Cardiology Flashcards
Most common cause of death in the US
Coronary artery disease (CAD)
Does stress affect risk for CAD?
Stress is not a clear risk factor since it cannot be measured properly
Sxs that signal something other than CAD
Pleuritic pain - PE, pneumonia, pneumothorax
Positional pain- pericarditis
tenderness- costochondritis
Chest pain. pain also occurs in epigastric area and is associated with a sore throat, metallic bad taste and cough
GERD- administer PPI
Alcoholic patient with chest pain. Nausea, vomiting, and epigastric tenderness
Ddx- pancreatic
Check amylase and lipase levels.
Chest pain and right upper quadrant tenderness. mild fever
Cholecystitis, cholelithiasis
order ABD sonogram for gallstones
abnormal finding: S3 gallop
cadriovascular
rapid ventricular filling using diastole.rushing blood cause “splash” or S3
aka: dilated left ventricle
Abnormal finding: S4 gallop
cardio vascular
the sound of partial systole into a stiff or non compliant left ventricle. before s1
AKA: left ventricular hypertrophy
abnormal finding: JVD oe holosystolic murmur (MR)
cardio vascular piece of physical exam
Jugular vein exam is in chest not HEENT on CCS
abnormal finding: rales suggestive of CHF
piece of physical exam: chest
abnormal finding: dishes patient, SOB, clutching chest
piece of physical exam: general exam
abnormal finding: edema
physical exam includes: extremities
Ischemic-type chest pain. Next step in management?
BIT: EKG
but choose treatment first (if made to choose)
CK-MB and troponin
Most accurate test but not initial.
Best to detect a reinfarction a few days after initial infarction.
When to order stress test?
When case is not acute and initial EKG/enzyme tests do not establish the diagnosis.
Stress test is a way to increase the sensitivity of detection of CAD beyond EKG and enzymes.
Action of Troponin C
Binds to calcium to activate actin:myosin interaction
Action of Troponin T
Binds to Tropomyosin
Action of Troponin I
Inhibits actin:myosin interaction
When is dipyridamole or adenosine thallium stress test or dobutamine echo the answer?
Pt cannot exercise to target heart rate >85% of maximum.
63yo woman abnormal stress, reversible ischemia. No risk factors CAD. BNS?
Angiography is the next diagnostic for “reversible” ischemia, followed by bypass.
“Fixed” defects (unchanged between exercise and rest) are scars and require no angiogram
Sestamibi nuclear stress testing
Used in obese patients and those with large breasts because of its ability to penetrate tissue.
Use of Nuclear Ventriculogram (MUGA scan)
most accurate method to evaluate ejection fraction
Mechanism of Thallium
Isotopes picked up by the Na/K pump of the normal myocardium. Cardiac tissue alive and perfused= high uptake.
Decreased uptake: damaged tissue
LOS:5 post MI. most specific method for establishing the diagnosis of a new infection?
CK-MB
troponin will be elevated for 2 weeks LOS
Best initial treatment for ACS
Aspirin administered PO.
Instant effect on inhibiting platelets.
Mortality reduction of aspirin for ACS
Reduces 25% mortality of acute MI
Reduces 50% for “unstable angina”
Other treatments for ACS
-Clopidogrel or ticagrelor (Acute MI)
-Prasugrel (angioplasty)
-Nitrates and morphine (no effect on mortality)
-O2 if pt is hypoxic.
Mechanism of P2Y12 Antagonists
Clopidogrel, prasugrel, and ticagrelor block aggregation of platelets to each other by inhibiting ADP-induced activation of the P2Y12 receptor.
Prevention Tx angioplasty or stent
Clopidogrel, prasugrel, and ticagrelor
(inhibit ADP activation of platelets)
Time critical Tx that lowers mortality in STEMI
Angioplasty preformed within 90 minutes of arrival at ED (does not depress mortality for stable angina)
If angioplasty cannot be preformed: thrombolytics wishing 30min of arrival at ED.
Indication for thrombolytics
chest pain <12hrs
ST elevations >1 leads
New LBBB
Tx that lowers mortality in STEMI
Beta Blockers (not time critical)
(prioritize aspirin, thrombolytics and angioplasty)
Mortality reduction of ACEi/ARBs
Will only lower mortality if there is left ventricular dysfunction or systolic dysfunction.
HMG CoA protocol for CAD/ACS
give HMGCoA to all patients with CAD or ACS.
regardless of LDL level, EKG, troponin or CK-MB level.
