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208 Cards in this Set
- Front
- Back
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Key point of flow vs flow velocity
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A vessel w/ large cross sectional area but same flow has a smaller flow velocity
Atherosclerotic plaque: decr area -> increased velocity Q = cm^3/sec V = cm/min = Q/Area = cm^3/sec/cm^2 |
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Mean Arterial Pressure
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(SP + 2DP) / 3
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Measurement of Cardiac Output
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Using doppler
A (cm^2) * V (cm/min) = Q (cm^3/min) Measure Q - coronary artery flow |
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Explain the diacrotic notch
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After peak pressure in arteries, as pressure is falling, the arteries recoil, creating a slight increase in pressure
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Holosystolic apical murmur
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Mitral regurgitation
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Systolic ejection murmur
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Aortic stenosis
(Harsh systolic ejection murmur over left parasternal intercostal 3-4 is VSD) |
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Normal chamber pressures
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RA: 2-6
RV: 15-30 / 2-6 PA: 15-30 / 6-12 LA/PCWP: 6-12 LV: < 130 / 10 |
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Continuous machine murmur
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Patent ductus arteriosus
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Ionic basis of phase 4 depolarization
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In the cardiac pacemaker MAP
Phase 4 = spontaneous depolarization: Decreased K+ current in due to increased membrane resistance + inactivation of K+ channels -> depolarization AP is carried by Ca+ in |
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Effect of catecholamines on prepotential phase 4 depolarization
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NE/E: B1 receptors -> incr cAMP -> inactivates more K+ channels to increase the slope of phase4 depolarization
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Effect of Ach on prepotential phase 4 depolarization
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Ach binds muscarinic receptors (GPCR) linked to K+ channels -> increases K+ conductance -> hyperpolarization
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Ionic basis of non pacemaker cardiac APs (5 phases 0-4)
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Phase 0 - Na+ channel activation is voltage dependent
Phase 1 - Na+ inactivation w/ slight repolarization and slight K+ channel opening Phase 2 - K+ channels close and Ca+ channels open for plateau phase Phase 3 - Ca inactivation and K activation Phase 4 - resting potential maintained by inward rectifying K+ channels which do not permit outward movement of K+ |
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Relationship b/w electrical and mechanical activity in myocytes
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Plateau phase 2 of MAP due to increased Ca+ also provides Ca for sarcomere activation and contraction
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Why is the T wave the same deflection as the P wave on lead I
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Because APs get shorter and shorter towards the ventricular apex, so the apical cells are the first to repolarize even though the last to depolarize
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Starling's Law of the Heart
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Relation b/w EDV/preload and Force or SV
Increased rest length/EDV increases Force/SV |
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How do positive and negative inotropic agents affect Starling's law?
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B1 agonist increases curve and B1 antagonist decreases curve
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Starling's Law: homeometric vs heterometric changes
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Homeometric: B1 agonist increases Force/SV at a given rest length/EDV
Heterometric: Force/SV increases w/ rest length/EDV |
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Mechanisms for Starling's Law heterometric change (2)
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1) Stretching myocytes makes increased overlap b/w thin and thick filaments
2) Longer muscles need less Ca++ to generate the same force |
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Initial velocity of shortening and afterload and inotropic affects
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As afterload increases, velocity of shortening decreases
Increases rest length (preload) makes muscle capable for shortening against a greater afterload) Inotropes increase the curve: for a given afterload there is increased velocity of shortening VMAX IS SAME FOR ANY GIVEN REST LENGTH |
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What cellular mechanisms explain the changes in VMax w/ inotropic agents?
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Epinephrine increases myosin ATPase and increases Ca delivery to contractile proteins
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What takes place during S3?
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1st rapid filling of ventricle when mitral valve opens
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What takes place during S4?
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Second rapid filling of ventricle when atria contract
abnormal to hear. |
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When does PCWP not equal LVEDP?
