Physio 1 USMLE Flashcards
Factors that affect rate of diffusion
Concentration, surface area, solubility, membrane thickness, molecular weight
Conditions that increase membrane thickness
Lung fibrosis, pulmonary edema, pneumonia, membranous glomerulonephritis
Conditions that affect surface area of the membrane
Exercise (increases SA), emphysema (decreases SA)
Osmoles Vs. mole Vs. mEq
150 mM of NaCl = 300 mOsm. Moles yield osmoles. 10 mOsm Ca++ = 20 mEq
Characteristics of protein-mediated transport
More rapid than diffusion, transport can be saturated (Tm), is chemically specific, substances compete for transporter
Types of protein transport
Facilitated (down a concentration gradient), active (against gradient, requires ATP)
Primary active transport
ATP consumed directly by the transporter. E.g. Na/K countertransport
Secondary active transport
Depends indirectly on ATP. E.g. Na/glucose cotransporter in the renal tubule depends on Na/K countertransporter
Constitutive endocytosis
Vesicles are continuously fusing with the cell membrane
Receptor-mediated endocytosis
The ligand binds receptor near clathrin-coated pits. More rapid and specific than constitutive endocytosis.
Simple diffusion curve in a graph
Linear. Slope increases if diffusion area or concentration increases. Slope decreases if membrane thickness increases
Facilitated diffusion curve in a graph
Reaches a plateau which represents Tm. Adding more transporters raises Tm, shifts curve up and right.
Amount of total body water
60% of weight in kg. 70kg = 42 L
Amount of intracellular fluid
2/3 of total body water or 40%. 42 L –> 28 L ICF
Amount of extracellular fluid
1/3 of total body water or 20%. 42 L –> 14 L ECF
Amount of interstitial fluid
2/3 of ECF. 14 L –> 10 L ISF
Amount of plasma volume
1/3 of ECF. 14 L –> 4 L plasma
Effective osmolarity
Represented by non-penetrating solutes such as Na. If effective osmolarity increases, cells shrink and vice versa.
Capillary membranes
Are freely permeable to substances dissolved in plasma except proteins. Separate ISF and plasma.
Isotonic fluid loss diagram
Decreased ECF, no change in ICF. Causes: hemorrhage, isotonic urine, diarrhea, vomiting
Loss of hypotonic fluid diagram (hypovolemia)
Decreases ECF and ICF, increases osmolarity. Causes: dehydration, sweating, diabetes insipidus.
Gain of hypertonic fluid diagram
Increases osmolarity and ECF, decreases ICF. Causes: salt tablets, mannitol, hypertonic saline, aldosterone
Gain of hypotonic fluid diagram
Decreases osmolarity, increases ECF and ICF. Causes: SIADH, drinking tap water, primary polydipsia.
Gain of isotonic fluid diagram
Osmolarity stays the same, ECF increases. Causes: isotonic saline infusion.
Loss of hypertonic fluid diagram
Osmolarity decresaes, ECF decreases, ICF increases. Causes: mineralocorticoid deficiency
↓ECF, no change in osmolarity or ICF, isotonic urine
Loss of isotonic fluid. Causes: hemorrhage, diarrhea, vomiting
↓ECF, ↓osmolarity, ↑ICF
Loss of hypertonic fluid or hyponatremic hypovolemia. Aldosterone deficiency.
↓ECF, ↑osmolarity, ↓ICF, little concentrated urine
Loss of hypotonic fluid or hypernatremic hypovolemia. Cause: Dehydration
↓ECF, ↑osmolarity, ↓ICF, lots of diluted urine
Loss of hypotonic fluid or hypernatremic hypovolemia. Cause: diabetes insipidus
↑ECF, no change in ICF or osmolarity
Gain of isotonic fluid. Cause: isotonic saline infusion
↑ECF, ↓osmolarity, ↑ICF
Gain of hypotonic fluid or hyponatremic hypervolemia. Causes: hypotonic saline, SIADH, tap water.
