ADVANCED ASSESSMENT Cardiovascular System
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Transcript of ADVANCED ASSESSMENT Cardiovascular System
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OBHG Education Subcommittee
ONTARIOBASE HOSPITAL GROUP
ADVANCED ASSESSMENT Cardiovascular System
2007 Ontario Base Hospital Group
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OBHG Education Subcommittee
ADVANCED ASSESSMENT Cardiovascular System
AUTHORS
Mike Muir AEMCA, ACP, BHScParamedic Program ManagerGrey-Bruce-Huron Paramedic Base HospitalGrey Bruce Health Services, Owen Sound
Kevin McNab AEMCA, ACPQuality Assurance Manager
Huron County EMS
References – Emergency Medicine
REVIEWERS/CONTRIBUTORSRob Theriault EMCA, RCT(Adv.), CCP(F)Peel Region Base Hospital
Donna L. Smith AEMCA, ACPHamilton Base Hospital
Tim Dodd, AEMCA, ACPHamilton Base Hospital
2007 Ontario Base Hospital Group
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CONSISTS OF: Heart (pump) Arteries and veins (container) Capillaries (site nutrient, gas exchange)
Cardiovascular System
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Transportation of oxygen and other nutrients to the cells
Removal of carbon dioxide and wastes Distributes hormones Control heat transfer
Functions
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Heart Anatomy
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Left Ventricle High Pressure More Muscle Systemic
Right Ventricle Low Pressure Less Muscle Pulmonary
Heart Anatomy
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Three Layers
Endocardium Myocardium Epicardium
Heart Anatomy
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Automaticity All myocardial cells can generate an
electrical impulse
Conductivity Intercalated discs
Contractility Functional syncitium
Heart Physiology
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1. Right atria via vena cava
2. Tricuspid valve into right ventricle
3. a) Pulmonic valve to pulmonary artery
4. b) Right and left pulmonary arteries
Blood Flow
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4. Pulmonary arterioles to capillaries = gas exchange
Blood Flow
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4. Left atrium via pulmonary veins
5. Mitral valve to left ventricle
6. Aortic valve to aorta
Blood Flow
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Arteries Arterioles Capillaries Venules Veins
Arteries & Veins
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Three Layers Intima Media Adventitia
Arteries & Veins
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Left Main Left Anterior
descending Circumflex
Right RCA Marginal Posterior
Decending
Coronary Arteries
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Limb Leads Chest Leads
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Lead Groups
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Contractility Conductivity Automaticity
Neuromuscular Electrophysiology
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Contractility Similar to skeletal muscle Interwoven muscle fibers
Contractility
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Muscle Fiber
Contractility
Thin Filament Actin Molecule
Troponin Tropomyacin
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Muscle Contraction
Ca2+ = Troponin =
Tropomyocin =
Contractility
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Cardiac versus Muscular
Contractility
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Specialized tissues conduct electrical impulses SA Node Intra-atrial pathways AV Node Bundle of His Lt and Rt Bundle Branches Purkinge Fibers
Conductivity
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Conduction System
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Cardiac Conduction
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Phase 0: Rapid Depolarization Phase 3: Relative Refractory Period
Phase 1: Early Repolarization Phase 4: Resting Membrane Potential
Phase 2: Plateau ( Absolute Refractory Period)
+ 20
- 100
0
-85
-65
PURKINJE FIBRE
Na+
K Na Cl Ca K K K K+ + ++ + + ++-
4 4
0 1 2
3
mV
INSIDE CELL OUTSIDE CELL
THRESHOLD
POTENTIAL
Action Potential
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Inherent ability of all myocardial cells to spontaneously depolarize
Primary Pacemaker - SA Node Secondary – AV Node, Bundle of His, Bundle
Branches, Purkinge Fibers Under stress all other cells can generate an
impulse
Automaticity
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Pacemaker Sites
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Phase 0: Depolarization Phase 3: Relative Refractory Period
Phase 1: Does not Apply Phase 4: Spontaneous Phase 4 Rise
Phase 2: Plateau ( Absolute Refractory Period)
- 100
- 85
- 65
0
+ 20
PACEMAKER CELL
33
444
30 00
2 2 2
SA Node
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Cardiac Output
=
