CVS Physiology

*Now most important value here to understand is Arterial barorceptor firing rate which is Decreased in our patient(In Hemorrhagic shock), because Baroreceptors are STRETCH receptors thus when you reduce the blood that circulates in vessels there will be less stretch and thus less baroreceptor firing, response of body to decreased baroreceptor firing is Increase in Efferent sympathetic firing and decrease in Efferent Parasympathetic firing that will lead to increased HR,Contractility to try and increase BP somehow, increased sympathetic tone /along with activation of RAAS in response to fluid loss will increase TPR,activation of RAAS will tilt systemic capillary fluid transfer in favor to ABSORBTION(Not filtration) to maintain alveolar O2 Pulmonary vascular resistance will also increase.

*Answer is EARLY diastole, as in late diastole, here you just need some IQ to realize that as more blood will end up in coronary arteries during early systole, there will be less additional blood flow as space is occupied and there is less negative pressure from previously dilated empty coronaries(in EARLY diastole) to suck blood from aorta in now filled arteries(in Late diastole)+as diastole ends eventually stress from myocardium(thus compression of vessels) will increase, hence less space for ur blood flow.

Purkinje fibers > atria > ventricles > AV node(0.03)*AV is slowest and it separates atrial and ventricular depolarization(Delays spread of impulse to ventricles) gives ventricles time to relax and fill up with blood.-if this delay didn't happen=atria and ventricles contracted the same time, valves(Tricuspid and Mitral) would close as ventricle contracted and blood wouldn't enter ventricle from atria.

*The radius was halved , so degree of stenosis 50%.(When you change the radius, for example decrease the halve it,resistance will increase in power of 4th to the change in the radius, so when you halved the radius you increased the resistance 16times=2x2x2x2)*remember resistance =Viscosity of blood x Length of blood vessel/radius of blood vessel in 4th power. *So the relationship between radius and resistance is inverse and in 4th power.

*PP is basically difference between Systolic and diastolic pressures(SBP-DBP)*High PP is very characteristic finding in Aortic Regurgitation(Diastolic,high-pitched murmur)-which leads to increased EDV>Increased Inotropy(Force of contraction)>Higher SBP.*contrast this with aortic stenosis( result of wear and tear(Resulting in dystrophic Calcification,stenosis)in aortic stenosis SV will be decreased which is DIRECTLY Proportional to PP(Because Decreased SV obv decreased Systolic BP, thus SBP-DBP would decrease which =PP), on the same principle we can deduce that anything that can decrease SV(Thus CO=HRxSV ) can DECREASE PP-thus Conditions like CARDIAC TAMPONADE,Cardiogenic shock,advanced HF can all DECREASE PP.*Very HY point is that PP is Directly proportional to SV while it is Inversely proportional to Arterial Compliance(e.g As we age we get increase in SBP and decrease DBP, because as we age we loose elastin/collagen,hence we Decrease Compliance of vessels(Like in Aortic STIFFENING) and thus we INCREASE PP, as in systole vessel can't accommodate the volume> we increase pressure a lot+ as we can't accommodate we get decrease in SV , thus less volume of blood will get back to the heart which is primary determinant of DBP which can be normal/decreased hence we get widened PP and ISOLATED SYSTOLIC HYPERTENSION as part of aging-with stiffening of vessels)*Hyperthyroidism,Obstructive sleep apnea,Exercise can result in> increased PP.( Thyroid hormone>Upregulates B receptors in heart>Increased Contraction force>Increase SBP,in obstructive sleep apnea we have increased sympathetic response due to hypercapnea stimulating chemoreceptors trough increase in H+,increased Sympathetic tone will increase SBP and hence the gap between SBP and DBP hence the PP,similiar mechanism accounts for increased PP during exercise-but here the effect is transient)

*MAP=CO(SVxHR)xTPR.*MAP=2/3 diastolic pressure+1/3 systolic pressure.*<Later formula is not tough at all, if you have bigger picture:MAP= the average arterial pressure during a single cardiac cycle, we spend most of cardiac cycle in diastole hence it contributes more(2/3 when compared to systolic 1/3)*Note that Diastole preferentially shortens with Increased HR, hence ventricular tachycardia can decrease CO which obv. can lead to syncope(Even though u increased HR, you did it too much and reduced time needed for diastole to fill ur ventricles hence u compromised SV)

*Initially you increase BOTH SV and HR, but later(Like after an hour of workout)you hit the stage when you can't increase SV anymore and thus you can only increase Cardiac Output by increasing HR further.

