Heart failure Flashcards
Heart Failure Pathophysiology
Interference with Co (such as preload, afterload, myocardial contractility, heart rate or metabolic state) leads to decreased ventricular function and heart failure. When the heart becomes overload the body resorts to compensatory mechanism that are aimed at maintain CO and BP. This occurs through the activation of the SNS which releases adrenaline and noradrenaline to increased HR, contractility and peripheral vascular constriction, initially this improves CO. eventually due to increased workload, the myocardium requires addition oxygen and CO falls as a result. The kidney’s notice this decrease in perfusion and activate the renin-angiotensin-aldosterone system which increases sodium retention in the kidneys(aldosterone) and increased peripheral vascular resistance (angiotensin) leading to an increased BP. In addition the brain notices a reduced CPP and secretes ADH to increase water absorption in the kidneys leading to a further increase in blood volume. Due to the increase in blood volume in the heart chambers the heart initially trys to compensate by stetching the ventricle walls (thinning), this works for a while until the muscle fibers become over streched and can no longer contract effectively leading again to a deduced CO. the compensate for this the walls of the ventricle thicken to give it more power, this increases CO and maintains perfusion but the muscles have a poor coronary artery supply and become prone to life threatening ventricular arrhythmias.
Define Heart Failure
A progressive condition of impaired cardiac function due to structure or functional disorder that decreases the ability of the ventricles to fill and eject. The heart cannot pump blood at a volume required to meet blood pressure requirements of the body.
Differentiate between clinical manifestations of L and R sided failure
LEFT: left heart failure means that the left ventricle is unable to pump the blood forward into the aorta causing the blood to back flow into the pulmonary system causing symptoms of pulmonary oedema (pink throthy sputum). At risk of pneumonia.
•Dyspnoea; orthopnoea (cant lie flat); dry hacking cough (cant bring up fluid); crackles on auscultation; nocturia; chest pain
RIGHT: right heart failure means that the right ventricle is unable to pump blood forward into the pulmonary vasculature causing blood to back flow into the venous system causing symptoms of peripheral oedema (pitting).
•Weight gain (sodium and water retention), GI bloating à nausea à anorexia, ascites (eventually), distended neck veins; behavioural changes
BOTH: suffer fatigue; tachycardia
Discuss Nursing management of chronic Heart Failure
Management is aimed at reducing the workload of the heart and preventing complications such as pleural effusion, arrhythmia, stroke from left ventricular thrombus, hepatomegaly from back flow of blood into the liver and renal failure from decreased perfusion.
•May require revascularisation (CABGS, Stents), pacemaker or heart replacement
Fluid volume excess
•Monitor urine output with strict fluid balance (renal function)
•Fluid restriction 1-1.5L per day
•Daily weight
•Dietary restriction (low sodium, high protein, smaller meals)
•Diuretics: thiazides (Hydrocholrothizide), loop diuretics (frusemide) or potassium sparing (spironolactone) which one will depend of other co-morbities.
Activity intolerance
•Encourage activity with regular rest periods as don’t want to over work the heart
•Cardiac rehab
•Paroxysmal nocturnal dyspnoea (additional pillows, positioning)
•Sleep disturbance: educate on effect of diuretics
Briefly explain indications of CABGs
Briefly explain indications
•Unstable angina that is not responding to medication or percutaneous coronary intervention (PCI)
•Left main coronary artery disease (wont do PCI as may occlude à massive AMI)
•Multi vessel disease ( don’t like doing multiple stents)
•Treatment of MI or heart failure
•Complications from PCI (coronary artery dissection post PTCA)
•Failed PCI
Differentiate between artery and vein grafts used
The selection of artery or vein from grafting will depend on the quality of the vessel, such as Peripheral Vascular Disease.
•Arteries: better quality and last longer, 90% patency at 10years. Have a risk of vasospasm then handling and take longer to re-stenose. Commonly the internally mammary or radial are used
•Veins: not as good quality, only have 60% patency after 10years but no vasospasm and are quicker to re-stenose. Commonly use saphenous (leg).
Discuss complications of CABGS
- High risk of bleeding (may need to return to theatre depending on cause) ?blood transfusion
- Cardiac tamponade (inflammation)
- Arrhythmias (heart doesn’t like be touched)
- Blood pressure alterations
- Electrolyte and metabolic disturbances (hypokalaemia due to diuresis due to release of ATN from atria due to hypertension during by-pass)
- Atelectasis (collapse of alveoli à pneumonia) : don’t want to deep breath due to pain
- Pleural effusion as lungs exposed
- Neurological (post anaesthetic delirium from long surgery), at risk of stroke.
