pulse ox and O2, 12 lead EKG
2) persistent brady and sxs (hypotension/shock, AMS, chest pain, acute heart failure, poor perfusion or heart is not working) - atropine 0.5 mg bolus q 3-5min (3.0 mg max) –> transcutaneous pacing OR dopamine or epi infusions –> consult and transvenous pacing
sinus brady can be nl (young, athletes, sleeping elderly), other causes - sick sinus, myocardial ischemia/infarct, osa, hypothyroid, cushings response, meds (bblockers)
- IV glucagon - reverse bblocker or CCB tox
counting rate - see picture
pulmonary HTN
P art pressure > 25 mm Hg at rest (nl < 20 mm Hg)
causes - HF, chronic lung disease, chronic thromboembolism
- primary pulm HTN - women, 40-50s
- treat based on etiology - ACEi and diuretics for HF, O2 and bronchodilators for chronic lung disease
- endothelin antagonists and PDEi for idiopathic PH
- graded exercise traning for all
sick sinus syndrome
SA node dysfunction
- fatigue, lightheadedness, palpitations, pre-syncope/syncope
- brady on EKG, can have brady with alternating tachys
anti-HTNs
ACEi/ARB - post-capillary venodilation
- normalize increased hydrostatic pressure
- angioedema
b-blockers - worsening of CHF, brady, increased airway resistance in asthmatics, generalized fatigue, sexual dysfunction
- OD* - bradycardia, AV block, hypotension, diffuse wheezing
- cardiogenic shock
- other effects - hypoglycemia, broncospasm, delirium, seizures
- tx - 1) IV atropine, 2) IV glucagon (increases intracellular levels of cAMP, helps reverse b-blockers and CCB tox)
CCB - peripheral edema is a common side effect
- preferential dilation of precapillary vessels –> increased capillary hydrostatic pressure –> fluid extravasation into interstitium
- amlodipine and nifedipine > dilt and verapamil
- other side effects - headache, flushing, dizziness
- CCB + ACEi/ARB reduces risk of peripheral edema
digoxin
action - blocks Na/K ATPase (3Na out, 2 K in) …. intracellular Ca increased
- bradyarrhythmias in young
- enhanced automaticity and tachyarrhythmias in elderly (who have underlying cardiac disease)
tox - fatigue, anorexia, nausea, diarrhea, blurred vision and disturbed color perception, arrhythmias (acute GI, chronic neuro and visual sxs)
- arrhythmia - atrial tachy with AV block
- inciting event is a volume depletion event - viral illness, excess diuretic use
- renally cleared, narrow therapeutic index, many DDIs (amiodarone, verapamil, etc.)
- hypokalemia (with loops) - potentiates digoxin
- check level, EKG (r/o arrhythmias)
WPW
px - palpations or (often) asx
depolarization from atria to ventricles that bypasses the AV node (AV node slows heart rate) - short PR (<0.12), wide QRS, delta wave (of QRS)
- if there is retrograde conduction from ventricles to atria –> can get re-entrant SVT
- afib occurs 10-30% of the time –> can deteriorate to afib
- for hemodynamically stable pts - immediately cardiovert
- stable - procainamide
- DONT use AV node blockers (adenosine, bblockers, CCBs, dig) - because this may promote increased conduction across accessory pathway
afib
afib with RVR (no P waves, narrow QRS) - symptoms are due to fast rate (rather than arrhythmia itself)
- ectopic foci is the pulmonary veins - normally cardiac tissue extends into the pulmonary veins and functions like sphincter to prevent backflow
- stable - b-blockers, dilt, verapamil, digoxin for rate control
- if hemodynamically unstable - cardiovert
- attempting cardioversion in pts with afib for unknown duration or for >48hrs without adequate anticoagulation increases risk of TE event
MANAGEMENT: rate vs rhythm control and need for chronic anticoagulation
CHA2DS2-VASc score for risk assessment in nonvalvular AF
- 2 points - age >75, stroke/TIA/TE
- CHF, HTN, DM, vascular disease, age 65-74, female sex
lone AF - afib in a person over 60 (no major heart disease, mild atrial dilation not considered major heart disease), CHA2DS2VASc 0
- risk of embolization is very low and anticoagulation is not needed
