Pathophys Flashcards Preview

Cardiology > Pathophys > Flashcards

Flashcards in Pathophys Deck (52)
Loading flashcards...

Function of the pericardium

- superficial fibrous outer layer: it protects, anchors, and prevents overfilling
- deep 2 layered serous pericardium: parietal and visceral (epicardium) layers that are separated by fluid that decreases friction


Layers of the heart wall?

- epicardium:visceral layer of serous pericardium
- myocardium: spiral bundles of cardiac muscle cells, and fibrous skeleton of the heart that anchors muscle fibers and supports vessels and valves, limits spread of action potentials to specific paths
- endocardium: continuous with endothelial lining of blood vessels


Vessels entering the right atrium?

- SVC and IVC
- coronary sinus


Vessels entering left atrium?

- right and left pulmonary veins


Difference in pressures: systemic and pulmonary circuit

- equal volumes of blood are pumped to the pulmonary and systemic circuits
- pulm circuit is short, low pressure circulation
- systemic circuit blood encounters much resistance in long pathways, high pressure


What is the shortest circulation circuit in the body?

- coronary circulation


What are the important coronary arteries?

- right and left coronary, marginal, circumflex and LAD


What are the branches off of the right coronary artery? Left?

- R: right marginal and posterior interventricular artery
- L: anterior descending and circumflex


During what period of the cardiac cycle do the coronary arteries receive perfusion?

- diastole


What is angina pectoris?

- thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium so cells become weakened


What is an MI?

- prolonged coronary blockage
- areas of cell death are repaired with noncontractile scar tissue


Different heart valves? function?

- ensure unidirectional blood flow through the heart
- AV valves::
prevent backflow into atria when ventricles contract, tricuspid and mitral
- chordae tendineae anchor AV valve cusps to papillary muscle
- semilunar valves: prevent backflow into the ventricles when ventricles relax, aortic and pulmonary semilunar valves


Why are there no valves going into R and L atria?

- no valves guarding Vena cavas and pulm veins because pressure is so low


Circulation of blood through the heart?

1. blood returning to heart fills atria putting pressure against AV valves which are then forced open
2. as ventricles fill, AV valves flaps hang limply into ventricles
3. atria contract, forcing additional blood into ventricles
4. ventricles contract forcing blood against atrioventricular valves cusps and the valves close, the papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria
5. As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves forcing them open
6. as ventricles relax and intraventricular pressure falls, blood flows back from arteries filling the cusps of the valves and forcing them to close


Why is there a fibrous insulator between the atrium and ventricle?

- keeps everything in order through specific pathways, keep ventricles from depolarizing at the same time


Describe cardiac muscle and contraction.

- has actin and myosin filaments
- has low resistance intercalated disks
- depolarization of the heart is rhythmic and spontaneous
- about 1% of cardiac cells have automaticity (self-excitable)
- gap junctions ensure the heart contracts as a unit
- long absolute refractory period (250 ms)


similarities b/t cardiac and skeletal muscle?

- both are triggered by action potentials that sweep across cell membranes
- 1% of cardiac fibers are auto rhythmic
- bulf of heart msucle however are composed of contractile muscle fibers responsible for heart's pumping action
- in these cells, the sequence of event leading to contraction is similar to that in skeletal muscle fibers


Describe systole and diastole?

- systole: ventricular muscle stimulated by action potential and contracting
- diastole: ventricular muscle reestablishing Na/K/Ca gradient and relaxing


What is the intrinsic cardiac conduction system?

- a network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart


Describe the electrical pathway of the heartbeat?

begins at SA node (pacemaker of heart) - goes down internodal pathway to AV node and impulse is delayed here to allow atria to contract before ventricles and AV bundle then takes impulse into ventricles through bundle of his and then down the left and right bundles of purkinje fibers that take impulses to rest of ventricles


Describe the autorhythmic cells?

