Cardio Flashcards
Infection of normal valves with a virulent organism (S. aureus)
Acute bacterial endocarditis
Difference in acute vs subacute bacterial endocarditis
Acute = Normal valves (S.Aureus)
Subacute = Abnormal valves with less virulent organism like (S. Viridans)
Duke Major criteria for endocarditis
Blood cx (x2 ; 12 hrs apart)
Echo = Vegetations seen
New regurg murmur
Dukes Minor criteria for endocarditis
Risk factors
Fever 100.5
Osler nodes
Janeway lesions
Roth Spots
Splinter hemorrhages
Clubbing
Tx of endocarditis normal valve + prosthetic valve
Normal valve = IV Vanc or Amp/Sulbactam PLUS aminoglycoside
Prosthetic valve = Rifampin
Which bacteria is seen in acute vs subacute vs IV drug user vs prosthetics
Acute + IV drugs = Staph aureus
Subacute = Sub → Not as bad = Staph Viridans
Prosthetic = S. Epidermidis
MC bug of endocarditis
Strep viridans = Late complication of valve replacement and presents as small vegetations and emoblic events
Gold standard dx for endocarditis?
TEE
Chest pain or discomfort, heaviness, pressure, squeezing, tightness that is increased with exertion or emotion
Stable angina
Chest pain or substernal pressure <10-15 min that is relieved with rest or w/ NTG
Stable angina
What is levine sign?
Clenched fist over sternum + teeth clenched = Stable angina
Workup for stable angina includes?
EKG = Normal (q waves before MI)
Cardiac stress test = reversible wall motion abnormalities
Coronary angio = DEFINITIVE diagnosis
Tx of table angina
NTG sublingual then IV nitro
Betablockers = make heart work less
Severe = angioplasty + by;pass
Main vessel involved in stable angina
Left main
Previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest
Unstable angina
Tx of unstable angina
Admit with continous monitoring, establish IV, O2
Pain control = NTG + morphine
ASA +/- Clopidogrel - Used together these reduce rate of MI compared to ASA alone
LMWH for 2 days
Bblockers
Revascularization if symptoms PERSIST WITH MEDS
Ace + statins go home with
What type of angina awakes pts from sleep and isn ot associated with clot?
Prinzmetal variant
Coronary artery vasospams causing transient ST segment elevation
Printzmetal angina
Known triggers of printzmetal angina
Hyperventilation, COCAINE, tobacco use, acteycholine, ergonivine, histamine, serotonin
Which type of angina is associated with nitric oxide deficiency?
Printzmetal - Lack of nitric oxide → Increases activity of potent vasoconstrictors + stimulators of smooth muscles
Is prinzmetal angina pain cyclical or noncylical?
Cyclical = Occurs most often in morning hours, no correlation to cardiac workload
What does Prinzmetal angina look like on EKG?
Inverted U waves; ST segment or T wave abnormalities
Tx of Prinzmetal angina
Stress test + Myocardial perfusion imaging or coronary angio
Once dx made = CCB + Long acting nitrates used for long term ppx like Amlodipine
Sawtooth pattern on EKG
Aflutter
Which type of pt is a.fib most commonly seen in?
Elderly, excessive alcohol use patients
What is the atrial rate of a. fluttler
250-350 BPM
What type of pt does a.fluttler most likely occur in?
COPD, CHF, ASD, coronary artery disease
What is the biggest concern in a pt with afib? What score assesses for this?
Clot/Stroke/DVT
CHADS2/VASc
How many points does a pt need to score on CHA2DS2 to qualify for anticoag regimen?
0 = Aspirin
1 = Aspirin or anticoag
2 = Anticoag
Which anticoag is used for pts with mechanical heart valves
Warfarin
1st degree AV block on EKG
PR interval is longer than 0.20 seconds
Rhythm is regular
What medication is contraindicated in any of the heart blocks/heart failure?
CCB because of the possibility of causing bradycardia and worsening cardiac output.
