Transport blood under high pressure from the heart to the capillary bed of tissues (high pressure/thick muscular walls)

Small branches of arteries that act as conduits between arteries and the capillary beds of tissues (muscular walls and sphincters)

Extensive lattice of vessels that supply blood to the cells/areas of substrate exchange (thin walled with pores for permeability)

Collect blood from the capillaries and coalesce to form veins

Transport blood from the Venules back to the heart. Act as a reservior (low pressure system, thin walls)

Anount of blood in venous system

LCA branches into?

Left Anterior Descending Artery provides blood to?

Circumflex Artery supplies blood to?

Right Coronary Artery supplies blood to?

Relaxation and Filling of the Heart

Contraction of the Heart

Flow (Q) through a blood vessel determined by?

Flow of blood to lungs: Flow of blood to body

Measurement of Vascular Resistance

<8 weeks of age = 8-10 woods/m2. >8 weeks of age = 1-3 woods/m2.

Infant = 10-15 woods/m2. 1-2 yrs old = 15-20 woods/m2. Child-Adult = 15-30 woods/m2.

How easy it is for blood to travel through arteries

Constriction and Relaxation of Smooth Muscle of Arteries and Arterioles controlled by:

Comparing Catecholamines

Comparing Catecholamines

Comparing Catecholamines

Volume of blood returning to the heart from systemic circulation = RA pressure or CVP

Systemtic pressure = pressure the heart must pump against to circulate blood = MAP

Contraction units of Cardiac Muscle

Thin protein filament, light band or I band (isotopic)

Thick protein filament, dark bands or A Bands (anisotropic), small projections from sides that form cross-bridges

Site of connecting myofibrils

Portion of myofibrils between two Z-Discs

Helix backbone, F-actin and G-actin

The active site for cross-bridges with myosin

Protein wrapped around F-actin, blocks active site

Three subunits of Troponin

Affinity for actin

Affinity for Tropomyosin

Affinity for Calcium

Two polypeptide chains wrapped in spiral forming a double helix

Globular polypeptide with associated light chains

Individual Myosin Molecules Bundled Together to Form the Body Where Cross-Bridge Hangs

Flexible Hinge and Arm Connected to Myosin Heads

Enzyme in Head for Energy Production

Myofilament and Actin Interaction

Walk-Along Theory

Potassium concentrations in cell

Diffusion of Potassium

Concentration of Sodium in the Cell

Diffusion of Sodium in the Cell

At rest cell has?

Leak of sodium into the cell, decreases the intracellular negativity. Opens voltage gated ion channel to generate more positive ion (Na and Ca) entry. Cell becomes more positive. Action potential is generated.

Potassium rapidly diffuses out of the cell and the intracellular negativity increases to resting state.

Phases of Action Potential

Time cardiac muscle is refractory to additional stimulation

Site of automaticity due to slow leak of NA ions (the most Na leak channels) that slowly increase intracellular charge until action potential is fired releasing Ca from the muscle fibers to cause myosin/actin contraction

Spread of depolarization through atria, followed by atrial contraction

Pause in Conduction at AV Node

Deopolarization of the ventricle, followed by ventricular contraction

Repolarization of the ventricles, happens just before the end of ventricular contraction

Amount of blood in a heart chamber after filling, before systole

Amount of blood ejected with each contraction of the heart

Amount of blood that remains in the heart chamber after systole

Percent of blood in chamber that is ejected with each systole

Amount of blood pumped into the aorta each minute

HR x Stroke Volume

P rate > 300, no PR interval, QRS variable, irregular rhythm. Decreased filling time causing fatigue? dizziness, dyspnea, irregular pulse

Associated with things that remodel the atria: (HF, ischemic CV disease, HTN, Obesity, OSA, rheumatic heart disease)

Early beats without p waves. Effects: decreased CO from loss of atrial contribution to ventricular preload resulting in heart fluttering, pounding, and palpitations. Associatied with abnormal potassium, hypercalcemia, hypoxia, aging, anesthesia, caffeine, tobacco, illicit drugs, exercise

Role of Lipoproteins

Dietary fat packaged in small intestine—> chylomicrons —> liver —> processed into:

Strong predictor of cardiac events

Indicator of cardiac risk but in context of other factors (age, diabetes, CKD)

Protective against atherosclerosis- want high level to remove access cholesterol from arterial walls

Primary causes of dyslipidemia

Secondary causes of Dyslipidemia

Chronic inflammation resulting in damage to arterial walls and plaque formation

Lesion in arteries filled with lipids and marcophages (stable or unstable)

Step 1 of Atherosclerosis

Step 2 of Atherosclerosis

Step 3 of Atherosclerosis

Unstable plaques prone to rupture

Atherosclerotic disease of the arteries

Pain without ambulation found in PAD

Contributes to blood pressure regulation, promotes cardiac contactility, controls arteriolar vasoconstriction (peripheral vascular resistance)

Responds to Catecholamines (epinephrine and norepinephrine), stimulates renin-angiotensin system (RASS)

Hypertension

95% of HTN caused my genetics and environment

Caused by underlying disease process (renal, pheochromocytoma, pregnancy) increasing PVR and CO

Vascular remodeling—> fibrosis of vessels—> organ injury (cardiac muscle, retina, kidneys, brain). LV Hypertrophy-> HF.

Rapid increase in SBP> 140mmHg—> cerebral arterioles cannot regulate blood flow to cerebral capillaries—> cerebral edema—> encephalopathy

Associated with pregnancy, cocaine and meth use, adrenal tumors, ETOH withdrawal

Supports Sodium Excretion

Deposited in tunica media and assists with vasoconstriction and increasing BP

Direct vasodilator lowering BP

Atherosclerosis of coronary arteries. Diminished blood supply.

Local, temporary oxygen depravation. Cells live but cannot function normally.

Persistent ischemia or complete occlusion of coronary artery. Commonly myocardial infarction.

Dyslipidemia, HTN, Smoking, DMII, Insulin Resistance, Obesity, Diet, Lifestyle

Age, male and post-menopausal women, family history

Transient inability of coronary arteries to deliver enough oxygen to myocardial cells (supply-demand mismatch). Begins after 10 secs (cells can survive 20 mins)

Times of increased O2 demand:

Times of decreaed O2 demand: