Compare and contrast skeletal, cardiac and smooth muscle with respect to striation, level of control, location, innervation and troponin content
Heart: striated, self controlled, located in heart, parasympathetic & sympathetic (autonomic - medulla) innervation, troponin, on nucleus.
Skeletal: striated, nerve supply control, located in skeletal muscle, motor neuron (somatic) innervation, troponin, multiple nuclei.
Smooth: not striated, self and induced control, located in organs, primarily sympathetic (autonomic) innervation, no torponin (calmodulin instead), one nucleus.
What is excitation-contraction coupling?
the process linking depolarization of the muscle cell surface membrane to the release of Ca2+ from the sarcoplasmic reticulum (SR). EC coupling controls [Ca2+] within the muscle cell; [Ca2+] controls force.
Describe excitation-contraction coupling in Cardiac muscle
Describe excitation-contraction coupling in skeletal muscle
What is the essential difference between cardiac and skeletal muscle excitation-contraction coupling?
Cardiac muscle requires extracellular Ca2+ while skeletal muscle will operate in the absence of Ca2+
Explain the physiological reason for the ability to auscultate an S1 and S2 heart sound.
S1 is the closing of the AV valves and S2 is the closing of the semilunar valves (aortic and pulmonary)
Describe the order of events in atrial and ventricular contraction, including the timing of opening and closing of heart valves.
Late diastole -AV valves open -blood flows into heart filling atria & ventricles ~70% of ventricular filling is passive Atrial systole -contraction of atria Ventricular systole -AV valves close -isovolumetric contraction -AV valves bulge into atria -Aortic & pulmonary valves open -ventricular ejection Early diastole -Aortic and pulmonary valves close
Describe the physiological mechanism behind a split S2 heart sound.
Split S2 sound is caused by the asynchronicity of the closure of the semilunar valves (aortic and pulmonary)
Describe the physiological mechanism behind the presence of murmurs/bruits.
When blood flow speeds up and is turbulent over an obstruction it creates these sounds.
bruit - mostly refers to the vessels … possible arthrosclerosis
murmer - incompetent valves of the heart or in large arteries … aneurysmal dialtion, arteriovenous fistula or patent ductus arteriosus
Describe the factors controlling cardiac output
controlled by stroke volume (SV) and cardiac rate (CR)
SV controlled by neural input - IONOTROPIC action (and EDV)
-sympathetic makes myocardial muscle fibers contract with greater strength = increased SV
-parasympathetic has the opposite effect = decreased SV
HR controlled primarily by autonomic nerves - CHRONOTROPIC action
-sympathetic increases HR
-parasympathitic decreases HR
Describe the factors controlling end diastolic volume (EDV).
- preload time
- increase in intrapercardial pressure = decrease EDV
- decrease ventricular compliance = decrese EDV
- increase ventricular stiffness = decrease EDV
- atrial contractions = increase EDV
- increase total blood volume = increase EDV
- constrictions of veins (reducing venous pooling) = increase EDV
- increase normal negative intrathoracic pressure - increase pressure gradient along which blood flows to heart = increase EDV
- standing - decrease venous return = decrease EDV
- muscular activity (pumping action) - incrase venous return = increase EDV
Predict the strength of contraction based on alterations to amount of stretch on the muscle fiber (preload) – Starling’s Curve
when muslce is stretched it develops tension to a maximum level then declines as stretch becomes extreme.
so strength of contraction increases with increased tension (up to a point)
Predict the response to adrenergic stimulation in blood vessels.
epinephrine interacts with beta 2-adrenergic receptors
the result will be vasodilation to vessels travelling to smooth muscle (organs and skin), and vasodilation to skeletal muscle.
Predict the response to adrenergic stimulation on the heart and describe the adrenergic innervation of the heart.
norephinephrine interacts with beta 1-adrenoreceptos, which are notable on SA and AV nodes, His-purkinje fibers and atrial & ventricular conractile tissue
result - increased stimulation results in increased HR (chronotropy), increased rate of transmission in conductive tissue (dromotropy) and increased ventricular contraction (inotropy)
Predict the response to cholinergic stimulation on the heart and describe the cholinergic innervation of the heart.
Acetylcholine interacts with nicotine receptors, which are notable on SA and AV nodes, His-purkinje fibers and atrial & ventricular conractile tissue
result - increased stimulation results in decreased HR, decreased rate of transmission in conductive tissue and decreased ventricular contraction
Predict the strength of contraction based on alterations to amount of stretch on the muscle fiber (preload) – Describe the location of baroreceptors and explain how they are involved in the regulation of blood pressure.
increased stretch/preload = increased strength of contraction.
Baroreceptors - stretch receptors
-located in the carotid sinus and aortic arch, in the walls of atria, entrance of superior and inferior vena cava and pulmonary veins.
-stimulated by distension of vessels. so increased firing with increased distention
BP effect…any drop in systemic arterial pressure, decreases the firing rate and will therefore increase BP and CO
…any rise in systemic arterial pressure will increase the firing rate causing dilation of the blood vessels and decreased CO, leading to decrease in BP.
**they compensate for abrupt changes in BP
Describe the local autoregulatory mechanisms that exist for local blood pressure control.
most vascular beds have intrinsic capacity to compnesate for moderate changes in vascular resistance –> autoregulation
-due to intrinsic contractile response of smooth muscle to stretch and vasodialtors
factors causing local vasodialtion
- decreased O2 tension
- decreased pH
- increased temperature
- increased K+
- increased lactate
- increased adenosine (in cardiac muscle)
Describe the electrical conducting system of the heart and the timing of how action potentials move throughout the conducting system
SA node - junction of superior vena cava and right atrium
AV node - in right, posterior portion og the interatrial septum
3 bundles of atrial fibers connect SA to AV
AV node continues with bundle of His and purkinje fibers
depolaorization initiated at the SA node and spreads radially through the atria ~0.1 seconds
Converges on the AV node ~0.1 seconds (AV delay)
From top of septum, wave depolorization spreads rapidly from left to right then down the septum to apex of the heart then to ventricular walls ~ 0.08-0.1 seconds
Compare and contrast the depolarization events in cardiac muscle and autorhythmic pacemaker cells
describe the anatomical location of each of the 12 leads used in 12 lead ECG
V1 - 4th inercostal space, right of sternal border - septal
V2 - 4th inercostal space, left of sternal border - anteroseptal
V3 - between V2 and V4 - anteroseptal
V4 - 5th inercostal space, left side midclavicular line - anterior
V5 - horizontally even with V4, anterior axillary line - lateral left ventricle
V6 - horizontally even with V4, mid axillary line - lateral left ventricle
I - right arm (RA) to left arm (LA) - lateral left ventricle
II - RA to LL (left leg) - inferior portion of left ventricle
III - RL (right leg) to LL - inferior portion of left ventricle
aVR - left to RA - square root of squat
aVL - right to LA - lateral left ventricle
aVF - arms to LL - inferior portion of left ventricle
Explain the basics behind why the ECG tracings appear different in each of the 12 leads.
different because they’re each taking a slightly different “electrical position” of the heart
Describe the underlying physiological mechanism associated with heart block.
disruption in the conduction of depolarization from atria to ventricles
1st degree - all atrial impulses reach ventricles but PR interval too long
2nd degree - not all atrial impulses conducted to ventricles, progressive lengthening of PR interval
3rd degree - complete block - atria and ventricles contract at completely different rates - atria faster
-AV nodal block - AV node disruption - remaining nodal tissue becomes pacemaker ~45 bpm
infranodal block - conducting systems below AV node disruption - pacemaker cells are located in periphery of heart ~35bpm
bundle of His interupted - excitation passes normally down unaffected side then sweeps back through the muscle to activate ventricle on other side - rate normal but prolonged and/or deformed QRS
Predict the changes in cardiac excitability based on alterations in blood concentration of potassium and calcium and describe the physiological basis for these changes.
Describe the mechanical events that occur with cardiac contraction and be able to synthesize this information with the electrical changes that occur on ECG along with the heart sounds that are heard on auscultation
…look at the notes, there is a figure with this…
Upon presentation of a normal lead II ECG tracing
Identify where S1 and S2 would be heard
Calculate the heart rate using the rule of 1500
Explain the electrochemical and mechanical events that occur at each phase of the ECG tracing (PQRST waves)
Measure the amplitude and duration of all waves and intervals
Upon presentation of an abnormal lead II ECG tracing
Recognize the characteristic patterns associated with first, second, Wenckebach, and complete heart block
Recognize the characteristic patterns associated with hyperkalemia and hypokalemia
Recognize characteristic ECG patterns associated with myocardial infarction.
Identify P waves, PR intervals, and QRS intervals that are abnormal with respect to duration and amplitude.
…use lab to study this…