1. objectives
    ventil/diff circulation, CO, neuronal control and cardiovascular addaptation impacts effective perfusion

    describe impairment and treatment revelant to altered perfusion
  2. perfusion
    forcing blood to other fluid to flow through a vessel and into the vascular bed of tissue to provide oxygen
  3. for effective perfusion
    adequate ventilation and diffusion- heart, brain, lungs

    • adequate circulation
    •      adequate blood volume and components

         pulmonary, systemic, and coronary circulation 

    adequate CO (cardiage cycle and conduction of impulses - AV nodes, SA nodes)

    • intact neuronal control and CV adaptation
    •    parasympathetic and sympathetic nervous sys

      blood pressure control
  4. circulation
    SVC, IVC, PV--> rt atrium--> tricuspid AV valve--->rt ventricle---> pulmonic SemiLunar valve---> pulm art------LUNGS---->pulm veins--->left atrium--->mitral AV valve---> left ventricle---> aortic SemiLunar valve---> aorta
  5. pulmonary circulation
    circ thru lungs

    • transfer o2 from atmosphere into to the body
    • o2 and co2 exchange
    • rights side of the heart
    • pulm arteries (carry deoxygenated blood), capillaries, veins (carry o2 to blood to left side of the heart)

    function at lower pressure than syst circulation: blood moves slowly to get more o2
  6. cardiac circulation
    blood flow to hear muscles supports hearts work in pumpin o2 blood to body

    • - part of syst circ
    •  heart pushes o2 blood to rest of body
    • heart- vital organ- perfusion is essential

    cardiac muscles req- constant supply of o2 and nutrients have little storage capacity
  7. systemic circulation
    o2 and nutrients are distributed to tissues

    • req- patency of blood vessels
    • not blocked or obstructed

    arteries transport o2 blood, capillaries incr SA

    chemical mediators<open, wide, capillary channels>

    • function @ high pressure bc blood must owrk against resistant to get to peripheral tissue
    • motored by left side of the heart- left ventricle (strongest pumping chamber)
  8. heart layers
    pericardium- outer covering, holds in place, minimizes friction w/ heartbeat

    myocardium- thick musc layer

    endocardium- inner lining of heart
  9. mvmt of blood- cardiac cycle
    • 1 contraction (systole) - forcefully remove blood out of ventricles
    • and
    • 1 relax phase (diastole)- allows bloods to fill ventricles

    systole begins w/ AV valves (mitral/ticuspid) closing FIRST HEART SOUND

    after AV valve closure, ventricles contract and pressure in ventricles becomes greater than in aorta and pulm artery

    • semilunar valves- open to eject blood from ventricles
    • once blood is ejected @ end of systole, ventricles relax (press now greater in aorta & pulm artery)
    • -closure of valves- SECOND HEART SOUND

    diastole- pressure also directs valves, ventricles empty and pressure in atria AV valves open and blood moves to ventricles 
  10. conduction of impulses
    electrical current of heart itself

    • depolarizaton- change in polarity- ions shift
    • - sudden change in voltage
    • fast sodium channels open as cell voltage peaks-> fast sodium
    • channel closes and cell moves into repolarization
  11. cardiac conduction system
    SA node- pace maker- generates rhythimia impulses in atria


    AV nodes - connects the conduction of imulses btwn atria and ventricles
  12. EKG/ECG
    • PQRST
    • p: first hump
    • q: first dip
    • r: highest pt
    • s: next dip
    • t: 2nd hump

    • p: atrial depolarization- contract
    • qrs- ventrical depolarization
    • t: ventricular repolarization
  13. relationships of determinants of CO
    • CO- cardiac output- amt of blood heart pushes out
    • HR x SV
    • stroke volume- how much blood iss getting pushed out
  14. preload
    pressure built up in the ventricle; the amt of volume generated in the ventricle

    - determined by the amt of blood return in centricle and blood left in ventricle after systole- preload volume
  15. afterload
    the resistant and impedance of blood in left ventricle

