Alterations In Cardiac Function

Front 1

Which side if most affected w/plaque and disease?

Back 1

LEFT

Front 2

When does the heart get oxygen and nutrients? systole or diastole?

Back 2

DIASTOLE

Front 3

What is the root of nearly all CAD?

Back 3

atherosclerosis

progressive narrowing of lumen by plaque

etiology: insult of microcirculation (inflam response + foamy macrophages)

poor perfusion pressure through coronary artery (hypotension, hypovolemia)

Front 4

occlusion

Back 4

leads to ischemia of myocardium (no delivery of O2 or nutrients)

Front 5

per cent occlusion

Back 5

clincical sx appear with a 75% occlusion of any of the 3 coronary arteries

Front 6

rupture

Back 6

atherosclerotic plaques with large lipid cores are fragile and rupture thereby exposing subendothelial proteins causing platelet migration-forming clots

Front 7

progressive plaque growth:

carry risk of?

two major damaging events can take place?

Back 7

carry risk of disruption of coronary blood flow >> ischemia >> MI

two major damaging events can take place?
- NARROWING of coronary lumen
- sudden RUPTURE of plaque

Front 8

atherosclerosis

Back 8

most common cause of ischemia

Front 9

atherosclerotic plaques

Back 9

lower the perfusion of the coronary arteries during diastole (narrowing of lumen)

Front 10

autoregulation

Back 10

does not occur (arterial)

Front 11

ATP storage

Back 11

myocardial cells are unable to store ATP. A large supply of oxygen is needed to synthesize ATP

Front 12

toxins

Back 12

circulating form from cigarette smoke, immune cells, infectious agents (group A b-hemolytic in peds)

Front 13

vasospasm

Back 13

caused by serotonin and thromboxane released by activated platelets (from inflam response)

Front 14

myocarditis

type of disorder?
onset?
histology?
pathogen?
prognosis?

Back 14

type of disorder? INFLAM
onset? ACUTE AND STORMY PICTURE
histology - NECROSIS
pathogen: VIRAL
prognosis - RECOVERY OR DEATH FROM NECROSIS

Front 15

cardiomyopathy

type of disorder?
onset?
histology?
pathogen?
prognosis?

Back 15

type of disorder? NON-INFLAM DISORDER
onset? EVOLVES INSIDIOUSLY OVER YEARS
histology? HYPERTROPHY OR ATROPHIED
pathogen? VIRUS, GENES, AUTOIMMUNE
prognosis? HEART FAILURE

Front 16

pericardial effusion

Back 16

> 50ml fluid in the pericardial sac

Front 17

cardiac tamponade

Back 17

fluid in pericardial sac that interferers with hemodynamics and becomes life threatening

decreased SV >> increased HR, JVD, pulsus paradoxus

Front 18

pericarditis

Back 18

inflam of the pericardium by viral or post MI

Front 19

factors that decrease blood supply?

Back 19

coronary plaque
decreased perfusion pressure
decreased arterial O2 content

Front 20

factors that increase myocardial oxygen demand?

Back 20

increased HR
increased preload
increased afterload
increased contractility

Front 21

factors that can lead to myocardial ischemia?

Back 21

coronary vasospasm
hypoxemia
low perfusion pressure from volume depletion or shock