Greatest single efficacy in lowering mortality in STEMI?
Angioplasty or PCI or Thrombolytics (unless contraindicated)
Mechanism of thrombolytics
Thrombolytics activate plasminogen into plasmin. Plasmin cleave fibrin strands into D-dimers.
Plasmin can only cleave fibrin prior to stabilization by factor XIII
Mechanism of BBlockers in MI
Prevents ventricular aTrrhythmia brought on by ischemia. Slower heart rate ^ time for artery perfusion. Increased left ventricular filling time increases both SV and CO
BB are anti-arrhythmic and anti-ischemic
72yo man. Chest pain 1hr. EKG: ST elevation leads V2-V4. Aspirin given.
most likely benefit patient?
Angioplasty will lower the risk of mortality most.
give metoprolol before sending home
ACS Tx that always lower mortality
Aspirin
Thrombolytics
Primary Angioplasty
Metoprolol
Statins
P2Y12 inhibitors
ACS Tx that only lower mortality in certain conditions
ACEi/ ARBs- low ejection fraction
Heparin- ST depression
ACS Tx that do not lower mortality
Oxygen
morphine
nitrates
CCBs
Lidocaine
Amiodarone
Pacemaker for acute MI
Third-degree AV Block
Second degree AV Block (Mobitz II)
Bifascicular block
New LBBB
Symptomatic Bardycardia
Aspirin Allergy Alternative
-grel (P2Y12)
Intolerance to Beta Blockers
-reaction
-alternative
Alternative: Verapamil or Diltiazem (CCB)
BB intolerance: Reactive Airway, cocaine - induced chest pain, coronary vasospasm
Prasugrel vs Clopidogrel
Prasugrel has grater efficacy but it increases bleeding in >75yo and <60kg
Sxs MI complication
All complications of MI lead to hypotension
Management of MI complication:
Cardiogenic Shock
Dx: Echo, Swan-Ganz (right heart), catheter
Tx: ACEi, urgent revasularization
Management of MI complication:
Valve Rupture
Dx: Echo
Tx: ACEi, nitroprusside, intra-aortic ballon as a bridge to therapy
Management of MI complication:
Septal Rupture
Dx: Echo, right heart catheter showing a step up in saturation from the right atrium to the right ventricle.
Tx: ACEi, Nitroprusside and urgent surgery
Management of MI complication:
Myocardial wall rupture
Dx: Echo
Tx: Pericardiocentesis, urgent cardiac repair
Management of MI complication:
Sinus Bradycardia
Dx: EKG
Tx: Atropine, followed by pacemaker if there are still symptoms
Management of MI complication:
Third-degree (complete) heart block
Dx: EKG, con “a” waves
Tx: Atropine and pacemaker even if symptoms resolve
Management of MI complication:
right ventricular infarction
Dx: EKG showing right ventricular leads
Tx: Fluid loading
Mechanism of septal rupture systolic murmur
Left ventricular pressure is grater than right ventricular pressure. Left to right shunt go oxygenated blood.
SaO2 increased RV compared to RA
Post MI wait for sexual activity
can resume sex within several days if there are no further symptoms of chest pain or dyspnea.
Management of Non- STEMI
-No thrombolytic use
-Heparin use routinely (LMWH > IV unfractionated)
-Glycoprotein IIb/ IIIa inhibitors lower mortality sp. with angioplasty
54yo Man. PMHx DM HTN. Substernal Chest Pain radiates Left Arm. Previously with exercise now on rest. EKG normal. Troponin elevated. Aspirin, O2, nitrates give. Most likely benefit?
LMW Heparin (Shown to lower mortality in NSTEMI)
GPIIb/IIIa
Angioplasty/ PCI
GPIIb/IIIa inhibitors
GPIIb/IIIa work best in combination with angioplasty and stent.
epitibatide
tirofiban
abciximab (doesnt benefit STEMI)
Mechanism of Heparin
Potentiates the effect of antithrombin.
antithrombin inhibits almost every step of clothing cascade. does not work with antithrombin deficiency. (only prevents new clots)
Chronic CAD Further Management
Aspirin & Metoprolol
Nitrates for angina pain (no benefit for mortality)
ACEi/ARBs (only for stable cases with CHF, systolic dysfunction, low ejection fraction)
Can initiate without doing angiography
Aspirin + metoprolol
Nitrates (pain)
ACEi/ARBs (low ejection fraction)
GPIIb/IIIa
Statins
Ranolazine (if pain persists)
Indications for CABG
Angiography needed to determine use of CABG
-three coronary vessels >70% stenosis
-Left main coronary artery stenosis >50-70%
-2 vessels in a diabetic
-2 or 3 vessels with low ejection fraction
Main difference between saphenous vein graft and internal mammary artery graft?
internal mammary artery graft remains open for 10 years.