score 1 - oral anticoagulant preferred (or ASA) - rivaroxaban
score 2 - warfarin or oral anticoagulants (rivaroxaban, apixaban, dabigatran)
rate control long term - amiodarone, flecainide
IVDA and heart disease
IVDA infective endocarditis
tricuspid regurg - systolic murmur (accentuated with inspiration)
- S aureus is the most common org
- septic embolic - round lesions in lungs, but will have fewer peripheral IE manifestations (like splinter hemorrhages, Janeway lesions)
- conduction abnormalities are uncommon
- another reason you can get tricuspid regurg - complication of implantable pacemaker
- 1 lead in RA, other lead passes through tricuspid and implants in RV
- can lead to damage to tricupsid leaflets –> TR
perivalvular abscess
- aortic regurg (early diastolic murmur), AV conduction block (abscess extending into conduction pathways)
wide complex tachy
AV dissociation, fusion/capture beats?:
yes - Vtach
- 1) stabilize pt
- 2) underlying cause? - electrolyte imbalance (diuretics cause hypoK and hypoMg), digoxin (side effects include arrhythmias, potentiated by hypok)
no - SVT with aberrancy
PAD
majority of patients with intermittent claudication
- 70-80% are stable at 5 yrs, 10-20% have worsening sxs
- 1-2% progress to critical limb ischemia (rest pain, nonhealing ulcer, gangrene)
pts with PAD and intermittent claudication are at high risk for MI and stroke
meds - cilostazol (PDEi, used for pts with intermittent claudication), smoking cessation is first-line tx
RAAS
ang 2 - vasoconstrictor, also promotes aldosterone production
remember feedback loops
decreased renal perfusion in CHF –> SNS RAAS activation
- ang 2 causes vasoconstriction of afferent and efferent arterioles –> increased renal vascular resistance –> decreased RBF
- preferential vasoconstriction of efferent renal arterioles to maintain GFR - increases intraglomerular pressure
- stimulation of Na reabsorption in proximal tubules and aldosterone secretion - decreased Na delivery to distal tubule
paroxysmal SVT
narrow complex tachy
- use adenosine to slow AV node conduction and interrupt re-entrant rhythm
- adenosine short acting
- can use carotid sinus massage - slows AV node
amiodarone
class 3 antiarrhythmic - used for ventricular arrhythmias, can also be used for pts with afib with LV systolic dysfunction
Side effects
cardiac - sinus brady, heart block, QT long and torsads
pulm - chronic interstitial pneumonitis (within mo - cough, fever, dyspnea, pulmonary infiltrates, restrictive lung disease)
endo - high or low thyroid
GI/hepatic - elevated transaminases, hepatitis
ocular - corneal microdeposits, optic neuropathy
derm - blue-gray skin
neuro - p neuroapthy
shock
low MvO2 when there is high CO - because of hyperdynamic circulation and inability of tissues to adequately extract to O2
septic shock - elderly with septic shock will NOT mount a fever
decreased cardiac afterload means low SVR
neurogenic shock - bradycardia
systolic heart failure
Chronic/clinic pxs
dilated cardiomyopathy - myocardial damage by toxic, metabolic, and/or infectious agents
- viral myocarditis (Coxsackie B)
- due to alcohol consumption (doe) - stop alcohol, LV function will normalize over time
- tx - supportive
concentric hypertrophy - due to increased afterload
eccentric hypertrophy - due to increased volume
Acute decompensated HF
- diuretics, inotropes
- avoid b-blockers - can worsen HF
Long-term management - b-blockers, ACEis/ARBs, spironolactone, and hydralazine + nitrates (in AAs) have shown mortality benefits in LV systolic dysfunction
rheumatic heart disease
immigrants
mitral stenosis - loud S1, mid-diastolic rumble, increased LA pressure
- sxs are usu precipitated by conditions that cause tachy (exercise, fever, anemia, pregnancy)
- OS and low pitched diastolic rumble (apex, pt lying on left in held expiration)
- over the course of years – L atrial enlargement –> L mainstem bronchus displacement, compression of recurrent laryngeal nerve, cough, hoarseness
