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Heart

QuestionAnswer
Heart in thoracic cavity or mediastinum
Mediastinum between the lungs
base superior to apex and at the level of 3rd rib
Apex inferior to based and between 4th and 5th ribs
Right side of the heart deflected anteriorly
Left side of the heart deflected posteriorly
Pulmonary circulation short and low-pressure
Systemic circulation high pressure and friction circulation
Heart coverings Outer Fibrous Pericardium & Inner serous pericardium
Outer Fibrous Pericardium Dense CT, protection, and maintain its position in the thorax
Inner serous pericardium Parietal & Visceral (epicardium) pericardium & Pericardial cavity
Parietal pericardium fused to the fibrous PC (outer layer)
Pericardial cavity filled w/ lubricating serous fluid; between epi & pericardium
Visceral pericardium (epicardium) fused to the heart
Layers of the heart Epicardium, Myocardium, & Endocardium
Myocardium made of cardiac muscle cells
Myocardium blood pump via heart and into major arteries
Myocardium left ventricle is significantly thicker than right ventricle
Endocardium endothelial lining of the BV
Endocardium covers the heart valves
pulmonary circulation VC & Coronary Sinus -> RA -> Tricuspid valve -> RV -> Pulmonary valve -> Pulmonary trunk -> Pulmonary arteries -> lungs
systemic circulation lungs -> 4 pulmonary veins -> LA -> Mitral valve -> LV -> Aortic valve -> Aorta
Coronary circulation small circulation for blood delivery to cardiac muscle cells & other part of heart; not continuous and it cycles
Coronary circulation at its peak heart relaxes
Coronary circulation nearly ceases heart contracts
Left coronary arteries circumflex and anterior interventricular artery
Right coronary arteries Marginal arteries (-> superficial of RV) and posterior interventricular artery (septum & portions of both ventricles)
Great cardiac vein follows the interventricular sulcus
Great cardiac vein drains the areas supplied by the anterior interventricular artery into the coronary sinus emptying into the RA
Anterior cardiac vein drains the anterior surface of the RV; drains directly into the RA
Cardiac veins collect deoxygenated blood from myocardium; drain the heart
Cardiac sinus (main pipe) vein that received blood from most cardiac veins, empty to RA
Atherosclerosis hardening of arteries from plaque
plaque cholesterol, connective tissue, WBC, & smooth muscle cells
Ischemia restricted blood flow, lead to hypoxia
Hypoxia insufficient # of oxygen to cells leading to cells might die -> MI
Blood pathway Great cardiac vein -> middle cardiac vein -> posterior cardiac vein -> coronary sinus -> RA
Valves ensure one-way blood flow & pressure
Coronary circulation how blood goes to heat muscles
Blood pathway Aorta -> Left and Right coronary arteries
Left coronary artery pathway Anterior interventricular artery & (Circumflex artery -> posterior interventricular artery)
Right coronary artery pathway Right marginal artery
SA node superior and posterior wall of RA
AV node inferior part of RA
Purkinje fibers apex to septum & base
SA node P wave
AV node PR interval
Bundle branches QRS complex
Purkinje fibers S wave
heart ap activity rapid depolarization, plateau phase (MP decline relatively slowly), & repolarization
Isovolumic relaxation AV valves closed; no enough pressure to open SL valves
Ventricular filling A & V in diastole
Ventricular systole A Atria in diastole/almost empty & ventricle depolarized
Ventricular systole B Depolarization lead to open SL valves -> ejection phase
Ejection phase blood leave ventricles
Epicardium scabbing would damage the heart
Endocardium thin layer of epithelial cells that line -> make blood flow smooth and continuous
incompetent heart valves not functioning properly -> valvular disease, range from benign to lethal
Prolapsed valve one of the cusps of valve is forced backward by blood force
Sterosis heart valves become rigid and may calcify over time
S1 heart sound closing of AV valves "lub"; ventricular depolarization
S2 heart sound closing of SL valves "dub"; ventricular repolarization
Cardiac output (CO) measure # of blood pumped by each ventricle in a min
Cardiac output (CO) HR x Stroke Volume (SV)
Cardiac output (CO) normal value: 5.25L/min
HR factors autonomic innervation, age, hormones, & fitness levels
SV factors heart size, contractility, fitness levels, contraction duration, gender, preload (EDV), & afterload (ressitance)
closed sl valves ventricles relaxed due to lack of pressure
open sl valves ventricles contract from blood force or increase bp
ventricular filling p wave occurs, ventricles depolarizes at the same time -> BP from atria open AV valves to ventricles
Isovolumetric contraction phase AV valves open and no enough pressure to open SL valves
Isovolumetric contraction phase in Ventricular Systole A
Ejection phase in Ventricular Systole B
Ejection phase blood leave ventricles: increase BP and open SL valve
End systolic volume (ESV) some blood remain ventricle
The plateau steady depolarized mp for longer contraction by squeezing the blood in ventricles
Refractory period can't double contract
The plateau slow Ca++ channels open and close, K+ channel open & faster open
Skeletal muscle fiber AP last 1-2 ms and contraction last 15-100 ms
Contractile muscle fiber AP last 200 ms and contraction last +200 ms
longer contraction in cardiac muscle fiber ensure efficient blood ejection and longer refractory period to prevent tetanic contractions
AV node delay the progress of AP since it has fewer Na+/K+ gates
AV bundle connect atria & ventricles
Bundle branches carry the signal toward the apex of the heart
Purkinje fibers extend through the myocardium from apex to septum & base
Passageway to Ap AV bundle, Bundle branches, & Purkinje fibers
Autonomic innervation Sympathetic innervation & vagus nerve
Medulla oblangata nervous control over HR
Pons control cardiovascular and respiratory
Sympathetic innervation force of stimulation SA, AV, & Purkinji fibers
Sympathetic innervation increase HR
Sympathetic innervation damage will make HR difficult to increase (HR will still happen but it can't increase it and person will tire easily)
Vagus nerve main mechanism is to decrease HR
Vagus nerve stimulate SA & AV
Vagus nerve damage heart won't relax
Autonomic tone both centers stimulate heart during rest
ECG tracing of electrical signal of heart
ECG AP and Contraction happen simutaneously, can delay
R point atrial completely repolarizes
PR interval atrial depolarization & ventricular depolarization; reflects delay @ AV node
ST interval ventricular depo & rep
PQ segment AV node hold/delay signal
RT segment plateau/ electrical signal pause
TP segment heart relaxes
Created by: FuirzH
 

 



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