Test 1 (Part 4) Flashcards
Electrocardiogram
- 12 Leads placed on skin surface at various locations on the torso
- Each records the VOLTAGE DIFFERENCE between itself and another location (s) on the Torso
- If there is a DIFFERENCE in VOLTAGE then there will be a DEFLECTION
- If there is NO DIFFERENCE then NO DEFLECTION
Characteristics of the ECG
- Illustrates changes of Electrical Activity of Cardiac Tissue produced by regions of DEPOLARIZATION or DEPOLARIZATION
- “Measures” EXTRACELLULAR Potential
- Only causes a DEFLECTION when:
A) Part of the CARDIAC EXCITABLE TISSUE is at a DIFFERENT Membrane Potential than the REST of the HEARTB) Current flow can OCCUR between those REGIONS - Does not cause a DEFLECTION when only the ATRIA and VENTRICLES are DIFFERING POTENTIALS
Characteristics of the ECG
- The ELECTRODES report Voltage differences in regions of EITHER the VENTRICLES of ARTIA
- Does NOT report differences between the ATRIA and VENTRICLES. WHY?
- We do not see a single based on current flow between the Atria and Ventricles - Plots changes in VOLTAGE DIFFERENCE with TIME
ECG Electrode Placements
- Each electrode looks at VOLTAGE CHANGES in the HEART from a different Direction
- One direction, referred to in the example is LEAD I, essentially looks at the HEART from LEFT to RIGHT
Voltmeter
1) Voltmeter Zero:
- Both cells Polarized with INSIDE Negative and OUTSIDE Positive. Electrodes (lead) see Outside
2) Voltmeter Charge:
- One cell DEPOLARIZE with POSITIVE inside and NEGATIVE outside. Positive electrodes sees Positive versus Negative on OPPOSITE Side
Cardiac Depolarization Path
- SA Node causes ATRIA to DEPOLARIZE from RIGHT to LEFT—-> P WAVE!!!!!!
- AV Node delays signal —-> PR INTERVAL!!!!!
- Ventricles Depolarize generally from Right to Left and from Apex to Base —-> QRS COMPLEX!!!!!!
- Action Potential PHASE 2 delays Depolarization of Ventricles —–> ST SEGMENT!!!!!!!
- Ventricles Depolarize generally from LEFT to RIGHT and BASE to APEX —–> T WAVE!!!!!
P Wave
- The P Wave represents PHASE 0 on the AP’s SPREADING through the ATRIAL Muscle
QRS Complex
- The QRS Complex represents PHASE 0 of the AP SPREADING throughout the VENTRICLES
T Wave
- The T WAVE represents PHASE 3 of DEPOLARIZATION of VENTRICULAR Muscle fibers spreading through the VENTRICLES!!!
Type of Information you Should Know
- Where are the Timed K+ gates opening in the Ventricles? —–> T WAVE!!!!
- When is Na+ MOST Permeable? —> P Wave and QRS
- Sketch an AP for SA and also AV Nodal Tissue
- **3 Types of K+ Channels:
1) Help Keep resting membrane Potential
2) Voltage Gated, causing PHASE 1 to occur
3) Close during DEPOLARIZATION and stay CLOSED for a FINITE period of time (TIMED)
- Closed during PHASE 2 and open during PHASE 3
Intervals and Segments
1) Segment represent she duration of a SINGLE EVENT on the ECG
2) An INTERVAL represents the duration of SEVERAL EVENTS
Segments
1) PR SEGMENT:
- End of ATRIAL DEPOLARIZATION until BEGINNING of QRS
2) ST SEGMENT:
- End of QRS until BEGINNING of T WAVE
Intervals
1) PR INTERVAL:
- Beginning of P Wave until BEGINNING of QRS
2) QT INTERVAL:
- Beginning of QRS until end of T WAVE
Why 12 Leads?
- Each LEAD displays VOLTAGE DIFFERENCES in the MYOCARDIUM seen from different perspectives by DIFFERENT ELECTRODES
AP Spreading
- As AP spreads through the HEART it is viewed by EACH LEAD from a DIFFERENT ANGLE
- If the AP is spreading towards the POSITIVE LEAD of the electrode set is PRODUCES a POSITIVE DEFLECTION. If going away, it produces a NEGATIVE DEFLECTION!!!
Labeling of Leads and Electrode Placements
1) STANDARD (Bipolar) Limb Leads use:
A) 1: Right Arm (RA) to Left Arm (LA)
B) 2: RA to Leg (LL)
C) 3: LA to LL
2) AUGMENTED Limb Leads:
A) aVF: Augmented Vector, Foot
- (RA+LA) to LL
B) aVR: Augmented Vector, Right
- (LL +LA) to RA
C) aVL: Augmented Vector, Left
- (LL + RA) to LA
3) Chest or Precordial Leads
- V1-6 (Vectors 1 through 6)
Standard Limb Lead Axis (EINTHOVEN’s TRIANGLE)
- Each lead is assigned a POSITIVE and NEGATIVE Polarity and the Voltage between them measured!!!
Augmented (a) Limb Leads
- One of the limb leads is assigned a POSITIVE POLARITY and the remaining 2 Electrodes are AVERAGED and ASSIGNED a NEGATIVE POLARITY
Chest or Precordial Leads
- Precordial leads are not assigned an AXIS
- Instead assigned REGIONS of the HEART
- Each lead acts as the POSITIVE ELECTRODE
Lead Assignments (IMPORTANT!!!!!!)