    • ex of high after load would be stenosis of the aortic valve
    • stenosis means its like a hardening of the valve...harder to push blood thorugh...harder to push means resistance..high afterload

    leads to HTN
  16. BP
    needed to perfuse vital organs

    • maintained by (4)
    • contraction of left ventricle
    • perioheral vascular resistance
    • elasticity of arterial walls
    • viscosity and volume of blood
  17. pushing pressure
    bp regulation req adjustment in cardiac output
  18. resist press
    bp regulation req adjustment in peripheripheral vascular resist
  19. sympathetic neruvous branch
    incr HR and cardiac contractility and can selectively produce artery and arteriole vasoconstriction to incr periph vasc resistant
  20. changes in BP
    • bc of 
    • Baroreceptors  (aler brain stem)and chemoreceptors in arteries
    • renin- angiotensin syst
    • kidneys

    brain stem acts on sympathic nerous syst to incr CO and cause vasoconstrict
  21. chemo receptors
    in aota and carotid arteries

    detect change in o2

    provide feedback to alter ventilation and promote vasoconstric as needed to maximize o2 organs
  22. BP depends on 
    • -force of contraction of heart- r/t how much heart muscles gets streteched by the incoming blood
    • - the degree to which the arteries and arterioles constric--incr the resistance to blood flow, req higher BP
    • - circulation blood volume-- higher circulation blood vol, the more the heart muscle gets stretched by incoming blood
  23. How Kidnes influence BP: arteries/veins constrict 1/2
    causing the arteries and veins to constrict:

    • when the BP drops, the amt of filtered sodium also drops
    • kidney release an enzyme called renin

    • renin converts andiotensinogen (a peptide, AA) into angiotensin I
    • antiogtensin I is then converted to antiogensin II by an angiotensin-converting enzyme (ACE), which is found mainly in the lungs.

    angiotensin II causes blood vessels to contract- the incr blood vessel constriting elevate the BP.
  24. How the Kidneys influence BP: incr the circulating blood volume 2/2
    antgiotensin II also stimulates the adrenal gland to secrete a hormone called aldosterone

    aldosterone stimulates more sodium reabsorption/ water follows

    the incr Na and H2O reabsorption reduces urine output and causes it to generate more pressure w/ each beat, thereby incr BP
  25. renin-angiotensin aldosterone
    • renin- an enzyme released by the kidney, turns a plasma protein
    • angiotensinogen (from liver) to antiotensin 1, which is then turned to antiogentsin II by another emzyne called angiotensin converting enzyme (ACE)

    • angII- is a remarkably powerly vasoconstrictor w/ epinephrine bieng the other. 
    • angII's stimulate the adrenal cortex to release the hormone aldosterone which elevates the renal retension of sodium and water.

    concl: RAA, plays a critical regulartory role in sustenance of BP

    characterized by being a slowly acting renal-hormone mech for BP regulation

    * BP and SNS part-take in RAA by eliciting renin release
  26. low blood volume vs high blood volume
    low blood pressure vs high blood pressure
  27. Altered perfusion
    the inability to adequately oxygenate tissues at the capillary level 
  28. factors that could alter perfusion
    V-Q mismatch- 1) respiratory disease 2) pulmonary ebolus

    impaired circulation 1) hemorrhage 2) obsttruction - Virchows Triad 3) inadequate blood comp/volume

    inadequate CO- 1) inadequate blod comp or vol  MI 2)impaired ventricular pumping 3) structural defects 4) excessives periph vasc reistant 5) conduction defects (Arrythmias)

    excessive perfusion demands- 1)prolonged exertion 2) metabolic alterations 3) anemia
  29. Alterred perf: general manif 
    • cyanosis, pain, hypotension or hypertension
    • heart murmur
  30. Altered Perf: Diagn
    echocardiography/ Dopple ultrasonography

    • ECG
    • chest x ray
  31. HTN
    progressive CV syndrome detected by an elecation in BP and/or presence of organ damage due to persistnt BP elevations
  32. HTN- Primary HTN
    can be essential or idopathic HTN

    • genetic and environmental factors
    • affects 95%, can be form insulin resistant (vasoconstrict), renal funct (angiotensin chain), or inflamm

    inflamm and angiotensin chaing leads to salt retension and water retention which causes high Blood volume--> high BP
  33. lets say BP falls
    baroreceptors alter kidneys--> renin activated--> and angiotensinogen makes angiotensin 1---> w/ ACE, make Angiotensin II

    Angtiotensin II--> increase BP

    Angiotensin II-->tells adrenal gland to produce aldosterone---> aldosterone goes to kidneys and tells to retain sodium/water---> leads to incr BP

    *baroreceptor also responsible for co2 and o2 management 
  34. 2 meds for BP
    ACE inhinitors- sotp conversion of Ang 1 to Ang 2

