Cvs Physiology

1. Patient presents after gunshot. He has hypotension, tachycardia, and appears pale. What is the arterial baroreceptor firing rate in this patient? What about pulmonary vascular resistance, total peripheral resistance, and systemic capillary fluid transfer?

Arterial baroreceptor firing rate is normal. Pulmonary vascular resistance, total peripheral resistance, and systemic capillary fluid transfer are all decreased.

*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.

Arterial baroreceptor firing rate is increased. Pulmonary vascular resistance, total peripheral resistance, and systemic capillary fluid transfer are all decreased.

Arterial baroreceptor firing rate is decreased. Pulmonary vascular resistance, total peripheral resistance, and systemic capillary fluid transfer are all decreased.

2. During which phase of the cardiac cycle is blood flow through coronary arteries maximized?

Peak systole

*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.

Mid diastole

Late diastole

During early diastole, there is maximal blood flow through coronary arteries as there is less compression from the myocardium. In late diastole, space in the coronaries is occupied and there is less negative pressure to assist blood flow. In peak systole, the myocardium exerts maximal contraction limiting blood flow. In mid diastole, the period between peak systole and late diastole, blood flow is not maximized as in early diastole.

Explanation

During early diastole, there is maximal blood flow through coronary arteries as there is less compression from the myocardium. In late diastole, space in the coronaries is occupied and there is less negative pressure to assist blood flow. In peak systole, the myocardium exerts maximal contraction limiting blood flow. In mid diastole, the period between peak systole and late diastole, blood flow is not maximized as in early diastole.

3. In the human heart, what is the correct order of speed of conduction from fastest to slowest?

AV node > ventricles > atria > Purkinje fibers

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.

Atria > Purkinje fibers > AV node > ventricles

Ventricles > AV node > Purkinje fibers > atria

The conduction system in the human heart follows a specific pathway to ensure proper blood flow and coordination of contractions. Understanding the speed of conduction helps in recognizing how the heart functions in various situations.

Explanation

The conduction system in the human heart follows a specific pathway to ensure proper blood flow and coordination of contractions. Understanding the speed of conduction helps in recognizing how the heart functions in various situations.

4. Degree of stenosis in vessel where flow is decreased 16 times compared to normal?

*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.

The length of the vessel increased, so degree of stenosis is 75%.

The radius decreased by 25%, so degree of stenosis is 25%.

The radius was doubled, so degree of stenosis is doubled.

When you change the radius of the blood vessel, the resistance increases in the power of 4 to the change in the radius. Halving the radius increases the resistance by 16 times (2x2x2x2) due to the radius to the power of 4 relationship with resistance.

Explanation

When you change the radius of the blood vessel, the resistance increases in the power of 4 to the change in the radius. Halving the radius increases the resistance by 16 times (2x2x2x2) due to the radius to the power of 4 relationship with resistance.

5. What is pulse pressure (PP) and how does it relate to SV (blood left in the ventricle after diastole - blood left in the ventricle after systole) and arterial compliance?

Low PP is characteristic of Aortic Regurgitation due to decreased ventricular filling

The difference between diastolic and systolic pressures is called the mean arterial pressure (MAP)

Conditions like aortic stenosis result in increased PP due to increased stroke volume

*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)

Pulse pressure is defined as the difference between systolic and diastolic pressures. The correct answer explains the relationship between PP, SV, and arterial compliance in various cardiovascular conditions. The incorrect answers provide misleading information about mean arterial pressure, the relationship between PP and conditions like Aortic Regurgitation and Aortic Stenosis.

Explanation

Pulse pressure is defined as the difference between systolic and diastolic pressures. The correct answer explains the relationship between PP, SV, and arterial compliance in various cardiovascular conditions. The incorrect answers provide misleading information about mean arterial pressure, the relationship between PP and conditions like Aortic Regurgitation and Aortic Stenosis.