2nd degree AV block type 1
Wenckebach
PR interval progressively lengthens until beat is dropped
PR gets longer
2nd degree AV block mobitz 2
P waves without QRS
Tx of 2nd degree Mobitz 2 block
Pacemaker
3rd degree AV block
P-P = Constant and the R-R is constant; Relationship between PR is erratic
3rd degree AV block tx
Pacemaker
You see regular P waves and regular QRS complexes, but they do not seem to have any correlation to each other. What is the diagnosis?
3rd degree block
Sx of AV block
Depends on severity; MC = As the electrical signal that controls one’s heartbeat is partially or completely blocked the heart beats slowly or skip beats and can’t pump blood effectively. Symptoms include dizziness, fainting, fatigue, and shortness of breath
MCC of AV blocks
- Idiopathic fibrosis and sclerosis of the conduction system (about 50% of patients)
- Ischemic heart disease (40%)
Stable vs unstable patient, what is the tx of AV block
Stable = Most likely benign; no tx
Unstable = Pacemaker
A 12-lead ECG showed sinus rhythm, rate 60, with an R and R’ (upward bunny ears) in V4-V6
Left bundle branch block
QRS looks like W in V1 and M in V6 it is LBBB (WiLLiaM)
Left BBB -
New LBBB + Chest Pain =
MI until proven otherwise
R and R’ (upward bunny ears) in V1-V3
Right bundle branch block
MCC of bundle branch blocks
In most cases, bundle branch block is caused by fibrosis or scarring, that either occurs acutely or chronically
-
Acute causes can be things like ischemia, heart attack, or myocarditis
- Chronic conditions include hypertension, coronary artery disease, and cardiomyopathies
An RSR prime in leads V5 or V6 should make you think of what diagnosis?
Left bundle
Which finding requires immediate attention: left bundle branch block or right bundle branch block?
New left bundle branch block is a STEMI equivalent. Right bundle branch block is usually not a problem.
Tx of bundle branch blocks
No specific treatment is indicated
- If there’s an underlying condition, such as heart disease, that condition needs treatment
- In patients with heart failure, a pacemaker also can relieve symptoms as well as prevent death
bnormal heart rhythm that occurs when a short circuit rhythm develops in the upper chamber of the heart in patients who have no other types of structural heart disease
Paroxysmal supraventricular tachycardia (PSVT)
What are the 3 causes of SVT?
AVNRT = AV nodal reentrant tachy
Wolff-Parkinson White
Atrial tachy
Hallmark sx of PSVT
- A regular but racing heartbeat of 120 to 230 beats per minute that starts and stops abruptly
- Palpitations, dizziness or lightheadedness, syncope, chest pain, weakness of fatigue
MC type of SVT
Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia and occurs when a small extra pathway exists in or near the AV node
MCC of Wolff-parkinson white
- Wolff-Parkinson-White (WPW) syndrome is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles (Bundle of Kent fibers). Hallmarks on EKG include a shortened PR interval, widened QRS, and delta waves
Atrial tachycardia is a type of SVT, but only occurs in 5%, why does this happen
- is responsible for about 5 percent of PSVTs. It occurs when an electrical impulse fires rapidly from a site outside the sinus node and circles the atria, often due to a short circuit.
Hallmarks of Wolff-parkinson white on EKG
hallmarks on EKG include a shortened PR interval, widened QRS, and delta waves.
How are PSVT most likely diagnosed?
Holter monitor to “catch” episodes while pt is symptomatic
Tx of PSVT
Try vagal maneuvers: carotid massage and Valsalva for stable patients
- Adenosine for symptomatic patients
- beta-blocker/calcium channel blocker (if regular)
- Definitive treatment: Radiofrequency ablation
- WPW - do not administer adenosine or calcium channel blockers
How is Adenosine dosed for psvt?