- CHF sxs, afib, thromboembolism
- afib causes a lack of atrial kick - acute worsening of mitral stenosis
- mimics can be ILD (reticular or nodular markings on CXR)
aortic stenosis or insufficiency - occurs but less frequently
aortic dissection
RFs - HTN, Marfans (young pts), cocaine
features - sharp tearing back pain, >20 mm Hg BP variation in between arms
- may not present classically - look for chest/neck pain, syncope, mediastinal widening
- many pts have sudden spike in BP that is associated with dissection
complications - stroke (carotid arteries)
- acute aortic regurg
- Horners
- acute MI/ischemia (coronary artery)
- pericardial effusion/cardiac tamponade - ascending aortic rupture into pericardial space (type A, surgical emergency) –> if pt was in cardiac tamponade/cardiogenic shock - urgent pericardiocentesis
- hemothorax
- LE weakness/ischemia (spinal or common iliacs)
- abd pain (mesenteric artery)
dx - CT angio in stable pts
- TEE in pts with hemodynamic instability or renal insufficiency
tx - pain control (morphine), IV b-blockers (labetalol, reduce SBP to 100-120, benefits of b-blocker include HR and contractility reduction), sodium nitroprusside for SBP > 120 (vasodilator), urgent surgical repair for ascending dissection
- note hydralazine is a vasodilator like Na nitroprusside - can cause reflex sympathetic tachy
syncope
syncope = LOC with loss of postural tone, followed by spont and complete recovery
vasovagal (neurally mediated) - nausea, diaphoresis, pallor, young women
- prodrome
- occurs in response to stress, pain, urination
- clinical dx
- tx - reassurance, avoidance of triggers, counterpressure techniques for recurrent episodes (supine position with leg raising, leg crossing with tensing of muscles, hand grip and clenched fists all increase venous return
exertional syncope - v arrhythmias, LVOT (blood flow obstruction)
- pts with fixed LVOT cant increase CO in response to exercise-induced vasodilation –> hypotension, cerebral hypoperfusion
- for valvular obstruction - preceding hx of exertional dyspnea, chest pain, fatigue
orthostatic hypotension - elderly, autonomic neuropathy, hypovolemic, diuretics, vasodilators, adrenergic-blockers, prolonged recumbence
carotid sinus hypersensivity - carotid sinus massage with reproduce the sxs
situational - triggers are cough, micturition, defecation
- prodrome
- alteration of autonomic response –> cardioinhibitory, vasodepressor, or mixed response
- increased PS tone (bradyarrhythmia), decreased SNS tone (vasodil, hypotension, syncope)
sick sinus syndrome, bradyarrhythmias, AV block - sinus pauses, long PR or long QRS
Torsades (acquired long QT) - hypokalemia, hypoMg, meds
- congenital long QT - FHx of sudden death, long QT with triggers (exercise, startle, sleeping)
CHF
signs - bibasilar crackles, pleural effusions (decreased breath sounds), wheezing (cardiac asthma)
BNP - elevated BNP, sensitivity >90% of heart failure (>400 pg/ml maybe 500 pg/ml rules in, <100 rules out)
- for systolic and diastolic HF
- can also get PCWP
physical exam findings - low sensivity
myocardial ischemia/infarct
- angina - stable and unstable
- MI and treatment
- complications
Stable angina - px - can occur with strong emotion
- triad: substernal, worse with exercise (or emotion), relieved with rest (or nitro) (atypical is 2/3 characteristics)
- ACS - S4 can be heard in most pts during acute MI or in ischemia-induced myocardial dysfunction
- RFs - CAD (SLE leads to accelerated atherosclerosis)
- prinzmetal angina - young pts, cigarette smoking is known RF, occurs at rest or during sleep, spont resolution in <15 min; ambulatory EKG will show ST elevation; tx with CCB and sublinguinal nitro
- dilt is a potent coronary vasodilator (weak systemic vasodilator)
- avoid ASA in pts with vasospastic angina - ASA inhbits prostacyclin production, worsens vasospasm (same with non-selective b-blockers like propranolol)
Stress testing