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Mitral stenosis
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Hemodynamic tracing: systolic LV > aortic
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Aortic stenosis
Systolic murmur |
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Hemodynamic tracing: diastolic LA > LV
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Mitral stenosis
Diastolic rumble murmur |
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Hemodynamic tracing: increased v wave
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Mitral regurgitation
Backflow of blood during systole into LA increases LA pressure |
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Cardiac output determinants
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CO = SV X HR
SV determinants: preload, afterload, contractility |
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Afterload definition
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Wall stress = pressure * radius / 2*wall thickness
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Shock: incr chamber pressure, decr CO, incr PVR
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Cardiogenic shock (MI)
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Shock: decr chamber pressure, decreased CO, incr PVR
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Hypovolemic shock (bleeding, dehydration)
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Shock: normal decr chamber pressures, incr CO, decr PVR
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Septic shock (toxins cause decreased PVR)
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Shock: decreased R but normal L chamber pressures, decr CO, incr PVR
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Pulmonary embolism
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Major characteristic difference b/w large and small arteries
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Large have elastic and small have muscle
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What is the main function of peripheral vasculature autoregulation?
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Tissue blood flow remains constant regardless of arterial pressure
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2 mechanisms of peripheral vasculature autoregulation
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Myogenic response - incr pressure stretches smooth muscle -> activates stretch channels -> incr Ca++ -> vasoconstriction
Dilator metabolite - incr flow -> dilution of dilator metabolites -> inhibition of metabolites' effect -> vasoconstriction |
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Why can't the myocardium incur an O2 debt? (3)
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1) Because O2 delivery is flow limited, muscle extracts all the O2
Only way to increase O2 supply is to vasodilate 2) Heart can only rest during diastole 3) LV myocardium has very limited flow during systole due to contraction |
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How does ventricular enlargement in disease affect O2 supply?
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Increased ventricle -> increased radius -> Law of Laplace: at a large radius it take more muscle (ATP) to generate enough pressure to contract
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Coronary circulation autoregulation (vasocontrictors and vasodilators)
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constrict: a1 receptors
dilate: adenosine released by muscle |
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Neural regulation of blood pressure
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Baroreceptors innervated by CN IX and X respond to wall stretch in aortic arch and carotid sinus -> medulla
Most sensitive b/w 75-125 mmHg -> incr firing rate -> decrease symp and increase parasymp tone |
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a1 receptor activation
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incr SVR
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B1 receptor activation
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increase HR and contractility
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Mechanisms leading to restoration of arterial BP from high pressure
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1. decr B1 adrenergic receptor activation
2. incr muscarinic @ SA node 3. decr a1 in blood vessels -> 4. vasodilation -> decr venous return -> decr SV and CO |
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Main risk factors for Coronary artery disease (5)
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HTN
DM Dyslipidemias FH Smoking |
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Main determinant of myocardial O2 supply
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Vascular resistance
NO is most important vasodilator, produced by the endothelium |
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Main determinant of myocardial O2 demand
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Heart rate
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Cardinal symptoms of CAD
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Angina and shortness of breath
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Pathophysiological consequences of myocardial ischemia
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Diastolic -> systolic dysfunction -> elevated ventricular filling pressures before ECG changes or symptom onset
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Unstable angina vs STEMI and NSTEMI
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UA does not have cardiac enzyme changes
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STEMI pathogenesis and treatment
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Disruption of a once stable plaque causing a complete/total occlusive thrombus
Rx - immediate thrombolytic therapy or balloon angioplasty |
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Pathogenesis of unstable angina and NSTEMI (5) and (differentiate from STEMI)
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(Incomplete occlusion is main contrast to STEMI) - occlusion due to:
Thrombosis Vasoconstriction Mechanical obstruction Increased myocardial O2 demand Inflammation |
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Hibernating vs stunned myocardium
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Both have to do with myocardium that doesn't contract.
Stunned happens after an MI while hibernating does not |
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Pathologic hallmark of acute coronary syndromes
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Coronary atherosclerotic plaque rupture or disruption a/w intraluminal platelet-fibrin thrombus
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MI macroscopic pathology at 4 time points
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After 24 hours - cut pallor surface
3-7 days - sharply outlined area with central pale, yellow necrosis 10-14 days - depressed, soft, gelatinous area > 14 days - healed infarcts are firm and necrotic |
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MI microscopic changes <24 hours
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< 24 hours - Non-contractile ischemic myocytes show wavy fibers, contraction band necrosis, deeply eosinophilic, wavefront
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MI microscopic changes 1-3 days
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Coagulation necrosis w/ loss of nuclei
PMNs Interstitial edema and hemorrhage |
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MI microscopic changes 5-10 days
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Few PMNs
Early granulation tissue Fibroblast proliferation w/ collagen deposition Lymphocytes and pigmented macrophages |
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RCA occlusion
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Inferoposterior LV
Posterior 1/3 of IV septum |
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LCircumflex occlusion
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Lateral wall LV w/o apex
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Mean Cardiac Vector (what does it mean?)