Heart Rate x Stroke Volume
Cardiac Output
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Intrinsic Preload
Extrinsic ANS Electrolytes Temperature Humoral/Chemical
Cardiac Function Control
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Preload Venous return to Heart 70 % blood volume Low Pressure
Intrinsic
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Autonomic Nervous System
Extrinsic influences on CO
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Electrolytes K+ - Increase will decrease rate and force Na+ - Increase will decrease force Ca++ - Increase will increase force
Temperature Low - Decreased rate Hi - Increased rate,Increased force
Humoral/Chemical Catecholamines – increase rate and force ADH – increased secretion increases preload Acids – increases in acids decreases function
Extrinsic influences on CO
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Rapid ANS
Baroreceptors Chemoreceptors
Blood Pressure Control
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Intermediate Renin/Angiotensin ADH
Slow Kidneys
Blood Pressure Control
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Lub closing of A-V valves S1
Dub Closing of aortic and Pulmonic valves S2
Heart Sounds “lub dub”
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When the heart is unable to pump the volume it receives it is said to be in failure
Right Sided Left Sided
Heart Failure
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Causes Pump Failure
Heart Failure
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Causes Cardiac ischemia Hypertensive event Rate related
Tachycardia Bradycardia
Valvular disease Prolapse Rupture
Heart Failure
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Acute Right Sided Failure associated with acute inferior wall MI hypotension normal to slow heart rate JVD chest clear
Treatment: fluid resuscitation
Heart Failure
Note: NTG contraindicated for HR < 60 and/or hypotensionNote: NTG contraindicated for HR < 60 and/or hypotension
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Volume overload inappropriate fluid resuscitation diligent monitoring of respiratory status required
when administering IV fluids
Heart Failure
Note: Auscultate chest q 250 cc in adults - q 100 cc in PaedsNote: Auscultate chest q 250 cc in adults - q 100 cc in Paeds
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CATEGORIZING FAILURE
• Left or Right sided heart failure
• Forward or Backward ventricular failure– Backward failure is secondary to elevated
systemic venous pressures.– Forward ventricular failure is secondary to
left ventricle failure and reduced flow into the aorta and systemic circulation
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LV BACKWARD EFFECTSDecreased emptying of the left ventricle
Increased volume and end-diastolic
pressure in the left ventricle
Increased volume (pressure) in the left atrium
Increased volume in pulmonary veins
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Increased volume in pulmonary capillary bed = increased hydrostatic pressure
Transudation of fluid from capillaries to alveoli
Rapid filling of alveolar spaces
Pulmonary edema
LV BACKWARD EFFECTS cont’d.
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LV FORWARD EFFECTS
Decreased cardiac output
Decreased perfusion of tissues of body
Decreased blood flow to kidneys and glands
Increased reabsorption of sodium and water and
vasoconstriction
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Increased secretion of sodium and water-retaining hormones
Increased extracellular fluid volume
Increased total blood volume and increased systemic blood pressure
LV FORWARD EFFECTS cont’d.
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RV BACKWARD EFFECTS
Decreased emptying of the right ventricle
Increased volume and end-diastolic pressure in
the right ventricle
Increased volume (pressure) in right atrium
Increased volume and pressure in the great veins
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Increased volume in the systemic venous Increased volume in the systemic venous circulationcirculation
Increased volume in distensible organs Increased volume in distensible organs (hepatomegaly, splenomegaly)(hepatomegaly, splenomegaly)
Increased pressures at capillary lineIncreased pressures at capillary line
Peripheral, dependant edema and serous Peripheral, dependant edema and serous infusioninfusion
RV BACKWARD EFFECTS cont’d.
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RV FORWARD EFFECTS
Decreased volume from the RV to the lungs
Decreased return to the left atrium and
subsequent decreased cardiac output
All the forward effects of left heart failure
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ONTARIOBASE HOSPITAL GROUP
Ontario Base Hospital Group
Self-directed Education Program
Well Done!Well Done!
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