- EKG - want pt to reach tHR of 85% of 220-age (contraindicated in LBBB, pacemaker)
- dobutamine stress echo - B1 agonist, increases HR and BP, use in reactive airway disease, DONT use in tachyarrhythmias
- EKG and dobutamine - increased myocardial demand
- pharm stress test with adenosine and dipyridamole - dilates coronary arteries with no increase in HR or BP (NOT for pts with reactive airway disease or pts on dipyridamole or theophylilne)
- blood flow in stenosed arteries does not increase as much as blood flow in normal arteries - difference in blood flow ~ ischemia (this is also the closest to the physiologic mechanism for angina)
Coronary angio for pts with high pre-test probability - men 40+ or women 60+ with typical angina
- and as a f/u to pts with high risk findings on stress testing
Meds
- b-blockers - first- line, decreases contractility and HR (O2 demand), alternative is nondihydropyridine CCBs (verapamil, dilt)
- dihydropyridine CCBs - add if needed, coronary artery vasodilation, decreased afterload by systemic vasodilation (monotherapy can result in reflex tachy)
- (long-acting) nitrates - decreased preload (dilates veins, decreased myocardial O2 demand), sx relief is immediate
- ranolazine - for refractory angina, decreased myocardial calcium influx
*********************************************************************
MI
first signs are T wave inversions
- trops dont rise fro 6-12hrs
immediate steps
1) restoration of coronary blood flow - PCI or fibrinolysis (goals are PCI within 90 min or 120 min if transfer is required), M&M benefits
Types
STEMI:
- inferior MI* - inferior leads are 2, 3, AVF
- -* RCA occlusion - 50% chance of involving the RV –> impaired RV filling –> hypotension and autonomic signs (diaphoresis, vomiting, increased vagal tone can lead to transient brady or AV block)
- avoid nitroglycerin (and diuretics and opiates) - venodilates –> will decrease preload and lead to profound hypotension
- JVD will be low - nl < 3cm
- give NS bolus (then inotropes)
Management - dual antiplt therapy (ASA and clopidrogrel), statin, anticoagulation, urgent revascularization
- PCI - within 12hrs of sx onset, 90 min from first medical contact
- O2, nitrates (caution in pts with hypotension, RV infarct, or severe aortic stenosis)
- following MI - ventricular remodeling occurs –> dilatation of LV and thinning of ventricular walls - ACEi have been shown to limit remodeling
–> start ACEi within 24hrs of MI
- statin therapy (possibly beta-blockers) - long-term management
Complications
stent thrombosis - localized ST elevation
- pt has to take ASA and plavix even if they have a drug-eluting stent placed
IV rupture vs free wall rupture - IV rupture will have holosystolic murmur at left sternal border, free wall rupture can present with PEA (low voltage EKG)
papillary muscle rupture and acute MR (can occur with inferior infarct) - murmur at apex
ventricular aneurysm - weeks-mo, will see localized ST elevation and deep q waves
- may present with HF, refractory angina, arrhythmias, embolism
acute pericarditis (in general, not just post-MI) - viral, idiopathic, uremia, autoimmune, early post-MI (risk factor is delayed coronary reperfusion), late post- MI (Dressler, weeks, elevated ESR)
- pericardial friction, diffuse ST elevation and PR deprssion (can have depression in aVR), pericardial effusion
- tx
- early post-MI - supportive, avoid anti-inflammatories (will disrupt collagen deposition…)
- late, Dressler - NSAIDs
- viral - NSAIDs and colcichine
pericarditis
diffuse ST elevation, positional pain
causes - viral (most common), bacterial
- surgery, trauma, radiation, drugs
- CT disease - RA, SLE
- Cardiac - Dressler
- uremic - BUN >60 (but degree of pericarditis does not always correlate with degree of elevation), doesnt have classic EKG findings, tx dialysis
- malignancy - cancer or chemorads
- for idiopathic or viral - NSAIDs and colchicine
pericardial effusion secondary to pericarditis (preceding URI, etc.)