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Mean direction of QRS vector
Eg it would be lead I in LV hypertrophy 1) add magnitude of QRS 2) drop perpendicular of magnitude on lead line Or simply find lead that has QRS summing to zero and the MCV is perpendicular |
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Pauses w/o P waves
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Sinus node dysfunction
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1st degree AV block (ECG feature and site)
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No block - P waves are all followed by QRS
Delay in conduction so that PQ interval is > 200 ms (1 large box) Site is at AV node |
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2nd degree AV block
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Only one P wave is blocked
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Mobitz I 2nd degree AV block
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Blocked P wave is preceded by a PR interval that is longer than the one that follows the blocked P wave
No Rx Site is AV node |
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Mobitz II 2nd degree AV block (2 ECG findings, site)
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PR intervals before and after non conducted P wave are fixed in length
Wide QRS Block is infra-nodal Can procede to complete AV block -> intervene w/ pacemaker |
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3rd degree AV block (complete block) (ECG findings, path of rhythm)
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All P waves are blocked - no relation b/w P and QRS -> escape rhythm:
if high block - narrow QRS escape @ 60 bpm if low block - wide QRS escape < 40 bpm -> life threatning |
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Evolution of MI on ECG (3)
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Acute - ST elevation
1 -2 Days - T wave inversion, Q wave deepens Weeks - ST and T normal, Q wave persists |
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PAC vs PVC
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Premature beats - ectopic
If preceded by P wave - atrial If wide and not preceded by P wave - ventricular |
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Bradyarrhythmias (2)
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Sick sinus syndrome
AV conduction abnormalities (2nd or 3rd degree) |
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Tachyarrhythmias (6)
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Supraventricular - AT, AVRT, AVNRT, Afib
Ventricular - Vtach, Vfib |
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Atrial fibrillation
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Irregularly irregular ventricular rhythm
Atrial rates at 350-600 bpm ECG - fibrillatory baseline w/ irregular activity, no discernible p waves |
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Atrial flutter (path, ECG)
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Macroreentrant tachycardia originating in right atrium involving tricuspid annulus
Regular ventricular rhythm Sawtooth ECG |
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Paroxysmal supraventricular tachycardia (3 types, most and least common?, ECG)
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AV node reentrant tachycardia (most common)
AV reciprocating tachycardia Focal atrial tachycardia (least common) ECG - P waves hidden, regular rhythm |
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Sinus node dysfunction (2)
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Sinus pauses > 3 s
Tachy-brady syndrome - atrial fibrillation terminating in a pause |
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How do AVNRT and AVRT differ from AT?
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AVNRT and AVRT are AV node dependent.
Interruption of AV node conduction terminates these tachyarrhythmias |
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Factors associated w/ Afib (1 main, 5-6 secondary)
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HTN
Age, cardiomyopathy, valvular disease, alcohol, OSA |
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Afib complications (3)
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Palpitations
Thromboembolism Heart failure |
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AVNRT vs AVRT path
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AVNRT - blocked fast pathway w/ reentry into slow pathway
AVRT - bypass tracts |
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Retrograde P waves in I, II, V1-V3
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AVNRT
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Wolff Parkinson White / Preexcitation
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Form of AVRT
Delta waves |
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SVT management (4)
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Vagal maneuvers
IV adenosine IV CCBs IV beta blockers |
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Mitral Stenosis Path and Signs
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Incr LA pressure -> incr pulm pressure -> eventually incr RV pressure -> RV hypertrophy
Elev JVP, pulm edema |
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Main cause of mitral stenosis?
