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Case Study: A patient has experienced a myocardial infarction resulting in…

- - - - Caused permanent damage to papillary muscle of left ventricle
        
        Resulting in mitral valve to close
        
        Other symptoms #
        
        Blood pressure is 95 / 55
        
        Normal blood pressure is 120/80
        
        Indication of hypotension
        
        Heart beat is 125 beats per minute
        
        Average HR at rest is 72-80 beats/min for women
        
        This is tachycardia
        
        Breathing rate is 30 breaths/min
        
        Breathing is labored
        
        Normal breathing rate is 12-16 breaths/min
        
        Gurgling is heard through stethoscope
        
        This murmur is indicative of valve problems
        
        An incompetent valve that fails to close properly creates blood backflow
        
        The fluid build-up could be the cause of the gurgling sounds indicated
  - - - DM II Diabetes mellitus II
        
        Possible factors leading up to MI
        
        Obesity
        
        Sedentary life style
        
        Calorie surplus
        
        Leading up to obesity
        
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        As well as unhealthy food choices
        
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        Information on DM II #
- - - - Ventral
        
        Thoracic
        
        Mediastial cavity
        
        Pericardial cavity (Contains serous fluid to reduce friction)
    - - Fibrous pericardium
        
        Loosely fitting superficial part of pericardium
        
        Composed of dense connective
        
        Function
        
        Protects heart
        
        Anchors it to surrounding structures
        
        Prevents overfilling of heart w/blood
      - Pericardium
        
        Double-walled sac in which heart is enclosed
      - Serous pericardium (Deep to FP)
        
        Slippery 2-layer membrane forming a closed sac around heart
        
        Types
        
        Parietal layer
        
        Lines internal surface of fibrous pericardium
        
        This then folds again to form
        
        Visceral layer AKA Epicardium
      - Heart wall layers
        
        Epicardium
        
        Same as visceral layer
        
        Myocardium
        
        Middle layer composed of cardiac muscle
        
        Arranged in spiral or circular bundles
        
        Links all parts of heart
        
        Layer that contracts
        
        Connective tissue fibers form cardiac skeleton
        
        W/out this, vessels & valves might become stretched
        
        Endocardium
        
        This is endothelium
        
        Squamous epithelium
        
        Lines heart chambers
        
        Covers fibrous skeleton of valves
    - - Heart has 4 chambers
        
        2 superior atria
        
        Receiving chambers
        
        Right atrium
        
        Has pectinate muscles
        
        Help w/ contractions
        
        Keep valves from blowing out
        
        Left atrium
        
        Mostly smooth
        
        Has pectinate muscles found in auricle only
        
        Fossa ovalis
        
        In interatrial septum
        
        In unborn babies, this bypasses the lungs
        
        2 inferior ventricles
        
        Right ventricle
        
        Anterior surface of heart
        
        Left ventricle
        
        Inferorposterior aspect of heart
        
        Has a THICKER wall than right ventricle
        
        Interventricular septum
        
        Separates the ventricles
      - Other structures
        
        Aorta
        
        Left common carotid artery
        
        Left subclavian artery
        
        Brachiocephalic trunk
        
        Pulmonary trunk
        
        Transmit O2-poor blood -> lungs for oxygenation
        
        Superior vena cava
        
        Return O2-poor blood from the head, neck, arm, & chest regions (Regions above the diaphragm) -> Right atrium
        
        Inferior vena cava
        
        AKA posterior vena cava
        
        Largest vein in body
        
        Brings O2-poor blood from regions below diaphragm -> Right atrium
        
        Right pulmonary artery
        
        Carries deoxygenated blood from right ventricle -> Lungs
        
        Right pulmonary veins
        
        Carry oxygenated blood from lungs -> Left atrium
        
        Fossa ovalis
        
        Foramen ovale becomes fossa ovalis as foramen closes
        
        Enables circulation & respiration independent of mother's placenta
        
        Technically a pulmonary bypass for unborn babies
        
        Pectinate muscles
        
        Increase power of contraction while providing cushioning to tendons
        
        They also keep valves from blowing out
        
        Tricuspid valve
        
        Keeps blood from back flowing into RIGHT atrium
        
        Chordae tendineae
        
        Also keeps valves from blowing out by anchoring them down to papillary muscles
        
        Left pulmonary veins
        
        Carry oxygenated blood from lungs -> Left atrium
        
        Mitral (bicuspid) valve
        
        Regulates blood flow from LEFT atrium -> left ventricle
        
        Aortic semi lunar valve
        
        Prevents blood from back flowing into left ventricle & keeps it moving in 1 direction towards body
        