- hypotension, syncope (decreased CO)
- tachy, distended neck veins, pulsus paradoxus, muffled heart sounds
- electrical alternans - variation in QRS amplitudes = specific not sensitive
- dx/tx 1) echo (if stable), 2) pericardiocentesis
cardiac tamponade
Becks triad: hypotension, elevated JVP, muffled heart sounds
large pericardial effusion - most often occurs from a viral illness (other causes include post-MI, trauma, uremia, autoimmune diseases, hypothyroidism)
- volume overload, clear lung fields, water bottle heart - inability to palpate PMI
- distinguishing between viral myocarditis - pts will have an audible S3 and pulmonary vascular congestion
hypertriglyceridemia
causes - familial, DM, obesity, hypothryoid, nephrotic syndrome, alcohol abuse
150-500
- lifestyle modifications (weight loss, moderate alcohol intake, exercise)
- add high-intensity statin for pts are high risk of CVD
>1000 - initial goal is pancreatitis prevention
- fibrates, fish oil, abstinence from alcohol
- fibrates are the most effective pharmacotherapy for lower TG levels - have increased adverse effects and no proven CV benefit (so they are not first line like statins)
statin: HMG-CoA reductase inhibitor - RLS, inhibits intracellular biosynthesis of cholesterol - decreased hepatic cholesterol –> activates LDL receptors on liver cell membranes –> circulating LDL is removed
- adverse effects - mild transaminitis, myalgias (2-10%)
- when to start statin - for 10 yr-ASCVD risk >7.5 (or pts with known MI, stroke, DM, CKD, or LDL > 190 indicative of familial hypercholesterolemia)
- high intensity v low depends on age and % risk
vitamin supplementation - has NOT demonstrated a benefit in lipid disorders of CVD
niacin - side effects are cutaneous flushing and generalized pruritis (usu improve in 2-4wks of therapy) - due to PG-induced vasodilation
- often prescribed with low dose ASA - counteracts PG-induced vasodilation
- used in hypertriglyceridemia
murmur and maneuvers
Manuevers
valsalva, standing, nitro - decrease preload
- HCM and MVP get louder with valsalva and standing, softer with other maneuvers
sustained hand grip - increases after load
squatting - increases afterload and preload
passive leg raise - increases preload
diastolic and continuous murmurs are always pathologic - get echo
- mid-systolic murmur by itself is benign in healthy, young adults
HCM - AD, sarcomere gene mutations, offer genetic testing to first degree relatives
- exertional sxs
- crescendo-decrescendo murmurs, biphasic pulse
- mitral valve leaflet moves abnormally and contacts thickened anterior septum –> LVOT
- EKG - LVH (tall R in aVL + deep S in V3), repolarization changes in anterolateral leads (1, avL, V4-V6)
bicuspid aortic valve
- ejection click and mid-systolic murmur
aortic stenosis - prolonged asx period, can present with syncope
- delayed carotid pulse (pulsus parvus and tardus)
- mid-late peaking systolic mumur that radiates to carotids - the later the murmur, the more severe the aortic stenosis
- soft single S2 - due to reduced mobility of aortic valve that closes at the same as the P2 (loud S2 is due to sudden aortic valve)
- most common causes - senile calcific (70 yo), biscuspid aortic valve, rheumatic disease
aortic regurg - causes are aortic root dilation (Marfans, syphilis), post-inflammatory, congenital biscupid aortic valve (fhx, will cause AR in young pts and aortic stenosis in older pts)
- best heard with expiration and leaning foward, waterhammer pulses, diastolic decrescendo murmur
- when it is due to root disease - best heard on RSB
- when it is due to valve disease - best heard on LSB
mitral stenosis - age-related calcification, asx or diastolic rumble
- rheumatic heart disease
- chronic mitral stenosis - RVH secondary to pulmonary HTN mitral regurg
- holosystolic, radiates to L axilla, loud S1
- decreases with decreased preload
MVP - myxomatous degeneration of mitral valve
- non-specific sxs - atypical CP, panic disorder…
- nonejection click and mid-to-late systolic murmur - murmur disappears with squatting - when LV is more filled –> delay in prolapse of valve
VSD - holosystolic murmurs
pulmonic stenosis - congenital (rarely acquired)
- severe will present in childhood, mild in adulthood
- crescendo-decresendo murmur that increases with inspiration (very specific for R-sided murmurs) (ASD is wide and fixed split S2)
- dx with echo
- tx - perc balloon valvulotomy, sometimes surgical repair
secondary causes of HTN
evaluate for secondary causes when a pt has resistant hypertension when on 3 anti-HTNs (one of which is a diuretic)
RAAS:
- renal parenchymal disease - elevated serum Cr, abnormal UA
- renovascular disease - renal artery stenosis, fibromuscular dysplasia (pts will worsen when put on an ACEi/ARB)
- signs - onset of severe HTN after age 55, resistant HTN (=persistent hypertension despite 3 or more agents)
- for renal artery stenosis - confirm dx with renal duplex doppler US, CT angiography, MRA
- primary aldosteronism - hypoK, hyperNa
Endocrine
- pheo
- Cushing SYNDROME
- adrenal origin
- hypothyroidism - … bradycardia (and reflex HTN?)