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Rheumatic heart disease
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Mitral Regurgitation/Incompetence Path
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Backflow of blood to LA -> LV has to work harder to maintain CO -> LV hypertrophy and failure
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Aortic Stenosis Path and Signs
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Decreased output -> angina and syncope
LV hypertrophy |
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3 causes of aortic stenosis
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Rheumatic 60-70 y/o
Calcification of abnormal bicuspid < 60 y/o Senile calcification > 70 y/o |
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Floppy Mitral Valve / Mitral Valve Prolapse
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Connective tissue anomaly -> mitral regurgitation
Young women Mid systolic click |
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Rheumatic fever pathogen (cause and path result)
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Group A beta hemolytic streptococcal pharyngitis
Aschoff nodules |
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Infective endocarditis (2 forms)
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Acute - normal valve, virulent organism -> high mortality
Subacute - abnormal valve, low virulence organism -> low mortality |
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Infective endocarditis: predisposing factors and path (4)
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RHD
Prosthetic / Abnormal valves Immunosuppression / IV drugs Sites of infection Path - bulky friable destructive vegetations occur anywhere on valve |
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Main differences b/w rheumatic and infective endocarditis (4-5)
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Rheumatic - small, minimal valve destruction, Aschoff, adherent
Infective - any site on valve, large, valve destruction, infl cells/organisms, friable |
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Two main functions of anti arrhythmic agents
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Maintain sinus rhythm after Afib
Reduce frequency of Vtach and Vfib |
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Triggered activity: early afterdepolarization (path and what drugs cause it?, what ecg does it result in?)
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Refractory period of cell is prolonged -> if too long spontaneous depolarization occurs from phase 3
Results in polymorphic Vtach Can happen form K+ blocking drugs |
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Mechanism of Vtach
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Reentry around scar from previous MI
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Mechanism of Afib
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microreentry in LA
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Main mechanisms of anti arrhythmic agents (4)
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Block Na channel (slow conduction)
Beta adrenergic receptor blockers (target AV > SA node to slow) Block K+ channel (extend refractory period) CCBs (target AV > SA node) |
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Use dependence vs reverse use dependence
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Use dependence - more effective/TOXIC when HR is rapid, Na blocers (drugs interact more with the receptors when they are in open or inactive states)
Reverse use dependence - more effective/TOXIC when HR is slow, K+ blockers (drugs interact with receptor in resting state) |
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Class I AAA (3 subclasses)
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IA - Na and K blockers; quinidine
IB - for Vtach; lidocaine IC - Na blockers; propafenone, flecainide; prevention of Afib- contraindicated in structural HD |
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Class II AAA (2 uses)
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Beta blockers
Control ventricular rate in Afib/flutter Prevent recurrence of PSVT |
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Class III AAA
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K+ channel blockers
Dofetilide, sotalol, amiodarone |
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Class IV AAA (2 uses)
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non-dihydropyridine CCBs
Diltiazem, verapamil Block AV node in pts w/ Afib/flutter Prevent PSVT recurrence |
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How to choose which AAA for AF?
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If not structural heart disease IC (Na blockers propafenone + flecainide)
If structural heart disease III - sotalol, amiodarone |
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How to choose which AAA for Vtach/Vfib?
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Heart failure status I-II sotalol (class III)
III-IV - amiodarone (class III) |
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Heart failure definition and Frank Starling curve
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heart's inability to meet metabolic demands w/o exceeding left and right filling pressures
With increased preload there is not a normal increase in stroke volume |
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Heart failure predisposing factors (3)
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Hypertension
CAD DM |
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Heart failure: systolic dysfunction
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Impaired contractility and decreased EF
LV dilatation and remodeling Causes: ischemic heart disease, chronic volume overload, cardiomyopathy |
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Heart failure: diastolic dysfunction
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Impaired ventricular filling during relaxation (impaired relaxation or increased stiffness or both)
LV shows concentric hypertrophy but not dilation Causes: HTN |
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Heart failure: ventricular remodeling and myocardial hypertorphy
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Response to increased pressure or volume to normalize wall stress
Continues unchecked resulting in abnormal myocyte proteins |
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Heart failure therapies (4)
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ACEi + ARB
aldosterone blockers Hydralazine + nitrates Beta blockers |
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Digoxin
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Heart failure therapy
Inhibits Na/K ATPase which increases intracellular Ca |
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What do high and low shear stress cause in the arteries?