- Lead electrode placements are denoted to Predominantly represent certain regions of the Heart
1) INFERIOR
- II, III, aVF
2) SEPTAL
- V1, V2
3) ANTERIOR:
- V2, V3, and V4
4) LATERAL
- I, aVL, V4, V5, and V6
Axis Deviation
- If general direction of AP spreads to UPPER LEFT then LEFT AXIS DEVIATION!!!!!!!
- If general direction is to RIGHT or Lower RIGHT then RIGHT AXIS DEVIATION
- Shifted by HYPERTROPHY, MI, Physical Placement of Heart
- Bundle Branch Block
Axis:
1) EXTREME RIGHT AXIS DEVIATION: Top Left Quadrant
2) LEFT AXIS DEVIATION: Top Right Quadrant
3) NORMAL: Bottom Right Quadrant
4) RIGHT AXIS DEVIATION: Bottom Right Quadrant
P Wave
- Anything changing NORMAL origin or PATH of AP through ATRIA will alter P WAVE such as:
1) ECTOPIC Focus/ Pacemaker in either ATRIUM or VENTRICLES2) ENLARGED ATRIA
P Wave:
- ATRIAL DEPOLARIZATION upright in 1,2, V4-V6, AVF inverted in AVR, Variable in 3, AVL, other Chest Leads
PR Interval
- Dependent on mainly HOW LONG AP takes to travel through AV Node
Can be altered by:
1) Autonomic Stimulation
2) Ischemia or Infarct
3) Structural Defect
4) Drugs Altering Conduction
QRS Interval and Complex
- Normal QRS means normal Distribution by bundles PURKINJE FIBERS and NORMAL PATH (Direction and Length) through MYOCARDIUM
Altered by:
1) If not originated from or near AV node
2) Blockage (Infarct) of BUNDLE
3) Cardiac Ischemia or Infarct
4) HYPERTROPHY
- Thicker Wall
- Dilated Ventricle
QT Interval
- Dependent on duration of PHASE 2 plateau of Myocytes
Altered by:
1) Heart Rate
2) Drugs
3) Malfunctioning timed K+ or Ca2+ gates which closed at Beginning of AP and open to TERMINATE AP
ST Segment
- ST Segment is best Representation of ISOELECTRIC POINT!!!!
- If it differs from “Baseline” is is actually the BASELINE which has shifted making it appear as though the ST Segment is DEPRESSED or ELEVATED
***Heart issues will always be able to Depolarize to a Normal Value, but it will not always be able to DEPOLARIZE to a Normal Value
Ischemia
- an Ischemic region of the Heart will REMAIN DEPOLARIZED during PHASE 4!!!!
- The Extracellular potential is LESS POSITIVE than tissue on other SIDE of HEART!!!
- An electrode facing the ISCHEMIC REGION will register a NEGATIVE VOLTAGE during Phase 4
- When the ENTIRE VENTRICULAR MASS is DEPOLARIZED during the ST Segment the VOLTAE will appear to become POSITIVE interpreted as an ELEVATED ST!!!!!!
T Wave
- Dependent on NORMAL DEPOLARIZATION sequence which is usually last to DEPOLARIZE if FIRST to REPOLARIZE!!!!!!
Altered by:
1) Abnormal Depolarization sequence
2) Drugs
3) Electrolyte Disturbance
Arteries
- High ressure
Arterioles
- Moderate pressure
- Smooth muscle walls can contract to control flow by changing resistance
Capillaries
- Large cross-sectional area
- Single endothelial lining
- Nutrient, waste, and gas exchange
***VELOCITY passing through the Capillaries is SLOW!!!!
Veins
- LOWEST PRESSURE
- Large Volume
- Can contract to move Blood to Arterial side to INCREASE BLOOD PRESSURE
Velocity of Blood Flow
- V = Q/A
- Can be calculated for SINGEL VESSEL knowing its CROSS Sectional AREA and FLOW
- Can also be determined knowing Total, Summed Cross Sectional Area of PARALLEL CIRCUITS and FLOW
Relationships between Blood Flow, Pressure, and Resistance
- Q (FLOW) = DP (Pressure Gradient)/ R (Resistance)
- Can be determined through individual vessel or segment of vessel or through entire system
- CO (Cardiac Output) = (Arterial Pressure - Venous Pressure) / TPR (Total Peripheral Resistance)
Resistance to Blood Flow
- Q = DP/ R
POISEUILLE’s LAW:
- Calculates RESISTANCE through a Section of Vasculature
- R = (8hl) / (pr^4)
- h: Viscosity
- l: Length of Vessel
- p: p
- r: VESSEL RADIUS!!!!
Resistance in Parallel or Series
- If Vascular Resistances are added in SERIES then simply ADD Individual RESISTANCES for TOTAL
- If Vascular Resistance beds are added in PARALLEL then formula for TOTAL RESISTANCE is more COMPLICATED
- Adding RESISTANCE beds in SERIES, INCREASES RESISTANCE
- Adding RESISTANCE beds in PARALLEL, DECREASES TOTAL RESISTANCE
Laminar Flow and Reynolds Number
- When VELOCITY is HIGH, Cross Sectional Area LARGE, density heavy and/or Viscosity is LOW BLOOD FLOW becomes MORE TURBULENT!!!!