- primary hyperparathryoidism - hypercalcemia sxs, usu parathyroid adenoma (in cases of significant HTN, consider MEN2, pt may also have pheo)
coarctation of aorta - HTN with brachial-femoral pulse delay
- machinery murmur over back
- px - headaches, epistaxis, blurred vision, elevated BP of UE
amphetamines - tachy, HTN, diaphoresis, hyperthermia, confusion
cardiac arrest
cardiac arrest –> CPR, O2, hook up to monitors, prepare defibrillators
- ACLS - CPR x 2 min, epi q3-5min, pulse and rhythm check q2min
A) VT/pulseless VT –> immediate defibrillation –> CPR
- mag sulfate for polymorphic VT with aquired long QT (torsades)
- amiodarone
B) PEA/asystole (non-shockable rhythm) –> CPR for narrow/wide complex tachyarrhythmia (afib, aflutter, VT with pulse) - cardiovert
OTHER:
vfib (see picture) - most common cause of sudden cardiac death during
acute MI pts with cardiac arrest can have arm twitching/seizure-like activity - due to cerebral hypoperfusion
tachycardia-mediated CM
tachy, palpatations + cardiac sxs (dyspnea, decreased exercise tolerance)
- other tachyarrhythmias can also causes this - a flutter, vtach, junctional tachy, AV node re-entrant tachy
chronic tachy causes structural heart changes - LV dilatation and myocardial dysfunction
dx - EKG, echo…
tx - aggressive rate control, restoration or normal sinus rhythm –> can lead to normalization of CM and systolic function
- AV node blockers, anti-arrhythmiccs, catheter ablation
ventricular arrhythmias
wide complex arrthythmias
lidocaine (occasionally amiodarone)
cocaine
inhibits NE reuptake system
- SNS overactivity (also enhances thrombus formation), CP, seizures, dilated pupils
- complications - acute MI, aortic dissection, intracranial hemorrhage
- for ACS - antiplts, nitrates, PCI
management of CP - benzos (for BP and anxiety), ASA, nitro and CCBs, fibrinolytics not preferred due to increased risk for intracranial hemorrhage, cardiac cath with reperfusion if needed
- NO b-blockers
coarctation
HTN, headaches, blurred vision, epistaxis, LE claudicaton
continuous murmur in L interscapular area - due to turbulent flow across collaterals
adenosine
blocks L type calcium channels - delays conduction velocity through AV node
pulsus paradoxus
systemic arterial pressure > 10 mm Hg during inspiration
ocurs in pts with cardiac tamponade - L and R ventricles have to compete for blood –> during inspiration, RV fills with blood –> bowing of IV septum and reduced end-diastolic volume
- also in asthma and COPD - drop in intrathoracic pressure is greatly exaggerated during inspiration –> pooling of blood in pulmonary vasculature
in severe aortic regurg - LVEDP is increased and prevents bowing of IV septum
- prevents pulsus paradoxus even in the setting of pericardial effusion and cardiac tamponade
AAA
screening x 1 - 65-75 M who have smoked, get abd US
diastolic heart failure
causes
- LV thickening diseases - HTN, restrictive CM, hypertrophic CM
- valvular disease, constrictive pericardial disease
- systemic disorders (high-output failure) - thyrotoxicosis, severe anemia, large AV fistula
tx - control BP and HR
- address concurrent conditions, treat volume overload, exercise training and cardiac rehab
exertional heat stroke
exertional heat stroke
RFs - anticholinergics, antihistamines, phenothiazines, TCADs
- impaired heat dissipation
- dehydration is also common - hemoconcentrated, hypotensive and tachy
px - T >40 immediately after collapse AND CNS dysfunction (confusion, irritabiliy, seizures), additional organ or tissue daamge (renal/hepatic failure, DIC, ARDs)
tx - rapid cooling (ice-water immersion), fluids
- no role for antipyretics - hyperthermia doesnt involve increased set point
non-exertional heat stroke - occurs in elderly, tx with evapoate cooling (spraying lukewarm water while fan blows air on pts skin)
- ice water immersion is associated with higher M&M in these pts
how to differentiate from anticholingeric tox?: wont have multiorgan dysfunction
- hot as a hare, blind as a bat, mad as a hatter, red as a beet, dry as a bone,
abberant rhythms
conduction blocks
First degree - long PR (>0.20), otherwise sinus
(2) Mobitz type 1 : progressive PR long, narrow QRS –> dropped QRS, group beating (3 P-QRS then drop..)