6. What is the relationship between Mean Arterial Pressure (MAP), Cardiac Output (CO), Total Peripheral Resistance (TPR), Systolic Blood Pressure (SBP), and Diastolic Blood Pressure (DBP)?

MAP=SBP-DBP

MAP=CO/TPR

*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)

MAP=HRxTPR+SV

7. How do we maintain cardiac output in early vs late phases of exercise?

C. Increase stroke volume (SV) in both early and late phases of exercise.

A. Increase only heart rate (HR) in the early phase and stroke volume (SV) in the late phase.

*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.

B. Maintain a constant heart rate (HR) throughout the exercise duration.

During exercise, the body adapts by increasing both stroke volume (SV) and heart rate (HR) to maintain cardiac output. While SV increases initially, it eventually plateaus, requiring further HR increases in the late phase to maintain cardiac output. This process allows the body to meet the increased oxygen demand during exercise.

Explanation

During exercise, the body adapts by increasing both stroke volume (SV) and heart rate (HR) to maintain cardiac output. While SV increases initially, it eventually plateaus, requiring further HR increases in the late phase to maintain cardiac output. This process allows the body to meet the increased oxygen demand during exercise.

8. What principle is described by the equation Cardiac output = Rate of O2 consumption / (Arterial O2 - Venous O2)?

Charles's law

Boyle's law

Hess's law

*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)

Fick's principle describes the relationship between cardiac output, rate of O2 consumption, and the difference between arterial and venous O2 content. It explains how any heart dysfunction that leads to decreased cardiac output can impact the flow of blood through vessels and the extraction of O2 by tissues.

Explanation

Fick's principle describes the relationship between cardiac output, rate of O2 consumption, and the difference between arterial and venous O2 content. It explains how any heart dysfunction that leads to decreased cardiac output can impact the flow of blood through vessels and the extraction of O2 by tissues.

9. Patient with Inferior wall MI, survives and comes for follow up, he has bradycardia, ECG is shown:

The ECG findings suggest a normal sinus rhythm with no abnormalities.

Inferior wall MI typically presents with ventricular tachycardia.

*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 .

The bradycardia is most likely due to a sinus node dysfunction.

The correct answer explains how the ECG findings are indicative of 2nd Degree AV block type I in a patient with Inferior wall MI. The incorrect answers are refuted by providing clarification on why they are not the appropriate diagnoses based on the given information.

Explanation

The correct answer explains how the ECG findings are indicative of 2nd Degree AV block type I in a patient with Inferior wall MI. The incorrect answers are refuted by providing clarification on why they are not the appropriate diagnoses based on the given information.

10. Patient has new onset Polyarthritis+Bilateral facial nerve palsy. He now complains of episodes of syncope, his BP is 94/64 and he has regular heartbeat 35 bpm. ECG is shown- what do you see? Diagnosis, most likely cause, treatment?

The patient is suffering from a severe allergic reaction that is causing the symptoms. Treatment includes antihistamines and steroids.

The patient has a rare autoimmune disorder affecting the heart and nervous system. Treatment involves immunosuppressants and corticosteroids.

The patient is experiencing a heart attack leading to bradycardia and syncope. The treatment involves immediate administration of thrombolytics and monitoring.

*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)

11. You note a prolonged PR interval (>200 msec) that does NOT change in length. What symptoms would you expect to find?

Irregular heart rhythm and fainting episodes

Elevated blood pressure and palpitations

*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.

Chest pain and shortness of breath

First degree AV block is typically asymptomatic and does not present with symptoms such as chest pain, shortness of breath, irregular heart rhythm, fainting episodes, elevated blood pressure, or palpitations.

Explanation

First degree AV block is typically asymptomatic and does not present with symptoms such as chest pain, shortness of breath, irregular heart rhythm, fainting episodes, elevated blood pressure, or palpitations.