REYNOLDS NUMBER:
- An equation which takes into account all these factors to predict when TURBULENCE will occur:
- Nr= rdv/hA) r: Density
B) d: Diameter
C) v: Velocity
D) h: Viscosity
***If GREATER THAN 2000 then considered to transition from LAMINAR to TURBULENT FLOW
- This leads to SOUND (BRUITS) and Lesions (ARTERIOSCLEROSIS)
Compliance of Blood Vessels
- Describes how easy it is to cause a vessel to EXPAND
- How much does the vessel EXPAND in response to a given change in LUMEN HYDROSTATIC PRESSURE?
COMPLIANCE: (Change in Volume)/ (Change in Pressure)
*****Smooth Muscle CONTRACTION causes shift in Compliance moving blood to Arterial Side and INCREASING PRESSURE!
**Compliance remains the same with Smooth Muscle CONTRACTION but SAME RESULT!!!
Pressures in the Cardiovascular System
- Pressure GRADUALLY drops through the Systemic Circulation
- PULSATILE nature at AORTIC END due to Compliance and Distension during EJECTION and RECOIL during DIASTOLE.
- **LOST BY ARTERIOLES!!!!!!!
Pressure Profile in Blood Vessels
- Clinically measure “Systolic Pressure” is GREATEST PRESSURE reached in LARGE ARTERY
- Clinically measure “Diastolic Pressure” is LOWEST PRESSURE reached in LARGE ARTERY
Presssure Profile in Blood
1) Systolic Pressure: 120
2) Diastolic Pressure: 80
3) Pulse Pressure: Systolic - Diastolic = 40
4) Mean Pressure: Diastolic + 1/3 Pulse Pressure = 80 + (40/3) = 93.3
Pulse Pressure and Compliance
- Since the PULSE PRESSURE is DEPENDENT on the ARTERIAL COMPLIANCE, a DECREASE in COMPLIANCE would cause it to INCREASE
- Systolic Pressure would INCREASE
- Diastolic Pressure may stay the same or could actually DECREASE
- What effect would INCREASED STROKE VOLUME have?
- What effect would INCREASED RESISTANCE have?
Answer: Increased Resistance would shift the ENTIRE CURVE UP with no Change in Shape or Pulse Pressure
Venous Pressure
- Low Pressure, High Compliance, Large Volume
Arterial Pressure
- Low and estimated by “Pulmonary Wedge Pressure”
- Since the measurement site is a little upstream from Atrium, it is a few mm Hg greater than ACTUAL left ATRIAL PRESSURE!!
P Wave
- ATRIAL Depolarization
- Upright in 1, 2, V4-V6, and aVF
- INVERTED in aVR
- Variable in 3, aVL, other chest leads
PR Interval
- Beginning of P wave to beginning of QRS Complex
- Time from SA NODE to VENTRICULAR MUSCLE FIBER 0.12-0.20 Seconds!!!!!
QRS Complex
- VENTRICULAR DEPOLARIZATION
- 0.05 - 0.10 Seconds DURATION
- Q Waves shouldn’t be more than 0.03 seconds in WIDTH
- Q Waves, Narrow/ Small, 1-2 mm is Normal
- In 1, aVL, aVF, V5, V6
ST Segment
- After the QRS Complex observe the LEVEL (Relative to baseline; ELEVATED or DEPRESSED) and SHAPE
- Normally it is ISOELECTRIC; sometimes normally elevated not more than 1 mm in STANDARD LEADS and 2 mm in CHEST LEADS; it is NEVER NORMALLY DEPRESSED more than 1/2 mm
- ST Depression: SUBENDOCARDIAL
- ST Elevation: SUBEPICARDIAL or TRANSMURAL Injury or ISCHEMIA
**ST Segment ELEVATION can be seen as Normal in a HEALTHY BLACK MAN
T Wave
- VENTRICULAR REPOLARIZATION
- Direction, Shape, Height UPRIGHT: 1, 2, V3-V6
- Inverted: aVR
- Variable: 3, aVL, aVF, V1-V2
- Height: Not Greater than 5 mm in STANDARD LEADS not Greater than 10 mm in PRECORDIAL LEADS
QT Duration
- LENGTH of Ventricular SYSTOLE
- Myocardial Ischemia
- Myocardial Injury
- Myocardial Infarction
T Wave: Ischemic pattern is associated with INVERTED T WAVES
ST elevation: Pattern of INJURY
Q Wave or QS Complex: Pattern of NECROSIS or INFARCTION
EKG Features to be examined
1) Rate
2) Rhythm
3) Axis
4) P Wave
5) PR Interval
6) QRS Interval
7) QRS Complex
8) ST Segment
9) T Wave
10) U Wave
11) QT Interval
How to find the Rate
- Find a QRS that lands on a DARK LINE and count how many lines until the next QRS
- Take that number and divide 300 by it!
PR Interval Variations
1) Normal PR Interval: 0.14 seconds
2) Short PR Interval: 0.10 seconds
- Hypertensive patient shortly after an episode of Atrial Flutter
3) Prolonged PR Interval: 0.30 seconds
- Shallowly INVERTED Tp Wave immediately following P Wave
QRS
Q: First Deflection DOWNWARD
R: First Deflection UPWARD
S: Second Deflection DOWNWARD
T Wave Variations
- Tall T Wave od MYOCARDIAL ISCHEMIA is a patient with ANGINA but without INFARCTION
- Tall upright symmetrical T Wave of INFERIOR INFARCTION
Rhythm: Basic
- Is the Rhythm a Sinus Rhythm?
