Mapa mental
Perfusion

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Perfusion
Definition
- Normal physiologic process, heart pumps enough CO, to deliver nutrients and oxygen to tissues via capillaries and arteries.
- Ischemia
- Insufficient tissue O2
- Infarction
- Tissue death
- Hypoxia
- Lack of O2
- Physiologic dead space
- No perfusion but oxygenation is there, lung is working fine
- cardiac problem or emboli
- No perfusion but oxygenation is there, lung is working fine
- Pulmonary shunt
- Proper perfusion, lack O2, lung problem, blood will shunt (redirect to area where there is more O2
- Arterial line
- To monitor BP and draw arterial blood gases
- Central line
- Tube that goes to superior vena cava
- give major volume of fluid, blood ,meds
- Tube that goes to superior vena cava
- Ischemia
- Normal physiologic process, heart pumps enough CO, to deliver nutrients and oxygen to tissues via capillaries and arteries.
Heart sounds
- Summation gallop" LUB-lub-dub-DUB (s3 and s4 present" Split S2: when pulmonic and aortic valves close at different times, audible during inspiration and expiration is abnormla, during inspiration and disappears w/ expiration is normal.
- S1
- "lub"
- Closure of AV valves. Normal. Best hear at tricuspid and apical area. S1-S2 is systole, shorter than diastole.
- "lub"
- S2
- "dub"
- Closure of semilunar valves at end of systole. S2-S1=diastole
- "dub"
- S3
- blood going into ventricles can cause vibrations, which causes s3 during diastole
- "DUB"
- Ventricular gallop, heard after S2. Normal in pregnant women, children, but not adults over 35-40yrs.
- Rapid ventricular filling. Right sided best heard over tricuspid,left over apical.
- Ventricular gallop, heard after S2. Normal in pregnant women, children, but not adults over 35-40yrs.
- S4
- "LUB"
- Atrial gallop, heard b4 S1, can be in healthy ppl, hear opening of valves.
- "LUB"
Perfusion
- Central perfusion
- Blood movement generated by CO
- Needs adequate cardiac fx, BP, BV
- CO=SV x HR
- SV: affected by contractility, preload, afterload
- Preload: fluids, diuretics afterload: antihypertensive, vasopressors decrease or increase CO
- MAP= (CO X SVR) + CVP
- mean arterial pressure: normal: (70-100mmHg) (below problem perfusing body) cardiac outpur systemic vascular resistance central venous pressure (passive, doesn't have a lot of impact)-dont usually include in equation
- Impaired central perfusion
- Low cardiac output, systemic effect d/t oxygenated blood not reaching tissues.
- Severe: shock. Untreated: ischemia, cell injury, cell death
- Cardiogenic
- MI,tissue death, heart not pumping enough
- Septic
- Third spacing fluid building in tissues
- Hypovolemic
- Change in tissue permeability
- Increase: RR,BP, HR to compensate,
- Decrease perfusion to periphery to go to central (preserve imp organs)
- Cardiogenic
- Severe: shock. Untreated: ischemia, cell injury, cell death
- Assessment
- head to toe (focus on body system taht seems to be affected most)
- Diseases: MI, HF, Stroke, Afib, HTN, ventricular septal defect,sx (hypovolemia)
- Effect
- On other organs-renal failure (urine output-30mL/hr), fluid reg...
- S&S: change in LOC, fainting, diziness, loss of sensation, decrease in T, pallor, diaphoresis, central cyanosis,pain
- chest pain
- Manifestations across the lifespan
- Infants
- growth and development, immature CV sys
- Poor feeding
- Poor weight gain
- FTT
- Dusky color
- Vs, health assessment, congenital abnormalities
- Toddlers and children
- Berlin heart- can be on it fro 2-3 years while waiting fro heart translpant, can do same for adult but for 24-48 hrs (ECMO)- Extracapurial memebrane oxygenation (replacec heart and lungs)
- Squatting to breath
- Easily fatigued
- Developmental delays (failure to hit milestones)
- Infants
- Low cardiac output, systemic effect d/t oxygenated blood not reaching tissues.
