Cardiac Section Flashcards
symptoms of arrhythmias
Asymptomatic Palpitations Dizziness: vertigo, disequilibrium, or pre-syncope Chest pain Dyspnea: trouble breathing Weakness Anxiety Note: sxs may be due to underlying heart disease (e.g. HF, ischemia)
sinus bradycardia: causes
normal (athletes), SA node dysfunction (called sick sinus syndrome if sxs), metabolic (including hyper or hypo-kalemia, hypercalcemia, and hyper- or hypothyroidism), drugs (beta-blockers, calcium-channel blockers, and lithium), neurogenic (vagal stimulation), cardiac ischemia (AMI), OSA, infection, inc. ICP
sinus bradycardia: treatment
stop meds causing slow HR; pacemaker
sinus tachycardia: causes
fever, sepsis, anemia, hypotention/shock, acute coronary ischemia/MI, heart failure, chronic pulm disease, hypoxia, pulm embolism, stimulants/illicit drugs, (nicotine, caffeine, OTC decongestants, cocaine), anxiety, pheochromocytoma
sinus tachycardia: treatment
target underlying disease
beta-blockers if not obvious dz
Guidelines for prevention of thromboembolism in A-Fib - moderate and high risk factors
moderate: > 75y/o, HTN, HF, DM
High: CVA, TIA, embolism, prosthetic valve
LBBB on EKG with ACS sxs
cannot R/O infarction - this is a STEMI (unless so elevation in cardiac markers)
variant (Prizmetal’s) angina: treatment
CCBs are 1st line
long-acting nitrates
Note: beta blockers are contraindicated
chronic stable angina: risk factor modification
LDL < 100 mg/dL
TG < 200 mg/dL
HDL > 40 mg/dL
BP < 130/85
chronic stable angina: life-style modifications
smoking, diet, activity, cholesterol, BP (salt intake)
chronic stable angina: medications
Beta-blockers (dec. oxygen demand)
Ca++ channel blockers (dec. afterload / demand)
Nitrates (inc. oxygen supply and dec demand)
Aspirin (ASA) (dec. vasoconstriction and platelet activity; 75-325mg/day) → reduced mortality
Statins (stabilize plaques): all pts w/ angina should be on statins regardless of LDL
suspect ACS: evaluation
Immediate EKG
MONA:
- Morphine sulfate: 2-4 mg IV, then 2-8mg every 5-15 min (Fentanyl)
- Oxygen
- Nitrates: SL nitroglycerin 0.4 mg q 5 minutes x 3
- ASA: 160-325 mg chewed
cardiac serum markers, CXR
NSTEMI management: low risk of progression to STEMI
Beta-blocker IV nitroglycerine (if pain persists) Heparin, low molecular weight = Enoxaparin (Lovenox): anti-thrombin effect Clopidogrel (Plavix): platelet inhibitor
NSTEMI management: high risk of progression to STEMI
*ST depression, persistent pain, unstable
Angiogram: diagnostic coronary arteriography (determines whether PCI is needed)
GP IIb/IIIa inhibitor: Abciximab (Reopro): platelet inhibitor, used prior to PCI
Percutaneous Coronary Intervention (PCI)
PTCA (Percutaneous Transluminal Coronary Angioplasty):“Balloon Angioplasty”
STEMI management
Beta-blocker
IV nitroglycerine (if pain persists)
IV Heparin
Clopidogrel (Plavix) (platelet inhibitor)
Primary PCI: goal less than 90 minutes
Thrombolysis with t-PA (tissue plasminogen activator): goal less than 30 minutes (if no PCI)
ACS: long-term risk factor modifications
smoking cessation weight, diet, exercise lipid lowering therapy (statin) fibrate or niacin if HDL<40 HTN control <130/80 control of hyperglycemia in DM Also medications: see below
ACS: long-term risk factor modifications - medications
Aspirin 75-325 mg daily
Clopidogrel (75 mg daily) when ASA is not tolerated (hypersensitivity, GI intolerance)
• Note: combined ASA + clopidogrel for 9 months after NSTEMI
Beta blockers unless contraindicated
ACE-I for pts with CHF, LV dysfunction (EF <40%), HTN, or DM
gold standard for coronary heart disease evaluation
coronary angiogram
- invasive and costly
- can consider stress test