Vein grafts start to become occluded after 5 years.
no difference in need for medications
Hyperlipidemia management standards
Statins- every patient with CAD abd strike. Most DM. Definitely the choice for >7.5% 10 year mortality.
Proprotein convertase subtilisin Kexin type 9 (PCSK9) inhibitor (no known mortality benefit)
Goal of Hyperlipidemia TX in CAD and diabetes
LDL <70mg/dL
CAD equivalents that require a statin for any level of LDL
PAD
Aortic Disease
Carotid Disease
Cerebrovascular Disease
Rick Factors in lipid management
-Tobacco use (cigarette smoking))
-HTN (>140/90 or on BP meds)
- Low HDL cholesterol (<40mg/dL)
-Fx early coronary heart disease (Fm <65, Male <55)
-Age (males> 45, females >55)
Statin liver toxicity
Liver Toxicity
Raised transaminases
(check LFTs)
Rhabdomyolysis (less common)
(check CPK)
mechanism of PCSK9 inhibitor
injectable medications which block the clearance of LDL by the liver from the blood.
works well in familial hypercholestolemia
PCSK9 inhibitor medications
Evolocumab and alirocumab
Erectile dysfunction post MI
cause: anxiety.
BB is mcc of medication related ED, Anxiety is the MCC of post infarction MI
ED post MI. going to start sildenafil.
First stop?
Nitrates
contraindicated with sildenafil.
together can cause severe hypotension
CHF symptoms
SOB
Edema
Rales on Lung
Ascities
JVD
S3 gallop
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue
Mechanism of rales
increased hydrostatic pressure develops in pulmonary capillaries from left heart pressure overload.
Transudation of liquid into alveoli.
During inhalation alveoli “pop” open
Worst manifestation of CHF
pulmonary edema (clinical diagnosis for CHF)
First step in management in pulmonary edema
more important than diagnostic tests is to remove volume from vascular system (thus from the lungs)
Sxs pulmonary edema
SOB
rales
S3
orthopnea
Pulmonary edema on CCS
move the clock forward no more than 15-30min at a time for all acutely unstable ICU or ED patients.
order:
CXR,
EKG,
Oximeter
Echo
Initial Therapy (O2, Furosemide, nitrates, morphine)
Mechanism of carvedilol
B1 B2 and A1 receptor antagonist
anti-arrhythmic, anti-ischemic and antihypertensive
Pulmonary edema on CXR
pulmonary vascular congestion
cephalization of flow
effusion
cardiomegaly
Pulmonary edema on EKG
Sinus Tachycardia
Atrial and ventricular arrhythmia
Pulmonary edema on Oximeter or ABG
Hypoxia
Respiratory Alkalosis
Pulmonary edema on echo
Distinguishes systolic from diastolic dysfunction
63yoW acute severe SOB, rales present, S3 gallop and orthopnea. Next Step?
Oxygen, Furosemide, nitrates and morphine.
mainstay treatment no mortality benefit.
If no response- positive inotrope
Mechanism of “cephalization” of flow
Bases of Bottom of the lungs are generally more “full” of blood because of gravity. Fluid build up fills the vessels from the bottom to the top (head/ cephalization).
Mechanism of Dobutamine, Inamrinone, and Milrinone
Phosphodiesterase inhibitors. Increase contractility, decrease after load.
Dobutamine less effective if Pt on BB
Mechanism of respiratory alkalosis in CHF
Fluid overload –> hypoxia –> hyperventilation –> decreased pCO2 –> alkalosis
hypoxia causes respiratory alkalosis
TX: Acute CHF
Preload reduction to control acute symptoms
if no response- positive inotrope.
Never use DIGOXIN for acute (slows CHF
TX: chronic CHF
Echocardiogram once stabilized to establish systolic vs diastolic dysfunction
Tx: CHF systolic dysfunction
ACEi/ ARBs & Beta Blockers
Digoxin
Mineralocorticoid receptor antagonist
if counterindicated or if not responding : Hydralazine + nitrates
