CO = SV X HR Normal CO: 5L/minute SV: how much blood you pump out with each beat • HR: how many beats in one minute • CO: how much blood pumped out in one minute. equal to blood FLOW The body tries to keep CO constant, so It will change SV, HR or both in order to do this. If a patient has tachycardia, give fluids, to ^SV, until the HR is back to normal.

Early exercise: CO is kept by ^HR and ^SV. Late exercise: kept by ^HR only (SV plateus)^HR leads to ^CO but also to v Diastole. ^^^HR >vvvDiastole(no time for blood to fill heart> vCOthis is why too much tachycardia(^HR) is bad!

TPR (total peripheral resistance), also called SVR (systemic vascular resistance) Is the resistance to flow of the peripheral circulation. Its an index of arteriolar resistance TPR = (Mean Arterial P. – Mean Venous P) /CO

* MAP= BP= left ventricle p. *MVP= p. outside of Right Atrium= CVP(central venous p) MVP is small and sometimes disregardedA v TPR due to arteriolar dilation (seen in exercise) will lead to an equal ^ CO (flow!) with little change in BP (MAP).

Arterioles- have most smooth muscle so constx and dilate most. Have B2(vasodilation) recept. #1 top auto regulator of BP, keeps it between 60-160 by changing TPR.

BP (also be called MAP (Mean arterial Pressure))is the average pressure (of syst and diast)coming out of your left ventricleBP=CO X TPRBP= SV x HR x TPRThese are the 3 causes of hypertension (=^BP) : • Volume: ^SV • Treat with diuretics (Blacks, Hispanics (high sodium diet)) • Rate: ^HR • Treat with B-blockers (Middle-aged Whites (stressed out)) • Resistance: ^TPR (Elderly (less compliance of arterioles))^SV- by ^ contrxn: thus by ^catecholam, and by ^Ca+in, v Na+out. With ^preload and v Afterload. **MI leads to death of myocardium(less muscle) and v contrxn, vSV.HR- by temp; Autonomic NS; SA node, thus also by Na and K levels. So all these factors if not compensated for, will affect CO and thus will affect BP.

MAP-ICP = CPPMAP= BP • ICP= the pressure created by gravity pushing on your brain • CPP= how much pressure is circulating through the brain, keeps the brain perfused.

Pulse pressure= Systolic - diastolic 120-80=40= Span of time during which blood is entering aorta, but has not flowed through it. 80: volume sitting on aortic valve Need 1 mmHg > diastolic p. to open up the aortic valve (= 81mmHg) 120: resistance in the aorta. Need 1 mmHg > systolic p. to make blood flow through the aorta (= 121 mmHg)

^ Pulse P = ^resist = hyperthyroid, Aort regurge, Ateriosclerosis, Sleep apnea, agingv Pulse P= ^vol = aortic stenosis, cardiogenic shock, tamponade, advance heart fail.

Normal BP= 120/80HTN= >135/85 -moderate HTN=>155/>100 -severe HTN= >175/>115

BP tells u if its resistance or volume problem!

DIASTOLIC= VOLUME (distention) -regurgitation or shunting

In order to get sustained contraction, the systolic pressure of the LV must be at least 20 mmHg above the resistance in the aorta. This is why the left ventricle is always the first one to give out in systolic hypertension (htn due to resistance problem).

Pulmonary Capillary Wedge Pressure (PCWP)Think of it as total volume in the lungs

EF= fraction of blood ejected in systole. = SV/EDV EF is an index of Ventricular contractility,

Systolic heart failure= less contraction prob. Dilated cardiomyopathy. MIDiastolic heart failure= less volume prob. Hypertrophyc cardiomyopathy

Systolic heart failure has v EF (and thus v SV) because heart is not pumping well.Diastolic heart fail has normal EF.