- EF
- percentage of blood pumped out by left ventricle (55-70%) normal
- SV: affected by contractility, preload, afterload
- CO=SV x HR
- Needs adequate cardiac fx, BP, BV
- Blood movement generated by CO
- Tissue or local perfusion
- Volume of blood that flows to tissues
- Requires: patent vessels, hydrostatic pressure, capillary permeability
- affected by wounds, burns, scars., pressure ulcers.
- Impairement
- D/t loss of vessel patency, permeability, central perfusion
- Localized effect, impaired perfusion to affected tissues.
- Ischemia, cell death if untreated
- Localized effect, impaired perfusion to affected tissues.
- S&S
- Decreased peripheral pulse, increased cap refill time, pain, necrosis, peripheral cyanosis, ischemia,emboli
- wound site, leg (DVT) popliteal, brachial, carotid, poste PE
- Decreased peripheral pulse, increased cap refill time, pain, necrosis, peripheral cyanosis, ischemia,emboli
- Assessment
- head to toe (focus on area that seems to be affected the most
- VS (what's going on?), LOC,GCS (esp stroke), CSMT, pulses, pain assessment, O2, edema, renal fx(hx)
- CIRCULATION, SENSATION, MOVEMENT, TEMPERATURE
- Diabetes (neuropathy), obesity, atherosclerosis, hyperlipedimia, peripheral vascular/artery disease, DVT
- D/t loss of vessel patency, permeability, central perfusion
- Requires: patent vessels, hydrostatic pressure, capillary permeability
- Volume of blood that flows to tissues
- Central perfusion
Populations at risk
- Middle aged and older adults,
- Infants and children (congenital),
- patent ductis arteriosis: hoel in heart taht does not close
- children and young adults (trauma),
- individual (risk factors)
- modifiable and non modifiable risk factors
- women over 55
- number one cause of death, more likely to die from heart disease than anything else
- Women and heat disease
- Altered perfusion
- Canada: women 16% more likely to die from heart attack than men
- stroke kills 32% more women than men
- Heart disease and stroke kills 7x as many women as breast cancer
- Women undiagnosed and untreated, different symptoms of MI,silent MI, indigenous pop, it's worse
- Risk factors
- Modifiable
- Smoking
- nicotine vasoconstricts, damage to BV
- Elevated serum lipids
- Atherosclerosis
- Sedentary lifestyle
- obesity
- Obesity
- atherosclerosis, increased risk of DMII
- DM
- Atherosclerosis
- HTN
- increase work of myocardium
- Smoking
- Non modifiable
- Age
- increses with age
- Gender
- men > women
- Genetics
- family hx
- Age
- Clinical management
- Primary prevention modifiable risk factors
- Smoking, nicotine use cessation
- Diet modification
- Reduce sodium, calorie
- Increase fiber, H2O
- Increase exercise
- Weight control
- Weight loss
- Screening
- 1.At what age should blood pressure screening begin? 2.How often should blood pressure screening occur? 3.Who should have lipid screening? How often?
