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Med-Surg II - wk 4
Nursing Management of Heart Failure
| Question | Answer |
|---|---|
| The "face" of HF | elderly, older you get the more likely you are to get HF. men and african-americans are more at risk. |
| Flow of blood through the heart | vena cave to RA, through tricuspid valve to RV, through pulmonic valve to the lungs, through pulmonary arteries to LA, through mitral valve to LV, through aortic valve, through aorta to the rest of the body. |
| Pre-Load | the volume of blood int he ventricles at the end of diastole. Means how much the heart is filling and stretching. |
| After-Load | force that the heart has to work against. Resistance. |
| After-Load: systemic vascular resistance | force the LV has to push against to push blood to the body |
| After-Load: pulmonary vascular resistance | force the RV has to push against to push blood to the lungs |
| Cardiac Output | HR x SV. normal is 3-6L/min. volume of blood per time. |
| CO: SV | pre-load, after-load, and contractility. |
| Frank-Starling Law | increased volume = more stretch; more stretch = more force of contraction. Rubber band: the more you stretch it, the further it will fly |
| Heart Failure is... | ventricular dysfunction. diminished quality of life (activity intolerance, fatigue, dyspnea). Impaired cardiac pumping or filling (or both). occurs when the heart is unable to meet the metabolic demands of the body |
| HF: most common causes/risk factors | diabetes; smoking; obesity; HTN (increases risk x3); CAD/MI; increased age. |
| Systolic HF | PUMP problem. contraction isn't working. Characterized by a decreased ejection fraction. |
| Systolic HF: main cause | MI. damage from MI causes ischemia, that part can't pump and starts to stretch due to increased end-diastolic pressure, further inhibiting it's ability to contract. Also caused by valvular disease and HTN. |
| Diastolic HF | problem of FILLING. cant get enough blood INTO the heart. muscle can be hypertrophied, less room for the blood in the Vs. Ejection fraction will be normal (~60%) (contraction is good, less blood is coming in, less volume pumped out, but the % is same). |
| Diastolic HF: main cause | chronic hypertension. increase after-load, vessels are clamped down and tight, causes the heart muscle to get very strong to get a bigger force of contraction, but this causes the muscle to hypertrophy. |
| Diastolic HF: other main cause | aortic stenosis. blood can't pass through the valve, gets stuck in the LV, causes it to try and pump harder, muscle hypertrophies. |
| R vs. L HF | determines the Sx the patient will have, determines the Tx. most of the time, pt's aren't one side or the other, they are a mixture of both |
| L Sided HF | blood backs up to the lungs/pulmonary system causing pulmonary edema, dyspnea, cough, crackles, etc. |
| L sided HF: causes | MI, HTN, cardiomyopathy (big floppy heart already having contraction problems). |
| L sided HF: Assessments | lung sounds (crackles); RR (expect to be high - tachypicnic). frothy sputum, productive cough. cyanosis (poor perfusion). increased cap refill. SpO2 may be low. |
| R Sided HF | blood backs up to the body, peripheral circulation |
| R sided HF: causes | L sided failure (blood just keeps backing up. L backs up to lungs, R pumps to lungs which are already full, R starts to fill as well). MI on RV. chronic pulmonary disease (i.e. COPD - high pressure system, hard for heart to pump against, blood backs up). |
| R sided HF: clinical manifestions | JVD. peripheral edema. hepatomegaly & spleenomegaly (sx: anorexia and nausea - GI syst congested w blood). weight gain. |
| HF: Compensation Mechanisms | body sense decreased CO (all HF has this). SNS activation. RAAS. Biomarker Response. Remodeling. Dilation. Hypertrophy. |
| Compensation Mechanisms: SNS activation | fight or flight. increased HR (to increase CO). vasoconstriction. increased contractility. this all increases O2 demand. |
| Compensation Mechanisms: RAAS | water & sodium reabsorption (aldosterone) - increases preload (volume). vasoconstriction (angiotensin) - increases after-load (resistance). this increases the work on the heart on an already weak, damage heart, which makes things worse. |
| Symptoms of decreased CO | kidneys: renal insufficiencies, oliguria, nocturia. brain: confusion, restlessness, change in LOC. |
| Sx of increased workload on heart | angina (doesn't have O2 supply to keep up with work). increased RR. dysrhythmias. fatigue. activity intolerance (r/t imbalance between O2 supply & demands). |
| Compensation Mechanisms; Biomarker Response | BNP (b-type naturetic peptide). overtime, as H is overstretched & overfilled, BNP is released. causes some vasodilation and minor diuresis (can help by nature! usually not enough to fix the problem). |
