Exam 5 Mon 4.18 Heart Anatomy review PP Flashcards
What type of circulation is the right side of the heart responsible for?
Pulmonary circulation - Pumps blood through the lungs
What type of circulation is the left side of the heart responsible for?
Systemic circulation - Pumps blood through the body
Deja vu review: long answer to Shappy’s question on our first day of PT school
- Rt. Atrium
- Rt. AV valve
- Rt. ventricle
- Pulm SL valve
- Pulm artery
- Lung: arteries>arterioles>venules>veins
- Pulm veins
- Left atrium
- Left AV valve
- left ventricle
- aortic SL valve
- aorta
- Organs: arteries>arterioles>capillaries>venules>veins
- vena cava
What is the mediastinum?
area above diaphragm, between lungs
3 parts of the heart wall
- Pericardium
- Myocardium
- Endocardium
A few things about the pericardium
- a double-walled sac
- Parietal (outer layer) and visceral (inner)
- Pericardial cavity and fluid separate them
What is the myocardium?
thickest layer, cardiac muscle
What is the Endocardium?
internal lining, connective tissue and squamous cells
Info about the valves of the heart: 2 big categories, sub-categories, and a little extra
- Atrioventricular valves:
- Tricuspid valve – R AV, 3 cusps (flaps)
- Mitral valve – L AV, bicuspid
- Semilunar valves:
- Pulmonic semilunar valve – RV to pulmonary artery (trunk)
- Aortic semilunar valve – LV to aorta
What are the great vessels? (4ish)
- Superior and inferior venae cavae
- Pulmonary artery (trunk)
- Right and left pulmonary arteries
- Pulmonary veins
- Aorta
What’s wrong with residual blood hanging out? (5)
- Can mean that there is a conduction issue
- could be due to “flabby” heart walls
- could be due to high volume of blood overwhelming heart
- residual blood could cause coagulation
- residual blood could cause infection
3 divisions of Right coronary artery
splits into:
- Conus
- Right marginal branch
- Posterior descending branch
2 divisions of left coronary artery
splits into:
- Left anterior descending artery
- Circumflex artery
List The Coronary Vessels, but you can omit coronary artery info b/c it’s on another card (4 plus 3 subvessels)
- Collateral arteries
- Coronary capillaries
- Coronary veins:
- Coronary sinus
- Great cardiac vein
- Posterior vein of the left ventricle
- Coronary lymphatic vessels
Some basic info about Coronary lymphatic vessels
- drain with cardiac contractions into mediastinal lymph nodes
- then into superior vena ca
Lub: what? where? how?
- Ventricular Contraction (Depolarization)
- S1 = Tricuspid and Mitral Valve closing
Dub: what? where? how?
- Ventricular Filling (Repolarization)
- S2 = Aortic and Pulmonic Valve closing
Things that control the heart electrically
- Cardiac action potentials- electric impulses
- Conduction system
- Sinoatrial node (SA)
- Atrioventricular node (AV)
- Bundle of His (AV bundle)
- Right and left bundle branches
- Purkinje fibers
SA node- location and electrical power
- in RA, just above tricuspid valve
- Generates ~75 action potentials/minute
AV Node- location and electrical info
- also in RA, superior to tricuspid valve
- near autonomic parasympathetic ganglia – these slow the impulse conduction through the AV node
Heart conduction sequence
- Normal excitation originates in the sinoatrial (SA) node then propagates through both atria.
- The atrial depolarization spreads to the atrioventricular (AV) node, and passes through the bundle of His to the bundle branches/Purkinje fibers.
- Note that the intrinsic pacemaker rate is slower in structures further along the activation pathway. For example, the atrioventricular nodal rate is slower than the sinoatrial nodal rate.
- This prevents the atrioventricular node from generating a spontaneous rhythm under normal conditions, since it remains refractory at rates
Propagation of cardiac action potentials (4)
- Resting membrane potential – voltage differential across the cell membrane
- Depolarization – electrical activation of the cell - inside of cell is less negatively charged; important fact as drugs that alter ion movement can affect heart rate
- Repolarization – electrical deactivation, reverse of above
- Hyperpolarization – too much extracellular K+, resting potential more negative
What is Refractory period?