- Renal impairment from hypoperfusion
- Coagulopathy à haemorrhage
- Infection of wound, donor site, ICC site and arterial line/CVC.
Discuss Nursing management of CABGS
Preoperative care
•Comprehensive assessment to obtain base line vitals, history to identify risk factors, CXR, ECG, Pathology (FBE, U&E, clotting)
•Education re: procedure and post-operative expectations (e.g. rehab, analgesia)
Post-operative care
•Usually ICU for first 24hours where they are intubated for first 6-12hours and have multiple haemodynamic monitoring devices (artline, CVC, intercostal x2, ETT)
•Breathing: chest auscultation, CXR, monitor pleural and mediastinal drains (UWSD)
•Circulation: monitor haemodynamic status
•CVC care
•ECG baseline on RTW then every 12 hours at least
•Monitor fluid balance (IDC for 24 hours usually)
•Atrial and ventricular pacing wire monitoring ? Remove in ICU
•Monitor GCS as at risk of stroke
•BGL – stress response
•Analgesia – lots plus splinting ( ribs fractured in theatre)
•Cardiac diet
•TED to prevent DVT
•Day 1 mobilisation with physio ( will start slow, maybe just sit in chair)
•Monitor wound Dx
•Monitor vitals as per hospital policy or surgeons preferences and as per patients condition (clinical decision)
Define APO
Is an abnormal accumulation of fluid in the interstitial tissue and alveoli that impairs gas exchange and lung expansion. This can be caused by fluid overload, left ventricular failure, prolonged airway obstruction, sepsis or aspiration. Characterised by hypoxaemia, crackles on auscultation, decreased oxygen saturation, and precence of infiltrates on chest x-ray. And pink frothy sputum.
Discuss Pathophysiology of APO
Discuss Pathophysiology
Increased hydrostatic pressure, decreased interstitial pressure or increased capillary permeability leads to a build of fluid in the interstitial space of the lungs which the lymphatics can normally drain, however if the fluid continuesp the lymphatic system becomes overwhelmed and fails to drain the fluid away, eventually this fluid along with red blood cells floods into the alveoli (alveolar oedema).
Clinical manifestations of APO
Altered LOC from hypoxia •SOB & Increased WOB •Hypoxaemia •Chest crackles on auscultation •Dullness to the base of lungs •Pink frothy sputum •Skin pale and diaphoretic
Discuss collaborative Management of APO
Discuss collaborative Management of APO
Aimed at reversal of the cause and interventions to treat the symptoms
•High flow Oxygen (consider intubation especially if pink frothy sputum)
•NIPPV/PEEP – high pressure to move fluid back and recruit alveoli
•Monitor ABG’s
•Chest x-ray
•Chest auscultation
•Frequent ECG and Cardiac monitoring
•Fluid balance chart ?IDC
•Monitor pathology – cardiac enzymes, FBE, U&E, lactate
•Cautious IVT
•Depending on cause morphine, digoxin, inotropes(hypotensive)
•Position in semi fowlers with legs dependent
•Diuretics +/-
•Fluid restriction depending on cause
Define Stroke
An acute neurovascular injury secondary to cerebrovascular disease that is either ischaemic of haemorrhagic of cause.
Differentitate and discuss
Ischaemic causes
Ischaemic causes
-Thrombus: caused by atherosclerosis, vasculitis, polycythaemia or infection
-Embolic: cardiogenic emboli (AF, AMI, atrial or ventricular septal defects), fat emboli or septic emboli
-Hypoperfusion: cardiac failure
Haemorrhagic such as a burst aneurism
Risk factors
Risk factors for stroke
HT, age (doubles every 10 years after 55), male, family Hx, smoking, hyperlipidaemia, diabetes, AF, recent AMI, endocarditis and carotid stenosis.
Clinical Manifestations for stroke
Clinical Manifestations
Think FAST
Facial weakness: facial symmetry when smiling
Arm movements: get patient to lift arms up, dose one drift down or drop rapidly, or turn
Speech change: slurred speech or is there difficulty finding correct words or phrases
T is for test
Discuss management of a diagnosed patient for stroke
Discuss management of a diagnosed patient
-Stroke management requires quick identification as patient may be eligible for thrombolysis.
