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The Heart (Cardiac Muscle (Anatomy (Sarcomeres (Organised along…
The Heart
Cardiac Muscle
Anatomy
Sarcomeres
Organised along myofibrils
T tubules :check:
Sarcoplasmic reticulum :check:
Terminal Cistane :red_cross:
Triads :red_cross:
Many Mitochondria (25% cell V)
Appearance
Striated
Branched network of interconnected muscle cells adjoined by intercalated discs
As a result of Actin and Myosin
Location
Only found in Heart
Composed of
Cardiocyte
Relative size
Cell that is smaller than skeletal muscle
Nucleus
Typically one central
Intercalated Discs
Function
Propagate Action Potentials
Interlocking Membranes held together by desmosomes and linked by gap junction
Stimulation
Stimulated by pacemaker cells
Cardiac Output (Stroke Volume x Heart Rate = Cardiac Output)
Terminology
Cardiac output
About 5-6 litres per minute in adults
the volume of blood pumped out by the ventricles in one minute
Stroke volume
The amount of blood pumped out of each ventricle with each contraction
SV
End-Diastolic volume minus End-Systolic volume
End-Diastolic volume
Amount of blood in the ventricles at the end of ventricular diastole
End-Systolic volume
Amount of blood in the ventricles at the end of ventricular systole
Factors that influence Cardiac Output
Autonomic innervation
Sympathetic and parasympathetic divisions of the autonomic nervous system innervate the heart via the cardiac plexus
Cardioacceleratory centre (sympathetic)
Cardioinhibitory centre (parasympathetic)
Hormones
Increase heart rate by their effect on the sinoatrial node
Epinephrine
Norepinephrine
Thyroid hormone
Increase heart rate by their effect on the contractile muscle cells
Epinephrine
Factors that influence Stroke Volume
End-Diastolic Volume
Filling time
Depends entirely on heart rate
fast = less filling time
duration of ventricular diastole
Venous return
the rate of blood flow back to the heart
Affected by
Velocity of blood flow
Pressure gradients
Sympathetic nerve activity
Skeletal muscle activity
Thoracic/abdominal pressure
Valves
End-Systolic Volume
Preload
the stretching of ventricular muscle cells during ventricular diastole (increase EDV, increased preload)
Contractility
the amount of force produced during a contraction (increased due to increased calcium entry into the cardiac muscle cells)
Affected by
Sympathetic NS increases contractility (positive inotropic action)
Parasympathetic NS decreases contractility (negative inotropic action)
Hormones (e.g. Epinephrine) have positive inotropic actions
Drugs have positive inotropic actions (e.g. Dopamine) and negative inotropic actions (e.g. Beta-blockers)
Afterload
tension required to force open the semilunar valves (increased by any factor that decreases blood flow)
Location
Relative to anatomy
Posterior to Sternum
1.2 cm to left
Base of heart at the level of the 3rd costal cartilage
Apex
at the 5th intercostal space
7.5cm to left
Rotated to the left
Anterior surface of heart is the right atrium and ventricle
Mediastinum
Pericardial Cavity
Pericardium
Layers
Visceral Pericardium
Function
Covers Heart
Perietal Pericardium
Function
Lines inner surface of pericardial sac
Associated Diseases
Pericarditis
Cardiac Tamponade
Heart Wall
Layers
Epicardium (outer surface)
Connects with Visceral Pericardium
Myocardium (muscle wall of heart)
Concentric Layers of cardiac muscle
Endocardum (Inner surface)
Simple Squamous Epithelium
Blood Supply
Coronary Circulation
Coronary Arteries
Right and Left Coronary Arteries
Cardiac Veins
Great Cardiac Vein
Coronary Sinus
Relative Disease
Coronary Ischemia
Causes
Reduced Blood flow to heart
Blockage of coronary circulation
Atherosclerosis
Atheromas
What is
1 more item...
Risks
Lead to Myocardial Infarction
Effects
Can lead to Hypoxia (Oxygen Deficiency)
Death of cells
Types
Temporary
Reversible
Myocardial Infarction (Heart Attack)
Statistics
Most common cause of premature death in Australia
40% Silent Infarcts
60% die before Reaching Hospital
Clinical diagnosis
Chest pain treated as heart attack
Symptoms
Pressure/squeezing pain radiating down from shoulder to arm
Causes
Blood Supply Blocked
Cells die from lack of oxygen (Infarct)
Risk Factors
Smoking
Diabetes
High blood pressure
High blood cholesterol levels
High circulating levels of low-density lipoproteins (LDLs)
Male (below 70)
Severe emotional stress
Obesity
Genetic predisposition
Sedentary lifestyle
Internal anatomy
Ventricles
Atrioventricular Valves
Relaxed (Open)
Papillary Muscles (Relaxed)
chordae tendinea
loose
Semilunar Valves
Closed
Contracting (Closed)
Papillary Muscles (Contract)
Chordae Tendinea
Taunt
Prevents blood from entering Atria
Semi lunar Valves
Open
Contraction
Terminology
Heart Beat
1 contraction of the heart
Pulse
the wave of blood forced out of the ventricles causing the artery walls to expand
Anatomy
Specialsed cells control contraction (Pacemaker cells)
Max Heart Beat
230 beats per minute
Max atrioventricular node can conduct
Relevant Conditions
Abnormal Pacemaker function
Tachycardia
(tachys = rapid or accelerated and kardia = of the heart)
Bradycardia
(brady = slowness and kardía = of the heart)
Cardiac Cycle
1
Atrial systole
2
Atrial diastole
3
Ventricular systole
4
Ventricular diastole
Vocabulary
Systole = contraction
Diastole = relaxation
Electrocardiogram (ECG)
Technetium pyrophosphate scanning
Cardiac Enzymes
Creatinine Kinase
Troponin I or T
Creates
Echo-cardiography
Waves
Types
QRS complex
ventricles depolarise.
Ventricles begin contracting after the R wave
Atrial repolarisation
is not seen as it occurs during QRS (ventricular contraction)
T wave
ventricular repolarisation
P wave
The atria begin contracting after the P wave
depolarisation of the atria.
Looking for
Height of waves
For example
Large QRS
enlarged heart
Smaller than normal
Heart mass has reduced
Duration of waves
Relationship between different waves
Amount of depolarisation in P wave and QRS complex
Segments
extend from the end of one wave to the start of the next
P-R interval
More than 200 msec = damaged conduction pathway
start of atrial depolarisation to start of ventricular depolarisation (QRS)
Q-T interval
Ventricular
de-polarisation
re-polarisation
Cardiac arrhythmias
Heart Sounds
“Lubb”
Start of ventricular contraction
when atrio- ventricular valves close
“Dubb”
Start of ventricular filling
when the semilunar valves closes