↑ECF, ↑osmolarity, ↓ICF
Gain of hypertonic fluid. Causes: salt tablets, mannitol, aldosterone excess
Volume of distribution formula
Vd = Amount given or dose / Concentration
Tracer to measure plasma volume
Not permeable to capillaries - albumin
Tracer to measure ECF
Permeable to capillaries but not membranes - inulin, mannitol, sodium, sucrose
Tracer to measure total body water
Permeable to capillaries and membranes - tritiated water, urea
Blood volume Vs. plasma volume
Blood volume is plasma plus RBC –> plasma volume / 1-Hct
Effect of urea solution on cell volume
If urea is the only solute, effective osmolarity is 0 –> cell swells.
Equilibrium potential
Electrical force required to balance the chemical force of an unequeal concentration of ions
Conductance
Permeability to an ion
Electrochemical gradient
Exists when the electrical and/or chemical forces are not balanced. Its what determines difussion of the ion.
Types of channels
Ungated, voltage-gated, ligand-gated
↑[K]o
Depolarization
↓[K]o
Hyperpolarization
↑gK
Hyperpolarization
↓gK
Depolarization
↑[Na]o
Depolarization
↓[Na]o
Hyperpolarization
↑gNa
Depolarization
↑[Cl]o
Hyperpolarization
↓[Cl]o
Depolarization
↑gCl
Depolarization
Characteristics of sub-treshold potentials
Proportional to stimulus stregth, not propagated, decremental with distance, summation
Characteristics of action potentials
Independent of stimulus strength, propagated unchanged in magnitude, summation not possible
Factors that affect conduction velocity of the action potential
Cell diameter and amount of myelination are directly proportional to conduction velocity
Absolute refractory period
No stimulus can depolarize the cell
Relative refractory period
A large stimulus can depolarize the cell
Neuromuscular transmission
Action potential travels down axon and opens pre-synaptic Ca channels –> calcium influx –> release Ach vesicles –> Ach diffuses and attaches to nicotinic ion channels –> ↑gNa –> end-plate depolarization (local) spreads to areas with voltage-gated Na channels –> depolarization of muscle fiber
Excitatory postsynaptic potentials
Transient subtreshold depolarizations due to ↑gNa –> summation reaches axon hillock at the junction of cell body and axon –> voltage-gated Na channels depolarize the axon
Inhibitory postsynaptic potentials
↑gCl or ↑gK hyperpolarize the cell and lower treshold for depolarization
Electrical synapse
Action potential transmitted from one cell to the next via gap junctions, without synaptic delay and in both directions. Cardiac muscle, smooth muscle.
Sarcomere A band
Contains overlapping actin and myosin. Does not shorten during contraction.
Sarcomere H zone
Contains thick myosin filaments. Shortens during contraction.
Sarcomere I band
Contains thin actin filaments. Shortens during contraction.
Sarcomere Z line
Within the A band.
Sarcomere M line
Within the H zone.
Actin
Structural protein of the thin filaments, contains attachment sites for myosin cross-bridges.
Myosin
Structural protein of the thick filaments, contains cross-bridges that attach to actin. Has ATPase activity to terminate actin-myosin cross-bridges. ATP decreases actin-myosin affinity.
Tropomyosin
Part of thin filaments. Covers the actin attachment sites for the myosin cross-bridges
Troponin
Part of thin filaments, binds calcium, which moves tropomyosin out of the way exposing actin binding sites for cross-bridges.
What happens if calcium is removed from sarcoplasmic reticulum?
Muscle goes back to resting state. Removal of calcium requires ATP.
Rigor mortis
Depletion of ATP - cycling stops with myosin attached to actin - (muscle contracted).