History exclusion >3hr, seizure, Bgl 22 mmol/. AMI >7 days < 3mth, stroke or serous head trauma < 3mth, major surgery 14 days, GIT urinary haemorrhage 21 days.
Pregnant, check haemorrhage risk INR, platelet, BP >185/>110,
Airway
-Remain NBM due to risk of aspiration
-Intubate if GCS less than 9 or sign of raised ICP
Breathing
-Supplemental oxygen if SaO2 below 95%
Circulation
-Manual blood pressure (must be accurate),
-ECG (may find T wave inversion -75%)
-Manage hypotension carefully
-Aggressive management of hypertension not recommended
-2 x large IVB
-Pathology: FBE, U&E, LFT, COAG, BGL and troponin (need to identify type of stroke)
-Maintain euvolemia with IVT
Disability
-Monitor neurovascular obs every hour at least (GCS, pupil size and reactivity)
-BGL every 2-4 hours (affect mortality), keep in range
-Elevate head of bed 30 degrees
-Urgent CT/ ?MRI
-Hypothermia can help decrease cellular metabolism and prevent secondary injury will need intubation and induced coma to stop shivering
-Anti-platelet therapy for ischaemic stroke (aspirin)
Example of ob for thrombolysis
•15mins for 2hrs
•30mins for 4 hours
•Hourly for 4 hours
•2 hourly for 12 hours
•4 hourly until r/v
Identify the inclusion and exclusion criteria for thrombolysis for a stroke
Onset of symptoms less than 3 hours (excludes those who wake up with symptoms)
-BSL must be over 2.7 and under 22mmol/L
-Seizure at onset excludes patient
-CT to determine cause (must illuminate haemorrhagic)
-Cant have had an AMI, stroke or serious head trauma within last 3 months,
-Cant have had major surgery within last 14 days as wounds will rebleed
-Cant have had GIT or urinary haemorrhage in last 21 days
-Not pregnant
-Need to check haemorrhage risk: warfarin INR needs to be below 1.7
-Cant have had IV heparin within last 48 hours or on herbal medicines and platlet/anticoags
-Need platlets above 100000/mm3
-Blood pressure below 185/110
NEED to stay in bed for first 24 hours as falling à haemorrhage
Minimise invasive procedures for 24 hours
No razors
Monitor for pressure areas
Differentiate and discuss
ØIntra-cerebral
- bleeding inside the brain
ØEpidural- bleeding between the dura mater (outer meninges) and the skull
ØSubarachnoid - bleeding in the subarachnoid (middle meninges) space that can lead to cerebral vasospasm and hydrocephalus (water on the brain)
- can be caused by ruptured cerebral aneurysm (treatment is to surgically clip or endovascular coiling)
ØSubdural - bleeding between the arachnoid mater and the dura mater (inner meninges)
- bleeding between the dura mater (outer meninges) and the skull
Differentiate and discuss extradural and subdural haematomas
Extradural haematoma is a neurosurgical emergency as the haemorrhage causes the dura to separate from the skull, it rapidly expands causing raised ICP and can lead to herniation.
Signs and symptoms
•LOC à consciousness àLOC
•Severe headache
•Hemiparesis
•Ipsilateral (same side) pupil dilation
A subdural is a collection of blood between the dura mater and the arachnoid mater and can be acute, subacute or chronic
Signs and symptoms
•Acute: LOC, hemiparesis, fixed and dilated pupils
•Subacute/Chronic: nausea and vomiting, altered LOC, headache
Define Intracerebral Haemorrhage
Intracerebral Haemorrhage
Bleeding within the brain tissue, manifestations depend on size and location (may or may not be operable), can lead to neuronal death, raised ICP and secondary ischaemia.
Factors affecting CCP
Decreased perfusion pressure -Decreased BP -Raised ICP Decreased oxygen or glucose delivery -Hypoxia -Anaemia -Hypoglycaemia -Decreased cardiac output
Increased metabolic demand on CCP
Increased metabolic demand
- Hyperthermia
- Seizures
- Agitation
Increased vascular resistance of CCP
Increased vascular resistance
- Vasospasm (post aneurism clipping)
- Thrombosis
- Cerebral oedema
- Hypocapnia (low CO2)