- Is there a P- Wave before every QRS Complex and Vice Versa?
1) PR
Rate
- Heart Rate > 100 = Tachycardia
- Heart Rate
Sinus Rhythm
- When we see a NORMAL P WAVE before every QRS Complex!!!
Rhythm
- P Wave precedes QRS
- P:QRS = 1
- Sinus Rhythm
- Are there other Rhythm? Yes
A) Ectopic Atrial RhythmB) Multifactorial Atrial TachycardiaC) Wandering Atrial PacemakerD) Others
Rhythm Cont
- P Wave follows QRS
- SVT (AV Nodal Re-entry Tachycardia)
- Junctional Rhythm
No P WAVES:
- ATRIAL FIBRILLATION, Atrial Flutter, Junctional or Ventricular Escape Rhythms, Junctional Tachycardia, VT
Six Limb Leads to the Standard EKG
Bipolar Limb LeadS:
1) I
2) II
3) III
Augmented Limb Leads
1) aVR
2) aVL
3) aVF
Axis
- Where is the Electrical Conduction living?
Quick and Dirty:
1) NORMAL AXIS: Positive Deflection in LEADS I and aVF
2) LEFT AXIS: Positive in LEAD I and Negative in aVF
3) RIGHT AXIS: Negative in LEAD I and Positive in aVF
Sinus Tachycardia
- Physiologic/ pathologic process
- LOOK FOR THE CAUSE
- Emotion, anxiety, fear, drugs, hyperthyroid
- Fever, pregnancy, anemia, CHF
- Hypovolemia
Atrial Arrhythmias
- Premature Atrial Contraction, also APC
- Seen in ABSENCE of significant heart disease; associated with Stress, Alcohol, Tobacco, Coffee, COPD, and CAD
Premature Beats
- An IRRITABLE FOCUS spontaneously fires a SINGLE STIMULUS:
1) Premature Atrial Beat
2) Premature Junctional Beat
3) Premature Ventricular Beat
Ventricular Rhythm Disturbances Principles of Treatment
1) Consider the setting:
- Normal, Stress, Hypoxia
2) Drugs:
- Nicotine, Caffeine, Thyroid, Aminophylline
- Digitalis, Intoxication
3) Heart Failure:
4) Acute Myocardial Infarction (AMI)
5) Ischemic Heart Disease
6) Cardiomyopathy
7) Electrolyte Disorder
- Hypokalemia, Hyperkalemia, Hypomagnesemia
Premature Ventricular Contraction (PVC)
- The QRS Complex and the ST Segment are going in OPPOSITE DIRECTIONS!!!
***A very IRRITABLE Ventricular focus ca EMIT CONSECUTIVE STIMULI
Atrial Fibrillation
ECG
- Atrial rate > 350-600/ min
- Undulating baseline
- No discernible P WAVES
- Irregular RR Interval (QRS Complex)
- “Irregularly Irregular” Ventricular Rhythm
Paroxysmal Ventricular Tachycardia
- 150 to 250/ min
- Suddenly, a very Irritable Ventricular focus PACES RAPIDLY!
Paroxysmal Supraventricular Tachycardia
- When you increase the HEART RATE the P Waves start to disappear
- The bumps seen are the T Waves
SUPRAVENTRICULAR TACHYCARDIA:
- Common in NORMAL Hearts
First Degree AV Block
- “Measure” PR by observation (ONE LARGE SQUARE)
- PR remains consistently lengthened cycle-to-cycle
Microcirculation
- Arterioles with Smooth muscle wall
- Metarterioles with limited Smooth muscle walls
- Capillaries with PRECAPILLARY SPHINCTERS
Exchange of Substance across the Capillary Wall
- Clefts allow passage of WATER SOLUBLE Substances such as Glucose, Electrolytes, etc
A) Very small in BrainB) Very large in Liver and Gut - Lipid soluble substances such as O2 and CO2 pass through Cell Wall
- Some LARGE MOLECULES may pass through in Vesicles
Fluid Exchange Across Capillaries
- The STARLING EQUATION calculates the FLOW of Water wither OUT of the CAPILLARY (+) or drawing it INTO the CAPILLARY (-)
- It is dependent on the NET FORCES influencing the MOVEMENT of WATER
- There are two types of FORCE both of which are found on BOTH SIDES of the Capillary Wall
A) IntravascularB) Extravascular or Interstitial - Hydrostatic Pressure (P)
- Osmotic Pressure (p)
