Perfusion Flashcards
The 4 layers of the heart
PERIcardium (2 layers w/ 20mL that LUBRICATE the heart surface to reduce friction during systole–ctx)
EPIcardium (lines the OUTSIDE of heart)
MYOcardium (heart MUSCLE fibers–> responsible for pumping)
ENDOcardium (lines INSIDE of heart & valves)
Cardiac tamponade
COMPRESSION OF THE HEART caused by accumulation of fluid in the pericardial space (pericardial effusion)
(>20 mL in the POTENTIAL SPACE) that
PREVENTS <3 from PUMPING EFFECTIVELY (chambers collapse) resulting in:
- -reduced ventricular filling (impaired diastolic filling)
- -subsequent hemodynamic compromise (decreased CO)
S/S:
HYPOtension, cyanosis, cold/clammy, JVD, impending shock
Cardiac tamponade TX
Tx: NEEDLE DECOMPRESSION (Pericardiocentesis) (aspirate until normal <3 rhythm returns)
or
PERICARDIUM WINDOW (drain to abdomen; for recurrent issue)
Diastole
“re-lax-a-tion” (di-as-to-le) 4
diastole = FILLING (P wave)
AV valves open, semilunar valves closed
<3 muscle RELAXES (early diastole) & VENTRICLES FILL (late diastole) from atria
**diastolic dysfunction**
IMPAIRED FILLING/RELAXATION=
S4 gallop (atrial gallop)
--"di-as-tol-ic" ("1-2-3-4")
--heard before S1
--stiff & thick heart muscle
--caused by atrial ctx. and ejection of blood in late diast.
<<>>
causes: HTN w/ LV hypertrophy, restrictive & hypertrophic cardiomyopathies, fibrosis, constrictive pericarditis, valvular dx, aging
Systole
“con-trac-tion” (sys-to-le) 3
systole = CONTRACT/PUMP (QRS complex)
atria contract»_space; then ventricles contract
**systolic dysfunction**
IMPAIRED CONTRACTILITY=
S3 gallop (ventricular gallop)
--"sys-tol-ic" ("1-2-3")
--heard after S2
--thin & weak heart muscle
--not that uncommon;
--is the sound of blood flowing into ventricles
>>>but indicates CHF in older pts<<<
causes: ischemic heart disease, chronic HTN, dilated cardiomyopathy, myocarditis, low EF
Normal Heart Sounds
p.1034
S1 = “LUB”
AV valves (M & T) close»_space;» b/c ventricles have been FILLED and they are ready to contract –>
BEGINNING of SYSTOLE
——————————–
S2 = “DUB”
Semilunar valves (A & P) close»_space;» b/c ventricles have EMPTIED blood into aorta and pulmonary arteries and the chamber are about to relax and fill –>
END of SYSTOLE –»begin diastole
Pulmonary circulation
p. 1036
–RIGHT side of heart + pulmonary artery/capillaries/veins
–low pressure system
Systemic circulation
p. 1036
–LEFT side of heart + aorta/branches, capillaries that supply tissues, systemic venous system, and vena cava
–high pressure system (responsible for moving blood)
Coronary circulation
p. 1036
–vessels that supply the heart muscle
–they perfuse the cardiac muscle DURING DIASTOLE (b/c there is less resistance)
–AORTA >
1–LEFT main coronary artery >
1a–Left Anterior Descending (LAD)
“widow maker”; covers most of the heart (LV)
1b–Left Circumflex (goes around the heart)
2–RIGHT main coronary artery (supplies RV)
2a–Posterior Descending (supplies back of heart)
Cardiac Output
amount of blood pumped by the VENTRICLES into circulation
IN 1 MINUTE
CO = SV x HR
–avg CO ranges from 4-8L/min
–INDICATOR of heart’s ability to function as a pump
–if heart cannot pump effectively, CO & tissue perfusion decr.
Stroke Volume
p. 1042
ranges from 60-100mL/beat; avg is 70mL/beat
affected by 3 factors:
1) PRELOAD: Amt of stretch at end of diastole (just before ctx)–Frank Starling Law (relationship b/t stretch & force of ctx to empty)
2) AFTERLOAD: force ventricles must overcome to eject their blood volume (resistance to ejection)
3) CONTRACTILITY: ability of cardiac muscle fibers to shorten; INCR. by catecholamines, SNS; DECR. by hypoxemia, acidosis
* *poor contractility = decr. fwd flow from the heart, incr. ventricular pressures, and decr. CO; incr. ctx. may stress <3
***ACIDOSIS decreases contractility
(CPR combats acidosis; cell death during MI releases K+)
Heart Rate
- -increased by SNS
- -decreased by PNS
- -also controlled by baroreceptors (reflex regulation of HR in response to systemic BP)
**increase HR = increased CO (even if no change in SV)
BUT rapid HR decr. time for vent. filling during diastole»_space;
..SO CO decreases b/c decr. fill time =decr. SV
** low HR = low CO (low # of cardiac cycles)**
Ejection Fraction
represents the fraction/percentage of DIASTOLIC VOLUME that is EJECTED from the heart DURING SYSTOLE
–normal EF ranges from 50-70% (** normal = > 60% **)
**low EF can be from cardiomyopathy (ex: thinning of LV)
Cardiac conduction system
“self excitation system”
p. 1042
1) SA node–
- -@ junction of SVC & RA
- -“natural pacemaker of <3”
- -60-100 impulses/min
2) AV node–
- -@ floor of interatrial septum
- -SLOW the impulse»_space;delay transmission to ventricles to allow them to fill properly
- -40-60 impulses/min
3) Bundle of His (AV bundle)
- -fibers b/t ventricles for electrical conduction
4) R & L Bundle branches
5) Purkinje Fibers–
- -located in ventricular muscle walls
- -in ventricle, so slower than atria
- -30-40 impulses/min
CONDUCTION:
path of electrical transmission produces a series of changes across muscle cell membranes
–electrical stimulus creates action potential
–exchange of Na, K, & Ca ions across membrane»_space; changes intracellular change to positive»_space; depolarization = heart ctx
–ion exchange reverses»_space; cells return to resting state of electronegativity»_space; repolarized = heart relaxes
Factors affecting pulse
- -age (decr. HR w/ age)
- -gender (men lower than women)
- -FEVER (incr. metabolic demand, so incr BP too)
- -HYPOVOLEMIA (incr. HR by triggering baroreceptors)
- -stress (incr. HR)
- -position changes (decr BP, but INCR HR)