- have unstable resting potentials (pacemaker potentials or prepotentials) due to open slow Na+ channels and closing of K+ channels
- at threshold Ca2+ channels open and explosive Ca2+ influx produces the rising phase of the action potential and depolarization occurs
- repolarization results from the inactivation of Ca2+ channels and opening of voltage gated K+ channels, this allows K+ efflux which brings the membrane potential back to its most negative voltage


Describe the sinus node and it's action potential?

- specialized cardiac muscle connected to the atrial muscle
- acts as a pacemaker because membrane leaks Na+ and membrane potential is -55 to -60 mV and when the membrane potential reaches -40 mV slow Ca2+ channels open causing action potential
- after 100-150 sec Ca++ channels close an K+ channels open more thus returning membrane potential to -55 mV


Electrical pathway?

1. SA node (pacemaker): generates impulses about 75 times/minute (sinus rhythm), depolarizes faster than any other part of myocardium
2. AV node: smaller diameter fibers, fewer gap junctions, delays impulses approx 0.1 sec
depolarizes 50 times/min in absence of SA node input, delays impulse from atria into ventricles
3. AV bundle (bundle of his): only electrical connection between the atria and ventricles
4. Right and left bundle branches: 2 pathways in the interventricular septum that carry the impulses toward the apex of the heart
5. purkinje fibers: complete the pathway into the apex and ventricular walls, av bundle (bundle of his) and purkinje fibers depolarize only 30x per minute in absence of AV node input


What are the homeostatic imbalances that may result in if there are defects in the intrinsic conduction system?

- arrhythmias: irregular heart rhythms
- uncoordinated atrial and ventricular contractions
- fibrillation: rapid, irregular contractions, useless for pumping blood


What may a defective SA node result in?

- ectopic focus: abnormal pacemaker takes over
- if AV node takes over, there will be a junctional rhythm (40-60 bpm)


What may a defective AV node result in?

- partial or total heart block
- few or no impulses from SA node will reach the ventricles


Describe the extrinsic innervation of the heart?

- heartbeat is modified by the ANS
- cardiac centers are located in the medulla oblongata:
cardioacceleratory center innervates the SA and AV nodes, heart muscle and coronary arteries through sympathetic neurons
cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerve (can control rate but not contractility)


Describe what the waves on an EKG mean?

- atrial depolarization which is initiated by the SA node, causes the P wave
- with atrial depolarization complete, the impulse is delayed at the AV node, ventricular depolarization begins at the apex, causing the QRS complex, and atrial repolarization occurs
- next ventricular depolarization is complete and repolarization begins at the apex causing the T wave, and ventricular repolarization is complete


What produces the first and second heart sounds?

- lubb: first heart sound (S1), this occurs during ventricular systole, due to AV vlaves closing - this signifies the beginning of systole
- dupp: second heart sound (S2), occurs during ventricular diastole when the pulmonary and semilunar valves are closing- beginning of ventricular diastole
- heart murmurs are often indicative of valve problems


Where on the chest are the valves heard opening and closing?

aortic valve: in 2nd intercostal space at right sternal margin
pulmonary valve: 2nd intercostal space at left sternal margin
tricuspid: right sternal margin of 5th intercostal space
mitral: over heart apex in 5th intercostal space (in line with clavicle)


What is occuring during systole? Diastole?

systole: heart is contracting
diastole: heart is relaxing


Describe the phase of ventricular filling?

- takes place mid to late diastole
- AV valves are open, 80% of blood passively flows into ventricles
- atrial systole occurs, delivering the remaining 20%
- EDV: volume of blood in each ventricle at the end of ventricular diastole


Describe ventricular systole?

- atria relax and ventricles begin to contract
- rising ventricular pressure results in closing of AV valves
- isovolumetric contraction phase (all valves are closed)
- in ejection phase: ventricular pressure exceeds pressure in large arteries forcing SL valves open
- ESV: volume of blood remaining in each ventricle at the end of systole


Describe isovolumetric relaxation that occurs in early diastole?