        Pulmonary semi lunar valve
        
        Prevents blood from back back flowing into right ventricle & keeps it moving in 1 direction towards lungs
        
        Papillary muscle
        
        Along w/chordae tendineae, these also act as tethers that anchor valve flaps
        
        They contract w/other ventricular muscles so they take up the slack on chordae tendineae
        
        Trabeculae carneae
        
        Ridges of muscle inside heart wall
  - - - Deoxygenated blood above the diaphragm returns to right atrium via superior vena cava
        
        Whereas, deoxygenated blood below the diaphragm returns to right atrium via inferior vena cava
        
        Deoxygenated blood from coronary veins empties through coronary sinus into right atrium
        
        All of this deoxygenated blood is then diffused down the tricuspid valve -> right ventricle
        
        Blood -> pulmonary semi lunar valve -> Pulmonary trunk
        
        -> 2 pulmonary arteries on the right & left sides of heart -> pulm. arterioles -> pulm. capillaries -> lungs to be oxygenated
        
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        Pulmonary circulation
    - - Listening to thorax w/stethoscope revels 2 sounds
        
        Lub-dup
        
        Lub associated w/ AV valves closing
        
        Point when ventricular pressure rises above atrial pressure
        
        Beginning of ventricular systole
        
        Tends to be longer, louder, & more resonant than 2nd sound
        
        Lub sounds
        
        Tricuspid valve
        
        Between 5th & 6th rib in right sternal area
        
        Mitral valve
        
        Between 5th & 6th rib over heart apex in line w/ middle of clavicle
        
        Dup associated w/ SLvalves snapping shut
        
        At beginning of ventricular diastole
        
        Resulting in a short, sharp sound
        
        Dup sounds
        
        Aortic valve
        
        Heard in 2nd -> 3rd intercostal in right sternal margin
        
        Pulmonary valve
        
        Heard in 2nd -> 3rd intercostal in left sternal margin
    - - Cardiac output (CO)
        
        Vol of blood pumped by each ventricle in 1 min
        
        Directly correlates w/blood pressure
        
        If CO increases, blood pressure increases & vice versa
        
        Unit
        
        L/min
        
        Average CO calculated by
        
        Ex: CO = HR x SV = 75 beats/min x 70mL/beat
        
        = 5250mL/min = 5.25L/min
        
        Norm blood vol = 5L
        
        Entire blood vol can be pumped out in 1 minute
        
        Cardiac reserve
        
        Difference between resting and maximal CO
        
        Gives you an idea of heart health
        
        CO in athletes during competition may be 35L/min, 7 times resting CO
        
        Max CO is 4-5 times resting CO in nonathletic ppl (20-25L/min)
        
        If max heart rate is similar to rest, heart is inefficient
        
        A high cardiac reserve is a good thing
        
        Homeostatic imbalance of CO
        
        In congestive heart failure (CHF)
        
        Occurs when blood circulation is inadequate to meet tissue needs
        
        This progressively worsening disorder reflects weakening of myocardium
        
        Common causes
        
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        W/heart being a double pump, each side can fail independently of each other
        
        Pulmonary congestion
        
        Left side fails
        
        The right side continues to propel blood to lungs
        
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        Peripheral congestion
        
        Right side fails
        
        Blood stagnates in body organs
        
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      - Stroke volume (SV)
        
        Vol of blood pumped out by one ventricle w/ each beat
        
        Correlates w/force of ventricular contraction
        
        Unit
        
        Vol per beat
        
        SV = EDV (Amount of blood that fills ventricle during diastole) - ESV (Amount of blood remaining in ventricle after contraction)
        
        Ex: SV = EDV - ESV
        
        120mL/beat - 50mL/beat = 70mL/beat
        
        Each ventricle pumps ~ 70mL of blood w/each beat ~ 60% of blood in chambers
        
        By altering EDV & ESV, 3 important factors are involved
        
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        EDV is normally ~ 120mL
        
        ESV ~ 50mL
        
        The higher atrial blood pressure, the higher ESV
      - Regulation of Heart rate (HR)
        
        Other characteristics
        
        In the unhealthy individual where blood vol drops or heart is weakened
        
        SV declines & CO is maintained by increasing HR & contractility
        
        In healthy ppl, SV is usually constant
        
        Positive chronotropic factors
        
        Increase HR
        
        Negative chronotropic factors
        
        Decrease HR
        
        Autonomic nervous sys. regulation of HR
        
        Sympathetic stimulation
        
        When emotional or physical stressors activate SNS
        
        Norepinephrine is released & causes HR to increase
        
        Enhances contractility & speeds relaxation
        
        When heart beats faster, there is less time for ventricular filling so low EDV
        
        Parasympathetic division
        
        Reduces HR
        
        Mediated by acetylcholine
        
        Which hyperpolarizes membrane of effector cells by opening K+ channels
        
        Has little effect on cardiac contractility
        
        Characteristics
        
        Heart exhibits vagal tone
        
        Due to both divisions continuously sending impulses though vagus nerves -> SA node
        