12. Contrast upper (Atrial Fibrillation) with lower (Sinus rhythm), how would patient most likely present? Most important predisposing factors, Complications? What you should consider/do before you attempt cardioversion?

Patient may present with fever, cough, and shortness of breath. Predisposing factors include smoking and obesity. Complications can include gastrointestinal bleeding and pneumonia.

Patient may present with dizziness and blurred vision. Predisposing factors include excessive caffeine intake and stress. Complications can include migraines and insomnia.

Patient may present with joint pain and rash. Predisposing factors include family history and age. Complications can include liver failure and kidney damage.

*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

13. A patient presents with fever, night sweats, chills, and increasing exertional dyspnea. They also experienced transient weakness in their arm a few weeks ago. On examination, they have low fever, tachycardia, low RR, and pulmonary consolidation with increased Tactile fremitus. Additionally, they have loud Split S1, loud P2, and S3 sounds. What is the most likely reason for these findings?

*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.

Pericardial effusion

Acute myocardial infarction

Pulmonary embolism

The patient's presentation and auscultatory findings are most consistent with Left atrial myxoma. This benign tumor of the heart can lead to various symptoms and characteristic heart sounds as described.

Explanation

The patient's presentation and auscultatory findings are most consistent with Left atrial myxoma. This benign tumor of the heart can lead to various symptoms and characteristic heart sounds as described.

14. What is the characteristic feature of Atrial Flutter on ECG?

*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)

Presence of wide QRS complexes

Absence of T waves

Inverted T waves

The characteristic 'Sawtooth' appearance in Atrial Flutter is due to rapid succession of identical back-to-back P waves, marking atrial depolarization on the ECG.

Explanation

The characteristic 'Sawtooth' appearance in Atrial Flutter is due to rapid succession of identical back-to-back P waves, marking atrial depolarization on the ECG.

15. Patient likely has Wolff-Parkinson-White syndrome where Bundle of Kent (Abnormal FAST Accessory pathway) Bypasses AV node and thus allows signals from atria to skip this rate-slowing step. PR Interval is shortened and QRS is prolonged due to earlier depolarization of ventricles through the accessory pathway. Does patient have Atrial/Ventricular Pre-excitation syndrome? What could be lethal for patient? Why don't we typically use class 2 and 4 antiarrhythmics during atrial fibrillation in those with WPW?

*Patient likely has Wolff-Parkinson-White syndrome where Bundle of Kent(Abnormal FAST Accessory pathway)Bypasses AV node and thus allows signals from atria to skip this rate-slowing step.*As ventricles begin to depolarize earlier they result in formation of classic Delta wave and shortening of PR Interval, now we began to depolarize ventricles earlier trough this accessory pathway,however Signal will eventually pass trough AV node too and will add upon the already started QRS-hence the prolongation(Or just think of D wave as addition to QRS:)*Remember that Wolff-Parkinson-white is an example of VENTRICULAR(Not atrial) pre-excitation syndrome.<In fact Most Common one and it is important to know that reentry circuits put the patients at higher risk for SUPRAventricular Tachycardia.*Want to know why excitation progresses faster trough Bundle of Kent?-because Myocytes(Make up this bund) contain Na channels while AV node contains Calcium channels.*PATIENTS WITH WPW can DIE from ATRIAL FIBRILATION because Crazy atrial rate(like 300s) now can transmit to Ventricles without AV delay and that frequency of contraction won't let ventricles fill up>Sudden Cardiac Death.*Class 2 and 4 antiarrhythmics aren't useful here because even though they act on AV node(Decrease speed of conduction and increase refractorness) they don't affect/INCREASE speed of conduction trough bundle of kent-hence they can make everything worse.(Increase ventricular repsonsivness to atrial fibrilation)Class1A is preferred in these cases.*Now for Cure of WPW we can use ELECTROPHYSIOLOGIC ABLATION-to abltate the accessory pathway.

The ECG findings suggest a normal conduction system in the heart, ruling out any pre-excitation syndromes.

