perfusion

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

describe impairment and treatment revelant to altered perfusion

forcing blood to other fluid to flow through a vessel and into the vascular bed of tissue to provide oxygen

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

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

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

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

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)

pericardium- outer covering, holds in place, minimizes friction w/ heartbeat

myocardium- thick musc layer

endocardium- inner lining of heart

• 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 

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

SA node- pace maker- generates rhythimia impulses in atria

then 

AV nodes - connects the conduction of imulses btwn atria and ventricles

• 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

• CO- cardiac output- amt of blood heart pushes out
• HR x SV
• stroke volume- how much blood iss getting pushed out

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

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

needed to perfuse vital organs

• maintained by (4)
• contraction of left ventricle
• perioheral vascular resistance
• elasticity of arterial walls
• viscosity and volume of blood

bp regulation req adjustment in cardiac output

bp regulation req adjustment in peripheripheral vascular resist

incr HR and cardiac contractility and can selectively produce artery and arteriole vasoconstriction to incr periph vasc resistant

• 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

in aota and carotid arteries

detect change in o2

provide feedback to alter ventilation and promote vasoconstric as needed to maximize o2 organs

• -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

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.

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

• 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

low blood pressure vs high blood pressure

the inability to adequately oxygenate tissues at the capillary level 

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

• cyanosis, pain, hypotension or hypertension
• heart murmur

echocardiography/ Dopple ultrasonography

• ECG
• chest x ray

progressive CV syndrome detected by an elecation in BP and/or presence of organ damage due to persistnt BP elevations

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

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 

ACE inhinitors- sotp conversion of Ang 1 to Ang 2

• ARD receptor blocker for angiotensin
•  beta blocker 1- heart
• beta blocker 2- lungs

• caused by systemic disease process that raises periphera vascular resistance or CO
• common causes: renovascular disease, DM, dysfunction of thyroid, cushings syndrome

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

• 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

• 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

CV changes- hypertrophy, pulm edema, heart fail

renal insuff: hematuria, proteinuria

several BP meas

• pre: 120-139/80-89
• HTN1:140-159/90-99
• consider ACE inhbitor
• HTN2+160/+100

• lifestyle
• drugs

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)

neuro sympt bc less o2 to brain

diag: BP change, over several times

treat: fludrocortisone

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)

• 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

• 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

• impaired pumping ability leads to backing up into the lungs
• - crackles cant be hear here

• CBC w/ differential, 
• INR/APTT, electrolytes,

HTN, smokng, hyper cholesterolemia, hyper lipidemia


exertional dyspnea, fatigue, syncope, nausea, and confusion

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

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.

Cardiac markers are biomarkers measured to evaluate heart function.

• Troponin Test
• CK-MB
• Myoglobin

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

• 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

• 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

• Emergency
• medical: MONA: morphine, o2, nitroglycerine, asprin

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

decr o2 delivery to tissues

caused by CAD, MI, HTN, valvular disease

incr w/ decr contractility or excess of plasma volume

incr preload eventually leads to outstretching o myocardium and leads to dysfunction and decr contractility

incr afterload is most common in incr of PVR- HTN

the heart responds to this by oding  hypertrophy of the left ventricle

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

when myocardium cant pump effectively enough to meet the bodies metabolic needs

pump failure usually occurs in left ventricle

• 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

make left ventricle larger...(lack of o2 to the ventricle + more muscle iss not good)

pain and tinglling in extremities

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

clinical manifestations, chest x ray, CBC

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

most commonly caused by a diffuse hypoxic pulm disease

• D- dyspnea
• A- anxiety
• N- nocturnal paroxysmal dyspnea
• G- gain in wt
• E- edema
• R- respiratory distress

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

tachy..everything

cool, clammy extremities

decr arterial blood pressure- late disn

no test is specific or sens for shock