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Low shear stress at bifuractions -> atherosclerosis
High shear stress (like post aortic arch) -> dilation |
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Claudication
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Pain experienced in limb upon activity and relieved w/ rest (cramping characters)
(vs rest pain - inadequate blood flow at rest, dull aching pain, pallor) |
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Arterial pathophysiology (what is the response to stenosis? (3))
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1) collateral pathways develop enlarge
2) arterial dilation (can cause rubor) 3) enhanced muscle metabolism and O2 extraction |
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Limb threatened ischemia
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In setting of thromboembolism from AF
Pain Pulseless Paralysis Pallor Parasthesia |
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Claudication Rx (5)
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Risk mod (smoking cess)
Exercise PDE inhibitors Endovascular therapy Bypass surgery |
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Abdominal Aortic Aneurysm (most common site, 2 types)
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Infra renal aorta is most common site
True - contains all 3 vascular layers, develops due to collagen degradation and weakening of matrix Fale - doesn't contain all 3 layers, usually complication of cardiac cath |
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Aortic dissection (path, 2 types)
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Spontaneous disruption of intima creates false channel
Type A - ascending aorta, immediate surgical intervention Type B - descending aorta, meds |
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Subclavian steal syndrome
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Occlusion of proximal subclavian -> retrograde vertebral flow
CNS symptoms w/ exercise but most asymptomatic |
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Risk of stroke if TIA from carotid
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13-30%
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DVT risk factors
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Virchow's triad - hypercoagulability, stasis, endothelial injury
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DVT Rx (3)
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Immediate anticoagulation w/ heparin -> coumadin 6 months
Leg elevation IVC filter |
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Secondary causes of dyslipidemia (5)
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Hypothyroidism
DM Obstructive liver disease Chronic renal failure Meds - anabolic steroids, glucocorts, progestins |
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What is the LDL goal of someone w/ FRS > 20%?
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< 100
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Statins SE (2)
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myalgias
rhabdo |
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Fibrates
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PPAR alpha agonists -> decrease TG by decreasing apo C-II for enhanced clearance of lipoproteins
(apo CII allows TG in VLDL to serve as a substrate for lipoprotein lipase in tissues) |
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Ezetimibe
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Blocks intestinal cholesterol absorption -> upregulation of LDL receptors
Minimal side effects Use in combo w/ statin |
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Anion exchange resins
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Bind bile acids in intestine -> excreted in stool -> liver uses cholesterol to make more -> increase LDL receptor
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Cholestyramine, colestipol, colesevalm
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Anion exchange resins
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Niacin
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B3
Raises HDL 30%, lowers LDL 15%, lowers TG 30% |
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CHD Risk factors (5)
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Smoking
HTN HDL < 40 FH (CHD in male < 55, female < 65 Age (male >45, female > 55) 2 or more = high risk |
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Fish oil
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Decreases VLDL and TG
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What drug for someone with low HDL?
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Niacin
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What drug for someone with high TG?
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Fibrates
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Congenital Heart Disease: Trisomy 21
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Complete AV canal defect
One AV valve instead of two |
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Congenital Heart Disease: Turner Syndrome
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Coarctation of aorta
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Congenital Heart Disease: DiGeorge
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Conotruncal and arch abnormalities
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What cells contribute to endothelial cushions?
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Neural crest cells
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Ventricular septal development (3 parts)
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1) septum of AV canal from AV canal cushions
2) muscular septum from ventricles 3) outflow tract septum (infundibular or conal septum) |
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Tetralogy of Fallot
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Most common cause of congenital cyanosis
Failure of septum to fully fuse -> VSD + Overriding aorta + Pulmonary stenosis -> RV hypertrophy |
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Transposition of great arteries (embryological cause)
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RA -> RV -> aorta -> RA
LA -> LV -> pulmonary -> LA Two separate loops Failure of normal septation of truncus arteriosus Must have a VSD or ASD to survive |
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Hypoplastic left heart syndrome
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Usually stenosis or atresia of mitral and/or aortic valves
Treat by surgically converting the RV to the main systemic ventricle |
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Eisenmenger's Syndrome
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ASD or VSD -> L-R shunting -> incr pulmonary blood flow -> incr pulm resistance -> decr pulm blood flow -> reversal of shunting to R->L
Aim of intervention is to prevent Eisenmenger's |
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Eisenmenger's syndrome a/w:
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Cyanosis
Hyperviscocity Brain abscesses Hyperuricemia Gall stones |
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Most common congenital heart disease in children
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ASD
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Most common congenital heart disease at birth
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VSD by a lot
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Atrial septal defect (results in, 2 symptoms)
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RV overload
Rarely causes Eisenmenger's Symtpoms: URTI, Afib |
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Ventricular septal defects (two types, what kind of murmur?)