The patient is experiencing atrioventricular nodal reentrant tachycardia, not Wolff-Parkinson-White syndrome.

The arrow indicates atrial flutter in this patient, leading to the described symptoms.

The correct answer explains the presence of Wolff-Parkinson-White syndrome, the potential lethal complication of atrial fibrillation in patients with WPW, and why class 2 and 4 antiarrhythmics are not typically used in WPW cases.

Explanation

The correct answer explains the presence of Wolff-Parkinson-White syndrome, the potential lethal complication of atrial fibrillation in patients with WPW, and why class 2 and 4 antiarrhythmics are not typically used in WPW cases.

16. Depolarization of T-tubules in phase 0 resulting in L-type calcium channel opening. Is that Calcium induced Calcium release?

*NOPE as here depolarizaiton happened by influx of Na channels and that resulted in opening of L-type calcium channels on sarcolemmalNot Sarcoplasmic Reticulum) membrane.<Now as these channels opened and calcium entered, this calcium will bind and open Ryanodine receptors which will result in Release of Calcium from Sarcoplasmic Reticulum<and that is called Calcium induced Calcium release.<Which can now bind tropomyosin, induce conformational change and displace it thus exposing binding sites for myosin on actin>Contraction.*Note that PLB and SERCA sit on Sarcoplasmic Reticulum.*SERCA is ATP ase that Pumps calcum back into SR.<KNOW THAT PLEASE.*PLB(Phospholamban) INHIBITS SERCA and thus Pumping of Calcium into SR.<U think that's the good guy? Naa SERCA is the long-term planner which pumps calcium into SR so next time you have signal for release you pump out enough as u have enough stores, but when PLB Inhibits it you basically deplete the stores and thus when it is the time for release, SR will release less Calcium>Less exposure of sites for myosin on actin>Less cross-bridge formation>less force of contraction.*NOW Sympathetic activity/B agonism (Trough action on B-adrenergic receptors on heart)>activation of these receptors >Activate Gs subunit >Activate Adenylate cyclase>Increase in cAMP>Activates Protein Kinase A>Phosphorylates L-type Calcium channel and PHOSPHOLAMBAN.*Phosphorylated Phospholamban can't inhibit SERCA-Hence we have more Calcium storage and upon Signal for release SR can release proper ammounts of Calcium+Phosphorylation of L-type calcium channels will promote Calcium induced Calcium release of SR, so B agonism is all for Increased Cytoplasmic Calcium>Hence we increase Contractility of the heart(Intrinsic ability of heart muscle to contract Which depends on number of myosin -actin interactions, which as we already know depend on intracellular calcium.)<So it makes sense that Exercise,Anxiety,B-agonists(NE,EPI) increase Contractility of heart.*Know this physilogy it will help you to undestand path/pharm, furtheroome here are some HY testable principles on their own...

Maybe

Yes

Not sure

Depolarization occurs by influx of Na channels leading to L-type calcium channel opening on sarcolemmal membrane, not Sarcoplasmic Reticulum. This calcium influx eventually triggers the release of calcium from the Sarcoplasmic Reticulum, known as Calcium induced Calcium release.

Explanation

Depolarization occurs by influx of Na channels leading to L-type calcium channel opening on sarcolemmal membrane, not Sarcoplasmic Reticulum. This calcium influx eventually triggers the release of calcium from the Sarcoplasmic Reticulum, known as Calcium induced Calcium release.

17. Patient with Cirrhosis presents with Dependent-pitting edema+Ascities. Why? What would his SerumNa, TBNa levels be?

Patient with Cirrhosis presents with Dependent-pitting edema + Ascites due to decreased Plasma Hydrostatic pressure in liver failure.

Patient with Cirrhosis presents with Dependent-pitting edema + Ascites due to increased Cardiac Output in liver cirrhosis.