cardiac stress testing
non-invasive approach involving stressing the heart (via exercise or meds) and measuring changes in response to stressors (via EKG or imaging - thallium or echo)
use for both diagnostic and prognostic assessment
indicated if pretest probability of CHD is INTERMEDIATE
poor R-wave progression on EKG: causes
Old infarct (previous MI)
Emphysema
COPD (heart sits lower)
Dextrocardia: heart on right
Note: R waves get progressively taller from V1 - V6
normal sinus rhythm: definition
P wave b/f every QRS and QRS after every P
Rate 60-100
P wave directions:
- Upright in II (current heading towards positive pool)
- Negative (inverted) in aVR (current heads towards negative pool)
- AVL is pretty flat (current directly 90 degrees from positive pool)
sign of junctional rhythm
P-waves negative in II, III, and aVF and upright in aVR
signs of ischemia on EKG
*ischemia: restriction of blood flow causing low oxygen to cells
flipped T waves
ST segment depression
Note: this is reversible
signs of myocardial injury (infarct)
ST segment elevation
signs of myocardial necrosis (death)
significant Q waves (wider than 1 small box; >1/3 size of QRS)
Note: q waves are usually very small
EKG sign of posterior STEMI
ST segment depression in leads V2, V3, V4 (since this would be elevation if leads were on patient’s back)
EKG clues to pulmonary embolism (PE)
tachycardia, RAD, inc. R’ over rt ventricle (aVR) = RBBB, T-wave inversion in anterior and inferior leads
EKG clues to pericardial tamponade
Low voltage EKG (often with low BP), SOB, tachypnea. Tachycardia
Electrical alterans: QRS in rhythm strip is higher and lower, higher and lower
EKG clues to myocarditis
*infection of heart muscle - much more serious than pericarditis
Low voltage in limb leads (I, II, III, aVR, aVL, aVF), tachycardia
Can also get positive Trop levels since cell death releases troponin
EKG clues to pericarditis
*infection in sac around heart; can be due to virus
GLOBAL ST segment elevation (all chest and limb leads)
syncope
transient loss of consciousness (T-LOC) due to transient global cerebral hypo-perfusion characterized by rapid onset, short duration (20-30 sec, <5min), and spontaneous complete recovery
4 types of neurally-mediated (reflex) syncope
vaso-vagal
situational
carotid sinus
atypical
prodromal sxs of vasovagal syncope
sweating, pallor, nausea
orthostatic hypotension (OH) syncope: causes
DAAD:
Drugs: vasodilators, vol. depletion, BP meds, diuretics, TCAs
Autonomic insufficiency: Parkinson’s, DM, adrenal insufficiency
Alcohol
Dehydration
cardiovascular syncope: causes
arrhythmias (bradycardia or tachycardia)
structural disease: valvular dz, AMI, HCM, masses, pericardial dz, prosthetic valve dysfunction
syncope on exertion or supine
WORRISOME for cardiac origin
syncope: basic work-up
History/Physical including orthostatic BPs
Medication Review
EKG
Carotid Sinus Massage (if age >40)
Note: all pts then risk stratified (high or low risk of short-term cardiac event)
Carotid Sinus Massage: what indicates a positive test for cause of syncope
bradycardia, hypotension, transient pause/asystole, or prodrome symptoms w/ massage
syncope: high-rise for ST cardiac event
Evidence of heart disease (heart failure (fluid), low LVEF, structural abnormality, previous MI)
Clinical: palpitations, syncope on exertion or supine
FH of sudden cardiac death or non sustained ventricular tachycardia
Hypotension (systolic <90 mmHg)
EKG features suggesting arrhythmia or abnormal
Comorbidities such as severe anemia or electrolyte disturbance
diagnosing essential / primary HTN
SBP ≥ 140 mmHg OR DBP ≥ 90 mmHg (2 or more readings spaced at least 2 wks apart)
