Quiz 3 - Cardio Physio, ECG, Acid/Base, O2/CO2, Chemical Reactions Flashcards
Epicardium
Outermost layer of heart, contiguous with visceral pericardium, simple squamous mesothelium that secretes fluid, supported by loose CT, contains coronary vessels, nerves, fat, ectodermal origin, contains keratins
Myocardium
Cardiac muscle, thicker in ventricles
Endocardium
Loose CT with smooth muscle cells, purkinje fibers, mesodermal origin, produces clotting proteins, contains vimentins
Mesothelium
Mesodermal origin, single cell layer protects body cavities and organs. Does not involve transportation of blood. Pleural (lungs), pericardial (heart), peritoneal (abdominal organs)
Atrium muscle
Thin epicardium, roughly equal myocardium and endocardium.
Ventricle muscle
Tiny endocardium, thick myocardium, thicker epicardium than atrium (mostly adipose)
Conduction system of the heart
Sinoatrial Node > Atrioventricular Node > Bundle of His > Left and right bundle branches > Purkinje fibers Nodes are modified cardiac muscle, bundle and fibers are conducting muscle fibers
Purkinje Fibers
Myofibers but larger than contractile muscle fibers, pale staining fibers, lack intercalated discs, don’t contract but conduct, contain lots of glycogen, mitochondria
Atrial Natriuretic Peptide
Synthesized by atrial myocytes, responds to high BP, acts to lower BP, Stimulates Na+ loss from blood into urine, relaxes vascular smooth muscle, prevents water retention hormones
Hypertrophy
Cells get bigger
Hyperplasia
Cells increase in number
Vasa Vasorum
Blood vessels that feed walls of large blood vessels
Tunica Intima
Innermost, thinnest layer, CT
Internal elastic lamina
Dense, elastic membrane that separates Tunica intima from tunica media
Tunica media
Thickest layer, contains smooth muscle, elastic fibers, connective tissue
External elastic lamina
Dense elastic membraane that separates Tunica Media from Tunica adventitia
Tunica adventitia
Connective tissue, nutrient vessels (vasa vasorum), autonomic nerves (nervi vasorum)
Aorta structure
Most of the wall is tunica media, smooth muscle cells synthesize elastic fibers to smooth out pressure pulses
Vernhoff stain
Stains elastic fibers
Azan stain
Stains collagen fibers
Muscular Artery
Thick, highly layered tunica media, regulates blood pressure
Elastic artery
Aorta, pulmonary artery, branches, carry blood to smaller arteries, tunica media has lots of elastic fibers, expand and recoil with systole and diastole
Small arteries
Contain up to 5-6 layers of smooth muscle,
Arterioles
Precapillary sphincters
Surround arterioles allow blood into capillary beds
Thermoregulation
High capillary flow = more heat dissipation, reduced flow = high conservation
Nitric Oxide
Released by vascular endothelial cells. Causes smooth muscle to relax, vasodilation
Endothelins
Released by vascular endothelial cells. Causes smooth muscle to contract, vasoconstriction
Continuous capillaries
Most common type. Endothelial cells linked by tight junctions
Fenestrated capillaries
Contain openings in endothelium that facilitate exchange. Found in kidney glomerulus, choroid plexus
Sinusoids
Have larger openings for greater exchange. Blood cells can squeeze through. Found in liver, bone marrow
Pericyte
Periendothelial cells. Critical for blood-brain barrier, small vessel hemostasis, contraction, phagocytosis, repair and regeneration
Transcytosis
Movement of big proteins, etc. through capillaries via vesicles
Venule and Muscular venule
Smallest of veins, major site of vascular permeability, particularly sensitive to histamine, small but less defined “roundness” than arterioles
Medium vein
Contain semilunar valves, have thicker Tunica Adventitia, small tunica media and tiny tunica intima
Large vein
Have thicker Tunica Adventitia, small tunica media and tiny tunica intima
Angiogenesis
Blood vessel formation, driven by multiple factors including Vascular Endothelial Growth Factors
Age and arteries
Elastic lamellae become fragmented and discontinuous, making vessels stiff
Arteriosclerosis
Hardening of arteries because of age, calcium salt deposits, thickening of TI
Myocardial Infarction