*Remember that anything that decreases Plasma Oncotic pressure-like Liver failure due to cirrhOsis,prOtein Malnutrition,nephrOtic syndrome can result in edema.+Note that when you have liver cirrhosis you are likely to have portal hypertension and thus increased Plasma Hydrostatic pressure which also will contribute to edema and Ascities.*Edema is due to accumulation of fluid in Interstitial space and it can happen as you decrease capillary oncotic pressure(So it can't keep protein inside) or when you increase capillary Hydrosatic pressure(You push fluid to leave capillary).*Note that Cardiac Output will decrease as you retain fluid in INTERSTITIAL space, and even though your kidney will try to compensate by RAAS to reabsorb more fluid/Na it will make everything worse because you can't keep fluid in vessel and it again adds up to interstitium>Makes edema worse, while heart still will have compromised preload and thus SV and thus Cardiac output will also be decreased.*BUT remember RAAS will increase Fluid/Na reabsorption-in our case slightly HYPOtonic fluid will be reabsorbed and hence Serum Na will go down while TBNa will go up(remember Serum Na= TBNa/TBW, you increased TBNa by reabsorbing it but you reabsorbed MORE TBW hence the ratio went down=Serum Na went down), now ECF will be expanded as you gained more fluid and ICF will be expanded too as fluid will move from Hyponatremia in ECF to higher solute in ICF and expand it too.*FOR Now make sure you undestand how Hydrostatic and Oncotic pressures fight and how/why you can get edema....*+Remember form general path that The fluid that is responsible for edema in HF,Na retention(Due to increased Hydrostatic pressure) and in CIRRHOSIS,Nephrotic syndrome,Protein malnutrition(Due to decreased oncotic pressure) is TRANSudate(HYPOcellular Clear fluid with Low protein and Low LDH-when compared to serum and with Specific gravity Less than 1.012)

Patient with Cirrhosis presents with Dependent-pitting edema + Ascites due to increased Plasma Oncotic pressure caused by liver cirrhosis.

18. How would you explain edema in patients with Lymphatic blockade in terms of Net fluid flow formula? What is the mechanism of the drug that can be used for treating Wuchereria bancrofti?

Diethylcarbamazine kills Wuchereria bancrofti by enhancing their smooth muscle movement and survival.

Decreased Capillary hydrostatic pressure leads to edema in patients with Lymphatic blockade.

*Because you Increase INTERSTITIAL(Not capillary) ONCOTIC pressure(pi), remember that Interstitial Oncotic pressure (in contrast to Capillary oncotic pressure) pulls fluid towards the Interstitial space.*When you have Lymphatic obstruction, lymphatic system can't clear interstitial space from proteins,solutes,junk and hence the Interstitial oncotic pressure(pi) will be increased and pull the fluid towards it>Edema.*Remember that diethylcarbazine-which blocks Arachidonic Acid metabolism(And thus removing prostaglandins needed for their smooth muscle movement and survival)can kill Filarial nematodes like wuchereria.But at least have association between this helminth,Lymphatic blockade and increased pi(INTERSTITIAL oncotic pressure) and the edema.*Also remember Lymphatic obstruction leads to formation of EXUdate(Cellular,Cloudy,protein-rich fluid with Increased LDH when compared to serum LDH and with Specific gravity >1.020.)

Lymphatic obstruction causes decreased Interstitial oncotic pressure leading to edema.

Lymphatic obstruction causes an increase in Interstitial oncotic pressure, not a decrease. Diethylcarbamazine kills Wuchereria bancrofti by blocking Arachidonic Acid metabolism, not enhancing their smooth muscle movement.

Explanation

Lymphatic obstruction causes an increase in Interstitial oncotic pressure, not a decrease. Diethylcarbamazine kills Wuchereria bancrofti by blocking Arachidonic Acid metabolism, not enhancing their smooth muscle movement.

