Heart Failure Mini Lecture PDF - University of Canberra

11857 Health Across Lifespan - High Acuity Mini Lecture – Heart Failure Kate Steirn 11857 Health Across Lifespan - High Acuity Lecture Objectives Defining heart failure Causes of HF Clinical manifestations of HF Physiological responses to heart failure Cardiogenic shock Diagnostic pro...

11857 Health Across Lifespan - High Acuity Mini Lecture – Heart Failure Kate Steirn 11857 Health Across Lifespan - High Acuity Lecture Objectives Defining heart failure Causes of HF Clinical manifestations of HF Physiological responses to heart failure Cardiogenic shock Diagnostic procedures/tests Pharmacological management of HF Heart Failure (HF) Heart failure is a complex clinical condition that is characterised by an underlying structural abnormality or dysfunction that results in the inability of the ventricle to fill with or eject blood. Also referred to as Congestive Cardiac Failure (CCF) or Heart Failure (HF) Left sided Heart Failure - Systolic heart failure - Diastolic heart failure Right Sided Heart Failure Causes of HF 1. CAD →  Blood supply 6. Rheumatic fever infarction and fibrosis from prolonged 7. cardiomyopathy ischaemia accounts for 2/3 systolic HF 8. Diabetes mellitus (diastolic HF) and a reduction in EF 9. Chronic HTN (diastolic HF) 2. Dysrhythmias 3. Valve disease Regurgitation stenosis 4. Cor pulmonale 5. Congenital heart disease (ASD, VSD) Systolic versus Diastolic Heart failure Systolic heart failure = problem with contraction Diastolic heart failure = filling problem  force of contraction / contractility /  inotropy  Preload small ventricles and large chamber  SV →  CO walls EF < 40% diagnosis of HF Myocardial hypertrophy Enlarged ventricles, chamber wall thinner Can have normal EF  Clinical manifestations LHF (L= Lungs) RHF ( R= rest of body)  PAP Peripheral oedema +/- Crackles on auscultation pitting oedema Pulmonary oedema Elevated JVP (congestion)  CVP Dyspnoea/orthopnoea Hepatosplenomegaly Pink frothy sputum Ascites Cough Weight gain Nocturia  BP,  CO  CI  S3 heart sounds  BP,  CO  CI Fatigue, weak, lethargic (not enough blood going forward) Fatigue, weakness, lethargy Decreased UO Rapid/irregular HR Rapid/irregular HR Decreased UO (Aitken, Marshall & Chaboyer 2019 and Bullock & Hales 2023) Physiological Responses to Heart failure 1. Sympathetic nervous system response 2. Renin-angiotensin-aldosterone system (RAAS) 3. Frank-Starling response FIGURE 23-43 Heather and Buckley 2011 p 635 Cardiogenic shock Acute and Chronic HF Acute heart failure is a sudden development of Chronic heart failure appears slowly over time, and symptoms, and is often severe gradually gets worse as heart function continues to Causes: deteriorate. myocardial infarction or an ischaemic, inflammatory or toxic insult It requires frequent assessment and adjustment of acute valve insufficiency or the management regimen pericardial tamponade Requires urgent evaluation and management Although a person with chronic heart failure may May respond to treatment and improve rapidly. have acute exacerbations from which they recover, It may occur as a decompensation of chronic heart the person’s heart function often continues on a slow failure. and incessant decline despite intervention. Diagnostic procedures ECG – basic interpretation of rhythm but should always be reviewed by MO within 1hr of taking. CXRAY – basic level of understanding and assessment required. Understand formal report findings - cardiomegaly - pulmonary oedema - ECHO – nurses do not undertake these but we need to be able to interpret the result and report findings - Dilation - Hypertrophy - Valves - Contractile force - EF % Management of HF 1. Treat underlying cause Fibrinolytic, cath lab, CABG, Valve replacement Lifestyle modification 2. Manage fluid volume overload Fluid restriction 1-1.5L/day ACE inhibitors, Diuretics (loop, thiazides), Daily weights fluid restriction, Reduce dietary sodium intake salt restriction Weight loss management 3. Improve ventricular function Smoking cessation Reducing preload, reducing afterload, improving contractility Limit caffeinated drinks Beta blockers (carvedilol, bisoprolol, metoprolol) Control diabetes ACE inhibitors Digoxin Antiarrhythmic drugs IV Calcium Inotropic therapy (dobutamine, milrinone, levosimendan) ACE inhibitors and ARBs Captopril Lisinopril Enalapril Ramipril Peridopril ACE inhibitors Angiotensin Receptor -Bockers (ARBs) Losartan Valsartan Candesartan Dobutamine Short term inotropic support – Acute HF or acute exacerbations of Chronic HF Used to treat HF, cardiogenic shock, sepsis with systolic dysfunction Onset of action 2-10minutes continuous IV infusion 250mg/250mls Mcg/kg/min 2-20mcg/hg/min Positive inotrope ( CO) and positive chronotrope ( HR) minimal Beta ()1 agonists activates – increase contractility leads to decrease in end systolic volume = increase SV Does have 2 and Alpha () 1 effects (minimal) 2 – vasodilation – Decreases afterload (SVR) - can sometimes be seen as a drop in BP initially should then