Muscle contraction steps
Action potential travels down T-tubules –> activates dihydropiridine voltage sensors –> foot processes are pulled aways from ryanodine calcium release channels of sarcoplasmic reticulum –> calcium is released –> calcium attaches to troponin –> tropomyosin moves exposing actin binding sites for myosin cross-bridges –> myosin binds actin –> myosin ATPase breaks down cross bridges producing active tension and shortening –> contraction terminated by active pumping of Ca into the sarcoplasmic reticulum.
Myosin ATPase
Hydrolizes ATP to supply energy for active tension and shortening. ATP decreases myosin-actin affinity
Sarcoplasmic calcium-dependent ATPase
Supplies energy to terminate contraction and pump Ca back into sarcoplasmic reticulum.
Source of calcium for skeletal muscle contraction
Sarcoplasmic reticulum. No extracellular calcium is involved because it doesn’t have voltage-gated Ca channels.
Source of calcium for heart and smooth muscle contraction
Sarcoplasmic reticulum and extracellular. Cardiac and smooth muscle have voltage-gated calcium channels.
Tetanus
Multiple action potentials increase release of calcium thus increasing contraction. Muscle cells have a short refractory period.
Preload
Stretch prior to contraction. ↑ preload –> ↑ prestretch of the sarcomere –> ↑ passive tension
Afterload
The load the muscle is working against. ↑ afterload –> ↑ cross-bridge cycling –> ↑ active tension
What is the best measure of preload?
Sarcomere length
Preload-length tension curve
It’s a function of the length of the relaxed muscle. A positive parabola.
Isometric contraction
Active tension is produced but length stays the same. Afterload is greater than active tension, load not moved.
How is active tension produced?
Calcium binds troponin –> tropomysion exposes actin sites –> myosin cross-bridges bond to actin –> myosin ATPase generates energy to break cross-bridge link –> cycle repeats –> active tension. The more cross-bridges that cycle, the greater the active tension.
Total tension
Passive (preload) tension + active (afterload) tension
Active tension curve
It’s a function of the number of cross-bridges capable of cross-linking with actin. Negative parabola.
What is L0?
The optimum length to produce maximum active tension. Beyond L0, muscle is overstretched; below L0, it’s understretched.
Isotonic contraction
Muscle contracts and shortens to move the load. Occurs when total tension equals the load.
Most energy demanding phase of cardiac cycle
Isovolumetric contraction. Active tension is generated. Equivalent to isometric contraction of skeletal muscle.
Relationship between load, muscle force and muscle velocity
↑ ATPase activity –> ↑ velocity; ↑ muscle mass –> ↑ force generated; ↑ afterload –> ↓ velocity
Regulation of skeletal muscle force and work
↑ frequency of action potentials, ↑ recruitment, ↑ preload and ↑ afterload –> ↑ force and work
Regulation of cardiac and smooth muscle force and work
Factors that regulate force and work are preload, afterload and contractility (which is altered by hormones). No summation nor recruitment.
Characteristics of white muscle
Large mass, high ATPase activity (fast muscle), anaerobic glycolysis, low myoglobin
Characteristics of red muscle
Small mass, low ATPase activity (slower muscle), aerobic metabolism (mitochondria), high myoglobin.
Characteristics of skeletal muscle
Actin and myosin form sarcomeres, sarcolema lacks junctional complexes, each fiber innervated, troponin binds calcium, high ATPase activity, triadic contacts by T-tubules at A-I junctions, no calcium channels on membrane
Characteristics of cardiac muscle
Actin and myosin form sarcomeres, gap junctions, electrical syncytium, troponin binds calcium, intermediate ATPase activity, dyadic contacts by T-tubules near Z-lines, voltage-gated calcium channels.
Characteristics of smooth muscle
Actin and myosin not organized in sarcomeres, gap junctions, electrical syncytium, calmodulin binds calcium, low ATPase activity, lacks T-tubules, voltage-gated calcium channels.