- ventricles relax
- backflow of blood in aorta and pulmonary trunk closes SL vlaves and causes dicrotic notch (brief rise in aortic pressure)
- closing of SL valves: Dupp


What is CO?

-volume of blood pumped by each ventricle in one minute
SV = volume of blood pumped out by a ventricle with each beat
- normal = 75x 70 m/beat = 5.25 L/min


What is the cardiac reserve?

difference between resting and max CO


What 3 main factors affect SV?

- preload
- contractility
- afterload


What is the ejection fraction?

- measurement of ventriculat systolic function
normal is 60%
get exact # with echo or cardiac catheterization


What is the preload?

- degree of stretch of cardiac muscle cells before the contract (frank-starling law of the heart)
- cardiac muscle exhibits a length tension relationship
- at rest, cardiac muscle cells are shorter than optimal length
- a slow heartbeat and exercise increase venous return
- increased venous return distends ventricles and increases contraction force
- increase preload = increase in SV
- increase after load= decrease in SV
- increasing contractile state shifts isovolemic pressure volume relationship leftward (decreasing ESV) increasing SV


What factors regulate contractility?

- contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV
- positive inotropic agents increase contractility: increased Ca2+ influx due o sympathetic stimulation, hormones = thyroxine, glucagon and epi
- negative inotropic agents decrease contractility: acidosis, increased extracellular K+, and Ca Channel blockers


What is the after load and what affects this?

- pressure that must overcome for ventricles to eject blood
- HTN increases afterload, resulting in increased ESV and reduced SV


Chronotropic factors?

- positive chronotropic factors: increase HR
- negative decrease HR


Sympathetic effect on heart?

- activated by emotional or physical stressors
- NE causes pacemaker to fire more rapidly and also increase contractility
- NE is released and this causes increased sinus node discharge, and increases rate of conduction of impulse and also increases force of contraction in atria and ventricles
- it increases pacemaker rate by decreasing K+ perm and increasing slow inward Ca2+ and Na+


Parasympathetic effect on heart?

- opposes sympathetic effects,
Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels
- heart at rest exhibits vagal tone (parasympathetic)
- doesn't affect contractility though
- Vagal nerves release acetylcholine at their endings, innervate SA node and AV juntional fibers prox to VA node. This causes hyperpolarization becuase of increased K+ perm in response to acetylcholine, this causes decreased transmission of impulses maybe temporarily stopping heart rate, ventricular escape occurs


What is the atrial (bainbridge) reflex?

- a sympathetic reflex initiated by increased venous return
- stretch of atrial walls stimulates SA node and also stimulates atrial stretch receptors activating sympathetic reflexes
- fast heart rate (tachycardia) can decrease C.O. because there isn't enough time for heart to fill during diastole


Explain how exercising can increase SV?

- exercise increases venous return, will have decreased heart rate to begin with so ventricles have more time to fill - this increases venous return and increases EDV which in turn increases SV, also producing Epi, thyroxine and excess Ca2+ which increases contractility and decreases ESV which increases SV


Explain how exercising or having anxiety can increase HR?

- increases sympathetic activity which increases HR and also contractility and decreases parasympathetic activity hence increasing HR
- increasing SV and HR = increase CO


How is the heart chemically regulated?

- Epi from adrenal medulla enhances HR and contractility
- thyroxine increases HR and enhances the effects of NE and E
- intra and extracellular ion concentrations (Ca and K) must be maintained for normal heart function


What other big factors influence heart rate?

- age
- gender (females have faster heart rate)
- exercise
- body temp


What is tachycardia?

- abnorm fast heart rate (greater than 100 bpm)
if this is persistent, it may lead to fibrillation


What is bradycardia?

- HR slower than 60
- may result in grossly inadequate blood circulation
- may be desirable result of endurance training


How can you assess perfusion at a pt's bedside?

- cold extremities indicate reduced perfusion (feel the feet0
- poor urine output also indicates poor tissue perfusion
- BP