19. How do the actions of Hydralizine, Nitroglycerin, ACE inhibitors, ARBs help you understand physiological principles?

ARBs and ACE inhibitors primarily increase preload and afterload.

Nitroglycerin primarily works by dilating postcapillary arterioles, increasing TPR, and increasing afterload.

*Well Hydralizine Works by Dilating Precapillary Arterioles>Decreased TPR>Decreased Afterload-Hence in idea it helps with prevention of Concentric Hypertrophy(that develops in response to increased afterload)*Nitroglycerin-Most effects of this drug is due to VENOdilatation(Decreasing Preload), thus in idea it prevents Dilated cardiomyopathy(Which is mainly due to increased Preload).*ARB/ACE inhbitors they Decrease Afterload(By decreasing AG2 medated Vasoconstriction of vessels)+They block RAAS system from reabsorbing more fluid/Salt thus decreasing Preload, hence they decrease BOTH preload and Afterload and are amazing drugs for preventing remodeling of the heart.*Remember that Preload depends on VENOUS tone and Circulating blood volume.*EDV can give rough idea about Preload and this is no BS.

Hydralizine works by decreasing preload, while Nitroglycerin increases afterload.

The correct answers explain the specific mechanisms of action of each medication and how they relate to preload and afterload, which are essential physiological principles in understanding cardiac function.

Explanation

The correct answers explain the specific mechanisms of action of each medication and how they relate to preload and afterload, which are essential physiological principles in understanding cardiac function.

20. What is EF, why do you check it? What is the normal range? Explain the difference between Systolic HF and Diastolic HF.

*Normal EF should be >55% and is frequently evaluated for prognosis of those with previous MI(If large area died/was replaced by fibrosis, contractile function will decrease which would obviously increase volume left in ventricle at the end of the Systole(ESV), now remember formula EF=EDV-ESV/EDS so obviously as we increased ESV we decreased EF, so really understand the formula and play with it.+ Easier way out would be to know : EF=SV/EDS, Contractility we compromised SV and hence the the ratio(EF) would decrease, remember that SV=EDV-ESV.*NOW HY point also is that in Diastolic HF the EF is usually normal while in Systolic HF it is DECREASED.*In Diastolic the EF(ratio) is normal because the Both the nominator- Blood Ejected(SV) and the denominator-Blood that enters heart(EDV) decrease proportionally hence the ratio(EF) remains the same(preserved).*Now in Systolic HF- we have Decrease in SV(EDV-ESV) as we can't pump enough blood and ESV increases, Hence the ratio will decrease as SV is the nominator.*REMEMBER: Ejection Fraction Best reflects CONTRACTILITY.<Most accurate test for measurement of EF is MUGA Scan(Nuclear ventriculogram)

Diastolic HF is characterized by increased EF, while Systolic HF is characterized by decreased EF.

The normal EF range is between 15-25%.

EF should ideally be

The correct answer explains the importance of EF, the normal range, and the differences between Systolic HF and Diastolic HF.

Explanation

The correct answer explains the importance of EF, the normal range, and the differences between Systolic HF and Diastolic HF.

21. What are the conditions that can result in Decreased Stroke Volume (SV) vs those that can increase SV and why?

*BOTH Diastolic and Systolic HF can DECREASE SV, EF remains normal in diastolic HF because EDV decreases proportionally.*SV is basically how much blood is pumped out by LV per Beat.*You should know all the factors that affect SV:*Preload,Afterload,Contractility (2 PAC)*Increase in Contractility leads to increase in SV, Increase in Contractility can be due to increased Activation of B adrenergic receptors due to B-agonists(like Isoproterenol),or just increased Sympathetic outflow due to anxiety,exercise.*Increase in SV can be due to increased Preload(Which can be due to increased Venous tone or as the case in pregnancy due to Increased volume of circulating blood)*Increased Afterload(Like in hypertension) on the other hand will decrease SV, this makes sense as Afterload is basically pressure AGAINST which heart must pump that blood during systole.*Hey that could explain why increased Afterload increases O2 demand, Basically as you reduce your SV(Due to increased Afterload), to keep your CO(SVxHR) you increase HR(Which increases O2 demand itself).But note that even though Hydralizine Decreases afterload, it can potentially cause significant drop in BP> reflex Increase in Sympathetic outflow to keep BP normal can result in increased HR(even SVT)>Increased O2 demand and that has more profound affect on O2 consumption than decreased Afterload.