***Albumin PULLS fluids out of the Interstitial and into the Capillary
**Hydrostatic Pressure in the Interstitial is VERY LOW!!!
**Hydrostatic Pressure in the LUMEN is POSITIVE because it is the Force pushing the FLUID OUT
***Colloid Osmotic Pressure is PULLING FLUIDS IN = NEGATIVE Value
Starling Equation
Jv = Kf [(Pc-Pi) - (pc-pi)]
= Kf [(Forces moving fluid out) - (forces moving fluid in)]
= Kf [(Pc + pi) - (Pi + pc)]
- Net driving pressure determine rate of fluid exit from or entry into the Capillary
- These forces (Pc, Pi, pc, and pi) can be altered and cause fluid shifts between the Vasculature and Interstitial
- Usually fluid leaves Capillary at Arteriolar end and some, but not all, RETURNS into the Capillary at the VENOUS END
- The NET EXCHANGE is a GRADUAL LEAKAGE of Fluid OUT of the Capillary and into the Interstitial which must be gathered up by the LYMPHATIC SYSTEM and returned to the Venous Circulation
Calculation of Forces
Jv = Kf [(Pc-Pi) - (pc-pi)]
= Kf [(Forces moving fluid out) - (forces moving fluid in)]
= Kf [(Pc + pi) - (Pi + pc)]
- Representative examples at the Arterial end might be: Pc = 30 Pi = 1 pc = 26 pi = 3
- Therefore (30 + 3) - (1 + 26) = 6 mm Hg
- This would mean that there is a net movement of FLUID OUT of the CAPILLARY
What can Alter these Forces- EDEMA
1) Pc by ELEVATED Venous Pressure (Heart Failure)
2) Pi by RESTRICTED Lymphatic Flow or INCREASED Driving Furce out of Capillary
3) pc by DECREASE in Albumin (Starvation, Liver Failure)
4) pi by RESTRICTED Lymph Flow or Inflammation
Lymph
- Excess fluid and proteins and other substances enter the Lymphatics via Valved Channels
- Muscle pumps push LYMPH through Lymph Node “SCRUBBERS”
- About 2 to 3 Liters/ day re-enters at SUBCLAVIAN VEIN
Special Circulations
- Already talked about how SYMPATHETIC CONTROL (Central Control) can GLOBALLY alter RESISTANCE (TPR) by stimulating the RESISTANCE BEDS
- Local beds have an ability to BREAK from this Control if need becomes GREATER than is being allowed (Local Control)
- Usually when a tissue “breaks” it is not sufficient to significantly alter TPR or other tissues compensate by FURTHER CONSTRICTION to MAINTAIN BP constant in the face of some tissues “Breaking” from Central Control
1) Myogenic Control (Autoregulation)
- If BLOOD PRESSURE is ELEVATED, which would other deliver MORE BLOOD than necessary, Arterial walls become STRETCHED and that causes VASCOCONSTRITION
- The opposite would also be true
2) Metabolic Control
- ACTIVE HYPEREMIA is Increasing Interstitial Concentration of metabolites such as CO2, H+, K+, Lactate, and Adenosine or reduction of O2 to INCREASING metabolic rate causes Smooth Muscle of Arterioles, Metarterioles, and Pre-Capillary Sphincters to RELAX Increasing flow through the area
- REACTIVE HYPEREMIA is when a Vascular Obstruction causes build up of Metabolites leading to Vasodilation. Therefore, if the obstruction is removed the area is Flooded with Blood
3) Methods of Local Control- SHEAR
- If Vascular Bed DILATES due to metabolic demand the flow through the Upstream Arterioles and small Arteries would Increase
- This would INCREASE the SHEAR or WALL FRICTION leading to the RELEASE of NO which would cause Vasodilation and Augment the DOWNSTREAM Metabolic Effect
Relative Contribution to Control of Blood Flow of Central (neural) versus Local Mechanisms
- Look at CHART on SLIDE 13 of MICROCIRCULATION LECTURE!!!!
Neural and Hormonal Control of Blood Flow
- SYMPATHETIC Stimulation causes Vasoconstriction. Decreasing Sympathetic stimulation causes Vasodilation
1) HISTAMINE and BRADYKININ
- Arteriolar Vasodilation
- Increase Capillary porosity (Kf) allowing escape of Large Molecules
- Causes EDEMA in response to Tissue Damage
2) SEROTONIN
- Vasoconstriction in response to Tissue Damage
3) PROSTAGLANDIN
- Mixed
Coronary Circulation
- Largely under METABOLIC CONTROL
- Sympathetic Innervation of Vasculature but usually ignored
- ventricular, especially LEFT VENTRICULAR CONTRACTION causes Constriction of Vasculature most notably near the ENDOCARDIAL SURFACE!!!
Cerebral Circulation
- Largely METABOLIC CONTROL
Pulmonary Circulation
- The HIGHEST Pressures of the PULMONARY Vascular System are found in the RIGHT VENTRICLE and PULMONARY ARTERY
- The Pressure in the RIGHT VENTRICLE varies from 24 mm Hg (Highest Reading) dow to between 0 to 4 mm Hg (Lowest Reading)
- The pressure changes are LESS in the Pulmonary Artery with the MAXIMUM the Same (24 mm Hg) but the MINIMUM being Grater at near 10 mm Hg to 16 mm Hg
- Average PRESSURE is up to 20 mm Hg in the Pulmonary Artery
Pulmonary Circulation
- What is the the resistance of the Pulmonary Vasculature compared to that of the Systemic Circulation?
- VIEW CHART on SLIDE 17 of MICROCIRCULATION LECTURE
Regulation of Pulmonary Blood Flow
- VASOCONTRICTION to Alveolar Hypoxia (Hypoxic Vasocotriction)
- Little Sympathetic Influence
- Arterial system much more compliant than Systemic Arteries.
