The Heart Flashcards
Mediastinum
Mass of connective tissue that cushions and protects the heart.
Extends from sternum –> vertebral column, diaphragm to first rib, and between the lungs.
Mass of heart
250 (female) to 300 (male) grams.
Apex of heart
Tip of left ventricle. Rests on diaphragm.
Anterior, inferior and lateral to left
2/3 of mass of heart lies left of midline
Base of the heart
Formed by atria (mostly left).
Posterior, superior and to the right.
Where big vessels connect.
Sides of heart
Anterior – deep to sternum and ribs
Inferior – between apex and right border. Mostly on diaphragm
Right border – faces right lung
Left border – Pulmonary border. Faces left lung.
Pericardium.
Membrane that surrounds and protects heart.
Maintains position of heart but also allows movement.
2 parts of pericardium
Fibrous
Serous
Fibrous pericardium
Superficial of the two layers. Strong, dense, inelastic, irregular connective tissue.
Anchors heart in mediastinum
Prevents over stretching of heart.
Protection.
Serous pericardium
Deep layer of pericardium.
Thin. Contains two layers:
- Parietal
- Visceral
Parietal layer of pericardium
Outer layer
Fused to fibrous pericardium.
Visceral layer of pericardium
Inner layer
AKA epicardium
Considered the outermost layer of the heart. Adheres to surface of heart.
Pericardial Cavity
The space between parietal and visceral layers of the serous pericardium. Houses pericardial fluid.
Pericardial fluid.
In pericardial cavity
Viscous fluid that helps reduce friction between between layers during heart contractions.
What are the layers of the heart?
Epicardium
Myocardium
Endocardium
Epicardium
External layer of the heart
AKA visceral layer of serous pericardium
Makes heart smooth and slippery
Myocardium
Middle layer of heart
Cardiac muscle layer
Makes up 95% of heart
Responsible for pumping
Endocardium
Innermost layer of heart
Thin layer of endothelium overlying thin layer of connective tissue
Provides smooth lining for chambers of heart and covers the heart valve.
Continuous with endothelial lining of blood vessels attached to heart.
Minimizes friction of blood
What are the chambers of the heart?
Right and left atrium
Right and left ventricles
Atria
Two superior chambers of the heart
Receive blood.
Have auricles located on anterior surface
Auricles (cardiac)
On anterior surface of each atrium
Help increase capacity/volume of blood.
Ventricles
Inferior surfaces of heart
Pumping chambers
Sulci (cardiac)
Small grooves that hold coronary blood vessels and fat.
Mark the external boundaries between chambers of the heart.
Coronary sulcus
“the belt of the heart”
Encircles the heart and separates atrium from ventricles
Anterior interventricular sulcus
Separates the two ventricles on the anterior side.
Posterior inter ventricular sulcus
Separated the two ventricles on the posterior side
Septum
Internal
Fibrous connective tissue that separates chambers
Inter ventricular and inter atrial.
Right Atrium
Forms right border of the heart
Receives deoxygenated blood.
Smooth posterior wall
Anterior wall rough due to pectin ate muscle
Blood passes from right atrium to right ventricle through tricuspid valve
Blood vessels to right atrium
Superior vena cava – from upper body
Inferior vena cava – from abdomen, lower body
Coronary Sinus – from heart
Pectinate muscles
Muscular ridges that extend into the auricle
Contributes to forceful arterial contraction.
Left atrium
Forms most of the base of the heart
Receives oxygenated blood from lungs from 4 pulmonary veins
Smooth posterior and anterior walls.
Auricle rough due to Pectinate muscles.
Blood passes to left ventricle through bicuspid/mitral valve.
Interatrial septum
Separated right and left atria.
Contains oval depression called fossa ovalis
Foramen ovale
Opening in interatrial septum of fetal heart. In adults closes and becomes fossa ovalis.
Right ventricle
Forms most of anterior surface if heart
Received deoxygenated blood from RA through tricuspid valve
Contain trabeculae carneae and chordae tendinae
Blood Passes through pulmonary valve (aka pulmonary semilunar valve)
Trabeculae carneae
Inside ventricles
Series of ridges formed
By raised bundles of cardiac muscle fibres
Some help with cardiac conduction
Chordae tendinae
In ventricles
Tendon-like cords that attach the cusps of the tricuspid and mitral valves to trabecular carneae called papillary muscles.
Help stabilize and strengthen the cusps and prevent them from everting during ventricular contraction.
Papillary muscles
Cone shaped trabecular carneae that the chordae tendinae attach to.
What does the pulmonary trunk split
Into?
Right and left pulmonary arteries
Left ventricle
Largest and strongest chamber
Has thickest myocardium and generates the most force during contraction
Forms apex of heart.