Pressure in the right ventricle
25/0 mmHg
Pressure in the pulmonary artery
25/8 mmHg
Mean pulmonary artery pressure
15 mmHg
Pulmonary capillary pressure
7-9 mmHg
Pulmonary venous pressure
5 mmHg
Left atrium pressure
5-10 mmHg
Left ventricle pressure
120/0 mmHg
Aortic pressure
120/80 mmHg
Mean arterial blood pressure
(Systolic - diastolic / 3) + diastolic = 93 mmHg
Skeletal muscle capillary pressure
30 mmHg
Renal glomerular capillary pressure
45-50 mmHg
Peripheral vein pressure
15 mmHg
Right atrium pressure (central venous)
0 mmHg
Systemic ciruit Vs. pulmonary system
Cardiac output and heart rate is the same as they’re connected in series. The systemic circuit has higher resistance and lower compliance therefore work of the right ventricle is lower.
Highest resistance segment of the systemic circulation
Arterioles. Also responsible for greatest pressure drop.
Largest and smallest cross-sectional areas of the systemic circuit
Largest: capillaries; smallest: aorta
Fastest and slowest velocities in the systemic circuit
Velocity is inversely proportional to cross-sectional area. Aorta has fastest velocity; capillaries have slowest velocity.
Largest blood volumes in the cardiovascular system
Systemic veins then pulmonary system have the largest blood volume. Both represent reservoirs due to high compliance.
Poiseuille equation
Q = P1 - P2 / R;
Determinants of resistance
R ∝ vL / r4; if radius doubles, resistance decreases to 1/16; if radius decreases by half, resistance increases 16-fold
Reynolds number
RN = diameter x velocity x density / viscosity. If > 2,000 –> turbulent flow; if < 2,000 –> laminar flow
Vessel with the most turbulent flow
Aorta - has large diameter, high velocity. In anemia (↓ viscosity) –> aortic murmur
Features of a series circuit
Flow is the same at all points; the total resistance is the sum of all resistances; adding a resistor decreases flow at all points and vice versa;
↓ resistance, ↑ capillary flow, ↑ capillary pressure
Arteriole dilation - beta agonists, alpha blockers, ↓ sympathetic, metabolic dilation, ACEIs
↑ resistance, ↓ capillary flow, ↓ capillary pressure
Arteriole constriction - alpha agonists, beta blockers, ↑ sympathetic, angiotensin II
↓ resistance, ↑ capillary flow, ↓ capillary pressure
Venous dilation - ↑ metabolism
↑ resistance, ↓ capillary flow, ↑ capillary pressure
Venous constriction - physical compression, ↑ sympathetic
↑ capillary flow, ↑ capillary pressure, no change in resistance
↑ arterial pressure - ↑ CO, volume expansion
↓ capillary flow, ↓ capillary pressure, no change in resistance
↓ arterial pressure - ↓ CO, hemorrhage, dehydration
↓ capillary flow, ↑ capillary pressure, no change in resistance
↑ venous pressure - CHF, physical compression
↑ capillary flow, ↓ capillary pressure, no change in resistance
↓ venous pressure - hemorrhage, dehydration
Characteristics of parallel circuits
The reciprocal of the total resistance is the sum of the reciprocal of the individual resistances. Connecting a resistance in parallel lowers resistance, total resistance is always less than individual resistances.
Parallel circuits with greatest resistance
Coronary > cerebral > renal > pulmonary
What happens if a parallel circuit is added?
TPR decreases, pressure would decrease but a compensatory increases in CO maintains same pressure. Obesity.
What happens if a parallel cuircuit is removed?
TPR increases, blood pressure increases, CO might decrease to compensate increased blood pressure.
Wall tension
T ∝ Pr. In aneurysm, tension is high due to greater radius.