- Therefore, relatively small changes in MEAN PRESSURE will significantly DILATE ARTERIES, RESUCE RESISTANCE, and HELP Maintain PRESSURE LOW in the Fact of LARGE CHANGES in FLOW
Skeletal Muscle
1) At REST under Central, Baroceptosr Control
- Norepinephrine to a Receptors
- When active, comes under LOCAL CONTROL:
A) Motor Centers also causes GENERALIZED INCREASE in Sympathetic Outflow causing INCREASE CO and Non-Muscle Vascular Resistance. This response compensates for an ANTICIPATED DROP in TPR by Skeletal Muscle METABOLIC DILATION and helps Maintain BP CONSTANT
2) During FLIGHT RESPONSE, Adrenal Glands SECRETE EPINEPHRINE which binds to Beta2 Receptors which causes VASODILATIOn
F- SKIN
- SYMPATHETIC Vasoconstriction to Baroceptosr Reflex
- SYMPATHETIC Inhibition and Dilation of SHUNT Pathways to EXCESSIVE BODY TEMPERATURE
Shunts
1) RIGHT to LEFT Shunt
- Blood passing from Systemic Veins to Systemic Arteries WITHOUT passing through Functional LUNG Tissue
2) LEFT to RIGHT SHUNT
- Blood passing from SYSTEMIC ARTERIES to SYSTEMIC VEINS WITHOUT passing through a CAPILLARY BED for Substance Exchange
Pressure Control Overview
- In order to meet metabolic needs of tissue adequate blood flow must be MAINTAINED
- Local arterial beds rely on a constant, high input pressure to control how much blood the tissue RECEIVES
- When metabolic demand is high, more blood is released through Capillary beds by REDUCING RESISTANCE of Arterioles
- This requires 2 general Control Mechanisms
1) One to MAINTAIN a CONSTANT, HIGH input Pressure
2) One to ALTER RESISTANCE to FLOW through individual VASCULAR BEDS
Pressure Control
- There are 2 general methods of Control of Arterial Pressure:
1) RAPID, NEURALLY mediated mechanism utilizing Pressure Sensors, a Control center and Pressure Control Mechanisms influencing the HEART and VASCULATURE (Baroreceptor Reflex)
2) SLOWER, HORMONALLY mediated mechanism again UTILIZING sensors and ALTERING cardiac and Vasculature FUNCTION. A large component of both the SENSOR and PRESSURE influencing ORGANS are the KIDNEYS
Baroreceptor Reflex
- A NEGATIVE FEEDBACK, as most of the reflexes are, which response to a CHANGE in ARTERIAL PRESSURE by invoking processes to return it to its original level
- Can act WITHIN SECONDS and LAST INDEFINITELY
Baroreceptors- The Sensory Structures
- BARORECEPTORS in CAROTID SINUS and AORTIC ARCH sense changes in Blood Pressure through the STRETCH it imposes on the Vessel Wall
- They INCREASE FIRING RATE in response to INCREASING VASCULAR WALL STRETCH and DECREASE FIRING RATE when PRESSURE FALLS!!
Brainstem- The Control Center
- Baroreceptors send input to the Control Center in the MEDULLA often referred to as the VASOMOTOR CENTER
- Within the center are Clusters of cells responsible for acting via OUTPUTS traveling either in the PARASYMPATHETIC (Vagus) Nerve or the SYMPATHETIC nerves on various aspects of the Cardiovascular System
Control Center- Vasomotor Center
- INCREASED FIRING of Baroreceptors (increased Pressure)
- DECREASES the SYMPATHETIC OUTFLOW and INCREASE PARASYMPATHETIC OUTFLOW
- DECREASED FIRING causes the OPPOSITE
Integrated Function of the Baroreceptor Reflex
BP= CO x TPR
CO = SV x HR
1) SV dependent on:
- SYMPATHETIC Stimulation of the HEART
- PRELOAD
2) HR dependent on:
- SYMPATHETIC stimulation
- PARASYMPATHETIC stimulation
TPR dependent on SYMPATHETIC Stimulation of ARTERIOLES!!!
Control Center
SYMPATHETIC System causes:
- CONSTRICTION of Arterioles and Veins (ALPHA Receptors)
- INCREASES HR and CONTRACTILITY (BETA-1 Receptors)
- Also causes FLUID Retention by KIDNYE due to AFFERENT ARTERIOLAR CONSTRICTION and INCREASED RENIN SECRETION
PARASYMPATHETIC System causes a DECREASE of HEART RATE:
- Muscarinic Receptors
- Acts on Sinoatrial Node
Renin-Angiotensin II- Aldosterone System (RAAS)
- The baroreceptor reflex occurs within seconds and attenuates somewhat with time
- For LONG TERM adjustments a HORMONAL RESPONSE is INVOKED and begins WITHIN MINUTES and can build over a PERIOD of DAYS or LOGNER if needed
Baroreceptors
- Baroreceptors reflexes are considered both SHORT and LONG TERM compared to HORMONE CONTROl which is generally considered to be more of a LONG TERM SOLUTION
Renin
- Renin is an enzyme secreted by the KINDYE into the BLOODSTREAM in response to a drop in BP
- If BP goes HIGHER than NORMAL then LESS RENIN is SECRETED
- Renin causes ANGIOTENSINOGEN to be converted to ANGIOTENSIN I in the Blood
- ANGIOTENSIN I is converted to ANGIOTENSIN II in the LUNGS to being the compensation Mechanism
- SYMPATHETIC STIMULATION also INCREASES SECRETION!!!!!