| BNP Lab | can be a lab valve to see what is happening to the heart. if they are releasing a lot of this peptide, then their heart is stretching a lot. |
| Compensation Mechanisms: Remodeling | either remodeling of dilation or remodeling of hypertrophy |
| Compensation Mechanisms: Dilation | Systolic increases pressures & increases chamber size. eventually leading to decreased CO. Systolic HF. |
| Compensation Mechanisms: Hypertrophy | increased muscle mass & wall thickness. also means it needs more O2 & coronary circulation. now at increased risk for dysrhythmias (electrical impulse may not get through the big thick muscle). Diastolic Hf. |
| HF Complications | Acute Decompensated Heart Failure. Dysrhythmias. Chronic HF. |
| ADHF | chronic patient becomes a more life-threatening situation. everything now is decompensated. Pulmonary edema. |
| ADHF: causes | L ventricular failure |
| ADHF: Sx | increased RR. decreased PaO2, SpO2. cool. slammy skin (poor perfusion due to dec CO). frothy blood-tinged sputum. crackles, wheezing, rhonchi. increased HR. anxious (feel like suffocating, can't breathe). exhausted. |
| ADHF: Treatment | determine the underlying cause, treat the cause |
| HF Diagnostics | ECHO. Labs. Chest X-Ray. |
| HF Diagnostic Labs | BNP (has the H stretched over time?). cardiac enzymes (have they had an MI?). ECG (rhythm? dysrhythmia? changes? trends?). LFT. CBC. CMP. |
| Nursing & Collaborative Care | positioning. oxygen. monitoring & continued assessments. drugs. anxiety reduction. teaching. priority actions. |
| Nursing & Collaborative Care: positioning | high fowlers, preferably feet dangling. decrease venous return and increases thoracic capacity. |
| Nursing & Collaborative Care: Oxygen | supplemental, nasal canula or mask, or ICU on a ventilator. |
| Nursing & Collaborative Care: monitoring & continued assessments | vitals (Q4H at least), hemodynamics status, central lines, IV, tele/continuous ECG, I/Os, daily weights. |
| Nursing & Collaborative Care: drugs | Lasix. Digoxin. Beta-blockers. Anti-coagulants. ACE inhibitors. Calcium-Channel blockers. vasodilators. Morphine. |
| Nursing & Collaborative Care: anxiety reduction | low stimulus (low lights). breathing exercises, calm breathing. let they know the plan for the day. be there with them, sit down and talk. |
| Nursing & Collaborative Care: teaching | daily weights (call if >5lbs in a week, or 2lbs in 1 day). energy conservation. exercise & activity. low Na diet. new drugs: medication teaching. BP checking. |
| Nursing & Collaborative Care: priority actions | Vitals. sit up, O2. ECG. IV. drugs. head to toe assessment. |
| Nrs Dx: Impaired gas exchange | R/T fluid in the lungs, alteration in alveolar capillary membrane AEB SpO2, PaO2, CO2, RR. |
| Nrs Dx: decreased CO | R/T alteration in preload or after-load, impaired myocardial contractility, L ventricular dysfunction AEB fatigue, pulses, cap refill, HR, urinary output. |
| Nrs Dx: activity intolerance | R/T imbalance between O2 supply & demand AEB SOB with minimal exertion. |
| Nrs Dx: fluid volume excess | R/T ventricular dysfunction |
| Goals of Care | decrease Sx. improve heart function. improve quality of life. decrease mortality and morbidity. |
| Lasix | loop-diuretic. decreases pre-load by decreasing intravascular volume. |
| Digoxin | positive inotrope. increases myocardial contractility (problem: increases O2 demand - can decrease survival). ordered for systolic HF only (diastolic has plenty of contraction, they can't fill, they need to relax the heart). |
| Beta-Blockers | block sympathetic NS stimulation. decrease HR and workload. some are non-specific (alpha and beta - also do some vasodilation), others are specific and only block beta. |
| Anti-Coagulants | in the pt has a dysrhythmia, the pooling blood puts them at risk for stroke. Lovenox or Heparin. |
| Anti-Coagulants: Potassium | lasix decreases K. |
| Digoxin: Potassium | when a pt has hypokalemia, they are more likely to have digitoxicity |
| Ace Inhibitor | blocks angiotensin I from converting to II, thereforce blocking aldosterone. blocks sodium and water reabsorption, decreasing intravascular volume. blocks vasoconstriction. decreases after-load, decreases pre-load, decrease intravascular volume. |
| ACE inhibitors: Side Effects | angioedema, dry cough |
| Calcium Channel Blocker | decrease amount of Ca in the cell, decreases contractility and HR. Verapamil. Vasodilation. |
| Vasodilators | not as common, but maybe Rx. nitroglycerin. decreases after-load which decreases pre-load. |
| Morphine | decreases anxiety. vasodilates the pulmonary AND systemic systems, helping with breathing. decreases work-load on the heart. |
Created by:
malysab14
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