Factors that increase systolic pressure
↑ stroke volume, ↓ HR, ↓ compliance
Factors that decrease systolic pressure
↓ stroke volume, ↑ HR, ↑ compliance
Factors that decrease diastolic pressure
↓ TPR, ↓ HR, ↓ stroke volume, ↓ compliance
Factors that increase diastolic pressure
↑ TPR, ↑ HR, ↑ stroke volume, ↑ compliance
Factors that increase pulse pressure
↑ stroke volume (systolic > diastolic); ↓ compliance (systolic increases and diastolic decreases)
Determinants of mean arterial pressure
MAP = CO x TPR
What happens to cardiac output and mean arterial pressure if TPR increases?
MAP increases and CO decreases
What happens to cardiac output and TPR if mean arterial pressure decreases?
TPR decreases, CO decreases but then increases to compensate and maintain blood pressure
Hemodynamic changes in hemorrhage
Loss of circulating volume and CO –> less firing of carotid sinus (↓ BP) –> reflex sympathetic ↑ in TPR and CO –> ↓ venous compliance –> ↑ circulating volume –> compensated CO and BP
Hemodynamic changes during exercise
Dilation of arterioles –> ↓ TPR –> ↓ BP –> less firing of carotid sinus –> reflex sympathetic ↑ in CO –> ↑ BP
Hemodynamic changes due to gravity
↑ venous pressure, ↑ pooling of blood in veins, ↓ circulating blood volume (CO), ↓ BP –> compensation via carotid sinus –> ↑ TPR, ↑ HR
Effects of inspiration on blood flow
↓ intrapleural pressure –> ↑ venous return –> ↑ right ventricle output –> splitting of S2 –> blood in pulmonary circuit increases –> ↓ venous return to left heart –> ↓ systemic pressure –> reflex increase in HR
Effects of expiration on blood flow
↑ intrapleural pressure –> ↓ venous return –> ↓ pulmonary blood volume –> ↑ output of left ventricle –> ↑ systemic pressure –> reflex bradycardia
What factor controls blood flow to capillaries?
↑ resistance of arterioles –> ↓ capillary flow and pressure; ↓ resistance of arterioles –> ↑ capillary flow and pressure
What factors affect capillary exchange?
Exchange is by simple diffusion only. Proteins do not cross the capillary membrane. Factors that affect diffusion rate are: surface area, membrane thickness, concentration gradient, solubility
When does the rate of uptake become perfusion-limited?
When concentration of the substance reaches equilibrium between capillary and tissue. ↑ blood flow converts perfusion-limited uptake to diffusion-limited again.
When does the rate of uptake becom diffusion-limited?
When concentration between capillary and tissue are not in equilibrium.
What forces favor reabsorption?
Capillary oncotic pressure and interstitial hydrostatic pressure
What forces favor capillary filtration?
Capillary hydrostatic pressure and interstitial oncotic pressure
What happens to filtration in lung capillaries when intrathoracic pressure decreases?
↓ intrathoracic pressure promotes filtration. In ARDS –> ↓ intrathoracic pressure –> pulmonary edema
Conditions that affect capillary hydrostatic pressure
Essential hypertension increases resistance and decreases capillary hydrostatic pressure. Hemorrhage decreases capillary hydrostatic pressure and promotes reabsorption.
Conditions that affect capillary oncotic pressure
Increased by dehydration. Decreased by liver and renal disease and saline infusion
Conditions that affect interstitial oncotic pressure
Increased by lymphatic blockage and increased capillary permeability to proteins (burns)
Conditions that affect insterstitial hydrostatic pressure
Increased by negative intrathoracic pressure in ARDS
Fick principle
Measures cardiac output. Flow = O2 consumption / O2 concentration difference across the organ
Intrinsic autoregulation of blood flow
Resistance of arterioles is changed in order to regulate flow. No nerves or hormones involved. Independent of BP.
Metabolic hypothesis of autoregulation
Tissue can produce a vasodilatory metabolite that regulates blood flow. Example adenosine in coronaries.
Tissues that have autoregulation of blood flow
Cerebral, coronary and exercising skeletal muscle circulations
Extrinsic regulation of blood flow
Controlled by nervous and hormonal influences. NE via β2 vasodilates, via α1 constricts (dose dependant). Angiotensin II constricts.
Tissues that have extrinsic regulation of blood flow
Resting skeletal muscle, skin
Lowest venous PO2 in the body
Coronary circulation due to maximal extraction of O2. To increase delivery of oxygen, flow must increase.
Factors that control coronary circulation
Coronary circulation occurs in diastole and its determined by stroke work of the heart. Exercise increases volume work and coronary flow. Hypertension increases pressure work and coronary flow. Vasodilation is mediated by adenosine.
Factors that control cerebral blood flow
Flow is proportional to arterial PCO2. Hypoventilation increases PCO2 and flow. Hyperventilation decreases PCO2 and flow. PO2 determines flow only if theres a large decrease in PO2.
Factors that control cutaneous blood flow
↑ sympathetic tone –> constriction of arterioles –> ↓ blood flow, ↓ blood volume in veins –> ↑ velocity (↓ cross-sectional area). Increased skin temperature –> vasodilation –> heat loss
Highest venous PO2 in the body
Renal circulation
Factors that control renal circulation
Small changes in blood pressure invoke autoregulatory responses. Sympathetic may influence blood flow in extreme conditions (hemorrhage, hypotension)
Characteristics of pulmonary circuit
Low pressure, high flow, low resistance, very compliant, hypoxic vasoconstriction.
Pulmonary response to exercise
↑ CO –> ↑ pulmonary pressure –> pulmonary vessel dilation (due to high compliance) –> large ↓ resistance –> ↓ pulmonary pressure
Pulmonary response to hemorrhage
↓ CO –> ↓ pulmonary pressure –> pulmonary vessel constriction –> large ↑ resistance –> less blood volume
Fetal circulation: percent O2 saturation in umbilical vein
80% O2 saturation
Fetal circulation: percent O2 saturation in inferior vena cava
26% O2 saturation. Mixes with hepatic vein blood –> step up to 67%
Fetal circulation: percent O2 saturation from inferior vena cava into right atrium
67% O2 saturation. Blood from inferior vena cava enters right atrium and passes through foramen ovale
Fetal circulation: percent O2 saturation in superior vena cava
40% O2 saturation. Mixes with blood from inferior vena cava (67%) and passes to right ventricle at 50% saturation
Fetal circulation: percent O2 saturation in right ventricle
Contains blood from superior vena cava mixed with IVC –> 50% saturation. Passes through pulmonary vein and 90% is shunted through the ductus arteriosus into aorta
Fetal circulation: percent O2 saturation in ascending aorta
Contains blood from inferior vena cava –> 67%
Fetal circulation: percent O2 saturation in brachiocephalic trunk
Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) –> yields 65%
Fetal circulation: percent O2 saturation in descending and abdominal aorta
Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) –> yields 60%
Ion channels present in the heart
Ungated K, voltage-gated fast Na, voltage-gated calcium, inward rectifying iK1, delayed rectifying iK
Voltage-gated Na channels of the heart
Open and close fast upon depolarization of the membrane
Voltage-gated calcium channels of the heart
Open upon depolarization, close more slowly than sodium channels. Partly responsible for the plateau (phase 2)
Inward rectifying iK1 channels of the heart
Open under resting conditions, depolarization closes them, they reopen during repolarization phase.
Delayed rectifying iK channels of the heart
Very slow to open with depolarization (late plateau), and close very slowly. Partly responsible for repolarization
Phase 0 of the ventricular action potential
Fast Na channels open, ↑ gNa causes depolarization. Inward rectifying iK1 channels close.
Phase 1 of the ventricular action potential
Slight repolarization due to transient potassium current and the closing of sodium channels
Phase 2 of the ventricular action potential
Slow Ca channels open, ↑ gCa, ↓ gK. Plateau phase is due to slow calcium current and decreased K current
Phase 3 of the ventricular action potential
Slow Ca channels close, the delayed rectifier iK reopen, ↑ gK. K efflux causes repolarization.
Phase 4 of the ventricular action potential
Voltage-gated and ungated potassium channels are open, ↑ gK. The delayed rectifiers close but are responsible for the relative refractory period.
Why can’t the heart be tetanized?
A long absolute refractory period extends through most of the contraction. Short relative refractory period.
How do premature ventricular depolarizations occur?
Action potential develops during the relative refractory period, but the earlier the potential, the shorter in amplitude and duration it will be
Funny current
In specialized cells of the heart. It’s a voltage-gated sodium channel the opens during repolarization and closes during depolarization. The sodium influx during phase 3 slowly depolarizes the cell towards treshold.
Phase 0 of SA nodal cells
Depolarization due to opening of voltage-gated slow Ca channels.
Phase 3 of SA nodal cells
Repolarization due to ↑ gK.
Phase 4 of SA nodal cells
Gradually depolarizes cell towards treshold due to funny current - ↑ gNa
Effects of sympathetics on pacemaker cells
Slope of phase 4 increases due to ↑ funny current and ↑ gCa. Action via β1 receptors.
Effects of parasympathetics on pacemaker cells
↑ gK causing hyperpolarization and ↓ sodium funny current decreasing slope of phase 4. Effect via M2 receptors.
Fastest conducting cells of the heart
Purkinje cells
Slowest conducting cells of the heart
SA nodal cells
PR interval
Due to conduction delay of AV node. 0.12 - 0.2 seconds or 120 to 200 miliseconds
QRS complex
Ventricular depolarization - should be less than 0.12 seocnds.
QT interval
Indicates ventricular refractorieness. Normal between 0.35 - 0.44 seconds.
Effect of hypercalcemia in ECG
Shortened QT interval (< 0.35 seconds).
Effect of hypocalcemia in ECG
Prolonged QT interval (> 0.44 seconds)
Drugs that shorten QT interval
Digitalis
Drugs that prolong QT interval
Quinidine, procainamide
Effect of intracerebral hemorrhage in ECG
Inverted T waves with prolonged QT interval
ST segment
Indicates conduction through ventricular muscle. Corresponds to plateau phase of action potential.
First-degree block in ECG
Slowed conduction through AV node. PR interval > 200 msec
Second-degree block in ECG
Some impulses not transmitted through AV node. Missing QRS complexes following P wave.
Third-degree block in ECG
No impulses conducted from atria to ventricles. No correlation between P waves and QRS complexes.
Sinus rhythms
Normal, bradycardia or tachychardia
Atrial flutter
Repeated succession of atrial depolarizations. Continuous P waves. Saw-tooth appearance.
Atrial fibrillation
No discernable P waves, irregular QRS
Ventricular fibrillation
No identifiable waves. Chaotic, erratic rhythm.
Causes of left axis deviations
Left ventricular hypertrophy or dilation, conduction defects of left ventricle, AMI on right side
Causes of right axis deviations
Right ventricular hypertrophy or dilation, conduction defect of right ventricle, AMI on left side
Initial AMI in ECG
ST segment depression, prominent Q waves, T wave inversion
AMI in ECG
ST segment elevation, T wave inversion, prominent Q waves
Resolving AMI in ECG
Baseline ST, inverted T waves, prominent Q waves
Stable infarct in ECG
Prominent Q waves
Indices of left ventricular preload
LVEDV, LVEDP, left atrial pressure, pulmonary venous pressure, pulmonary wedge pressure (swan-ganz)
Sarcomere length in skeletal muscle Vs. heart muscle
In skeletal muscle it’s close to L0. In heart muscle, sarcomere legth is below optimal, therefore increased preload moves sarcomere legth towards optimal for maximal cross-bridge linking
Factors that increase slope of cardiac function curve
↑ inotropy, ↑ heart rate, ↓ afterload
Factors that decrease slope of cardiac function curve
↓ inotropy, ↓ heart rate, ↑ afterload
Factors that shift vascular function curve up and to the right
↑ blood volume, ↓ venous compliance
Factors that shift vascular function curve down and to the left
↓ blood volume, ↑ venous compliance
Factors that increase slope of vascular function curve
↓ SVR
Factors that decrease slope of cardiac function curve
↑ SVR
What is contractility and what influences it?