Renin Production
- Renin is secreted by JUXTAGLOMERULAR (JG) CELLS in walls of RENAL AFFERENT Arterioles
- In RESPONSE to LOW BP and in RESPONSE to SYMPATHETIC STIMULATION
Angiotensin II
1) Causes SECRETION of ALDOSTERONE from Adrenal Cortex
- Causes Na+ and H2O RETENTION by KIDNEY
- Increases BLOOD VOLUME, PRELOAD, STROKE VOLUME, CO, and therefore BP!!!!
2) Acts directly to INCREASE Na+ and H20
- Increases PRELOAD and BP
3) Increases THIRST
4) Stimulates SECRETION of ANTIDIURETIC Hormone (ADH)
- Reduces URIN Production (Fluid Retention)
- Increases BLOOD VOLUME and BP
- Binds to ARTERIOLAR receptors to cause CONSTRICTION and INCREASE TPR (now called VASOPRESSIN)
5) Causes GLOBAL VASOCONSTRICTION of Arterioles via specific receptors
- INCREASES TPR and therefore BP
BP= CO x TPR
Angiotensin II- Pharmacological Intervention
- ANGIOTENSIN CONVERTING ENZYME INHIBITORS (ACE) prevent the conversion of ANG I to ANG II in LUNGS
- Side effect can be COUGHING because of accumulation of BRADYKININ. AND II breaks down BRADYKININ
- Arteriolar ANG II Receptors can also be BLOCKED by ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)
Other Regulatory mechanisms
- CEREBRA ISCHMEIA causes increased Sympathetic OUTFLOW from VASOMOTOR CENTER
- PROTECTIVE if blood pressure i dropping and not enough to adequately PREFUSE BRAIN- Can cause HYPERTENSION if INTRACRANIAL PRESSURE reduces FLOW to VASOMOTOR Center (CUSHING REACTION) or if Stroke leaves Vasomotor Center Ischemic
- Other Central Regions can ACTIVATE or DEPRESS Sympathetic or Parasympathetic OUTFLOW
- Respiratory Center via CHEMORECEPTORS
- MOTOR CORTEX
- MICTURITION CENTER
Vasopression
- Previously said to be SECRETED in response to ANG II
- Also secreted in response to receptors in ATRIA in the PRESENCE of LOW PRELOAD
- Increasing OSMOLARITY of blood will also INCREASE SECRETION
- Causes INCREASED TPR and Water Retention
Natriuretic Peptide
3 formes names:
1) ATRIAL (ANP)
2) BRAIN (BNP)
3) C-Type (CNP)
- Secreted by EXCESSIVE PRELOAD of ATRIA and VENTRICLES
Causes:
1) Arteriolar Dilation: DECREASES TPR
2) Increases Fluid Loss: DECREASES PRELOAD
3) Inhibits Renin: DECREASES both TPR and PRELOAD
- Protects against OVERDILATION or OVERSTITCHING of CARDIAC CHAMBERS
Principles of Clinical ECG Cases
1) Treat the patient- not the ECG
2) Establish urgency of treatment - responsiveness, ABCD survey differential diagnosis, treat reversible causes (Hypoxia, Hypokalemia, Hypovolemia)
3) Access hemodynamic stability (LOC, BP, HR)
4) Antiarrhythmic/ electrical therapy
Arrhythmias
Palpations- skips, pounds, irregular
Lightheadedness- faint like
Syncope (near syncope)
Chest pain
Dyspnea
Sudden Death
Stress:
- Ischemia
- Hypoxia
- Metabolic Acidosis
- Infection: endocarditis
- Inflammation- Myocarditis
Sinus Tach
- Physiologic/ pathologic process
- Look for cause
- Emotion, Anxiety, Fear, Drug, Hyperthyroid
- Fever, Pregnancy, Anemia, CHF
- Hypovolemia (Need Volume)
Sinus Node
- Normally, the dominant Cardiac Pacemaker because of its Intrinsic Discharge rate it the HIGHEST of all POTENTIAL CARDIAC PACEMAKERS
- Bradycardia:
Sinus Bradycardia
- P Wave represents FORMATION of SINUS IMPULSES, Each Atrial Impulse is FOLLOWED by VENTRICULAR BEAT
- Rate
Medical Condition/ Situations Associated with Bradycardia
- Normal People
- Healthy Althea: well trained, goo physical endurance
- Physiologic component to Sleep, Fright, Carotid Sinus Massage, Carotid Hypersensitivity, Avoid tight collars, shave neck lightly, massage or ocular pressure (glaucoma), mental control - yoga training
- Obstructive jaundice: effect of bile salts on SAN
- Sliding Hiatal hernia
- Valsalva Maneuver: lifting heavy object, straining bowels
Medical Condition/ Situations Associated with Bradycardia
- Ischemia
- Decrease pO2
- Increase pCO2
- Decrease pH
- Increase BP
Treatment of Sinus Bradycardia
- Depends on Clinical Setting/ DX the cause: may not need to be TREATED
- Depends on Hemodynamics/ Impaired
- Depends on Circulation
- Maybe no or few symptoms: no RX
If hemodynamically Compromised may get combination of:
1) Decr BP
2) Decr CO, Decr SV, Decr Renal Perfusion : OLIGURIA
3) SOB, Decr Cerebral Profusion: CONFUSION
4) CP, Cool, Clammy, Diaphoretic
5) Syncope, Dizziness, Fatigue
6) Fatigue
Treatment of Sinus Bradycardia Cont
- Commonly seen in S.B. in ACUTE INFERIOR MI: especially in the first few hours. This is related to SN Ischemia or to a VAGAL REFLEX Initiated in the ISCHEMIC AREA
- RX: if HR
Treatment of Sinus Bradycardia Cont
ATROPINE: 0.3 —> 0.5 —> 2 mg IV
- Repeat 10 min
Use caution in GLAUCOMA: can IOP
Side effects of Atropine:
- Urinary Retention
- ABD Distension
- Transient
Epinephrine 1-10 ug/ min
Isoproterenol (1 mg in 500 cc D5W —> 1-4 ug/ min IV
Pacemakers!!!!
