Cardiovascular Function and Diseases Flashcards
Heart wall (inner to outer)
- Endocardium
- Myocardium
- Epicardium (or visceral pericardium)
- Pericardial cavity
- Parietal pericardium
Endocardium
Innermost layer
Myocardium
Thickest layer of cardiac muscle
Cardiac myocytes (muscle cells) provide contractile force to propel blood
Epicardium
Inner layer of the pericardium that lies against the heart surface
Also called visceral pericardium
Parietal pericardium
Outer layer of the pericardium that is in contact with lungs and the structures in the chest cavity
Pericardial cavity
Space between the visceral and parietal pericardium layers
Contains pericardial fluid (approx. 20 ml)
Functions:
- Prevents displacement of heart during movement
- Protects heart from infection/inflammation from lungs and other surrounding tissue
- Contains receptors that can control HR and BP
Heart chambers
RA
RV
LA
LV
Atria are smaller and thin-walled; “storage units” and passageways to the ventricles
Ventricles are larger and thick-walled; pumping chambers
Atrioventricular valves (AV)
In-between each atria and ventricle:
- Right AV valve: tricuspid valve (TV)
- Left AV valve: mitral valve (MV)
Function as a unit to simultaneously allow blood flow from atria into ventricle, and prevent back flow into atria from ventricle when the ventricle contracts
Semilunar valve (SV)
In-between RV and pulmonary artery, and LV and aorta
Open to allow blood to flow from ventricles into greater vessels, and close to prevent back flow into ventricles
Coronary arteries
Supply myocardium and other heart structures with oxygenated blood
Originate from the aorta, and divide into smaller RCA and LCA branches
Coronary veins
Coronary sinus: empty deoxygenated blood from heart into the RA
Cardiac cycle
One heartbeat accounts for one contraction (systole) and one relaxation (diastole)
Systole: contraction (blood leaves the ventricles)
Diastole: relaxation (ventricles fill)
Cardiac conduction
- SA node (“pacemaker” of the heart), located at junction of RA and SVC, generates action potential (AP; 60-100/min)
- Atria contract
- AP travels through myocardium to the atrioventricular (AV) node where they pass to the ventricles
- Bundle of His, located in the interventricular septum, divides into right and left bundles which conduct impulses to the ventricular apex
- Purkinje fibers are the end branches of the bundles
- Ventricles contract
Myocardial AP
Depolarization: electrical activation of muscle cells
Repolarization: deactivation of muscle cells
Caused by movement of ions (Na2+, Ca+, K+, Cl-) across the cardiac cell membrane that results in a voltage difference (membrane potential)
AP phases
Phase 0: depolarization (rapid Na+ entry into cell) (+30 mV)
Phase 1: early repolarization (slow Ca2+ entry into cell)
Phase 2: plateau; continued repolarization (slow Na+ and Ca2+ entry into cell)
Phase 3: late repolarization (K+ moves OUT of cell)
Phase 4: return to resting membrane potential (-70 mV)
PQRST EKG wave
P-wave: atrial depolarization
QRS complex: ventricular depolarization and atrial repolarization
T-wave: ventricular repolarization
Myocytes (cardiac cells)
Characteristics:
1. Intercalated disks with gap junctions allow electrical impulses to spread quickly from cell to cell
- More mitochondria due to increased ATP need
- Increased T-tubules (invagination of muscle membrane) allow faster access to Na+ and K+; conduct impulse to sarcoplasmic reticulum (smooth ER within myocytes) that store Ca2+
Atherosclerosis
Chronic inflammatory condition characterized as thickening and hardening of vessels
Characteristics:
- Endothelial (blood vessel lining) dysfunction
- Plaque development/narrowing, and/or instability
Consequences (vascular events): MI, stroke, renal artery disease, aneurysm, PAD, CAD
Development of atherosclerosis
- Chronic endothelial injury
- Immune response adheres to injury
- Inflammatory response
- LDL cholesterol penetrates vessel wall and becomes trapped
- Macrophages with lipids inside accumulate and form a “fatty streak” that release inflammatory cytokines
- Cytokines stimulate vessel smooth muscle growth
- Plaque forms over the fatty streak
- Plaque can calcify and obstruct blood flow, OR rupture (a “complicated plaque”)
- Plaque rupture exposes vessel underneath, and thrombus forms rapidly, which can obstruct the vessel (angina, infarction)
Lipids
Necessary for life (cell membranes, hormone development, bile production)
Types of lipids:
1. Chylomicrons: consist mostly of triglycerides; transport dietary fat from intestine to liver and peripheral cells
- Triglyceride: major form of lipid; used for energy
- Very Low Density Lipoproteins (VLDL): triglycerides and protein
- LDL (“Bad”): cholesterol and protein; delivers cholesterol from liver to cells (cell membranes, steroid hormones)
- HDL (“Good”): phospholipid and protein; returns excess cholesterol from cells/artery walls to liver to be converted to bile salts
Risk of CAD (r/t dyslipidemia)
Linked to:
1. High triglycerides, VLDL, and LDL
- Low HDL
HTN
Consistent, sustained elevation of BP >130 mmHg systolic OR >80 mmHg diastolic
Increases risk of atherosclerotic disease and MI
BP classification
Normal: <120/<80
Elevated: 120-129/<80
HTN Stage 1: 130-139/80-89
HTN Stage 2: >140/>90
Goal for BP in pts with diabetes and/or renal disease is <130/80 (below HTN stage 1)
Primary HTN (95% of cases)
HTN that is NOT related to another disorder
Risks: FHX, age, gender, ethnicity, high dietary sodium, glucose intolerance, tobacco, obesity, heavy alcohol consumption, low dietary intake of Ca2+, K+, and Mg2+