Also contains trabecular carneae and chordae tendinae
Blood passes through to ascending aorta through aortic valve.
Interventricular septum
Separate right and left ventricles
Ligamentum arteriosum
Connects aortic arch and pulmonary trunk.
Remnant of ductus arteriosus (temporary blood vessel that shunts blood from aortic arch and pulmonary trunk during fetal development)
Fibrous skeleton of the heart
Four connective tissue rings that surround the valves of the heart.
Prevent over stretching of valves
Point of insertion for bundle of cardiac muscle fibres.
Electrical insulator between atria and ventricles.
Myocarditis
Inflammation of the muscles of the heart
Usually due to viral infections, rheumatic fever, or chemical or pharmacological agents.
Endocarditis
Inflammation of the endocardium, usually due to bacterial infections.
Usually involve heart valves
Pericarditis
Inflammation of the pericardium
Wet or dry.
Most common is acute (dry). Symptoms can mimic heart attack. May involve pericardial friction rub.
Chronic (wet) – gradual build up of pericardial fluid (effusion). May leave to cardiac tamponade.
Cardiac tamponade
Build up of fluid causes compression of heart.
Valve prolapse
Eversion of heart valves
What causes heart valves to open and close?
Pressure changes and chambers contract and relax.
Atrial-Ventricular Valves: open
When open, rounded ends of cusps project into ventricle. Papillary muscles relaxed. Chordae tendinae slack. Blood moves down pressure gradient from atrium to ventricle.
AV Valves: closed
Cusps up. Ventricles contracted.
Pressure if blood in ventricles drives cusps upward.
Papillary muscles contract, chordae tendinae tighten to prevent valve prolapse.
Semilunar valves
Separate ventricles from pulmonary artery (right) and aorta (left)
Composed of three crescent moon shaped cusps; free border of each cusp opens into lumen of artery.
Valves open when pressure in ventricle exceeds pressure in arteries.
What is the pressure required to open SL valves,
Diastolic. LV 80 mmHg.
RV 25-30 mmHg
Stenosis
Narrowing of heart valve that restricts blood flow. Can increase BP
Valve insufficiency or incompetence
Failure of valve to close completely.
Mitral Valve Prolapse
Failure of the mitral valve to close completely.
Allows backflow of blood from LV to LA.
Affects 30% of population
Rheumatic fever
Infectious disease that damages heart valves, most often left side.
Usually occurs after strep throat.
Cardio-Pulmonary Pathway
Aorta
Systemic arteries
Systemic arterioles
Systemic capillaries
Systemic venues
Systemic veins
Superior/inferior vena cava
Right atrium
(Tricuspid/right AV valve)
Right ventricle
(Pulmonary semilunar valve)
Pulmonary arteries
Pulmonary arterioles
Pulmonary capillaries
Pulmonary venules
Pulmonary veins
Left atrium
(Left AV/bicuspid/mitral) valve
Left ventricle
(Left/aortic semilunar valve)
What does the aorta feed?
Ascending – coronary arteries
Aortic arch – upper body
Descending aorta – divides into thoracic and abdominal (which itself divides into common iliac arteries)
Cardiac circulation
Ascending aorta feeds right and left coronary arteries
Left coronary artery divides into: anterior intraventricular and circumflex branches
Right coronary artery supplies right atrium and then divides into posterior intraventricular branch and marginal branch.
Great cardiac vein, middle cardiac vein, small cardiac vein – all empty into coronary sinus.
Anterior cardiac vein drains into RA.
Left coronary artery
Branches off ascending aorta
Passes inferior to left auricle and divides into anterior intraventricular branch (or Left Anterior Decending – LAD) and circumflex branch.
Anterior intraventricular branch or LCA
AKA Left Anterior Descending
Supplies blood to both ventricles
Circumflex branch of LCA
Lies in coronary sulcus
Feed left atrium and left ventricle
Right coronary artery
Supplies right atrium
Continues inferior to right auricle and divides into posterior intraventricular branch and marginal branch.
Posterior intraventricular branch of RCA
Follows posterior intraventricular sulcus.
Feeds both ventricles
Marginal branch of RCA
Lies in coronary sulcus
Supplies right ventricle
Coronary sinus
Located in coronary sulcus
Received deoxygenated blood from myocardium (all veins except anterior cardiac) and empties into RA.
Great Cardiac Vein
Lies in anterior interventricular sulcus
Drains areas of heart supplied by LCA (RV, LV, LA)
Empties into coronary sinus
Middle Cardiac Vein
Lies in posterior interventricular sulcus
Drains areas of heart supplied by posterior interventricular branch of RCA (LV, RV)
Small cardiac vein
Lies in coronary sinus
Next to RCA
Drains RA and RV
Empties into coronary sinus
Anterior cardiac vein
Drains RV and opens directly into RA.