    • ARD receptor blocker for angiotensin
    •  beta blocker 1- heart
    • beta blocker 2- lungs
  35. HTN- Secondary HTN
    • caused by systemic disease process that raises periphera vascular resistance or CO
    • common causes: renovascular disease, DM, dysfunction of thyroid, cushings syndrome
  36. HTN- Isolated systolic HTN
    elevations of systlic pressure are caused by incr in CO, total peripheral vascular resistance or both

    causes decr coronary blood flow and eventually left ventricular ypertrophy (low preload), coronary ischemia, and heart failure

    • >140/<90 for BP
    • common in elderly bc of aortic stiffening bc of vascular calcifiaction

    also due to elastic fibers
  37. HTN- complicated HTN
    • chronic HTN damage to walls of systemic blood vessels
    • smooth muscl cells undergo hypertrophy and hyperplasia w/ fibrosis of the tunica intima and media- layers of arteries

    • sustained HTN leads to one of these:
    •  left ventr hypertrophy, CAD, angina pectoris, congestive heart failure (left heart failure), MI. 

    • incr in heart size means more demand for o2 delivery over time
    • contractilit of heart is impaired and the person is at risk for heart failure---> could lead to aneurysm of coronary arteries---affects renal syst bc it pushes the blood TOO fast
  38. HTN- Malignant HTN
    • rapidly prgressive HTN
    • diastolic press +140
    • causes profound cerebral edema, and encephalopathy

    • see los of consciousness
    • high presure makes fluid go thru the capillaries and into the interstitial space---causing edema
  39. HTN clin man
    CV changes- hypertrophy, pulm edema, heart fail

    renal insuff: hematuria, proteinuria
  40. HTN diagn
    several BP meas

    • pre: 120-139/80-89
    • HTN1:140-159/90-99
    • consider ACE inhbitor
    • HTN2+160/+100
  41. HTN - treatment
    • lifestyle
    • drugs
  42. Orthostatic hypotension
    decr in syst and diast BP upon standing

    lack of normal BP compensation in response to gravitational changes on circulation

    acute: cause by alteration in body chemicals, drugs, prolonged immob, venous pooling

    chronic: disease,idopathic (unknown cause), secondary to endocrine disorder (adrenal insuff, DM)
  43. Orthostatic hypotenston: clin man/ diag/ treatment
    neuro sympt bc less o2 to brain

    diag: BP change, over several times

    treat: fludrocortisone
  44. MI
    happens in Acute coronary syndrome

    • when coronary blood flow is interrupted for a long time
    • necrosis occurs--leads to MI
    • plaque (athersclerosis) occludes vessel for longer time...leads to necrosis

    • if ST elevation: need immediate care!!!
    • if its a t wave inversion- then will have a sudendocardial infarction (a myocardial infarction that involves the innermost layer and, in some cases, parts of the middle layer of the myocardium but does not extend to the epicardium)
  45. MI- what happens?
    • things form where the coronary artery has an injury like the foam cells, fatty streaks, and oxidized cholesterol
    • leads to narrowing of artery which leads to decr perfusion

    scar tissue formf rom MI will lead to reduced efficiency of heart
  46. MI- hypoperfusion
    • leads to epinephrine relese which incr HR
    • damage cells release things into the blood stream

    the conduction syst goes out of whack and you dont pump right
  47. MI- pumping
    • impaired pumping ability leads to backing up into the lungs
    • - crackles cant be hear here
  48. MI- lab tests
    • CBC w/ differential, 
    • INR/APTT, electrolytes,
  49. MI- risk factors
    clin manif
    HTN, smokng, hyper cholesterolemia, hyper lipidemia

    exertional dyspnea, fatigue, syncope, nausea, and confusion
  50. MI- facts
    Women- late bloomers

    women more likely to delay treatment than men 

    #1 cause of death in women over 35

    kills 6 as many women as Breast CA
  51. MI- Diag crit
    angiography- imaging technique used to visualize the inside, or lumen, of blood vessels and organs of the body, with particular interest in the arteries, veins and the heart chambers. This is traditionally done by injecting a radio-opaque contrast agent into the blood vessel and imaging using X-ray based techniques such as fluoroscopy.
  52. Serum cardiac markers (3)
    Cardiac markers are biomarkers measured to evaluate heart function.

    • Troponin Test
    • CK-MB
    • Myoglobin
  53. Toponin Test
    The most sensitive and specific test for myocardialdamage. Because it has increased specificity compared with CK-MB, troponin is a superior marker for myocardial injury.