Blockage of Coronary artery kills cardiac muscle cells, scar tissue replaces it, blood leaks into epicardium
Electrocardiography
Records electrical activity of heart
Diastole
relaxation of heart chambers which fill with blood
Systole
Contraction of heart chambers
Ventricular filling
mid to late ventricular diastole
S1 heart sound
Lub, closure of AV valves at beginning of ventricular systole
S2 heart sound
Dub, closure of semilunar valves at beginning of ventricular diastole
Pacemaker cells
SA node, AV node, Bundle of His, Bundle branches, Purkinje fibers, have intrinsic rhythmnicity
Working myocardial cells
Most of heart cells
Normal Activation Sequence
SA node > Atria > AV node > His > Bundle > Purkinje > Ventricles
Fast-response Action Potential - Plateau phase prolonged by Ca2+
Slow-Response Action Potential - in Pacemaker cells, slowly depolarize in Phase 4 to automatically trigger AP
Excitation-Contraction Coupling in Cardiac Muscle
Action potential travels along sarcolemma (plasma membrane) and into T tubules, causing Ca2+ to enter cells. Ca2+ triggers opeining of Ca2+ release channels in sarcoplasm. Ca2+ binds to tropomyosin, allowing myosin fibers to bind to actin and trigger contraction. “Ca2+-induced Ca2+ release”
Cardiac Output
= Stroke Volume X Heart Rate
Stroke Volume
= End Diastolic Volume - End Systolic Volume
Usually about 70-80 mL
Total Peripheral Resistance
Sum of the resistance of all peripheral vasculature in the circulatory system
Blood Pressure
= Cardiac Output X Total Peripheral Resistance
Baroreceptor Reflex
Responds to change in arterial pressure by increasing or decreasing heart rate as needed
Bainbridge Reflex
Responds to changes in blood volume. Increases heart rate when there is increased arterial presure.
Normal Sinus Rhythm
When the SA node is acting as the pacemaker.
Normal Heart Rate
60-100 beats/min.
Tachycardia - >100 beats/min.
Bradycardia - <60 beats/min.
Electrocardiogram
Machine to measure heart’s electrical potential.
Lead - electrical potential difference between two electrodes
P Wave
Atrial depolarization
PR Interval
Atrioventricular conduction. (0.12-0.2 sec)
QRS Complex
Ventricular Depolariation 0.06-0.1 sec
ST Segment
Index of ventricular AP plateau 0.14-0.16 sec
QT Interval
Ventricular Action Potential 0.3-0.4 sec
R-R Interval
Interval between ventricular beats, varies with heart rate, used to calculate HR
T Wave
Ventricular Repolarization
ECG Abnormalities with MI
ST elevation
T wave inversion
Exaggerated Q waves
ST depression
Dipole Orientation
If the + end of dipole approaches + electrode, signal up
If + end of dipole approaches - electrode, signal down
If electro
ECG time scale
Each large box is equivalent to 0.5 mV and 0.2 seconds.
Each small box is equivalent to 0.1 mV and 0.04 seconds.
HR in beats per minute on ECG
=60/R-R interval
Lead 1
- electrode on RA, + electrode on LA
Lead 2
- electrode on RA, + electrode on LL
Most closely paralells average dipole during QRS wave.
Lead 3
- electrode on LA, + electrode on LL
Einthoven’s Law
Lead I + Lead III = Lead II
Dipole calculation
Amplitude of a lead = (+) deflection + (-) deflection
Augmented Vector Right
Perpendicular to lead III
Augmented Vector Left
Perpendicular to Lead II
Augmented Vector Feet
Perpendicular to lead I
Atrial Fibrillation
No clear P waves, absence of isoelectric baseline
Second Degree AV block
Type 1 and 2. Dropping QRS wave. More frequent in Type 2
Third Degree (Complete) AV block
Dropped QRS wave, needs pacemaker immediately
Ventricular Tachycardia
Deep inverted Rs repeating
Long QT syndrome
QT interval elongated, can lead to ventricular tachyarrythmias, can be congenital, aquired from medications, or from hypokalemia
Torsade de Pointes
ECG turns into big squiggly lines around baseline, twisting of ventricle muscle
Physiological pH
7.4
Bronsted-Lowry Acids/Bases
Acids donate protons, Bases accept protons
Strong Acids/Bases
Completely Dissociate in solution. Ex.) HCl, NaOh
Weak Acids
Donate relatively few of their H+/OH- ions. Ex.) H2S, NH3
Reason for pH regulation
Proteins, ions, muscle contraction, etc. all rely on specific pH range.