secondary HNT: causes
hints: severe, resistant to tx, sudden onset, young age (w/ no FH or obesity)
OSA: #1 cause tied w/ meds
meds: OCPs, NSAIDS, simulants, Calcineurin inhibitors, antidepressant (venlafaxine)
Heavy EtOH use
renal: renal vascular or primary renal dx
rare dz: pheo, primary aldosteronism, Cushings, coarctation, hyper- or hypothyroidism, primary hyperparathyroidism
hypothyroidism - signs
fatigue, unintentional weight gain, cold intolerance, constipation
5 P’s of pheochromocytoma
palpitations perspiration pallor pounding HA inc. BP
labs to R/O secondary causes of HTN
electrolytes (Na, K, Ca) - hyperaldosteronism, hyperparathyroidism creatinine - renal dz TSH - hypo/hyperthyroidism
HTN evaluation: target organ damage
neuro: HA, neurologic sx
ophthalmology: cotton-wool spots, AV nicking
CV: CP on exertion, dyspnea, claudication, dec. pulses
Pulm: rales, fluid (HF)
HTN evaluation: risk stratification
Assess other CV disease risks:
- Smoking, Type 2 Diabetes (T2DM)
- Hyperlipidemia
- Known vascular disease history
Labs:
- lipid panal
- EKG: LVH
HTN management: lifestyle modifications
Weight maintenance/loss: ↓10kg = ↓BP 5-20 mm Hg
30 minutes exercise/day: ↓BP 4-9 mm Hg
Sodium <2400 mg/day: ↓BP 2-8 mm Hg
Restrict EtOH (1/day W or 2/day M): ↓BP 2-4 mm Hg
HTN management: medications
JNC8 first-line agents
- Thiazide-type diuretic
- ACE-I OR ARB
- CCB
JNC 8 second-line agents
- Beta Blocker (BB)
- Aldosterone antagonist (e.g. spironolactone)
thiazide and loop diuretics: actions and side effects
decrease total body salt and water
dehydration
hypokalemia
worsens insulin resistance i
increases uric acid (gout)
Contraindicated in pregnancy
ACE-I: actions and side effects
Inhibits activation of RAAS - leads to dec salt/water retention by kidney and dec peripheral vascular resistance
hyperkalemia
cough
urticaria/angioedema
Contraindicated in pregnancy
Decreases incidence of DM in hypertensive individuals
ARBs: actions and side effects
inhibits RAAS one step later than ACE-I
hyperkalemia
urticaria/angioedema
Decreases incidence of DM in hypertensive individuals
Calcium channel blockers: actions and side effects
Dipines (DHP): vasodilate peripheral blood vessels
Cardiac (non-DHP): lower heart rate
Edema
Bradycardia (non-DHP)
CHF exacerbation (non-DHP)
Beta blockers: actions and side effects
lowers heart rate and decreases peripheral vascular resistance mediated by SNS
Bradycardia
CHF exacerbation
Masks signs of hypoglycemia in DM; some inc. insulin resistance
Contraindicated in asthma
aldosterone antagonists
competes with aldosterone at distal renal tubule, conserves potassium and excretes sodium/water (diuretic)
hyperkalemia
dehydration
chronic kidney disease: best HTN drug
ACE-I or ARB
DM: best HTN drug
ACE-I or ARB preferred (avoid beta-blockers since mask hypoglycemia)
Black: best HTN drug
diuretic or CCB
All races (other than black): best HTN drug
diuretic or ACE-I/ARB or CCB preferred
pregnancy: best HTN drug
1st-line: Methyldopa (long track record)
2nd-line: Labetalol (beta-blocker)
Additional options:
- nifedipine
- hydralazine
chronic kidney disease: parameters
GFR < 60 ml/min
OR
microalbuminuria > 30mg / gram creatinine
hypertensive urgency: treatment
decrease BP <160/100 over 3-6 hours
- usually use a diuretic
hypertensive emergency: assessing for end organ damage
Neuro/optho: reversible encephalopathy, hemorrhagic stroke, retinal exudates/ hemorrhages, papilledema
CV: unstable angina/MI, HF (pulm edema), aortic dissection
Renal: proteinuria, hematuria, acute renal failure
Pregnancy only: preeclampsia/eclampsia
hypertensive emergency: treatment
ADMIT: ED/ICU
Lower DBP by MAX of 25% in 2-6 hours
