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Cardio Vascular Disease 1st Half

The document discusses Peripheral Vascular Disease (PVD) and its pathophysiology, highlighting the differences between Peripheral Venous Disease (PVD) and Peripheral Artery Disease (PAD). It outlines risk factors such as obesity, smoking, diabetes, and hypertension, which lead to atherosclerosis and complications like ischemia and necrosis. Additionally, it covers pharmacological treatments and nursing care strategies for managing heart failure and angina.

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Raheem Mohsin
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27 views16 pages

Cardio Vascular Disease 1st Half

The document discusses Peripheral Vascular Disease (PVD) and its pathophysiology, highlighting the differences between Peripheral Venous Disease (PVD) and Peripheral Artery Disease (PAD). It outlines risk factors such as obesity, smoking, diabetes, and hypertension, which lead to atherosclerosis and complications like ischemia and necrosis. Additionally, it covers pharmacological treatments and nursing care strategies for managing heart failure and angina.

Uploaded by

Raheem Mohsin
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF or read online on Scribd
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Cardiovascular Disorders PVD: Peripheral Vascular Disease Ill Satta Pathophysiology Course BE + Doppler ultrasound + ABI- ankle brachial index (for PAD) Clan Pvp & PAD C-Constriction AVOID PVD ExConstreive dothing PAD esac an VEINS = ELEVATE csonivinned oxtybyor, ARTERIES = HANG ineapere (Away) PHARMACOLOGY AC anm-ctoccine oF arteries [A\ANT PLATELET (ani Clumping) AOASA C-Clopidogrel , ; 10%: Bleedin = PVD with varicose veins, wear compression cinieenieedng socks & limit standing to aid with blood C chotesTeRoL LoweRING return to the heart. Lovastatin “stay clean” CAUTION: Liver Toxic, NO grapefruit PVD: Peripheral Vascular Disease I JEEEN CEH Pathophysiology Course. rr iro Think of anything that scars the lining of the blood vessels. Modifiable * Obesity (BMI over 25)- puts pressure on the blood vessels. + Sedentary “sitting” lifestyle - makes the vessels stiff. + smoking chemicals scar the lining of the vessels. jabetes DM (uncontrolled) think the blood is turned to mud (like syrup) from HIGH sugar && this scrapes & scars the blood vessels. @ + High cholesterol - fatty deposits stick to the vessel walls making, b. them narrow & hard (plaque). . + Hypertension HTN (High blood pressure) - Uncontrolled over a long Period of time will damage & stretch out the vessels. + High stress - leads to high blood pressure, ig St cnt ty or C7 ge Greens Atherosclerosis Atherosclerosis AtheroscARosis Atherosclerosis - After the scarring & stretching occurs (from the risk factors) small fatty deposits, calcium, & even macrophages settle 1 AerosARis into these tiny tears in the blood vessels (called plaque) Hlerrine sropaeie te aed making the arteries hard & narrow. This plaque can also burst, leading to a blood clot which can kill the client! PATHOTIP. com Atheromas (plaque) in large arteries [Abdominal Aorta Uipids, calcium & possible clots) ie Arteries Atheromas (plaque) = Main Sites: Femoral Arteries + Abdominal aorta fr cs + Carotids arteries (neck arteries) cen + Femoral arteries on seas Hr hebeteie PVD: Peripheral Vascular Disease Es) Pathophysiology Course Pathophysiology Peripheral Vascular Diseate la condition where there is scarring Enarroungot the perpheralblood vessets wens areres)ine. = PVD. PAD those in hw legs Eventualy the blood vessels becore smal Of paengtumaunmy making very dificuk fr blood to get and from the extremes, PRIPRERALISCULAR SESE 2 different conditions for Peripheral Vascular Disease VEIN ARTERY + Pvp: Peripheral Venous Disease - narrowed Veins * PAD: Peripheral Artery Disease - narrowed Arteries VEINS ARTERY BADE) VACUUM = AWAY — pvp ® 8 vase | | mo & cs vein A Ve ARTERY Veins pull or Arteries push oxygen rich blood Vacuum deoxygenated blood back to the