The initial dose of adenosine in treating acute PSVT is 6 mg given by rapid i.v. bolus injection, followed in one to two minutes by up to two additional 12-mg boluses if necessary.
Adenosine has been found to be effective in terminating PSVT and thus offers an alternative to verapamil
How does Adenosine work for PSVT?
It acts on receptors in the cardiac AV node, significantly slowing conduction time
What are the 3 types of premature beats?
Three types: Premature atrial (PACs), ventricular (PVCs), and junctional (PJCs) contractions
What type of premature beat is this: Early wide “bizarre” QRS, no p wave seen
PVC= Premature ventricular contraciton
What type of permature beat is this: Early, abnormally shaped P wave
Premature atrial contraction
What type of premature beat is this:Early, narrow QRS complex, usually measured at 0.10 sec or less, no p wave or inverted p wave
Premature junctional contraction
These arise from the region of the AV node, so the ventricles are usually activated normally.
Which premature beat is MC in pts with COPD
PAC
Dx of premature beats
EKG, holter monitor testing, exercise stress testing, echo
Tx of premature beats
None or beta-blockers/calcium channel blockers if symptomatic
- PAC: Usually benign, provide reassurance if symptomatic treat with beta-blockers or calcium channel blockers
- PVC: If symptomatic, look for cause and treat with calcium channel blockers/beta-blockers first then consider radiofrequency catheter ablation
- PJC: Treatment only if greater than ten per minute or they are multifocal – can use lidocaine or an antiarrhythmic
What causes torsades?
- Etiology: QT prolongation may occur secondary to multiple drug effects, electrolyte abnormalities and medical conditions; these may combine to produce TdP
- Drug-induced long QT can be remembered by the mnemonic (ABCDE):
- AntiArrhythmics (class IA, III)
- AntiBiotics (e.g., macrolides)
- Anti”C“ychotics (e.g., haloperidol)
- AntiDepressants (e.g., TCAs)
- AntiEmetics (e.g., ondansetron)
- Drug-induced long QT can be remembered by the mnemonic (ABCDE):
Torsades may cease spontaneously or
- This arrhythmia may cease spontaneously or degenerate into ventricular fibrillation
Tx of torsades
- Treatment is with IV magnesium and measures to shorten the QT interval
Hemodynamically unstable pt with torsades, what is the tx
Unsynchronized cardioversion
uncoordinated quivering of the ventricle with no useful contractions
Ventricular fibriation
- Presentation: Unstable patient
- EKG: No discernible heart contractions
Vfib
What is the tx of V.Fib
Treat with unsynchronized cardioversion
- Unsynchronized cardioversion - start CPR
- Give 3 sequential shocks (120, 150, 180); assess rhythm
- If VF persists –> do CPR and intubate
- Administer two doses amiodarone 2-4 min. Administer 1 mg IV bolus epi every 3-5 minutes (will ↑ myocardial blood flow and ↓ cerebral blood flow and ↓ defib threshold)
Implantable cardioverter-defibrillator may be necessary
three or more consecutive ventricular premature beats
V. tachycardiac
VT is frequently a complication of
Acute MI or Dilated cardiomyopathy
Unstable patients with monomorphic VT should be immediately treated with
synchronized direct current (DC) cardioversion, usually at a starting energy dose of 100 J (compare this to ventricular fibrillation which is treated with non-synchronized cardioversion)
Tx of V. tach
Stable: Stable patients have adequate vital end-organ perfusion and thus do not experience signs or symptoms of hemodynamic compromise
- Treat with amiodarone → lidocaine → procainamide (in this order)
-
Unstable: Unstable patients have signs or symptoms of insufficient oxygen delivery to vital organs because of the tachycardia. Such manifestations may include chest pain, dyspnea, hypotension, and altered level of consciousness
- Unstable patients with monomorphic VT should be immediately treated with synchronized direct current (DC) cardioversion, usually at a starting energy dose of 100 J
- Unstable polymorphic VT is treated with immediate defibrillation. The defibrillator may have difficulty recognizing the varying QRS complexes; therefore, synchronization of shocks may not occur.