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Restrictive - small VSD, loud murmur, no Eisenmenger
Non-restrictive - large VSD, no murmur, Eisenmenger PE: holosystolic murmur |
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Coarctation of aorta (symptoms, one PE sign)
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HTN, lower body fatigue
Back bruits |
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AAA for rate control (3)
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Beta blockers
Non dihydro CCBs Digoxin |
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AAA for restoring and maintaing sinus rhythm
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Class Ia,c, III
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Dilated cardiomyopathy (pathophys, most common cause, clinical)
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By far most common cardiomyopathy (90%)
All four chambers are dilated w/ hypertrophy (esp LV) Chronic alcoholism Insidious 20-60 y/o |
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Dilated cardiomyopathy (path and hist)
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Globoid heart, flabby+pale myocardium
Hypertrophic and atrophic myocytes w/interstitial fibrosis |
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Etiologic factors a/w dilated cardiomyopathy (4)
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Chronic alcoholism
Viral infections Anthracycline (vacuolar degeneration of myocytes) Peripartum |
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Hypertrophic cardiomyopathy (genetics, epi)
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Autosomal dominant B-myosin heavy chain defect
Young males |
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Hypertrophic cardiomyopathy (path and hist) (3)
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LV hypertrophy
Septal thickening Myofiber disarray in IV septum |
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Restrictive cardiomyopathy (define and 2 common causes)
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Myocardium infiltrated w/ material that impairs ventricular filling
Common causes: amyloidosis and hemochromatosis |
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Hemochromatosis
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Abnormal iron deposition in myocytes
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Myocarditis: 3 main causes
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Idiopathic
Infectious - viral, bacterial, rickettsial, chlamydiae, fungi, parasites Non-infectious - hypersensitivty and immune related (SLE, RHD), radiation |
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Viral myocarditis path
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Hx - URTI
Patchy or diffuse interstitial infiltrate of T lymphocytes, macrophages, w/ focal myocyte necrosis |
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Myocarditis in AIDS
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Cardiac disease in upto 50% of AIDS pts
Most patients are asymptomatic |
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Chagas disease path
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T. Cruzi infection transmitted by reduviid bug
Myocardial involvement in 10-40% of infected individuals |
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Chagas two clinical forms
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Acute: 1-2 wks post infection -> chagoma w/ fever and swollen lymph. 2-3 wks, parasitemia, pseudocysts in myocardium
Chronic: 32% of infected have fatal damage to heart and GI tract -> ventricular dilation, chronic inflammation w/ myocyte necrosis |
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Aortic stenosis pathophys
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LV pressure overload -> concentric hypertrophy (incr wall thickness) to normalize wall stress
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Aortic regurgitation etiology (2)
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Primary valve etiology - eg Congenital heart disease, RHD, endocarditis
Primary aortic root dilatation - rheumatoid syndromes, marfan's, athero |
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Aortic regurgitation pathophys
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Chronic volume overload in LV ->
Eccentric hypertrophy Dilation and hypertrophy A large EDV can somewhat compensate for the reduced SV |
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Bounding pulses and wide pulse pressure
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Aortic regurgitation
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Mitral stenosis pathophys
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Incr LA pressure ->
Dilation -> Incr pulm pressure -> pulm edema and SOB ->-> eventually RV hypertrophy and failure |
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Loud S1 w/ opening snap
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Mitral stenosis
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Mitral regurgitation etiology (6)
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Rheumatic HD
MVP Papillary muscle dysfunction Endocarditis LV dilation Marfan's |
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Mitral regurgitation pathophy
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LV volume overload -> hypertrophy and dilation ->
incr LAP -> incr pulm pressures and RV failure |
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Tricuspid regurgitation (secondary to?)