*Cardiac output = Rate of O2 consumption/difference between arterial and venous O2 content(Arterial O2-Venous O2)*Any heart dysfunction like HF that leads to Decreased Cardiac Output.<Hence flow trough vessel decreases,Hence Tissue has MORE time to EXTRACT that O2 and hence the blood that passed tissues and now entered Vein will have LOWER O2.So in terms of formula ratio of Rate of O2 consumption/Ao2-Vo2 will decrease as we decreased Vo2 and thus inceased the denominator(Hence the ratio goes down)and that decrease in ratio obviously reflects decrease in CO(Once more CO=Rate of O2 consumption/Ao2-Vo2)

*Patient most likely has 2nd Degree AV block type I(Mobitz type 1=Wenkebach).*Note the IRREGULAR PR intervals(In IRregular pattern, no particular pattern-hence the "irregularly Irregular") and progressive lengthening of PR intervals untill the beat is dropped(P wave isn't followed by QRS complex.)<Contrast this with mobitz type 2-sudden loss of impulse conduction without a corresponding change in PR interval(PR is constant) and contrast these with type 1 AV block(Not mobitz typ 1=type2 AV block) where we see no Dropped beats.(QRS always follows P)*Remember that in most patients AV,SA nodes are supplied by RCA(likely affected in inferior wall MI that he survived)*On that note remember that type 2 can progress to type 3 (COMPLETE)AV block-where there is no conduction trough AV node and ventricles beat at their intrinsic pace, Atria and ventricles beat independently, thus on ECG we see dissociation of P and QRS .

*Well he probably cought Borrelia burgdorferi when he went for hiking in woods,travel to NORTHEASTERN U.S(They won't tell you this story always:), vector for this spirochette is ixodes deer tick(Yes they want you to know that).*Our patient likely has early disseminated form of the disease(Stage2)-characterized by migratory myalgias/transient arthritis,facial nerve palsy,carditis and AV Block.DISSOCIATION between P and QRS complexes(Signal from atria is not conducted trough AV Node and ventricles beat at their own pace), characteristically Atrial rate>Ventricular rate.*They love to ask management of Type 3 block-Pacemaker.*To prevent all this sht you should prevent getting the spirochette from Ticks(avoid travel, or wear long light closes to notice the tick) or actually proper treatment Doxycycline is 1st line(Frequently asked)

*Most likely None, First degree AV block is mostly asymptomatic and is characterized by prolonged PR interval(>200msec), with no drops in QRS complexes.*No treatment is required.(And yes they can ask this).It is HY to know that PROLONGED PR(corresponds to AV conduction) Interval can be sign of Calcium channel blocker/B-blocker overdose.

*Lightheadedness, palpitations, anxiety, pallor,diaphoresis often accompany atrial fibrilation.*HYPERTENSION and CAD are common important predisposing factors.*On ECG:we can see loss of P waves, Chaotic baseline with IRREGULARLY SPACED QRS complexes, PR interval can be absent and QRS<0.12s.*They love to ask complications and that is Thromboembolic events(esp. STROKE)<Irregularly irregular uncoordinated atrial contractions can lead to tachycardia and stasis of blood in the left atrium>Thrombi formation>Embolizaiton.*Rate control with B-blockers like metoprolol,Digoxin,Caclcium channel blockers(All delay AV node conduction),anticoagulation,rhythm control by Class1C,III antirarrhythmics,cardioversion are all possible components of management.HOWEVER:till you do cardioversion you should be sure that patient has no thrombus in atria and that you won't promote embolization,Transesophagial echocardiogram can be used for screening of left atrial thrombus, or patient should be on oral warfarin for several weeks until cardioversion is done....but to prevent paradoxical coagulation(As protein C and S-anticoagulants are more rapidly depleted than 2,7,9,10), don't forget to begin IV-heparin(Antithrombin3 activator) for short-term atnicoagulation

*She could have Left atrial myxoma-which accounts for Most cases of benign tumors of the heart and arises from mural endocardium, minor cases are familial and follow autosomal dominant pattern.. *her Transient weakness in her arm few weeks ago was likely due to EMBOLIZATION-common complication of atrial myxoma.*For now at least understand changes on heart auscultation:Splitting of S1 is increased as the tumor is extruded from the mitral orifice.(Remember S1 is due to AV valve closure-Specifically Mitral valve closure)*Loud P2 sound(Closure of pulmonary valve)-could be caused by this tumor as it can compromise. pulmonary venous return and more blood will back up and hit the pulmonary valve as it closes, Very characteristic finding in atrial myxoma is S3 heart sound with early diastolic rumbling murmur.<(due to Plopping of the tumor in the atrium during diastole)*Remember mechanism for signs of inflammation in atrial mxyoma(Like fever)-This tumor produces IL6.

*Rapid succession of identrical back-to-back P waves(Mark atrial depolarization)- this creates characteristic "Sawtooth" appearance of Atrial FLUTTER on ECG.*Definitive treatment is catheter ablation.(procedure used to selectively destroy areas of the heart that are causing a heart rhythm problem)

*Well because this erratic rhythm without identifiable waves is classic of ventricular fibrilation and is easy to recognize, however patient is in BIG TIME problem, because without Immediate CPR/Defibrilation he can DIE pretty soon.