        Sensory input is generated by baroreceptors
        
        Which respond to changes in systemic blood pressure
        
        Atrial (bainbridge) reflex
        
        An autonomic reflex initiated by increased venous return & increased atrial filling
        
        If you have more blood coming back from heart & stretch of SA node causes it to fire
        
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        Blood pressure regulation often involves reflexive controls of HR
        
        Chemical regulation of HR
        
        Hormones
        
        Epinephrine
        
        Enhances HR & contractility
        
        Thyroxine
        
        Increases metabolic rate & increases production of body heat
        
        Causes sustained increase in HR when released in large quantities
        
        Acts directly on heart but also enhances effects of epinephrine & norepinephrine
        
        Ions
        
        Plasma electrolyte imbalances are dangers to heart
        
        Other factors that regulate HR
        
        Age, gender, exercise, and body temp also influence HR
        
        Resting HR is fastest in fetus
        
        140-160 beats/min & gradually declines throughout life
        
        HR is faster in females
        
        72-80 beats/min
        
        HR in males
        
        64-72
        
        Exercise raises HR through SNS
        
        It also increases blood pressure
        
        However HR in the physically fit tends to be substantially lower (Ex: 40beats/min)
        
        Heat increases HR by enhancing metabolic rate of cardiac cells
        
        Cold directly decreases HR
- - - - A failed valve would allow for back flow of blood into left atrium
        
        The same blood gets pumped over & over
        
        This increases hearts workload & can weaken the heart over time # # # #
        
        This can cause the low blood pressure that the patient is experiencing (95/55)
        
        Due to the reason that blood could flow in either direction
        
        Therefore, lowering pressure in one direction
  - - - Respiratory system
        
        The failed mitral valve could be the cause for the patient's labored breathing in that not enough O2 is -> rest of the body
        
        Regurgitation of blood occurs in that its getting backed up into left atrium -> left pulmonary veins preventing more O2 from getting into ventricle
        
        Therefore the patient has to breath harder to blow off excess CO2
        
        & Being that the patients breathing rate is 30 breaths/min, this occurrence is indicative of previous observation
        
        Normal breathing rate is 12-16 breaths/min
        
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        This is considered hyperventilation
        
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        If this issue is not rectified, it could lead ->
        
        Blood backing up further into pulmonary veins
        
        Which can back into venules -> lungs
        
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      - Nervous system
        
        In this case, the heart is weakened, therefore, SV declines & CO is maintained by increases HR & contractility
        
        This is indicative of the 125 beats/minute ( tachycardia) that the patient has
        
        Autonomic NS is affected b/c
        
        The sympathetic division detects a physical stressor
        
        & reacts by releasing norepinephrine
        
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        There is a possibility that the hearts pumping action at this point is not maintaining CO & venous return well
        
        Due to the blood congestion from the mitral valve malfunction, the amount built up in veins returning -> heart could cause Congestive heart failure (CHF)
        
        Where the heart is such an inefficient pump that blood circulation cannot meet tissue needs
        
        Another way for this to occur is if patient has multiple MIs
      - Urinary system
        
        Being that the heart also pumps oxygenated blood -> kidneys, the kidneys remove wastes & regulates water & electrolytes
        
        Therefore, the kidneys cannot do their job effectively
        
        When the heart is not pumping efficiently, it becomes congested w/blood
        
        This causes pressure build up in main vein that is connected to kidneys
        
        Leading to congestion of blood in kidneys
        
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        If kidneys cannot remove enough wastes from blood, this can lead to kidney failure
        
        This can create a positive feedback loop in that if the kidneys are impaired, they cannot remove necessary substances from blood
        
        Such as H2O for example
        
        Thereby increasing blood pressure more and causing heart to work even harder
    - - Possibly irreversible beyond 30 minutes if issue is not resolved
        
        Being that the left side failed, pulmonary congestion occurs
        
        Right side continues to propel blood -> lungs
        
        But b/c the left side is not properly ejecting the O2 blood into systemic circulation, pressure increases in vessels
        
        Fluid leaks from vessels into lungs causing pulmonary edema
        
        If untreated
        
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