Next to marginal branch of RCA
Myocardial ischemIa
Lack of blood supply due to partial obstruction of vessel. Causes hypoxia
Angina pectoralis
Chest pain associated with myocardial ischemia
Neck, chin, left arm to elbow
Cardiac vs skeletal muscle tissue
Shorter Less circular Branching One centrally located nucleus (usually) Larger and more numerous mitochondria Transverse tubules wider and less abundant. Smaller sarcoplasmic reticulum Involuntary Intercalated discs (thickening of sarcolemma)
Same arrangements of actin and myosin, bands, zones, z discs
Intercalated discs
Irregular transverse thickening of sarcolemma
Connect neighbouring cardiac muscle fibres
Contain desmosome and Gap junctions
Role of desmosomes in cardiac tissue
Tight cell-to-cell junctions create stability.
Hold fibres together
Role of gap junctions in cardiac tissue
Tubular cell-to-cell junction that allow for transmission of substances and signals.
Allow muscle action potentials to conduct from one muscle fibre to its neighbour –> allows atria/ventricles to contract as a single coordinated unit.
What percentage of muscle fibres are autorhythmic?
1%
Two main characteristics of the cardiac conduction system
1 pacemaker
2 conduction system
Steps of cardiac conduction.
- Firing of SA node (natural pacemaker)
- AP conducts along atrial fibres, and reaches AV node in interatrial septum.
- Signal propagates to AV bundle (Bundle of His)
- Signal splits into left and right bundle branches that travel down interventricular septum
- At apex of heart, conducted through Purkinjw fibres, which stimulate ventricular contraction.
Sinoatrial (SA) node
Natural pacemaker. Creates approx 100 AP/minute
Posterior wall of right atrium.
Signal propagates to LA via gap junctions. Both atria contract simultaneously.
What is the only site where APs can conduct from atria to ventricles?
Bundles of His (the AV bundle)
What happens at AV node?
Signal slows before relating to Bundle of His. This allows time for Atria to empty blood into ventricles.
What modifies the timing and strength of the heartbeat?
ANS impulses, blood borne hormones (epinephrine)
Do not affect rhythm!
Resting potential (cardiac)
Membrane potential of a resting, non contracting muscle cell
-90mV
Plateau phase
Period of sustained contraction due to simultaneous/concurrent release of calcium.
Stages of cardiac action potential
Resting potential Depolarization Plateau phase Re polarization Refractory period
Depolarization (cardiac)
Action potential increases to threshold
Voltage gated channels open
Na+ moves into cytosol. Rapid depolarization.
Signal to contract – not actual contraction
Plateau.
Period of maintained depolarization.
Ca+ channels open and calcium comes in from SR.
Contraction triggered
Repolarization
K+ channels open and restore negative membrane potential
Refractory period (cardiac)
All stages except rest
Cardiac ATP production
Mostly aerobic
In heart attacks, cardiomyopathy causes Creatine kinase to spill into blood. Tested for after heart attack.
Electrocardiogram is used to determine:
If conduction pathway is abnormal
If heart is enlarged
If certain regions of the heart are damaged
Cause of chest pain.
Normal ECG
P Wave – atrial depolarization
QRS Complex – rapid ventricular depolarization (and thus contraction)
T Wave: ventricular repolarization.
P-Q interval
Atrial depolarization and contraction; AP travelling to Purkinje fibres.
Time can lengthen due to scar tissue
S-T interval
End of QRS to START of T wave
Plateau phase of depolarization of ventricles.
Elevated in acute MI, depressed with low O2
QT interval
Beginning of QRS to END of T Wave
Start of ventricular depolarization to end of ventricular repolarization.
Lengthened by myocardial damage, ischemia, conduction abnormalities.
Range for aortic pressure
80-120 mmHg
Range for LV pressure
0-120 mmHg
Atrial pressure is ________ than the ventricles, and the right side is always _______ than the left side.
Much less
Less
Atrial systole
Marked by P wave
SA node fires; both atria contract.
Atrial pressure increases; ventricular pressure low.
Blood ejected through AV valves (tricuspid and mitral) into ventricles.
AP propagates down through bundle of His into Purkinje fibres.
Atria relax and atrial pressure drops.
End diastolic volume
The amount of blood in the ventricles at the end of atrial systole/ventricular diastole.
105ml + 25ml (from atria) = 130ml
Determined by: 1. Duration of ventricular diastole. 2. Venous return.
Ventricular systole
Begins part way through QRS (just after R)
As pressure in ventricles rise, AV valves shut.
Semilunar valves open. Ejection lasts about .25 second. About 70ml ejected.