- no new cardiac action potential can be initiated
- gives time for channels that permit Na+ and Ca++ to re-enter cell
- Abnormal refractory periods, due to heart disease, can cause dysrhythmias
What is Electrocardiogram?
sum of all cardiac action potentials
What is Automaticity?
generating spontaneous depolarization to threshold so that the SA and AV nodes generate cardiac action potentials without any stimulus
What is Rhythmicity?
SA sets the pace because it’s usually the fastest (60-100/min); AV (40-60/min) takes over if SA damaged; conduction cells in atria usually take over for the AV node; Purkinje fibers can also conduct (30-40/min)
6 parts of an EKG reading and what they are
- P wave – atrial depolarization
- PR interval – onset of atrial activation to ventricular activation
- QRS – ventricular depolarization and atrial repolarization
- ST interval – ventricular depolarization
- QT interval – time between ventricles contracting and refilling
- T – ventricular repolarization
Cardiac Innervation and ANS involvement (4)
- Autonomic system influences the rate of generation of action potentials, depolarization/repolarization, strength of contraction, diameter of coronary vessels.
- Sympathetic nerves – activation happens quickly, so that “fight or flight” response can be activated when needed
- Parasympathetic nerves – through the vagus nerve (Cranial nerve X) to slow heart rate; acetylcholine decreases heart rate and slows conduction from AV node
- Adrenergic receptor function – increases contractile strength of the heart
- Beta-adrenergic receptors
- Norepinephrine or epinephrine
Why do we care about Calcium channels in myofibrils?
site of action for calcium blocker medications – work by:
- blocking contraction
- dilating blood vessels
- prescribed for hypertension and migraines
Points about Myocardial metabolism
- like all muscles, ATP required
- Myocardial oxygen consumption (MVO2) measures cardiac work, which is linked to cardiac energy requirements
- MVO2 determined by:
- Systolic blood pressure (amount of wall stress in systole)
- Heart rate (duration of systolic wall tension)
- Contractile state of the myocardium, for which no clinical measurement exists; is assumed in measurements
- MVO2 can increase dramatically with exercise
- O2 to myocardium is delivered by coronary arteries – 70-75% is used immediately, very little reserve; any increased energy need must be met by increasing blood flow
What is Cardiac output?
amount of blood flowing through the systemic or pulmonary circuit/minute, usually 5 L/min at rest
What is Ejection fraction? -and some additional info
- amount of blood ejected in a beat. Can be estimated with echocardiography
- Stroke volume – volume of blood ejected during systole
- EF = Stroke volume/end-diastolic volume
- Normal is around 50-75%
- Decreased EF is sign of ventricular failure (36-49%, below normal; <35%, severe)
What is Preload?
- volume and pressure in ventricle at end of diastole
- Called left ventricular end-diastolic volume
What is Laplace law?
length/tension relationship – affects size of ventricle and the ability to produce a forceful contraction
What is Frank-Starling law of the heart?
myocardial stretch determines the force of myocardial contraction. The greater the stretch, the stronger the contraction
What is Afterload?
resistance to ejection of blood from the ventricle
- Load muscle must move after it starts to contract
- Determined by system vascular resistance in aorta, arteries, and arterioles
True or False: Changes in preload, afterload, and contractility all interact to determine stroke volume and cardiac output
True
Review of the components of the RAAS
Renin-Angiotensin-Aldosterone System
- Renin- released by kidney due to decrease in blood pressure
- Angiotensin I released systemically due to renin in circulation
- Angiotensin I converted to Angiotensin II in lung by ACE
- Angiotensin II causes vasoconstriction and decreased excretion of salt and water by the kidneys by increased release of aldosterone
- Aldosterone- produces reabsorption of salt and water
- If elevated BP (hypertension and potential long term CHF)
- Drug: ACE inhibitor
Norms for BP and numbers for the different stages of hypertension
- Normal BP 120/80 (systolic BP and diastolic BP)
- Prehypertension - 120-139 mmHg and 80-89 mmHg
- Stage 1 HTN 140-159 mmHg and 90-99 mmHg in stage 1
- Stage 2 160-179 mmHg and 100-109 mmHg
- Stage 3 greater than 180 mmHg and greater than 110 mmHg
The Two major categories of hypertension
-
Essential hypertension (EH)- unknown cause in 95%
Genetics or stress hypothesized -
Secondary hypertension- result of known cause
kidney or bladder infection, Cushing’s syndrome, arterial disease