Preload is approximated by EDV (Related to Right Atrial P.) Rubber band. How much you stretch before contrxn)Afterload is approx. with BP (p. coming out of left ventr). Resistance in aorta preventing blood from going in. Thus: VEnodilators v PrEload★ and VAsodilators v Afterload★vPreload= vCO BUT! In CHF venodilators cause vPreload which ^CO (heart v overstretch)

Chronic HTN(^BP) which implies a ^afterload, will cause LV hypertrophy to overcome aorta p.Can HTN cause dilated heart?? From like ^^CO?

Pulsus Alternans: seen with dilated cardiomyopathy, MIAlternating strong and weak beats (contxns). MCC is left vent systolic failure.v L.vent contxn > ^EDV> ^muscle distention (preload)> ^L.vent contxnPulsus Paradoxus: tamponade, pericarditissystolic BP ≤10mmHg during inspirationMCC is v Left vent capacityKussmaul sign: seen in Konstrictive pericard, restrict cardiomy, Right heart tumor^ JVD on inspiration (instead of only in expiration). MCC is v R. ventricle capacityblood backs up in Venae Cavae> JVD * can also be seen in tamponade*

ORTHOSTATIC HTN:When you stand ^gravity causes ^venous blood pooling and vCO and vSV.Baroreceptors normally compensate for this. B-block and a-block screw compensation!vCO causes vArterial BP, if Cerebral blood flow v enough, u get orthostatic hypoten.

SA node: = sinus rhythm and controls HRHR: normal: 60-100*Max possible sinus Heart rate? 220- age (Anything above this is an ARRHYTHMIA!)*HR increases 10 points for every temp. degree above 100F. So this must be substracted to see ACTUAL HR. (Ex. HR= 90 and 104F. subtract 40 from 90 = 50 HR. Heart block!)

SYSTOLIC= RESISTANCE -stenosis

If both numbers are high, assume VOL prob. Yet, The # with the biggest change is most responsible.

BP

Arterial CLOTS: HTN> high velocity in artery > endothelial damage> platelets aggregation> Arterial clotsTx. ASPIRIN! DOC (block PlATELETS!)Venous CLOTS: stasis> v s︎keletal movem.> ^blood accum> clotting factors build up and form Venous clotsTx. HEPARIN! DOC (stop clotting factors)

HYPOVOLEMIA: Controlled by NE . Veins have MORE α 1 than arteries! and thus Veins constrict first.   GI and Skin veins have the most   α 1 keeping the least blood! (this explains ileus after surgery and stress ulcers (v blood= v acid protection)So... Hypovolemia:^NE> #1 venoconstx #2 arteries constrix #3 arterioles dilate (NE stim B2. so ur tissues get food)As a vessel NARROWS BP INCREASES

 CAPILLARIES:• FF= Hydrostatic v + Oncotic v  (v=vessel)

• BM has HEPARAN SULFATE (- charge)• Has FENESTRATIONS:     EDEMA          Transudate = mostly water outside of vessel.          Exudate = mostly protein outside of vessel.

AORTA: Has special armor (SQUAMOUS cells, strong collagen BM, Vasa vasorum(blood v.)• Blood passes at ~200 m/h. This speed cleans up possible placks.• Dilated Cardiomyopathy > ↓ veloc blood→  less cleaning t4 more atherosclerosis• With age armor weakens→exposed muscle(media) weakens t4 ↑   risk of aneurysm/

dissection• Collagen dzs, BM dzs, syphilis, takyasu ALL cause weak armor t4 ↑ risk of

aneurism/dissection.

NITROGLYCERIN:Dilates both Arteries and Veins! Thus blood of arteries moves faster! but Veins go against gravity so blood moves up more slowly. = less EDV and ESV

HTN:• ↑ risk of Atheroscler., LVH, lacunar strokes, CHF, renal fail. and Aortic Dissec.Atheroscler then ↑ risk of Aneurysm!.

CO= (BP X r4)/ viscosity Diabetes, Polycyth,Obesity= ↑ Viscosity >↓ flow ! Arterioles will ↓ resistance (↑radius) to keep BP and CO. they will dilate till short of stasis b4 contracting. HTN follows eventually