A buildup of fluid between the pericardial sac and the heart; constricts the heart
Cardiac tamponade
Pathophys behind cardiac tamponade
- Heart unable to pump normally → blood flow through chambers obstructed → cardiac output decreases → hypotension → lower tissue perfusion → heart rate increases
MCC of cardiac tamponade
- Acute onset: trauma, myocardial infarction, aortic dissection, pericardial effusion
- Slow onset: cancer, chronic inflammation, uremic pericarditis, hypothyroidism, connective tissue disease
Becks triad
The 3 D’s: D istant heart sounds, D istended jugular veins, and D ecreased arterial pressure
Beck’s triad:
- Hypotension
- muffled heart sounds
- elevated neck veins (JVD)
What is pulsus pardoxus
(drop 10 mmHg in systolic pressure on inspiration), narrow pulse pressure) Commonly seen in → Cardiac tamponade
consecutive, normally-conducted QRS complexes alternate in height) and low voltage QRS complex
Electrical alternans → Seen in cardiac tamponade
Also pulsus paradoxus
What is the CXR finding in cardiac tamponade
Water bottle heart = Huge enlarged water filled heart
Tx of cardiac tamponade
Pericardiocentesis
5 causes of acute chest pain in ED
- Pericarditis: chest pain that is relieved by sitting and/or leaning forward
- ACS: chest pain with shortness of breath, with possible radiation to the neck, jaw, arms, shoulders, and back
- Pulmonary embolism: dyspnea (most common) and pleuritic chest pain. Spiral CT is the best initial test
- Pneumothorax: ipsilateral chest pain and dyspnea with decreased tactile fremitus, deviated trachea, hyperresonance, diminished breath sounds
- Thoracic aneurysm/dissection: severe, tearing (ripping, knife-like) chest pain radiating to the back
myocardial necrosis (evidenced by cardiac markers in the blood; troponin I or troponin T and CK will be elevated) WITHOUT acute ST-segment elevation or Q waves
NSTEMI
Tx of NSTEMI
TX: Beta Blockers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion
- Reperfusion via percutaneous coronary intervention (not thrombolysis)
- Less time-sensitive than in STEMI
STEMI =COMPLETE BLOCK OF
St-segment elevated MI is myocardial necrosis (evidenced by cardiac markers in the blood; troponin I or troponin T and CK will be elevated) WITH acute ST-segment elevation or Q waves
- Coronary artery completely blocked; full thickness of myocardial wall involved
I, AVL, and V2 to V6 in EKG STEMI =
Anterior wall
ST elevation in the lateral leads (I, aVL, V5-6). Reciprocal ST depression in the inferior leads (III and aVF).
Lateral wall MI
ST depressions in V1 to V3
Posterior wall MI
Tx of STEMI
TX: Beta Blockers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion
- Aspirin and Clopidogrel are given at once
- Very time sensitive - Immediate (within 90 minutes) coronary angiography and primary PCI
- Thrombolytic therapy within the first 3 hours if PCI not available
Absolute contraindications for fibrinolytic use in STEMI include the following:
- Prior intracranial hemorrhage (ICH)
- Known structural cerebral vascular lesion.
- Known malignant intracranial neoplasm.
- Ischemic stroke within 3 months.
- Suspected aortic dissection.