heart ‘Avay from the heart PAD = problem pushing oxygen rich blood Away from PVD = problem Vacuuming deoxygenated blood backto the heart. the heart! Blood begins to pool in the legs manifesting Oxygen can't get to legs! WORSE PROBLEM leading to: oss Varienan Vel ~ Ischemia (low oxygen) & + Necrosis (tissue death) _ Signs & Symptoms _ fa ‘Absent Halr (Shiny) = Cool legs VVOLUMPTUOUS PULSES - Warr lens R ROUND, RED SORES (blood pooling) EEDEMA (blood pooling) ‘TTOES & FEET PALE or BLACK "Eschar” [IRREGULAR SHAPE SORES (Exotic pools) 'S SHARP CALF PAIN NNO SHARP PAIN (Dull pain) (intermittent Claudication) ‘Y YELLOW & BROWN ANKLES E- Exerdise- E-levation (recliner chai) PAD Intermittent severe caif pain when muscles are depleted of oxygen. cation common with: ClAudication common with: + E- Elevating legs (recliner chair) Intermittent CAf Pain Heart Failure II ACNE ae Pharmacology & Care AACE & ARBS ino slnopl «Losartan A -ACTS on BP only (not HR) A -ACE (rip Lisinopril chill pri 1st choice ‘enol ‘A -ARBS ( sartan) Losartan ‘relax men" 2nd choice ‘A-Avwid Pregnancy ‘A-AAngioedema (Airway Risk) *only Ace dine, Carey, Vrapai €-Cough tonly Ace DIGOXIN tomrts E-Elevated K+ (normal 35-5.0) B - BETA BLOCKERS (4) AtenoLOL “LOL = LOW" Corde Genie or Blocks both BP & HR (AVOID Low HR & BP) Caution: HOLD IF: Sea B-Bradycardia LESS than 60) & BP Low (90/60) only hold ifthe patient isin an acute exacerbation of CHF B-Breathing problems “wheezing” (Asthma, COPD) ota Wasting & Sparing Bad for Heart Failure patients Mikione otopic dup AST LINE therapy-alative care B-Blood sugar masking “hides S/S" (Diabetics) C -CALCIUM CHANNEL BLOCKERS Calms BP & HR (AVOID Low HR & BP) QE xeie ae (Nifedipine) -dipine “declined BP & HR PU a TPE Ey -amlodipine “chill heart” D - piurerics Drain Fluid [BD DIET tow setme ri c+ ott) D-Drains Fuld “Dhirese “Dried” Gq Risk For FALLS! stow K+ Wasting-Furosemide & Hydrochlorothiazide bla (caution: Low kt, Eat melons, banana & green leafy veg) EE] BP & BNP ssteasnorbeinceane) K+ Sparing-Spironolactone “Spares potassium" {AVOID Salt Substtues, melons & green leafy veg) FY ELEVATE LEGS onpenermen gexec LB) DAILY WEIGHTS (20s 05217 aays= Nitropycerin, Isosorbide BisXcusancen. Nitroghycerin "Nitro = Pitow forheart” Caution: NO Viagra afi" Sidenafil = DEATH! EEISTOCKINGS 120 oe cess bod pots systolic BP below 90 or 30 mmHg Drop Temove ca Adverse effect: HA= side effect Low BP= adverse effect (SLOW position changes) D - DIGOXIN (inotropic) TNO OTC meds (Cough or Flu, Antacids Digs fora DEEP contraction ‘or NSAIDS) INEUEXT Increased contractility No Canned or packaged foods (chips, sauces, meats, Apical Pulse x1 minute cheeses wine) Toxic (over 2.0) Vision changes, NA’ TESTTIP Potassium 3.5 or less (higher r/t toxicity) NEVER massage calves (CHF patients) [NELERTIP) Heart Failure Pathophysiology Course. aos The heart falls to maintain adequate cardiac output (oxygenated blood pumped OUT to the body) due to Impaired pumping abilty. + HE - Heart Failure (fallure to pump blood forward) + HE - Heavy Fluid (backs up in lungs / body) Weight Gain = Water Gain R-RIGHT-sided HF L-LEFT sided HE R- ROCKS BODY with fluid LUNG fluid + Pulmonary Edema + Craekles in lungs + Peripheral Edema + Weight Gain = Water Gain + IND (big neck veins) “Rales that don't dear with + Abdominal Growth ‘a cough” ‘Asdtes luld in abdomen) | * Pink Frothy “blood tinged” - Hepatomegay (big tver) sputum + Splenomegaly (bigspleen) | + Orthopnea - ear choke Ace Lsonap¢l pe ants nat nStDN as soxoruss ( vo.sEro. i ae cee 50 gets risky" (not INR, not PTT) =a Araihypertensive (BP ONLY) "HOLD: Low GF (not HR). a commas Pet apie = Tet eae chatter onengstatr eer iia tetany Sarr FE cose © eee wma 9 13 Ao popu see ee er eae tp yc stor “eet ‘Muscle pain (Rhabdomyolysis risk) "Beiisemuct catpe spar, tae atone iim ace Congenital Heart Defects VI SimpleNursing Pathophysiology Course. Cirrus ‘They include medications to lower biood pressure and control heart rate, heart devices, cardiac catheter procedures. Surgery is the ultimate solution in most