- BP screening
- start at 18
- Every 1-2yrs
- Lipid screening
- 12 Lead ECG
- Asuscultation
- Adventitious heart sounds
- Valvular dysfx can lead to regurgitation
- back flow of blood in heart
- Which may lead to HTN, hypertrophy of a chamber, pulmonary HTN, cardiomyopathy, HF
- Valvular dysfx can lead to regurgitation
- Adventitious heart sounds
- Interventions
- Independant
- Based on nurse's assessment, clinical judgement
- Collaborative
- Dietition, nutritionist CABG:goals for discharge: be able to walk 2 flights of stairs w/o getting out of breath with unasistance Berlin ehart- children Ideal- whats least invasive MI- want to decrease CO Cardiac arrest: want to increase CO Risk factor MI: emotional stress, heavy meals, strenuous activity, smoking
- TX strategies depend on pt condition
- Diet and smoking sensation
- Increased activity
- Pharmacotherapy
- Impaired central perfusion
- Inotropes
- Positive
- Increase contractility
- Digoxin
- Cardiac glycoside, Antiarrythmics Slow electrical conduction at AV node- used tx arrithmias Antidote: Digibind N&V 1st sign of toxicity Narrow TI, long T1/2
- Block Na+/K+ ATPase pump, clock exit 3Na+, influx 2K+= high Na+ intracelular
- Activates Na+/Ca2+ exchanger= increase Ca2+, increase 3NAa+=contractility
- Calcium
- increase hr,co, contractility
- increase contractility, hr, co
- Epinephrine
- Dopamine
- Digoxin
- Increase contractility
- Negative
- Decrease contractions and HR
- Tx: arrythiax, HTN, angina, afib,
- CCB
- Decrease BP, vasodilate (increase blood flow), smooth muscle relaxation (coronary and vascular)
- Cardio selective: decrease HR, CO, COntractility- optimize contrctions,
- Cardio-selective: Verampil (isoptin), Diltiazem (Cardizem)
- Decrease BP, vasodilate (increase blood flow), smooth muscle relaxation (coronary and vascular)
- Decrease contractions and HR
- Positive
- Antihypertensives
- ACE inhibiors (prils)
- 1st line tx HF Potent, works fast, short T1/2 can cause severe hypotension
- Decrease BP (vasodilation), BV
- Enalapril (Vasotec), Captopril (Capoten), Monopril, Ramipril (Altace)
- BB
- Decrease HR (negative chronotropy), decrease conduction rate, contractility (negative inotrophy)
- Atenolol (b1), metoprolol (b1,b2), propanolol (b1,b2)
- Decrease HR (negative chronotropy), decrease conduction rate, contractility (negative inotrophy)
- CCB
- NItrates
- Nitroglycerine (NitroStat), Nipride (Nitroprusside),
- Vasodilator,MI, decrease SV, relax heart, decrease chest pain (angina)
- Nitroglycerine (NitroStat), Nipride (Nitroprusside),
- Diuretics
- Loop, thiazide (hypokalemia), Spironolactone (potassium sparing)
- ACE inhibiors (prils)
- Antiarrythmics
- Decrease Na influx to decrease action potential
- Amiodarone (Cordarone)
- Procainamide
- Antianginal agents
- Nitroglycerine
- Vasopressors
- cardiac arrest
- Increase SVR to increase BP, vasoconstriction, work on alpha adrenergic receptors
- Dopamine
- Epinephrine
- NE
- Vasodilators
- O2
- Nitroprusside (Nipride)
- H and T of cardiac arrest
- Hypovolemia
- Hypoxia
- Hypo/hyperglycemia
- Hypothermia
- Hydrogen (acidosis)
- Toxins/Tablets
- OD
- Tension pneumothorax
- compress vena cava, lungs
- Thrombosis (MI)
- Thromboemoblism (PE)
- Trauma
- Tamponade (cardiac)
- Inotropes
- Impaired local perfusion
- Anticoagulants
- Heparin
- LMWH
- Enoxaparin (Lovenox)
- Dalteparin (Fragmin)
- Apixaban
- Block thrombin receptor and factor Xa DVT
- Dabigatran (Pradaxa)
- Block thrombin receptor and factor Xa Prodrug
- Warfarin (Coumadin)
- Inhibit hepatic formation fo certain factors
- Thrombolytics
- Act on t-PA which converts plasminogen to plasmin in order to break up clot T1/2: 13-16 min IV within 6 hrs of onset of S&S
- Trauma, stroke, STEMI, Ischemic stroke, PE, DVT,
- Ateplase
- Reteplase
- Lipid lowering agents
- Statins, Vit B
- Vasodilators
- Antiplatelets
- Aspirin
- 81mg acute MI
- Aspirin
- Anticoagulants
- Impaired central perfusion
