cardiac Flashcards
HEART STATISTICS
72 beats per min 103,680 per day 728,252 per wk 3,155,760 per month 37,869,120 per year 2,900,000,000 per lifetime 7,568 litres/day 53,162 l/wk 230,370 l/mo 2764445 l/yr 211,700,000 l/lifetime 1,331,552 barrels/ lifetime
trace a drop of blood through the heart
superior vena cava- right atrium- through tricuspid valve- right ventricle- pulmonary semi lunar valva- pulmonary arterie- lung- pulmonary vein - left atrium- mitral valve (bicuspid)- left ventricle- aortic valve- to the body
coronary arteries
supllies blood to the heart
Systole
when the heart contacts with ejection of blood
what is the most common deseases in western world
cardiovascular disease (atherosclorosis, then hypertensive heart desease)
Ischemic vascular disease
Atherosclerosis
coronary heart disease
Main Regions and Pathology Resulting from Atherosclerosis
Systemic Inflammatory Disease affecting Arteries
brain, aorta, peripheral vascular (gangrene- diabetic)
Atherosclerosis, CAD (specific to the heart starts with ischemia then injury then necrosis)& IHD- start off with ischemic episode- leads to heart failure
Coronary arteries supply blood and nutrients to the heart muscle
Coronaries fill during diastole
Atherosclerosis of the coronary arteries = Coronary Artery Disease (CAD)
CAD = Ischemic Heart Disease
Ischemic Heart Disease can lead to Heart Failure
Pathogenesis of Atherosclerosis
Endothelial injury: is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA
Pathogenesis of Atherosclerosis!!!!!!!
hallmark is Endothelial injury!!!!!! (hypertension, diabetes, obesity): is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA
first layer in the lumen is the subendothelial matrix then the smooth muscles
athelrosclorosis affects the endothelial injury- circulating LDL gets into the endothelial injury
monocytes adhere on the lumena nd enter the endothelium and act on the cytochines - become macrophages and engulf the LDL and are now stcuk - gets into foam cells - become fatty steak and then become palque and can be ruptured - miocardial infarction
can recover from ischemia if not too long
if too long- necrosis- no coming back
angina pectororis
chest pain
Types of Ischemia
(1) Tolerable ischemia, which has a low degree of reduced blood flow
(2) Critical ischemia, which reflects a modestly severe flow reduction
(3) Lethal ischemia, which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction
Tolerable ischemia
which has a low degree of reduced blood flow
Critical ischemia
which reflects a modestly severe flow reduction
Lethal ischemia,
which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction
atherosclorosis start in the
first decade of life and continuously grows - usually gets too big at aroud the fourth decade
risk factor!!! modifiable and non modifiable
Non-modifiable Increasing Age Male gender Heredity (genetic predisposition) Potentially modifiable Hyperlipidemia Hypertension Physical inactivity Smoking Obesity Stress Diabetes mellitus
Symptoms of Coronary Stenosis!!!
know the desease (pathology)- the symptoms-
Angina pectoris Asymptomaticv( Arrhythmia (cardiac rhythm abnormalities) Sudden death Myocardial infarction Congestive heart failure
Angina Pectoris
2 types- stable and unstable
Transient discomfort in the chest or adjacent area caused by myocardial ischemia brought on by exertion: no myocardial necrosis.
Two types: Stable Unstable Pain of ischemia Precipitated by exercise Relieved by rest, nitroglycerine (vasodilator)
Complications of CAD
Myocardial Infarction (MI)
Sclerosis: hardening due to collagen deposits surrounding the atheroma
Thrombosis: surface of atheroma may ulcerate and sometimes sudden death without previous warning symptoms
Aneurysms: a weakened wall may dilate and rupture (ruptured aneurysm- bleed out) (weakening of wall of the blood vessle- blood can stagnant )
Myocardial infarct (MI)
Heart Attack
Blockage of a vessel causes tissue to become ischemic ( lack of oxygen to tissue bed)
The ischemia causes tissue necrosis (infarction: death)
Dead tissue: subjected to normal body processes of removal and repair with formation of scar tissue.
Diagnosis may be clinical: cardiac biomarkers, ECG,
Cardiac catheterization, post mortem
MI Clinical symptoms
Choking or pressure like pain most commonly in left chest extending up neck, down left arm.
However, can be anywhere above umbilicus to teeth in lower jaw down either arm to wrist & between shoulder blades.
May become unconscious
Sweating, pallor
Symptoms of shock – weak or imperceptable pulse
The most common cause of death from Acute MI is !!!!
an Arrhythmia: Ventricular Fibrillation
- first rythm is v tact