- impaired conduction of AV node (digoxin, bblockers, CCBs are AV node blockers)
- CCBs prolong PR (increase AV node refractory period)
- asx, benign in young pts with good ventricular function, low risk for complete heart block
- improves with exercise, worsens with carotid massage
(2) Mobitz 2: below AV node (usu bundle of His)
- PR constant, intermittent nonconducted P waves
- worsens with exercise, improves with carotid massage
- high risk for complete heart block, indication for pacemaker
Third degree/complete heart block - P-P and R-R intervals are constant, P has no relation to QRS (may be buried in QRS)
- dizziness and worsening angina
- immediately place pacemaker - investigate cause (myocardial ischemia T wave inversions, vagal tone, hyperkalemia, AV node blockers)
Pacs - p wave that doesnt look like the others (originates from somewhere other than the SA node)
- occur earlier in the cardiac cycle - RR will be shorter, still followed by QRS
fibromuscular dysplasia
pathophys - noninflammatory, nonatherosclerotic dz
- abnormal cell development in arterial wall –> vessel stenosis, aneurysm, dissection
- disrupted blood flow –> down stream effects
px:
- brain ischemia - amaurosis fugax, Horners, TIA, stroke
- renal artery - HTN due to secondary hyperaldosteronism (aldosterone:renin < 20)
- carotid, vertebral artery involvement - non-specific sxs - can involve other arteries
dx - CT angio of abd or duplex US
pts will have increase in Cr after starting ACEi/ARB
non-pharm treatments for HTN
Treatments - all have shown reduction in SBP
- weight loss to BMI < 25 (5-20 mm Hg drop in SBP for every 10 kg loss)
- DASH - high fruits and veggies, low in fats
- exercise - 150 min/wk
- dietary sodium <3g
- alcohol intake - 2drinks/d in men, 1 in women (alcohol use is a common cause of refractory HTN)
- drugs - thiazides are first line
- others - ACEi/ARB, CCBc
drugs that can increase BP - NSAIDs, decongestants, glucocorticoids
when do you screen for secondary causes - pts have resistant HTN with 3+ anti-hypertensives in young, nonobese, non-AA pts
paradoxical splitting
when A2 closes after P2
occurs in pts with fixed LVOT - aortic valve stenosis, LBBB, RV paced rhythm
vasculitis
systemic sxs
Takayasu - aorta and major arteries off aorta
adult tachy algorithm
HR > 150
- ABCs and treat underlying cause
- persistent tachy causing instability - hypotension, AMS, signs of shock, ischemic chest discomfort, acute heart failure –> cardiovert (times shock so that pts is not shocked during QRS, vs defib which will shock at any time and is indicated for v fib)
- sedation
- if regular narrow complex, consider adenosine
- if QRS > 0.12 s - IV access and 12 lead ekg, adenosine for regular and monomorphic, consults
- if QRS < 0.12 s - IV access and 12 lead, vagal maneuvers, adenosine, b-blocker/CCB, consults
long QT
>450 ms in M
>470 ms in F
increased risk for sudden cardiac death due to torsads or polymorphic V tach
SVTs
SVT - means tachy that originates above His bundle
- pt will be symptomatic - palpitations usy
narrow QRS complex tachy, no regular P waves (can be retrograde, seen at beginning or end of QRS complex as spikes)
- narrow means QRS < 0.12
paroxysmal SVTs have abrupt onset/offset - AVNRT, AVRT, atrial tachy, junctional tachy
- for stable pts - id type of SVT with vagal maneuvers or IV adenosine (slow conduction through AV node –> unmask P waves or will terminate AV node dependent arrhythmias)
acute limb ischemia
causes - embolism (sudden development of sxs, afib, post-MI, septic emboli from infective endocarditis), arterial thrombosis, trauma
- embolism vs dvt - dvt pain is dull and aching
- arterial thrombosis - pts have PAD, collateral circulation has developed
6Ps - pain, pallor, paresthesias, pulselessness, poikilothermia (cool extremity), paralysis (late)
tx - anticoagulation (heparin), thrombolysis vs surgery
- during this time, dx - arterial doppler to confirm
cholesterol crystal embolism
RFs - hypercholesterolemia, HTN, DM2, cardiac cath or vascular procedure