Goal DBP 100-105 mm Hg within minutes to 2 hours
use vasodilators, beta-blockers, dopamine-1 agonist
-nitroprusside, labetalol, fenoldopam, hydralaine
3 determinants of stroke volume
preload
afterload
contractility
cor pulmonale
isolated rt sided heart failure (not caused by left-sided)
CHF: 3 ways patients usually present
asymptomatic (cardiac enlargement)
dec. exercise tolerance (inc. fatigue)
sxs of fluid retention (lungs, periphery)
right-sided heart failure: what you see on PE
JVD, peripheral edema (bilateral), RUQ tenderness / hepatomegaly
left-sided heart failure: what you see on PE
tachycardia, tachypnea, dyspnea (nocturnal), orthopnea, nocturnal cough, pulmonary rales, pneumonia, S3 gallop
CHF: risk factors (call can cause remodeling)
HTN Valvular Disease Diabetes Myocardial infarction Atherosclerosis Cardiomyopathy Arrhythmias/LBBB COPD Cardiotoxic drugs (smoking, alcohol, cocaine, ephedra, long-term NSAIDs use)
CHF: diagnostic imaging
Echocardiogram
- most important test (establishes baseline, help when change of sxs)
- tells EF, LVH, structural abnormalities
EKG: LBBB, LVH, atrial fibrillation (evidence of prior MI or arrhythmia)
CXR: cardiomegaly, pulmonary infiltrate
CHF: laboratory testing
BMP and CBC are standard
UA (kidney) A1C: DM can lead to vascular dx Lipid Panel: dyslipidemia can lead to vascular dx Hepatic Function (ALT/AST) Thyroid Function Transferretin: iron HIV
heart failure: stages
Stage A: people at risk for HF (see risk factors)
Stage B: begin to have structural heart disease (valve changes, EF), but no signs of systemic symptoms
Stage C: begin to have systemic symptoms
Stage D: end-stage disease
heart failure: tx based on stage
stages A and B:
- ACE-I / ARB
- Beta-blockers (esp. if post MI)
stages C and D:
- optimize ACE-I/ARB and beta-blocker
- begin diuretics (loop, HCTZ)
- aldosterone antagonists
- digoxin
stage A: treat risk factors
stage D: palliative care, heart replacement
heart failure: meds to avoid
NSAIDS: cardiologists hate Cold meds containing pseudo ephedrine (Sudafed) Na containing antacids: alka-seltzer Anti-arrhythmic agents CCBs
heart failure: when to refer to cardiologist / work with cardiologist
stage c = symptomatic conduction abnormality suspect prior/unknown MI suspect CAD evidence of pulmonary HTN
heart failure: acute exacerbation
presents as acute pulmonary edema
LMNOP:
- lasix
- morphine
- nitrate
- oxygen
- pressors (vasoconstrict)
heart failure: home monitoring
Patient and family education:
- warning signs of worsening
- weight monitored daily (fluid)
- medication regimen
- diet adjust (salt restrict)
- moderate physical activity
Vaccinations:
- pneumovac
- influenza
bacterial endocarditis: definition and types
infection of the endothelial lining of the heart (including, but not limited to the valves)
- Acute Bacterial Endocarditis (ABE)
- Subacute Bacterial Endocarditis (SBE)
Acute Bacterial Endocarditis (ABE): sxs
infection of normal or abnormal valves with a virulent organism (e.g., Staph Aureus);
- Abrupt onset: high fever, chills, night sweats
- Prominent leukocytosis
- Rapid, severe valve destruction
- Apical heart murmur (not always in R-sided)
- Often complicated by heart failure
Subacute Bacterial Endocarditis (SBE): sxs
indolent infection of abnormal valves with a less virulent organism (e.g., Strep Viridans)
- Indolent onset (wks-mos): fever, night sweats, weight loss
- Apical heart murmur (not always in R-sided)
- Minor endocardial damage
- Leukocytosis often minimal or not present
bacterial endocarditis: high risk groups
Abnormal cardiac structure (anatomy or “foreign bodies)
- congenital heart disease (VSD, PAD, etc.)