T wave marks onset of ventricular repolarization.
Isovolumetric Contraction
In ventricles, the 0.05 seconds when both AV and semilunar valves are shut.
Muscles exerting force and contracting but not shortening.
Also occurs during relaxation phase.
Pressure required to open semilunar valves
LV 80 mmHg (continues to rise to 120 mmHg)
RV 20 mmHg (rises to 25-30 mmHg)
End systolic volume
The volume of blood remaining in each ventricle at the end of systole. About 60 ml.
Stroke volume
The amount of blood ejected per beat
SV = EDV - ESV
At rest: SV = 130 - 60 = 70 ml.
Dicrotic wave
The sound blood makes when it bounces off closed valves.
lub (AV) dub (semilunar)
(Aortic valve closes around 100 mmHg)
When do AV valves open?
When ventricular pressure drops below atrial pressure. Passive ventricular filling before atrial contractions = 105 ml
What are the two heart sounds inaudible by stethoscope?
S3 & S4 –blood turbulence during ventricular filling and atrial contraction (Systole).
Heart Murmur
Any abnormal sound heard during, before or after normal heart sounds.
Common in kids; in adults may indicate a valve stenosis or other disorder.
Cardiac output
Blood ejected/minute
Stroke volume x BPM.
Average SV = 70ml
Average BPM = 75
Average CO = 5250 ml/min
Cardiac reserve
The difference between max CO and resting CO
Average 4-5x
Greater in athletes; almost none in severe asthmatics and people with heart disease.
Three main factors that regulate stroke volume
Preload
Contractibility
Afterload
Preload
The degree of stretch on the heart before contraction
More blood enters ventricles, greater the stretch, more powerful the contraction.
Frank-Starling Law
Preload volume is proportional to the EDV.
–> equal pumping of blood between ventricles.
Contractability
Strength of contraction of muscle fibres.
Inotropic agents
Positive – increase contraction (sympathetic NS, digitalis, anything that increases Ca)
Negative – decreases contraction (parasympathetics, anoxia, Ca blockers)
Congestive heart failure
Loss of pumping efficiency
Increased EDV (preload) –> contracts less forcefully –> increases EDc
LV. Pulmonary Edema
RV peripheral edema.
Most important regulators of HR
ANS (medulla oblongata) and hormones released by adrenal medulla.
Medulla oblongata and HR
Receives sensory input from baro, chemo and proprioceptors.
Sympathetic signals sent through cardiac accelerator nerves in T-spine region
Parasympathetic signals sent through vagus nerve (CN X)
Chemical factors affecting HR
Reduction: hypoxia, acidosis, alkalosis, K+ (block AP), Na+
Increase: calcium, (nor)epinephrine, thyroid hormones
Arrythmias (dysrhythmias)
Abnormal heart rhythm due to defect in conduction system.
Asynchronous contraction –> abnormal blood pumping.
Coronary Artery Disease
Results from accumulation of artherosclerotic plaque in coronary arteries.
Artherosclerosis
One form of arteriosclerosis (thickening of arterial walls and loss of elasticity) Formation of lesions (artherosclerotic plaques, made of cholesterol/fat) in arteries.
CAD surgical treatment
Coronary artery bypass grafting (CABG)
Percutaneous Transluminal Coronary Angioplasty. (PTCA) 30-40% failure within 6 months without stent.
Coarctation of aorta
Congenital narrowing of aorta
Patent ductus arteriosus
Ductus arteriosus doesn’t close at birth. Aortic blood flows into pulmonary trunk, increasing load on ventricles.
Septal defect
Atrial – foramen ovale fails to close
Ventricle – incomplete development of septum. Oxygenated and deoxygenated blood mix.
Tetralogy of Fallot
Combination of: Intraventricular septal defect Dextrapositioned aorta Stenosed pulmonary valve Hypertrophied right ventricle
Cardiac arrest
Cessation of effective heartbeat
Cardiomegaly
Enlarged heart
Cor Pulmonale (CP)
RV hypertrophy secondary to lung condition.
Paroxysmal tachycardia
Tachycardia with sudden onset and end.
When does the heart begin to develop?
From mesoderm on day 18/19
Most development occurs between W5-9
Afterload
The pressure required to open SL valves
Left (aortic) 80mmHg
Right (pulmonary) 20 mmHg
Depolarization
Voltage gates Na+ gates open
Na+ rushes in –> rapid depolarization
Plateau
Period of maintained depolarization
Opening of voltage gated Ca+ channels in sarcolemma
Triggers contraction
Slow outbound leak of K+
Repolarization
Recovery of resting membrane potential (-90 mV).
More K+ channels open. Outflow of K+ restores resting potential.