px - livedo reticularis, blue toe syndrome, acute/subacute kidney injury, ocular involvement (Hollenhorst plaques), CNS and GI findings
labs - elevated serum Cr, eosinophilia, hypocomplementemia, bland urine sed
high output heart failure
congenital - PDA, angiomas, pulmonary AVF, CNS AVF
acquired - trauma (stab wound to the leg), iatrogenic (femoral cath), atherosclerosis (aortocaval fistula), cancer
other - thyrotoxicosis, Paget, anemia, thiamine deficiency
sxs - widened pulse pressre, strong arterial pulsation (brisk carotid upstroke), systolic flow murmur, tachy, flushed extremities
- eventually - cardiac function begins to decompensate, considered heart failure as circulation is unable to meet O2 demand of peripheral tissues
dx - doppler, tx - surgery
orthostatic hypotension
idiopathic orthostatic hypotension - due to degeneration of postG sympathetic neurons
Riley-Day syndrome - Ashkenazi Jews, gross dysfunction of autonomic NS
AVNRT
reentrant circuit that is formed by 2 separate conducting pathways within the AV node
- one fast and one slow
- suddent onset and termination, tachy, regular, narrow QRS, no P waves
a flutter
reentratnt circuit around tricuspid annulus
factors associated with poor outcome after witnessed out of hospital sudden cardiac arrest
most common cause is vtach/vfib due to acute myocardial ischemia or infarct
- very poor prognosis
- bystanders should perform compression-only CPR prior to arrival to ED
time elapsed before CPR/defibrillation
inital rhythm of PEA or asystole, absence of vitals
prolonged CPR (>5 min), persistent coma after CPR, need for intubation or vasopressors
advanced age, prior hx of cardiac disease, 2+ chronic illnesses
PNA or renal failure after CPR
sepsis, CVA, class 3/4 HF
anti-arrhythmics
class 1 - block Na channels - flecainide, propafenone
- fine when pts have a slow HR –> when pts have tachy, the drug has less time to dissociate from Na channels –> high number of blocked channels and slowed impulse conduction –> long QRS with tachy
- above is called use-dependence - this is why class 1C are good for use against SVTs
class 3
- dofetilide - risk of torsades
chronic venous insufficiency
venous HTN, leg edema that is worse in the evening or after prolonged standing
- venous dilation, skin discoloration, lipodermatosclerosis, skin ulceration (medial malleolus)
- RFs - advancing age, obesity, others
tx - leg elevation and compression stalkings
cardiac myxoma
sxs
- constitutional sxs (due to overproduction of IL6) - fever, weight, Raynaud phenomenon
- CV symptoms - mitral disease (tumor plop sound), heart failure, myocardial invasion..
- embolization
- lung invasion - can mimic bronchogenic carcinoma
dx and tx - echo and prompt surgical resection
aortic branches
R–>L
brachiocephalic (R subclavian, R carotid) - L carotid - subclavian
subclavian steal syndrome - decreased pressure in distal subclavian that steals blood from ispilateral vertebral artery
- exercise vasodilates distal subclavian - worsening the problem
- L subclavian is more commoly affected - due to sharper curvature, more turbulent, high risk of atherosclerosis –> ischemia of affected upper extremity
- pts with concurrent atherosclerosis of the circle of willis will develop vertobrobasilar ischemia
- dx - doppler or MRA
- tx - lifestyle changes, sometimes stent
coronary arteries
anterior MI - LAD - V1-V4
inferior MI - RCA/LCX - 2, 3, AVF
- RV MI - ST elevation in leads V4-V6R
- think RV MI if pt presents with signs of a heart attack and hypotension
- in 90% of pts, RCA also supplies blood to the AV node - infarct will lead to heart block
posterior MI - LCX or RCA, again can get a combination of ST depression/elevation depending on which vessel is affected
lateral MI - LCX, diagonal - ST elevation 1, avL, V5, V6
- ST depression in inferior leads
Chagas disease
T. cruzi - protoza, Latin America
px - megacolon, megaesophagus, and cardiac disease
v. s. other forms of myocarditis
- giant cell myocarditis - rare, severe px, and fatal