Sinus Arrhythmia
Sinus Arrhythmia- SAN forms impulses IRREGULARLY
- Waxes/ Wanes with PHASES of RESPIRATION
- HR Increases with INSPIRATION
- HR Decreases with EXPIRATION
- Sinus Arrhythmia is NORMAL FINDING
Multifocal Atrial Tachycardia
- 3 or more DIFFERENT P Waves
- PR Interval varies
- Irregular Ventricular Rhythm
- Atrial Rate > 100
- ASSOCIATED with LUNG DISASE (COPD, Pneumonia, Ventilator Theophylline), Beta Agonists, Electrolyte Abnormalities (Decr K, Decr Mg) Digitalis Toxicity, Sepsis
Multifocal Atrial Tachycardia
IRREGULAR RHYTHM
- P Wave shape varies
- Atrial Rate exceeds 100
- Irregular Ventricular Rhythm
Atrial Fibrillation
- Atrial Rate > 350-600/ min
- Undulating Baseline
- No discernable P Waves
- Irregular RR Interval (QRS Complex)
- “Irregularly Irregular” ventricular Rhythm
Atrial Flutter
- “Saw tooth Appearance”
- Leads II, III, aVF, V1, Often Best Leads
Supraventricular Tachycardia
- No P Waves, so it is a JUNCTIONAL AVNRT!!!
- QRS Complex NARROW
- Any Tachycardia SHORTENS Diastole (No P Waves)
Premature Ventricular Contractions
Etiology:
- Normal Heart
- CAD, MI, HF, Myocardial Ischemia, Hypoxia
- Valvular Heart Disease, Congenital heart Disease
- Cardiomyopathy, Electrolyte Abnormalities
- Acid Base Imbalance
- Hyperthyroid
- Drugs
Premature Ventricular Contractions Cont
ECG Characteristics of PVC:
- Premature, Bizarre, Wide QRS
- No preceding P Wave; may produce a RETROGRADE P wave in ST Segment
- ST-T Wave moves in OPPOSITE DIRECTIOn of QRS
- Usually FULL Compensatory pause
Treatment of PVCs
- If stable no RX
- If Symptomatic or in setting of ACS: METOPROLOL 2.5 - 10 mg IV
- If unstable: AMIODRANE, LIDOCAINE (1-1.5 mg/ kg up to 3 mg/ kg)
PROCAINAMIDE
Ventricular Tachycardia
- 3 or more Consecutive Bizarre QRS Complexes
- Ventricular Rate 120 - 200 (100- 250)
- Usually regular, wide QRS (> 0.12 Sec)
- P Wave OFTEN LOST; if seen no RELATIONSHIP to QRS (AV Dissociation)
- Lasts owner than 30 Seconds (SUSTAINED)
Ventricular Fibrillation (VF)
- Disorganized Depolarization
- Noneffective Pump
- Clinical setting: AMI, HF, IHD, K+ Disturbance (Low or High)
Treatment of Ventricular Fibrillation
CPR
- Defibrillation
Torsades de Pointes
- “TWISTED RIBBON”
- Twisting of the Points
- QRS Swings from Positive to Negative Direction
- May be INHERITED (Prolonged QT) or acquired (Class I, II Antiarrhythmias, Alcohol, TCA, Electrolyte Imbalance - K, Ca, Mg)
Torsades de Pointes Treatment
- DC Cardioversion
- MgSO4, 1-2 Grams IV Bolus
- Overdrive Pacing
- ISOPROTERENOL
Hypokalemia
- Very common in HOSPITAL or office
Etiology:
- DIURETICS
- Metabolic Aklalosis (Transcellular Shift of K+ into Cell
- High ALDOSTERONE (Conn’s CUshings)
- Beta-agonist overdose, Diarrhea, Renal Loss
ECG:
- U Waves inc QT Interval, FLAT or INVERTED T WAVE!!!!!
Hyperkalemia
- Renal Failure (Insufficiency)
- Metabolic Acidosis
- DKA
- Cell Breakdown (Hemolysis, Rhabdomyolysis)
ECG:
- Peaked T Wave, Wide QRS, Inc PR Interval, Loss of P Wave
Treatment of Hyperkalemia
- Dialysis
- Insulin and Glucose
- Na HCO3
- Albuterol
- Resin Binding Agents
- Calcium Glutinate/ Chloride
None
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