Contractility is the force of contraction at a given preload or sarcomere length. Due to changes in intracellular calcium
Indices of contractility
dp/dt (change in pressure/change in time); ejection fraction (stroke volume/EDV)
Changes to the action potential induced by increased contractility
↑ slope (↑ dp/dt), ↑ peak left ventricular pressure, ↑ rate of relaxation, ↓ systolic interval
Changes to the action potential induced by heart rate
↓ diastolic interval
Cardiac function curve in hemorrhage
↓ preload (down); ↑ contractility to partially compensate (left)
Cardiac function curve in excersice
↑ contractility (up, same preload)
Cardiac function curve in volume overload
↑ preload (right); ↓ contractility (slightly down)
Cardiac function curve in CHF
↓ contractility (down); ↑ preload (right)
Afterload
Force that must be generated to eject blood into aorta. ↑ afterload in hypertension, ↓ afterload in hypotension. Acute ↑ in afterload –> ↓ stroke volume, ↑ EDV, ↑ preload
Parasympathetic innervation of SA and AV nodes
Left vagus predominates in AV node, right vagus predominates in SA node
Effect of inspiration on heart rate
Inspiration makes intrathoracic pressure more negative –> increase venous return –> Brainbridge reflex (stretch receptors in the right atrium) –> tachychardia
Baroreceptor reflex
Baroreceptors in the aortic arch send afferents via vagus nerve; baroreceptors in the carotid sinus via glosopharyngeal; baroreceptor center is in the medulla. ↑ firing of baroreceptors is sensed as ↑ blood pressure –> ↑ parasympathetic, ↓ sympathetic
Acute reflex changes when blood pressure increases
↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic
Acute reflex changes when blood pressure decreases
↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic
Acute reflex changes with occlusion of the carotid
↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate
Acute reflex changes with a carotid massage
↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate
Acute reflex changes if baroreceptor afferents are cut
↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate
Acute reflex changes in orthostatic hypotension or fluid loss
↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate
Acute reflex changes in volume overload
↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate
S1 heart sound
Closure of mitral and tricuspid valves; terminates ventricular filling, starts isovolumetric contraction
S2 heart sound
Closure of aortic and pulmonary valves; terminates ejection phase, begins isovolumetric relaxation
Isovolumetric contraction
Beginning of systole, ventricular pressure is increasing but aortic and mitral valves are closed. Most energy consumption occurs here
Ejection phase
Aortic valve opens when isvolumetric contraction generates high enough pressure; ventricular volume decreases. Most work done here.
Isovolumetric relaxation
Ventricular pressure decreases; volume is end-systolic volume; aortic and mitral valves are closed
Filling phase
Opening of the mitral valve passes volume to ventricle followed by atrial contraction
Stroke volume
EDV - ESV
Ejection fraction
Stroke volume / EDV
a wave of the venous pulse
Produced by contraction of the right atrium
c wave of the venous pulse
Bulging of the tricuspid valve into the right atrium during ventricular contraction
v wave of the venous pulse
Wave rises as the atrium is filled; terminates when the tricuspid valve opens
y wave of the venous pulse
Opening of tricuspid valve and atrial emptying
Aortic stenosis
Increase in afterload. Systolic murmur, concentric hypertrophy.
Aortic insufficiency
↑ preload, ↑ ventricular and aortic systolic pressures, ↓ aortic diastolic pressure, diastolic murmur, eccentric hypertrophy
Mitral stenosis
↑ pressure and volume in left atrium, enlargement of left atrium, diastolic murmur
Mitral insufficiency
↑ atrial volume and pressure; systolic murmur