- Active bleeding or bleeding diathesis (excluding menses)
Dyspnea on exertion in the ER should make you think of two areas ⇒ the cardiac and pulmonary systems
Cardiac system:
- Coronary heart disease
- Heart failure
- Myocarditis
- Pericarditis
- MI
- ACS
Pulmonary system:
- Asthma
- COPD
- Pneumonia
- Pulmonary Hypertension
- Obesity, kyphosis, scoliosis (restrictive lung disease)
- Interstitial lung disease
- Drugs (e.g., methotrexate, amiodarone) or radiation therapy, cancer
- Psychogenic causes
What is the pathophysiology behind dyspnea on exertion for Heart, lungs, Blood
HEART → not pumping blood out to the lungs during exertion causing shortness of breath
LUNGS → not functioning properly and dyspnea on exertion is because the lungs cant exchange oxygen
Blood → Anemia is also another cause of shortness of breath usually a chronic problem and can be easily worked up with routine blood work (CBC)
Main causes of edema seen in ED
- In other words, when patients in the ER have edema either the heart is failing as a pump (CHF) or the fluid is backing up such as with kidney or liver disease
- Always remember medications such as calcium channel blockers and Alpha-1 blockers vasodilate the vessels making the fluid come out and will go down to the feet due to gravity
Main sx of heart failure
- Exertional dyspnea (SOB), then with rest
- Chronic nonproductive cough, worse in a recumbent position
- Fatigue
- Orthopnea (late), night cough, relieved by sitting up or sleeping with additional pillows
- Paroxysmal nocturnal dyspnea
- Nocturia
Physical exam findings of heart failure
- Cheyne-Stokes breathing - periodic, cyclic respiration
- Edema: ankles, pretibial (cardinal)
- Rales (crackles)
- S4 = diastolic HF (ejection fraction is usually normal)
- S3 = Systolic HF (reduced EF) with volume overload - tachycardia, tachypnea. (Rapid ventricular filling during early diastole is the mechanism responsible for the S3)
- Jugular venous pressure: >8 cm
- Cold extremities, cyanosis
- Hepatomegaly Ascites, jaundice, peripheral edema
CXR finding in heart failure
Kerley B lines
Best test for dx heart failure
Echocardiogram (BEST TEST): diagnose, evaluate, manage Most useful, differentiates HF ± preserved LV diastolic function
New York Heart failure Classification
- Class I (< 5%) without any limitation of physical activity
- Class II (10-15%): Patients with slight limitation of physical activity, they are comfortable at rest
- Class III (20-25%): Patients with marked limitation of physical activity they are comfortable at rest
- Class IV (35 - 40 %): Patients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or anginal syndrome even at rest
Tx of systolic vs diastolic heart failure
Systolic left heart failure: Ace Inhibitor + β-blocker + Loop Diuretic
Diastolic heart failure: Ace inhibitor + β-blocker or CCB (do not use diuretics in stable chronic diastolic failure)
- Lasix—for diuresis
- Morphine—reduces preload
- Nitrates (NTG)—reduce preload O2
- ACE inhibitor + diuretic (unless contraindicated)
- CCB in diastolic HF
- Poor prognosis factors: chronic kidney disease, diabetes, lower LVEF, severe symptoms, old age
- 5-y mortality: 50%
- BP usually >180/120 WITH impending or progressing end-organ damage
HTN Emergency
HTN Urgency
- BP usually > 180/120 WITHOUT signs of end-organ damage
Tx of HTN urgency vs emergency
- Hypertensive emergency = sodium nitroprusside (drug of choice)
- Hypertensive urgency = clonidine (drug of choice)
MCC of cardiogenic shock
Common causes: acute MI, heart failure, cardiac tamponade
Tx of cardiogenic shock
- Treatment: Fluid resuscitation, pressors (dopamine), and treat the underlying cause
Drop of > 20 mm Hg systolic, 10 mmHg diastolic, 15 BPM increase in pulse 2-5 minutes after a change from supine to standing
Orthostatic hypotension
Cardiac vs pulmonary causes of orthopnea
Cardiac causes:
Pulmonary causes
- COPD and cor pulmonale
- Pulmonary hypertension
- Indirect causes such as kidney failure and liver failure (will cause fluid back up into the lungs)
Pathophys behind pulmonary vs cardiac causes of orthopnea
Heart = fluid is in the pulmonary space either by the heart not pumping or failing as a pump (CHF) or the heart is injured (MI).
