Ejection Fraction
percentage of total ventricular end-diastolic volume ejected with each beat (normal is 50-75%)
decrease indicates heart failure
SA node
“pace maker”
where electrical impulses come from causing the contraction of the atria
AV node
conducts action potentials to the ventricles
Bundle of HIS
right and left bundle branches, bridge from atria to ventricles
Nervous System and Cardiac
Sympathetic: increase conductivity and strength of contraction
Parasympathetic: Slow HR and conduction, reduce strength of contraction, release of acetylcholine
B1 Receptor Cardiac
found in SA node, AV node, cardiac monocytes
increases HR, automaticity, contractility
B2 Receptor Cardiac
Blood vessel walls
causes vasodilation
Alpha 1 Receptor Cardiac
Postsynaptic in the systemic and coronary arteries
causes vasoconstriction
Preload
volume/pressure inside ventricle at end of diastole
left ventricular end-diastolic volume (LVEDP)
Laplace law: tension directly related to amt of fluid, wall thickness, and radius of space
Afterload
Resistance to ejection of blood from left ventricle
load muscle must move after it starts to contract
determined by system vascular resistance in aorta
Myocardial Contractility
myocardium’s ability to stretch and contract in response to filling of the heart with blood
stroke volume and preload
Cardiac Output
Stroke Volume x Heart Rate
Vascular Endothelium Functions
Filtration
Vasomotor: contract and relax
Inflammation: where the changes happen during inflammation
Angiogenesis: creation of new blood vessels
Laminar Blood Flow
parabolic-shaped velocity of blood flow that is straight
Turbulent Blood Flow
associated with bruit, blood flowing in many directions
Chronic Venous Insufficiency
Inadequate venous return over a long period due to varicose veins or valvular incompetence
causes venous stasis ulcers from pooling blood (from breakdown of endothelial wall)
can cause deep vein thrombosis
Stages of Venous Insufficiency
C1: Telangiectasias “spider veins” - little blue veins
C2: Varicose Veins
C3: Edema
C4: Skin Changes - pigmentation, hardening, patterns
C5: Healed venous ulcer (from breakdown of endothelial wall)
C6: Active venous ulcer
Primary Hypertension
Essential or idiopathic hypertension (92-95% of HT)
risk factors:
high sodium intake
natriuretic peptide abnormalities
inflammation
larger body habitus
insulin resistance
Secondary Hypertension
More acute
Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output
Arteriosclerosis
Chronic disease of the arterial system, abnormal thickening and hardening of the vessel walls
Atherosclerosis
Form of arteriosclerosis where vessel walls are thickened and hardened by accumulation of lipid-laden macrophages in the arterial wall, plaque development
*arethomas
Disorders of the pericardium
Acute pericarditis (often infection)
Pericardial Effusion, associated with decreased heart sounds
- Tamponade - no room for filling, cannot beat effectively
Cardiomyopathies
disorder of the myocardium
dilated cardiomyopathy (congestive cardiomyopathy
hypertrophic cardiomyopathy
restrictive cardiomyopathy (stiff)
Disorders of the Endocardium
Valvular Stenosis
- Aortic stenosis (could be congenital)
- Mitral stenosis
Valvular Regurgitation
- Aortic (can be congenital or degenerative), Mitral, Tricuspid (more common, can be caused by rheumatic heart disease
Mitral Valve Prolapse Syndrome (most common heart disorder)
- palpitation, tachycardia, chest pain, headiness (possible)