- abnormal cardiac valves (prosthetic valves, mitral or aortic valve regurgitation)
Abnormal risk of bacteremia (IV drugs or IV access)
Age > 60
Immune compromised
abnormal risks of bacteremia
IV drug use (IVDU) Indwelling central venous catheter Chronic hemodialysis Poor dentition/dental caries Colon cancer/IBD
bacterial endocarditis: typical pathogens
80% Gram Positive Cocci (GPC)
∗ 32% S. Aureus
∗ 18% S. Viridans
∗ 11% Enterococcus
IV drug users: 60% Staph Aureus, 20% Strep Viridans
Prothetic valves: 30-35% S. Epidermidis (usually non-pathologic skin flora)
bacterial endocarditis: signs and sxs
fever, rigors (chills), night sweats, arthralgia / bone pain / septic joint, malaise/weakness, weightless, SOB, abd pain, rashes/skin changes
Hx of predisposing structural cardiac abnormalities / bacteremia risk
bacterial endocarditis: PE findings
fever, skin conditions, CV (new murmur, CHF signs), GI (splenomegaly, abd tender to palpation), MSK (bone TTP), neuro (neuologic signs, Roth spots on fundoscopic exam)
Note: sxs all over body
bacterial endocarditis: skin conditions associated
Petechiae: soft palate or extremities
Janeway Lesions: non-tender erythematous/hemorrhagic macular/nodular lesions on palms/soles
Osler’s Nodes: painful, immune-complex related inflammatory nodules on finger pads
- more common in SBE
Splinter Hemorrhages: linear, red hemorrhages in nails
- more common in SBE
bacterial endocarditis: lab findings and tests
Blood cultures x 3 sets (minimum) prior to giving antibiotics
CBC: leukocytosis (ABE), normocytic anemia
ESR: elevated, often > 100 (specific to only a couple conditions – one is endocarditis)
Creatinine: assure renal fx preserved
Urinalysis: microscopic hematuria (common), glomerulonephritis (proteinuria, RBC casts = GN = not common = big hint)
EKG: heart blocks
bacterial endocarditis: imaging
Trans-esophageal echocardiogram is best: 81.4% positive for vegetation on valve
bacterial endocarditis: Modified Duke Criteria
Major Criteria:
- Sustained bacteremia (3/4 sets 1 hr apart OR 2 sets 12 hr apart)
- Endocardial involvement: vegetation (oscillating intracardiac mass), valve abscess/ perforation, prosthetic dehiscence (come undone) OR New Valvular regurgitation
Minor Criteria:
- Predisposing medical condition (abnormal valve or bacteremia-prone)
- Fever (>38°C)
- Vascular phenomena (septic emboli, mycotic aneurysm, Janeway lesion)
- Immune phenomena (glomerulonephritis, Osler’s nodes, Roth spots, RF+)
- Blood cx + or evidence of infection
bacterial endocarditis: diagnosis
Definite pathologic: micro-organism demonstrated in vegetation or cardiac abscess OR pathology of vegetation shows active endocarditis
- rare, need heart surgery
Definite clinical: 2 major OR 1 major/3 minor OR 5 minor criteria
Possible: 1 major/1 minor OR 3 minor
bacterial endocarditis: treatment
6 weeks of IV ABX:
Native valve ABE: empiric therapy while waiting for cx results
- Nafcillin/Gentamicin (tx staph - most common) OR Vancomycin/Gent (if suspect MRSA)
Native valve SBE: likely wait for return of cx results (Ampicillin/Gentamicin)
Prosthetic valve: Vanco/Gent/Rifampin
bacterial endocarditis: surgical indications:
Incompetent valve causing CHF despite maximal medical therapy (must fix valve)
Heart block worsening (due to conduction system involvement)
Cardiac abscess (must go in and drain)
Recurrent emboli on medical therapy
Fungal infection: indication to remove valve, esp. if prosthetic
bacterial endocarditis: meds to avoid
Anticoagulation (heparin/Coumadin) contra-indicated: potential for hemorrhage from emboli
However, anti-coag is generally accepted (despite ↑ risk) in following conditions:
o Prosthetic heart valve
o Acute coronary syndrome
bacterial endocarditis: prophylaxis
Amoxicillin (clindamycin if pcn-allergic) prior to dental procedures for at-risk patients:
- congenital Cyanotic Heart Disease: unrepaired or repaired with residual defects
- prosthetic valve
- prior endocarditis hx
- heart transplant recipients who develop “valvulopathy”
pericarditis: definition and causes
infection of pericardium
1/3: infectious (viral, TB, fungal)
2/3: neoplastic, immune-mediated (post-cardiac surgery – called “Dressler’s Syndrome, etc.), uremic (end-stage renal disease), idiopathic, drug-induced, traumatic (MVI / chest trauma), immediate post-MI (larger infarcts)
pericarditis: clinical presentation
Positional pleuritic chest pain: better leaning forward, worse supine
Fever (esp. if infectious cause)
Pericardial friction rub (classic finding; brown paper bag crumpling)
If pericardial effusion is present: distant heart sounds, fainter friction rub
pericarditis: EKG findings
diffuse ST elevation (acute pericarditis)
pericardial effusion: low voltage throughout all leads
pericarditis: diagnosis:
2 or more of the following 4:• Chest pain
Pericardial friction rub
Appropriate EKG changes
Pericardial effusion
pericarditis: expanded lab and test work-up
EKG (as seen already)
Labs: thyroid testing (TSH): thyroid dz can cause, renal function (creatinine), ANA, rheumatoid factor (b/c SLE or RA can cause)
Consider TB/fungal evaluation in appropriate pt (immunosuppressed, TB exposures)
Consider evaluation for recent MI (e.g., wall motion abnormalities by ECHO, troponin less helpful because often ↑ in pericarditis)
HIV testing: if at risk
Cancer W/U:
pericarditis: treatment
Non-steroidal anti-inflammatory medications (NSAIDs) – consistent w/ viral infection
- treatment is for sxs / tolerance to sxs (not to fix issue)
Colchicine or Steroids (Prednisone) (if NSAIDs ineffective)
pericarditis: medication to avoid
anticoagulants: may cause hemorrhage and cardiac tamponade (same as for endocarditis, but for different reason – potential for hemorrhage from emboli in endocarditis)
• Caveat: if immediate post-MI period continue aspirin/heparin unless pericardial effusion > 1 cm or tamponade sx develop
cardiac tamponade: sxs and tx
complication of pericarditis (10-15% of acute pericarditis)
Sxs: “Becks triad” – distant heart sounds, hypotension, JVD; pulsus paradoxus; pericardial friction rub
tx: pericardiocentesis
constrictive pericarditis: sxs and tx
chronic pericardial inflammation causes fibrosis and scar
sxs: HF, normal BP, elevated JVP - similar to cardiac tamponade but slower in progression
Dx: CXR and Echo give hints; dx via heart catheterization
Tx: surgical resection of pericardium
