CARDIO Flashcards
Digoxin MOA
- slows ventricular rate during afib by ENHANCING VAGAL TONE
- leads to inhibition of AV nodal conduction
- positive inotropic effect via INHIBITION of the Na+/K+-ATPase pump=INC intracellular calcium and greater contractility
WPW CP
- palpitations
- no CP or dyspnea
- AV conduction tract bypasses the AV node (accessory pathway bypasses AV node and directly connect atria and ventricles)…triad:
- short PR inteval
- widening of QRS interval
- slurred and broad upstroke of QRS complex=DELTA WAVE
mechanicla complications of acute MI
- RV failure (acute)
- hypoTN, clear lungs, Kussmaul sign
- papillary muscle rupture (3-5days)
- acute, severe pulm edema
- severe/acute onset MR with flail leaflet
- interventricular septum rupture defect (3-5d)
- hew holosystolic murmur
- stepped-up oxygen level between right atrium and ventricle
- L-R shunting
- free wall rupture (5-14d)
- pericardial tamponade (hemopericardium), JVD, distant heart sounds
- tamponade leads to profound hypoTN and shock with rapid progression to pulseless electric activity + DEATH
- pericardial tamponade (hemopericardium), JVD, distant heart sounds
myxomatous changes (with pooling of proteoglycans)
- where? MEDIA layer of LARGE arteries in cystic.MEDIAL.degeneration
- predisposed to aortic dissections and aortic aneurysms
- seen in young indivs with Marfan
media action in giant cell arteritis vs. cystic medial degeneration
- cystic medial degeneration: myxomatous changes with pooling of proteoglycans in MEDIA
- GCA: granulomatous inflam of MEDIA and fragmentation of internal elastic lamina
PDA + Eisenmenger syndrome
- differential clubbing ad cyanosis (toes) sans blood pressure or pulse discrepancy=LAGE PDA complicated by Eisenmenger syndrome
- Eis=reversal of shunt flow from L-T to R-L
- (severe coarctation of the aorta can cause lower extremity cyanosis)
- R-L shunting in pts with large septal defects and ToF=WHOLE body cyanosis
What are the FIVE (5) things on the differential diagnosis for chest pain
- coronary artery disease (CAD)
- substernal, radiation to arm/shoulder/jaw
- pulmonary/pleuritic (pleurisy, pneumonia, pericardities, PE)
- sharp stabbing pain, WORSE W/ INSPIRATION
- pericarditis: worse when lying flat
- PE, pneumothorax: respiratory distress, hypoxia
- aortic (dissection, intramural hematoma)
- SUDDEN SEVERE tearing pain radiates to back in old men
- GI/esophageal: NOCTURNAL pain in upper abdo and substernal; non-exertional
- CW/musculoskeletal
- persistent, prolonged
- worse with movement/chang ein position
- often follows: REPETITIVE ACTIVITY
chronic transmural inflamm (AAA) vs. cystic medial necrosis vs. focal intimal tear (FIT)
- chronic transmural inflamm (AAA)
- focal dilation of abdo aorta (infrarenal mc)
- RF: >60, smoking, HTN, men
- TRANSMURAL INFLAMM of the aortic wall
- chronically leads to degradation of elastin and collagen by proteases
- causes LOSS of ELASTIN and loss of smooth mu cells
- end up with ABNML collagen remodeling and crosslinking
- final product: weaken and expand aortic wall=ANEURYSM
- cystic medial necrosis
- loss of smooth mu, collage, elastic tissue
- formation of cystic mucoid spaces in aortic media
- marfan syndrom: cystic medial degeneration=rf for ascending AA and dissection
- focal intimal tear
- primary event of aortic dissection
cardiac tissue conduction velocity
- park at venture avenue
- fastest–>slowest=purkinje, atrial mu, ventricular mu, AV node
- AV node is slowest conductor-delay allows ventricules to completely fill with blood d/r diastole
sans significant PERICARDIAL dz what are the most frequent causes of pulsus paradoxus
- asthma and COPD exacerbation
- immediate relief:
- beta-adrenergic agonists cause bronchial smooth muscle relaxation via INC intracellular cAMP
RV MI
- general
- CP:
- systemic hypoTN (and shock)
- elevated JVP
- clear lungs
- mc occurs in setting of acute inferior wall MI
- d/t occlusion of proximal RCA
- hemodynamic assessment:
- elevated RA and CVP
- reduced PCWP
- reduced CO
mc primary cardiac neoplasm
- MYXOMAS
- 80% are in LA
- pedunulated and gelatinous
- CP: emboli, mid-diastolic rumbling murmur heard best at apex, positional CV s/s (dyspnea, syncope)
- histo: scattered cells within a mucopolysaccharide stroma
- abnml blood vessels
- hemorrhaging
Pulmonary artery HTN
- definition: pulm arterial pressure >/=25 (nml: =20)
- 2 hit hypothesis
- abnml BM.PR.2 gene predisposes to xs endothelial and smooth mu cell proliferation
- dz process:
- vascular remodeling
- elevated pulm vascular resistance
- progressive pulm HTN
paradoxical embolization (stroke in the setting of venous thromboembolism)
- PP: conditions that raise RAP>LAP (Valsalva) can produce transient R-L shunt across PFO
- usually: septum primum and septum secundum flaps all up on eachother and fuse cloed
- ASD: missing primum or secundum…less common than PFO in health adults
A fib and thromboembolism
- afib is assoc with INC r/o systemic thromboembolism
- LA appendage=mc site of thrombus formation
hemodynamics of severe AORTIC stenosis
- impaired LV output
- higher systolic pressures cause LVH
- atrial contraction necessary for filling of stiffened LV
- end up with: hypoTN and pulm edema
- may cause afib, cardioversion indicated
coronary sinus and RA
- CS runs transversely in LAV groove on posterior heart, communicates freely with RA
- CS gets dilated by any factor that causes RA dilation
- mc: secondary to pulm HTN
Constrictive pericarditis
- Etiology
- idiopathic or viral
- cardiac sx or radiation therapy
- TB (in endemic areas)
- Path:
- thickened, rigid pericardium noncompliant casing a/r heart=limited ventricular expansion d/r diastolic filling
- Hemodynamic signs:
- INC JVP
- KUSSMAUL
- pulsus paradoxus
- pericardial knock knock who’s there?? (early in diastole)
Tet of Fallot SVR:PVR
- pulm stenosis and overriding aorta cause low ration of SVR:PVR (systemic and pulmonary vascular resistance)
- low ratio=deoxy RV output take low-resistance route (via LV) to SYSTEMIC circulation=acute hypoxemia (Tet spell)
- fix with SQUAT!
- quickly INC SVR (sans changing PVR)=INC ratio
- INC SVR=more RV output goes to PULM circulation, oxygenate in pulm cap beds, INC arterial oxygen concentration…yay!