Increased Afterload always leads to an increase in SV.

Only Diastolic HF can decrease SV.

Increased Preload always leads to a decrease in SV.

Stroke Volume (SV) is affected by factors like Preload, Afterload, and Contractility. Both Diastolic and Systolic Heart Failure (HF) can decrease SV due to various reasons as discussed in the correct answer. Increased Afterload, such as in hypertension, will decrease SV because it is the pressure the heart must pump against during systole. On the other hand, an increase in Contractility results in an increase in SV, showing the opposite effect.

Explanation

Stroke Volume (SV) is affected by factors like Preload, Afterload, and Contractility. Both Diastolic and Systolic Heart Failure (HF) can decrease SV due to various reasons as discussed in the correct answer. Increased Afterload, such as in hypertension, will decrease SV because it is the pressure the heart must pump against during systole. On the other hand, an increase in Contractility results in an increase in SV, showing the opposite effect.

22. How do low levels of Extracellular Na affect Heart contractility, and how can this principle help you understand the mechanism of digoxin?

Digoxin acts by inhibiting the Na/Ca exchanger, promoting the movement of Na into the cell and resulting in decreased contractility.

Low levels of Extracellular K disrupt the normal gradient, leading to increased intracellular calcium and decreased contractility.

High levels of Extracellular Na enhance the normal gradient, leading to decreased intracellular calcium and decreased contractility.

*Low levels of Extracellular Na disrupt the normal gradient(For Na to move from high concentration outside to lower concentration in the cell), this gradient normally is utilized by Na-Ca exhcanger(as Na would go in, Calcium would go out), so as gradient is not there due to low extracellular Na, This exchanger can't pump out Na and can't utilize energy derived from that movement down the gradient to pump the calcium IN, as we know Low intracellular calcium>Decrease in Contractility(As Calcium makes myosin binding spots on actin available by displacing tropomyosin)*Now as we said maintaining the high Na outside the cell is important and that is done by our friend Na/K pump which Needs ATP, DIgoxin blocks this Na/K atpase, so we can't pump Na out, hence Na/Calcium exchanger is inhibited which now can't pump Na in as Na/K atpase didn't create gradient for Na outside to promote its entry into the cell, as this exchanger is not ATPase it needs that movement of Na down the gradient to pump calcium out, so as these processes are inhibited more calcium stays in the cell>increased intracellular calcium>Increased contractility.<Thus in contrast NON-Dihydropyridine calcium channel blockers can cause decrease in Contractility-as they block calcium channels in the heart, now contrast this with Dihydropyridine calcium channel blockers which are way more selective for Vascular calcium channels and by causing vasodilation can cause reflex increased Sympathetic response >Increased Contractility.

The correct answer explains how low levels of extracellular Na disrupt the normal gradient, affecting the Na/Ca exchanger and resulting in increased contractility. The incorrect answers provide misleading information that does not align with the mechanisms discussed in the correct answer.

Explanation

The correct answer explains how low levels of extracellular Na disrupt the normal gradient, affecting the Na/Ca exchanger and resulting in increased contractility. The incorrect answers provide misleading information that does not align with the mechanisms discussed in the correct answer.