gradually improve due to 1 effects CO = HR X SR therefore if we SV & HR + SVR = CO → Preserved systemic BP References Aitken, L., Marshall, M & Chaboyer, W. (2019) ACCCN’s Critical Care Nursing (4th ed) Elsevier Buckley, T. (2023b). Alterations of Cardiovascular Function Across the Lifespan. In Craft, J., Gordon, C., Huether, S.E., McCance, K.L., & Brashers, V.L (Eds) Understanding Pathophysiology (3rd ed. p 610-679). Elsevier. Craft, J., Gordon, C., Huether, S.E., McCance, K.L., & Brashers, V.L (Eds) Understanding Pathophysiology (3rd ed) Elsevier Knights, K., Rowland, A., Darroch, S., & Bushell, M., (2018). Pharmacology for health professionals (6th ed). Mosby Elsevier. Tiziani, A. (2018) Harvard’s Nursing Guide to Drugs (11th ed) Elsevier Wagner, K., Hardin-Pierce, M., Welsh, D., & Johnson, K. (2015) High-Acuity Nursing global edition, (6th ed.) Pearson  The University of Canberra acknowledges the Ngunnawal people, traditional custodians of the lands where Bruce Campus is situated. We wish to acknowledge and respect their continuing culture and the contribution they make to the life of Canberra and the region. We also acknowledge all other First Nations Peoples on whose lands we gather. The University of Canberra acknowledges the Ngunnawal people, traditional custodians of the lands where Bruce Campus is situated. We wish to acknowledge and respect their continuing culture and the contribution they make to the life of Canberra and the region. We also acknowledge all other First Nations Peoples on whose lands we gather. 11857 Health Across Lifespan - High acuity care needs Mini Lecture – Haemodynamic monitoring Kate Steirn 11857 Health Across Lifespan - High Acuity Lecture Objectives Students will be able to identify, gather and analyse health data in high-acuity contexts including: Understanding Haemodynamics Non-invasive haemodynamic monitoring Invasive haemodynamic monitoring Arterial lines Central lines Pulmonary Artery (PA) catheters Continuous cardiac monitoring Pathology results Haemodynamic Assessment and Monitoring Haemodynamics – measuring and monitoring factors that influence the force and flow of blood Haemodynamic monitoring is used to assess cardiovascular function in the critically ill or unstable patient. It is indicated when standard vital signs measurements are not adequate to evaluate changes in cardiovascular status. Haemodynamic monitoring provides the full range of information required to enable individualised goal directed therapy Non-Invasive patient assessment Look Listen Feel Pathology When Cardiac Output (CO) drops and there is inadequate perfusion to the tissue or organs, it doesn’t affect each organ simultaneously. There are compensatory mechanisms in place to preserve CO to vital organs Comprehensive assessment of haemodynamics therefore needs to go beyond assessment of ‘circulation’ Need to go beyond BP, HR and peripheral vascular assessment. Signs of inadequate perfusion/ compromised haemodynamics Primary (skin and GIT) Secondary (kidneys, liver, lungs) Final (Brain, Heart) Cool, clammy skin, > cap refill Concentrated urine Decreased or altered LOC Pallor, cyanotic skin Decreased UO Disorientation Decreased Bowel sounds Increase BUN/Cr/Potassium Slow reacting pupils Diarrhoea /constipation Increase in ALT/AST/Coags Chest pain Increased NG output Increase RR and effort Tachycardia/bradycardic/ectopics SOB ST elevation Decreased PaO2 decreased SpO2 Continuous cardiac monitoring + ECG Continuous cardiac monitoring 5 lead continuous cardiac monitoring Allows for rapid assessment and constant evaluation (2 lead display preferred) Nurse needs to be skilled at interpretation of rhythms (SR, AF, SVT, ST elevation, 1st, 2nd, 3rd degree heart blocks, Bundle Branch blocks (BBB) atrial and ventricular ectopics, VT, VF, and asystole) 12 lead ECG Pharmacology knowledge Electrolyte levels Mean Arterial Blood Pressure (MAP) The definition of mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole. MAP is influenced by cardiac output and systemic vascular resistance, each of which is influenced by several variables Is a risk indicator and is regarded as perfusion pressure MAP values less than 60-65mmHg should be avoided Low perfusion pressure can lead to tissue hypoxia with associated complications A common method used to estimate the MAP is the following formula: MAP = DP + 1/3(SP – DP) Where DP is the diastolic blood pressure, SP is the systolic blood pressure. Invasive patient assessment and monitoring Arterial Catheters Insertion sites Brachial artery Large easy to place Invasive way to continuously monitor BP Easy to control bleeding Arm mobility more restricted Limited collateral circ Radial artery 2nd increased risk thrombus Most common/ preferred Max mobility Bleeding control easy Collateral circulation Femoral artery Risk to nerves 2nd most common High risk infection close to perinium Mobility affected Bleeding control not easy Increase risk of thrombus Arterial lines Advantages Complications Continuous assessment of systemic arterial BP