cases & serious cases may require a heart transplant. erirmenrcne inn fe + Aleryotedne 1 Thou “haus hire) Shorr MPO state ft) + Reon th newex ~ i ag | > Pry Assen "sued cath ‘Norma Weak pulse NCHEXTIP: ‘NOT nat Coote paleexrenty 2, Sealpnteg for 4-8 hours Sinesion site ‘Asis torbleeding ‘infection baths Garr Chest tubes are placed during cardiac surgery to help drain excess fluid & air for lung expansion. After surgery it remains in place to drain excess blood. EEETTET report to HCP INCLEXTIP! . ‘© Lhour: Over 5~ 10 mL/ka, ‘© 3hours: Over 3 mL/kg/hr Indicates: severe bleeding, & cardiac tamponade 1 For example ‘Child weighs 6 kg hour: 30- 60 mL/kg, Ld © Shours: 6 kgx3 mL = 18mL/hr ame (54 mLin 3 hours) ions ere ac ‘Atter surgery the nurse should always elevate the head of bed to reduce respiratory effort Surgical sites - infection! Report fever, warm surgical site, smelly purulent drainage & no heavy lifting or strenuous activity for the first 3 to 4 weeks, gu Bl Congenital Heart Defects V See hag Pathophysiology Course. Stenosis (stiff valve) When blood flow attempts to leave the heart it meets resistance from this narrowed valve. This blocked blood flow now backs up Ea inthe heart resulting in Decreased cardiac OUTput meaning Less oxygen-rich blood OUT to the body + S-Stenosis + S- Suit & narrow Ey stevoss st rarow Decreased caine OUTput Uz one blod OUT o the Body Ginna + Pulmonary valve: stiff, smal, narrow valve, “Simotoms: * Right ventricular ypertrophy * Loud 'sjstolcefection” > > heart murmur “eatiments * Balloon angioplasty # Surgical repair Vaotomy) ec Portic valve: narrowing "Symptoms ‘Decreased cardiac output Decreased 02 blood OUT to the body ‘Activity intolerance Vitals: Low BP, Tachycardia “Left ventricular hypertrophy ‘Pulmonary congestion Cees Narrowed aorta: decreased cardiac OUTput {Decreased 02 blood OUT to the body) /Symptoms- ‘* Upper extremities: High BP, Bounding pulses * Lower extremities: Cool, low BP & diminished pulses Symptoms ‘* Balloon angioplasty Balloon Stents * Stents angioplasty Congenital Heart Defects IV SR Pathophysiology Course OTe NCLEX TRICK YOU Closes naturaly 1 Surtees vsD == Qe Patent Ductus Arteriosus * Opening that corners sorta to psnoery wary “Symptom * Lo machin: She murmur NELBRTIR amor TEK Lod machune tke DUCK. “Treatment indamethach (NSAID) Sa + oth ASD & VSD 1 hoes Atria & Ventre Congenital Heart Defects Sameer Pathophysiology Course. An Thisis an abnormality in the heart that develops before birth, where one or a Genetics more problems with the heart's structure changes the way blood flows through "e Family hi the heart & out to the body. Family history ‘* Down Syndrome = During pregnancy &: ‘dD * Infection (Rubella) Me # Alcohol/Drug abuse A a * Diabetes Congenital Heart Defects types is Torievalestenosis Courdationofthesorta Ebsteiisanomaly Patent ductus arteriorus Ve Septal detects Tingleventride detects Tevalogy of Fallot “etal ancmalous venous “Tanspasition ofthe great "anc arteriosus pulmonary connection arteries V-Veins = Decreased cardiac V- Vacuum blood back to heart OUTput meaning s Less oxygen rich blood ‘Asyou know in a NORMAL heart, deoxygenated blood Is vacuumed back to the OUT to the body heart va the Veins through the vena cava into the right side of the heart. ‘Then pushed into the lungs to get oxygenated. After that - this oxygenated blood is pushed into the LEFT side of the heart to be pumped OUT to the body - wANINN this is cardiac OUTput, oxygen-rich blood OUT to the body. AY But with these heart problems less blood is pumped OUT of the heart resulting in dcreased cardiac OUTput meaning Less oxygen-rich blood OUT to the body, resulting & “j in the big complications like abnormal heart rhythms, murmurs, heart failure & hypoxia low oxygen in the blood Congenital Heart Defects II Sannasy Pathophysiology Course Gres Lay er er asec enter Ponies feta | om ena ae cony chateitetet nt coo Signs & symptoms ae a + Cyanosis (ue ski) HE Heor Fi , 1 Poor feeding & weight gain

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