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Usually secondary to RV and annular dilation
Endocarditis in IVDA Large V waves and venous congestion |
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Pericarditis (common symptoms and causes
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Sharp, well localized pain relieved by leaning forward
Acute viral or idiopathic |
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Pericarditis ECG and Rx
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ECG - diffuse ST elevation
Rx - NSAIDs |
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Pericardial tamponade signs and symptoms (4 important signs)
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Fatigue and SOB
Pulsus paradoxus Beck's triad - hypotension, incr JVP, muffled heart sounds CXR - cardiac sillhuoette |
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Constrictive pericarditis signs and symptoms
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JVP w/ Kussmaul sign (changes in JVP w/ respiration)
Prominent y descent and square root sign pericardial knock |
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2 indications for heart transplant
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Ischemic heart disease
Dilated cardiomyopathy |
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3 problems influencing course of heart transplant patients
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Acute allograft rejection
Cardiac allograft vasculopathy Infections |
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Acute allograft rejection (pathophys, path)
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Recipient recognizes graft antigens
Interstitial lymphocytic infiltrate -> necrosis and vessel injury |
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Graft atherosclerosis
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Vascular disease effecting all vessels of graft heart
Concentric, diffuse thickening of intima -> occlusion |
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V wave
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Pressure in atria before mitral/tricuspid valve opens
If regurgitation -> increased V wave due to increased blood |
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Aspirin (use and SE)
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Secondary prevention (for people who already had events)
Not for primary prevention b/c of SE: GI/CNS hemorrhage |
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Aspirin mechanism
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Irreversibly blocks cyclooxegenase mediated synthesis of thromboxane A2 (platelet aggregator)
Does not block irreversibly in endothelium b/c endo can regenerate COO |
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Adenosine diphosphate (ADP) blockers
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Adjunctive therapy in acute coronary syndromes
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Nitrates mechanism
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Reduction in preload via venous dilation
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Nitrates interactions
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Don't use with PDE5 inhibitors since both increase cGMP -> excessive vasodilaiton
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Beta blockers mechanism
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Decrease myocardial oxygen consumption by lowering heart rate and contractility
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Beta blockers use
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Chronic angina and post MI
Especially good for SNS like anxiety |
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Beta blockers ISA
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Can't use in patients w/ cardiovascular disease since they have intrinsic sympathomimetic activity
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CCBs type I vs type II (effects and use)
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Type I - electrophysiologic and dilatory effects
Used for tachycardic arrythmias Type II - no electrophys effects, just vasodilators so used in angina |
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Main angina therapy
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Aspirin and prn nitrates
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Nidefipine, amlodipine
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Type II CCBs used to treat angina
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Commonly used conduits for CABG
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Left internal mammary artery (best long-term patency)
Saphenous vein Radial artery (rarely) |
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Hibernating myocardium
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Impaired LV myocardium that can recover after ischemia if revascularized as long as myocardium retained its viability
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Aortic and mitral valve repair or replacement?
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Aortic - replace
Mitral - repair |
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c-ANCA
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cytoplasmic (to proteinase-3)
Wegener |
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p-ANCA
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perinuclear (to myeloperoxidase)
Microscopic polyangitis (hypersensitivity vasculitis) Churg-Strauss |
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Medium arteries, usually carotid branches)
Focal granulomatous inflammation w/ internal/external elastic lamina destruction Elev ESR |
Temporal (Giant cell) arteritis
Rx - steroids |
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Female < 40 y/o
Medium - large arteries Aortic arch Weak pulses Focal granulomatous inflammation |
Takayasu's arteritis
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Young adults
Nodular lesions (OF DIFFERENT AGES) of small or medium muscular arteries Fibrinoid necrosis Spares lung and spleen |
Polarteritis nodosa
A/w hepB Rx - corticosteroids |
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40 y/o
c-ANCA Necrotizing or granulomatous vasculitis small vessels |
Wegener's
Rx - steroids |
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Acute necrotizing inflammation of small vessels
All lesions of same age Skin lesions p-ANCA |
Hypersensitivity vasculitis/Microscopic polyarteritis
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Middle aged w/ new onset or worsening asthma
Peripheral neuropathy p-ANCA Eosinophilia |
Churg Strauss
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Child
Rash on buttocks and legs IgA immune deposits in small vessels |
Henoch-Schonlein Purpura
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< 35 y/o smoker
Small - medium vessels Gangrene Granulomatous inflammation leading to thrombosis and microabscesses |
Buerger's disease
Rx - smoking cessation |
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What is the most common primary cardiac tumor? (adults vs children)
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Adults - Myxoma "ball-valve" obstruction in LA -> syncope
Children - rhabdomyoma (a/w tuberous sclerosis) |
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When is rupture of LV wall most likely to happen after MI?
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5-10 days
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When is arrhythmia most likely to happen after MI?
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1-4 days
(ventricular arrhythmia after weeks) |
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Descrescendo diastolic murmur over left 2nd interspace
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Aortic regurgitation
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Holosystolic murmur w/ S3 gallop over apex
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Mitral regurgitation
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