23. How does squatting alleviate cyanosis in children with Tetralogy of Fallot?

*2 mechanisms really but you should really know this one:When you squat you Obstruct your femoral arteries>Increased PVR which means that LV has to work against higher pressure=Increased afterload, remember that these patients have RV hypertrophy(Due to pulmonary hypertension)-which gives the Heart "Boot Shaped appearance" but more importantly this hypertrophy+Pulmonary hypertension result in INCREASED right to Left gradient and deoxygenated blood from RV goes LV trough VSD and we end up with>Cyanosis because even less blood is oxygenated in pulmonary circuit and the deox.blood meant to enter Pulmonary vasculature begins to enter the system trough LV, so when they squat as they increase Pressure against which LV has to work the gradient of Right over left ventricular pressure decreases and shunt reverses hence less Deox. blood reaches systemic circulation and we also get better Pulmonary blood flow thus better alveolar perfusion and thus oxygenation, all this >Less cyanosis.*Also know that during squating we decrease Right over left ventricular pressure by decreasing Preload(When u obstruct femoral VEINS more blood remains in those veins and less reaches the right heart)>Less Right to left shunting torugh VSD >Less symptoms.

Squatting reduces pulmonary blood flow, exacerbating cyanosis

Squatting increases the right over left ventricular pressure gradient, worsening cyanosis

Squatting increases the left ventricular afterload, leading to increased cyanosis

24. How can they describe the mechanism of the S3 heart sound in CHF?

*Rapid ventricular filling after opening of mitral valve.*Remember S3 is often sign of fluid overload in ventricle, as more blood from atrium enters ventricle, fast deceleration takes place as that blood encounters already too much fluid stuck there(Can be due to lack of Contractility as you can't pump blood out or can be due to increased Preload-like in the case with Volume expansion in pregnancy)

Delayed closure of the aortic valve.

Contraction of the atrium during diastole.

Decreased blood flow from the lungs to the heart.

The S3 heart sound in CHF is primarily caused by rapid ventricular filling after opening of the mitral valve, not by contraction of the atrium during diastole, delayed closure of the aortic valve, or decreased blood flow from the lungs to the heart.

Explanation

The S3 heart sound in CHF is primarily caused by rapid ventricular filling after opening of the mitral valve, not by contraction of the atrium during diastole, delayed closure of the aortic valve, or decreased blood flow from the lungs to the heart.

25. What is the mechanism by which B-blockers decrease SV? How does understanding this mechanism aid in the treatment of B-blocker overdose?

B-blockers increase cAMP levels, leading to decreased cytoplasmic calcium levels, increased contractility, stroke volume, and heart rate. The antidote for B-blocker overdose is nitroglycerin, which counteracts the effects of B-blockers by dilating blood vessels.

*B-blockers decrease cAMP thus decrease Cytoplasmic Calcium>Decreased Contractility,SV,HR+varying degrees of AV block.*Antidote for B-blockers is very important-Glucagon as it increases intracellular cAMP>Increased intracellular calcium>Hence increase in Contractilility,SV,HR and increase in SA node firing , these effects are mediated by acting on GPCR and glucagon's effects are INDEPENDENT of adrenergic receptors.

B-blockers inhibit the release of acetylcholine, resulting in increased cAMP levels, increased cytoplasmic calcium levels, increased contractility, stroke volume, and heart rate. The antidote for B-blocker overdose is atropine, which blocks the effects of B-blockers on acetylcholine release.

B-blockers increase cAMP levels, leading to increased cytoplasmic calcium levels, increased contractility, stroke volume, and heart rate. The antidote for B-blocker overdose is epinephrine, which further enhances these effects.

Understanding the mechanism of action of B-blockers and their effects on cAMP and calcium levels is crucial in determining the appropriate antidote for B-blocker overdose. The key is to counteract the effects of B-blockers on these pathways in order to restore cardiac function and hemodynamics.

Explanation

Understanding the mechanism of action of B-blockers and their effects on cAMP and calcium levels is crucial in determining the appropriate antidote for B-blocker overdose. The key is to counteract the effects of B-blockers on these pathways in order to restore cardiac function and hemodynamics.