- SX
- Other
- Central perfusion
- Pacemaker insertion
- Electrical cardioversion
- Electrical current to reset heart rythm
- Ablation therapy
- Tumor
- Intra aortic ballon pump
- Deflated on systole, inflates on diastole
- heart gets more circulation, MI
- Deflated on systole, inflates on diastole
- Cardiac valve sx
- Ventricular assistive device
- Cardiac transplantation
- HF
- Local perfusion
- CABG
- bypass or graft sx
- PTCA
- widen arteries, balloon and stent cardiac catheterization, femoral artery
- Endarterectomy
- Remove plaque
- CABG
- Central perfusion
- Independant
- Primary prevention modifiable risk factors
- Modifiable
Common dx tests
- Lab test(blood)
- Myoglobin: heme protein helps transport O2, cardiac and skeletal muscles. Onset: 1-3hrs Peak:4-12hrs Return to normal:12 hrs Negative result help rule out acute MI, increase doesn't help to indicate if there has been an MI-not specific
- Electrolyte panel
- Na, Ca, K+,Cl-, Mg, PO4,Glucose
- Hemoglobin A1C
- Over last 2-3 months, dx diabetes (6.5% or greater)
- Hemoglobin A1C
- Na, Ca, K+,Cl-, Mg, PO4,Glucose
- Cardiac markers
- Peak, duration, check for MI
- CK-MB
- CK are isoenzymes, CK-MB is specific to the heart Onset:4-8hrs Peak:12-24hrs Return to normal: 3-4days Mass essay: (MB,MM,BB) onset: 2-3hrs Peak:10-18 hrs Return to normal: 3-4days Confirmation rather than diagnosis as peak is much later
- Damage to cardiac cells
- Troponin I
- regulates myocardial contractin
- Released c death, specific to heart
- released 3-4hrs after, lasts 7-10days Three isomers: C, I ,T I and T are specific to the heart Reliable and critical markers Onset:3-4hrs Peak:4-24 hrs Return to normal: 1-3wks
- LDH
- Lactic dehydrogenase
- Lactic acid build up
- check for tissue death, not specific to heart
- BNP
- Brain natriuretic peptide
- Sent by brain to stimulate ventricle to pump harder
- HF, in increased ventricular workload high, low normal
- Homocysteine
- amino acid get from eating meat
- Rise in heart disease
- atherosclerosis, high,low or normal
- CRP
- Biomarker of inflammation
- cancer, CAD, tumor, obesity, nonspecific high low or normal
- Biomarker of inflammation
- Serum lipids
- cholesterol, LDL, HDL, VLDL, Triglycerides
- CBC
- Hematocrit, platelets, hemoglobin, RBC
- Coagulation panel
- Coag Panel
- PT
- PTT
- INR
- Time it takes for blood to clot
- Affect perfusion, can lead to DVT, too slow- at risk for bleeding (hypovolemia)
- Radiographic studies
- Chest X-Ray (CXR)
- Arteriogram
- ECHO
- U/S of heart
- Evaluate ventricular fx, can be used to measure EF, dx MI
- U/S of heart
- TEE
- Transesophageal exhocardiogram
- Pt is sedated to visualise heart blood flow
- U/S probe is swallowed, u/s of heart is taken from oesophageous
- V-Q scan
- Looking for PE, pulmonary shunt, dead space- check pulmonary perfusion
- MITI
- Myocardial perfusion test
- Exercise + contrast dye + exercise to see changes in perfusion
- Chest X-Ray (CXR)
- Cardiac stress test
- Exercise or pharmacological
- ECG, walk, run, check normal sinus rythm normal ECG)
- 12 Lead ECG
- T wave inversion, ST elevation, normal or depressed, abnormal Q wave
- Acute MI, chest pain
- T wave inversion, ST elevation, normal or depressed, abnormal Q wave
- Lab test(blood)
Key takeaways
- ▪Perfusion affects everything! Reflect on how it affects previously discussed concepts: gas exchange, pain, tissue integrity. ▪Start learning your common medications that impact perfusion (eg. antihypertensives, etc.) – know their mechanism of action ▪Focus on prevention, health promotion, and patient teaching wherever possible ▪Think about how perfusion affects other conditions, eg. Myocardial infarction and the concepts that apply
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- Descripción
- NURS 224 Mapa Mental sobre Perfusion, creado por Mag Mag el 22/02/2020.
- Creado por
- Mag Mag
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