    • onset 4-5 hrs
    • peak 18-24 hrs 
    • duration- 10 days
  54. CK-MB
    • It is relatively specific when skeletal muscle damage is not present.
    •  Since it has a short duration, it cannot be used for late diagnosis of acute MI but can be used to suggest infarct extension if levels rise again. This is usually back to normal within 2–3 days.

    • onset- 4-12 hrs
    • peak- 18-24
    • duration 2-3 days
  55. Myoglobin
    • low specificty
    • Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly,rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis

    • onset 1-2 hrs
    • peak 8-10 hrs
    • duration- 24 hrs
  56. MI- treatment
    • Emergency
    • medical: MONA: morphine, o2, nitroglycerine, asprin
  57. Heart Failure
    impaired punping ability of heart

    gneral term used to decribe servial typs of cardian dysfucntion that results inadequate perfusion of tissues w/ blood borne nutrients
  58. heart failure results in  and caused by
    decr o2 delivery to tissues

    caused by CAD, MI, HTN, valvular disease
  59. Heart Failure- preload
    incr w/ decr contractility or excess of plasma volume

    incr preload eventually leads to outstretching o myocardium and leads to dysfunction and decr contractility
  60. Heart Failure- afterload
    incr afterload is most common in incr of PVR- HTN

    the heart responds to this by oding  hypertrophy of the left ventricle
  61. Heart Failure: renin angiotensin aldosterone systm
    activation of  RAAS due to MI- creates incr in angio 2 and aldost---> angio 1 does vasoconstri and aldos incr fluid volume--> incr after load, BP, Hr

    ventricular remodeling- hypertrophy of the ventricle that impair contractility
  62. Heart Fail- myocardium, L ventricle
    when myocardium cant pump effectively enough to meet the bodies metabolic needs

    pump failure usually occurs in left ventricle
  63. Heart Fail also due to
    • mitral stenosis
    • rheumatic heart disease
    • constricive pericarditis

    excessive fluid will also lead to volume overload or pressure overload

    can result from mitral or aortic insuff
  64. Heart Fail- incr work load/ end diastolic volume
    make left ventricle larger...(lack of o2 to the ventricle + more muscle iss not good)

    pain and tinglling in extremities
  65. Heart fail: decr inleft ventr
    make blood ppol in left ventricl and it back up into pulm veins and cap's

    getdyspnea on exertion

    • as circul becomes more engorged you get sodium and water being pushed into interstital space in the lungs causing pulm edema
    • this incr PaCO2

    fluid builds up in extremities- will rush to heart...left ventricle is already sucking so if yo add more work to it then it will get gg'd--> mor epum edema

    right vent starts failing bc of incr pressure it has to push againts form the pulm edema in heart

    • right vent starts to get bigger and push more blood
    • buffing up fails...and blood still pools in Rt vent and rt atrium ----> causing pressure in vena cava and systemic circ----> this is when you see JUGULAR DISTENTION  and elevvated central venous pressure

    • liver and spleen enourged bc of blood back flow into body,  causes anorexia, nausea
    • also causes wt gain, edema, nocturia
  66. Heart Fail: diag crit
    clinical manifestations, chest x ray, CBC
  67. Congestive Heart Failure- (left heart fail)
    syst heart fail- inabilty of hear tog enerate adequteCO for tissues, backs up in lungs

    • diast heart fail- pulm congestion despite normal stroke volume and CO due to decr compliance of left ventr
    • creates pulm edema

    left venr cant relax and fills improperly during diastole and stroke volume falls
  68. Right sided heart fail
    most commonly caused by a diffuse hypoxic pulm disease
  69. Warning Signs
    • D- dyspnea
    • A- anxiety
    • N- nocturnal paroxysmal dyspnea
    • G- gain in wt
    • E- edema
    • R- respiratory distress
  70. Shock
    condition of circ failure and impiared perfsion of vital organs

    • sources of impaired perfusion:
    • ineffective cardiac pumping: cardiogenic shock

    decr blood volume: hypovolemic shock (lost a lot of blood)

    massive syst vasodilation 1) septic shock- incr HR - infections 2)neurogenic shock- stim imp, from brain/spinal cord HR norm 3) anaphylactic shck- type 1 hypersensitivy
  71. Shock clinical manif

    cool, clammy extremities

    decr arterial blood pressure- late disn
  72. shock- diag crit
    no test is specific or sens for shock
Card Set
pathophysiology- ch 14