Carbonic Anhydrase
Converts CO2 to carbonic acid to dissolve it into the blood
Ways to control H+ ion concentration in the serum
Lungs: remove CO2
Kidneys: Removes H+, Retains HCO3-
Buffering: Resists pH change (does not remove H+ ions)
Volatile Acid
Can be released in gas form. CO2/Carbonic acid
Nonvolatile Acid
Acids that are not released in the blood. Lactic acid, etc.
Acidemia
High concentration of H+. Acidosis decribes conditions leading to acidemia
Alkalemia
Low H+ concentration in blood. Alkalosis is term for conditions leading to alkalemia.
pH regulation in Lungs
Increase in pH from 7.4-7.0 results in 4-5X increase in alveolar ventilation. Raised pH causes respiratory depression.
Lungs only deal with volatile acid
pH regulation in Kidneys
Slow acting
Kidneys can excrete or retain acids (H+ or NH4+)
Kidneys can excrete or retain HCO3- or generate it from Glutamine
pH regulation in Buffers
Bicarbonate: in extracellular fluid
Phosphate: in intracellular fluid
Henderson-Hasselbach Equation
pH = pKa + log [A-]/[HA]
Buffers are most effective when pH = pKa
Intracellular pH regulation
Low IC pH: Na+ gradient pushes H+ out and HCO3- in
High IC pH: Cl- gradient pushes HCO3- out and OH- out
H2PO4- buffer
Respiratory Acidosis/Alkalosis
Hyper/Hypoventilation causes Alkal/acidosis
Involves lungs and volatile acids (CO2)
Metabolic Acidosis/Alkalosis
Disturbances in HCO3 because of Kidney function or other systems.
Abnormal loss or retention of HCO3
Mixed Acid-Base Disorder
Acid-base disorders are rarely just one thing. Respiratory acidosis can exist at the same time as metabolic alkalosis
^G Free Energy
Released or consumed by a chemical reaction to perform work
Free Energy Equation
^G = ^H - T^S
^H = enthalpy (heat) change
T = Temperature
^S = Entropy (disorder)
(+)^G decreases entropy
(-)^G increases entropy
Anabolism
(+)^G
Going “Up” from precursor molecules to macromolecules
Catabolism
(-)^G
From energy containing macromolecules to their end products with the release of energy
5 main types of chemical reactions
- Making and breaking carbon bonds
- Molecular Rearrangements
- Free Radical Reactions
- Group Transfers
- REDOX reactions
Condensation Reactions
Make carbon bonds, water is major byproduct
Carboxylation/Decarboxylation
Addition/Removal of Carboxyl Group (CO2)
Molecular Rearrangements
Change in shape of a single structure
Ex.) cAMP –> AMP
Free Radical Reactions
Molecule containing an unpaired electron, highly reactive
Ex.) Dopamine can become a superoxide radical in right conditions.
Ex.) Vitamin E functions as antioxidant to neutralize free radicals by donating an electron, then rearranging its molecules to reduce charge
Group Transfers
Adding or removing a functional group
Phosphorylation – Kinase
Ubiquitination – Ubiquitin Ligase
Acetylation – Acetyltransferase
Methylation – Methyltransferase
Hydroxylation – Hydroxylase
How does ATP function?
Transfers Phosphate group.
Higher concentrations of ATP relative to ADP cause a greater release of energy.
Energy released usually by transfer rather than hydrolysis
Protein Kinase A
Phosphate transfer drives signal transduction
REDOX Reactions
Involve a Reduction and an Oxidation
Reduction: Load molecules with electrons (+)^G
Oxidation: Remove electrons from a molecule (-)^G
Carbon Oxidation state
Reduced Carbons energy rich
Long saturated carbon chains
Beta Oxidation
Conversion of long lipid chains into Acetyl-CoA for use in citric acid cycle and electron transport chain
NAD+
Major carrier of electrons for REDOX transfer of electrons