Lungs = Pulmonary causes mean the lungs are failing to move the blood so the fluid leaks out. Causes like pulmonary hypertension and COPD (secondary cause of pulmonary hypertension)
Same symptoms as acute pericarditis except patient will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternans, distant heart sounds and an echocardiogram showing a collection of pericardial fluid
Pericardial effusion
Intermittent claudication, Ankle-brachial-index (ABI) < 0.9
Peripheral vascular dz
Sx of Peripheral vascular dz
- Lower extremity loss of hair, brittle nails, pallor, cyanosis, claudication, hypothermia
- Ulcers are pale to black, well-circumscribed and painful, located laterally and distally
Gold std for dx of peripheral vascular dz
Ateriography
Tx of peripheral vascular dz
- Definitive treatment: Arterial bypass
- Medical treatment: Antiplatelets, anti lipids, manage risk factors, cilostazol Aspirin, and Plavix
Transient loss of consciousness/postural tone secondary to an acute decrease in cerebral blood flow
Syncope
Harsh systolic ejection crescendo-decrescendo murmur at the right upper sternal border (aortic area) with radiation to the neck and apex heard best by leaning forward with expiration
Aortic stenosis
Soft, early diastolic blowing murmur along the left sternal border with the patient sitting leaning forward after exhaling
Aortic regurge
Diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with the patient in the lateral decubitus position
Mitral stenosis
Holosystolic high-pitched blowing murmur at the apex (mitral area) that radiates to axilla with a split S2
Mitral regurge
Flank pain, hypotension, pulsatile abdominal mass
Abdominal aortic aneurysm
Tx of AAA
- Surgical repair if > 5.5 cm or expands > 0.6 cm per year
- Monitor annually if > 3 cm. Monitor every 6 months if > 4 cm
- Beta-blockers
sudden arterial occlusion
Remember the P’s of arterial emboli: P ain, P allor, P ulselessness, P aresthesia, P aralysis, P oikilothermia
Arterial embolis or thrombolism
Gold std tx of arterial embolism/thrombolism
Angiography
Tx of acute arterial occlusion
- Treat with IV heparin if not limb-threatening then call the vascular surgeon for angioplasty, graft or endarterectomy
Why does phlebitis occur
Spontaneous or after trauma, or IV/PICC lines
Tx of phlebitis/thrombophlebiits
- Treatment: Symptomatic: NSAIDs, warm compress
three different atrial ectopic foci (at least 3 different P wave) depolarize to pace the heart
MAT
Multifocal Atrial Tachycardia
- Associated with older patients and those with COPD
- Rate will be 100–200 beats/min
- PR interval will differ
- Notable feature: at least three different P wave forms
- Treatment is to treat the underlying cause, calcium channel blockers
What is the name for an occasional contraction generated from a single ectopic atrial focus?
Premature atrial contraction
Which med is contraindicated in right ventricular infarct
Nitroglycerin → which is commonly used in acute myocardial for its preload and afterload reducing effects, should not be used in right ventricular infarction because it can precipitate critical hypotension and cardiovascular collapse.
Anterior & Septal leads for ECG
V1-V4 = LAD
Inferior leads of ECG what artery
Right coronary artery 70%
Which leads are lateral leads of ECG?
I, avL, V5-V6
AVL → L= LATERAL
Tx of afib
- Treatment
- Unstable: cardioversion
- Stable: rate control is mainstay (diltiazem, metoprolol)
- > 48 hours: anticoagulate for 21 days prior to cardioversion
- Determine the need for anticoagulation by using CHA2DS2-VASc score
S4 gallop and a harsh (as opposed to soft blowing) systolic murmur loudest in early or mid-systole, best heard at the apex, and diminishing before S2
Mitral regurg
- PE
- Acute: unique, harsh, midsystolic murmur best heard at apex that radiates to the base rather than the axilla
- Chronic: blowing holosystolic murmur best heard at apex with radiation to axilla
