Flashcards in CV 1 Deck (58):
Mitral valve regurgitation
Myocarditis due to acute rheumatic fever
- Develops after untreated strep
- Aschoff bodies on microscopy (interstitial myocardial granulomas)
- Aschoff bodies contain plump macros w/ abundant cytoplasm and central, slender ribbons of chromatin
Supine hypotension syndrom in preggers
=> Supine/right lateral decubitus position
=> Compression of IVC
=> reduced venous return
=> reduced preload
=> decreased CO
Sx resolve when standing or sitting
- Directly inhibits Na-K-ATPase in myocardial cells
- Causes v in Na efflux => ^ intracellular Na levels => reduces Na-Ca exchanger => ^ intracellular Ca => improved myocyte contractility and left ventricular systolic function
Go review blood vessel anatomy around the heart
V1-V2 ST elevation. Which coronary artery?
Left anterior descending
V3-V4 ST elevation. Which coronary artery?
V5-V6 ST elevation. Which coronary artery?
LAD or LCX
I, aVL ST elevation. Which coronary artery?
II, III, aVF
- Irregularly irregular rhythm
Precipitated by acute systemic illness, increased sympathetic tone, excessive alcohol consumption (holiday heart syndrome)
ECG of Afib
- Absence of P waves
- Irregularly irregular rhythm with varying R-R intervals
- Stimulates alpha-adrenergic and serotonergic recetpors
- In pts w/ pinzmetal's angina, low doses can induce coronary spasm, chest pain, and ST elevation
IV drug users and heart issues
- Tricuspid (right sided) endocarditis
- S. aureus (1) and P. aeruginosa (2)
- Can develop multiple septic emboli in lungs
- Pulm infarcts are almost always hemorrhagic
Turner syndrome cardiac anomalies
- Aortic coarctation
- Bicuspid aortic valve
Aortic coarctation presentation
- Cyanosis of LE
- Severe form
- Decreased femoral pulses
- Pain/cramping in legs during exercise
- More common w/ Turner syndrome
Which part of the heart makes up the anterior surface?
Penetrating injury to RV occurs where?
Left sternal border
Fourth intercostal space
Which layers would a penetrating injury to RV go through?
1) Skin/subcutis 2) Pectoralis major m.
3) External intercostal membrane
4) Internal intercostal m
5) Internal thoracic a. & v.
6) Transversus thoracis m
7) Parietal pleura
9) R. ventricular myocardium
Pleura of lungs is injured but not the actual lungs (no middle lobe on left side)
- Peripheral neuropathy of distal L/UEs
- Sensory/motor impairments
- Dry beriberi plus cardiac involvement
- Cardiomyopathy, high-output CHF, peripheral edema, tachy
Subfascial space in upper thigh:
- Inguinal ligament (superior)
- Adductor longus (medial)
- Sartorius (lateral)
Path of LAD
- arises off l. main a.
- courses along anterior aspect in the anterior interventricular groove toward apex of the heart
Pathogenesis of atherosclerotic plaques
- Release of PDGF from locally adherent plts, endo cells, and macros
- Promotes migration of SMCs into intima
Which part of the body has the highest O2 extraction?
Drains into coronary sinus
Nitroglycerin affects which vessels?
Decreases preload => decreases ventricular wall stress => decreasing CO demand
Large veins are most susceptible
What does the pulm cap wedge pressure measure?
L. atrial end diastolic pressure (LAEDP)
LAEDP = LVEDP in normal conditions
Go review the LV pressure-volume relationship
DiGeorge - lack of development of which embryologic structure
- Third & Fourth branchial/pharyngeal pouch
Deletion of chr 22
Absent thymic shadow, hypocalcemia, cleft palate, mandibular deformity, low-set ears, aortic arch abnormalities
presents in neonate period after pulm vascular resistance has declined (so not at birth)
Prussian blue stains what?
Gold cytoplasmic granules in macros that turn blue with Prussian blue staining?
hemosiderin laden macrophases (siderophages)
What is the significance of hemosiderin laden macros?
- Indicates chronic elevation of pulm cap hydrostatic pressures
- Most commonly due to left-sided HF
Bicuspid aortic valve?
Common cause of aortic stenosis
- harsh, cres-descres systolic ejection murmur
- heard best at R. 2nd intercostal space`
adenosine and dipyridamole
Selective vasodilators of coronary vessels
What is coronary steal?
- Blood flow to ischemic areas (after an MI) is reduced
- Because of arteriolar vasodilation in nonischemic areas
- Can lead to hypoperfusion and worsening existing ischemia
Right heart failure => ^ed CVP
What happens after that?
- Increased cap hydrostatic pressure
- Increased net plasma filtration
- Increased interstitial fluid pressure => increased lymphatic drainage (prevents peripheral edema development)
Cardiac AP (speed of conduction) slowest to fastest
Blood flow radius and resistance
- Directly proportional to vessel radius^4
- BF is innersely proportional to radius^4
Where do K sparing diuretics act on the kidney?
Blocks absorption of Na
Blocks excretion of K, H
Where do loop diuretics act?
Thick ascending limb of loop of Henle
Blocks absorption of Na, Cl, K
Where do thiazide diuretics act?
Distal convoluted tubule
Blocks absorption of Na, Cl
Beta blocker MOA
- Inhibits renin release from renal juxtaglomerular cells through antagonizing beta-1 receptors
- Prevents activation of RAAS pathway => decreased vasoconstriction & renal Na &H20 retention
- Beta- adrenergic agonist
- Predominantly B1 receptors
- Increases HR, contractility => increase myocardial O2 consumption
- ^ NO in VSMCs => ^ in cGMP and SM relaxation
- Dilates veins >>> arteries
- Decrease preload
- Reflex tachy
- "Monday disease"
Where is the MI with a ST elevation of II, III, aVF?
Presentation: hypotension, distended jugular veins, clear lungs
Hemodynamic assessment of RVMI
- Elevated RA and CVP
- Reduced PCWP
- Reduced CO
- Inhibits NaCl resorption in early DCT
- Decreased Ca excretion
- Hypokalemic metabolic alkalosis
Coadmin of ACEIs and diuretics
Significant first-dose hypertension
ACEIs must be initiated at low doses to decrease the reaction
Pros of using mineralcorticoid receptor antagonists (e.g. spironolactone, eplerenone) in pts with HF?
- Improve survival
- Regression of myocardial fibrosis & improvement of ventricular remodeling
Used in pts w/ decreased LVEF
In transient ischemia, why do myocytes increase in size?
No O2 = No ATP
- Can't stimulate Na(going out)/K (going in) pump
- Can't maintain Na (going in)/Ca (going out) exchange
MOA of statins
HMG-CoA reductase inhibitors
Lower total cholesterol and LDL
Most effective for prevention of CV events REGARDLESS of baseline lipid levels
Anatomical findings in tetralogy of Fallot
1) Pulm infundibular stenosis
2) R. ventricular hypertrophy
3) Overriding aorta
Cause of TOF
Anterosuperior displacement of infundibular septum
Clinical Presentation of TOF
Early childhood cyanosis
Squatting: ^ SVR, v R-to-L shunt, improves cyanosis
Harsh systolic murmur (pulm stenosis)