EXAMPLES Flashcards
Know the signs of raised ICP early and late
Early - Confusion, drowsiness headaches.
Late - vomiting, seizures, hypertension, irregular RR, bradycardia
Congestive heart failure is?
Inability of the heart to maintain CO to meet the body’s needs
Your patient has had a STEMI and: is tachypnoeic (RR > 21) is tachycardic (HR>101) is oliguric has chest pain (6/10)
He goes on to become SOB with a cough
How does the underlying pathophysiology relate to these signs and symptoms?
A STEMI results in myocardial cell death, reduced myocardial contractility and reduced CO (the myocardium is not pumping as efficiently as it should)
In an attempt to maintain an adequate CO the SNS & RAAS respond causing the ↑RR, ↑HR,↓UO
SOB & the cough relate to L)sided heart failure → hydrostatic pressure forces fluid into the lungs → impaired gas exchange
What is the goal of management of angina or a MI?
Increase oxygen supply to the myocardium → give nitrates and consider O2 if SpO2 < 93%
Relieve pain, reduce O2 demand & signs of ischaemia
Effects of hypercapnia are
Tachypnoea (↑ RR) to “blow off” excess CO2
Use of accessory muscles to increase chest expansion and help with forced exhalation to expel CO2 and recruit O2
Effects of hypoxaemia are
Tachypnoea once PO2 < 60mmHg to recruit more O2
Activation of SNS response (↑ HR, BP) to increase O2 circulation to tissues
Peripheral vasoconstriction (poor peripheral perfusion) to preserve O2 for vital organs
Name two compensatory systems in HF?
SNS and RAAS
How are SNS and RAAS the two compensatory systems in HF?
Baroreceptors in the aortic and carotid arteries sense a drop in the BP
The sympathetic nervous system (SNS) releases adrenaline and noradrenaline
Low cardiac output and vasoconstriction results in decreased renal perfusion → renin is released by the kidneys
This initiates the renin angiotensin aldosterone system (RAAS)
SNS activation results in:
↑ Heart rate and ↑ contractility which ↑ blood pressure
Neuro-hormonal activation results in:
↑ blood volume (related to aldosterone & ADH secretion) which ↑ preload angiotensin II ↓ vascular capacity which ↑afterload
NEURO - state 4 assessments with interventions linked
Perform vital signs to get baseline/Administer prescribed oxygen to reverse hypoxaemia and help prevent cerebral hypoxia
AX: GCS to assess LOC. Record and report changes in GCS to implement early intervention
Rapid Ax to guide interventions/Administer prescribed medication [beta blockers] to maintain BP within set parameters To prevent further hypertension and rise in ICP
Respiratory assessment*positioning/Maintain head of bed at 30◦ to facilitate venous drainage and prevent rise in ICP
RESP = state 4 ax and interventions
Vital signs to ax RR, depth etc - Administer oxygen as prescribed to reverse hypoxaemia
Posterior chest Ax to assess WOB, accessory muscle use [AMU], Administer bronchodilators/corticosteroids as prescribed for relaxation of smooth muscle in airways to facilitate gas exchange
Assess positioning- Ensure patient upright to optimise air entry and facilitate gas exchange
Rapid Ax - to guide prioritised interventions. Encourage pursed lip breathing to facilitate exhalation of CO2 (reduce gas trapping)
If asthma is one of them what one intervention and ax would be good to mention
If Asthma make sure you add - Posterior chest Ax to assess WOB, accessory muscle use [AMU], Administer corticosteroids as prescribed for relaxation of smooth muscle in airways to facilitate gas exchange, through spacer for more delivery of medication to lungs.
using spacers more effective as it delivers more of the medication to the lungs.
EVALUATION for RESP ax and interventions. how would you know they worked?
Medications were administered as prescribed with good effect - ↓ RR ↓ WOB ↑ PF
Oxygen titrated as required to maintain 02 saturations as charted
Patient maintained upright position with good air entry, mobilised as able
Vitals recorded and reported to RN. NZEWS recorded and acted on as needed
Reassurance/education provided to patient and family as appropriate
Effective use of spacer noted.
If GTN doesn’t work for chest pain[angina] what is your next step? What would you administer, how does it work and some nursing considerations for this medication
An opioid acting primarily on receptors that perceive pain, morphine also acts as a vasodilator, reducing ventricular preload and cardiac oxygen requirements
Also reduces anxiety thus reducing myocardial oxygen demand
Nursing considerations: withhold if RR < 12, decreased level of consciousness/sedated, hypotension
What class is aspirin? and what is it’s mechanism, how does it work
Aspirin is NOT an anticoagulant or a ‘blood thinner’
Its an ANTIPLATELET/NSAID
Be sure to understand its mechanism – it inhibits platelet formation, thus preventing a thrombus forming/developing further
What three classes of medication are your front lines for HEART FAILURE?
Ace inhibitors, beta blockers and diuretics.
How do ace inhibitors work?
ACE inhibitors promote vasodilation and diuresis by decreasing afterload and preload thus decreasing the workload of the heart
- What are three medications commonly used in acute chest pain management?
GTN, morphine and aspirin
For patients with heart failure: Diuretics activate the SNS and RAAS so best used with a _______ to prevent this occurring
ace inhibitor
CARDIAC - state 4 ax and interventions
Vital signs - assess RR depth and pattern, Sp02 to measure blood within the body.
Rapid Ax - to assess pt’s presenting concerns. Evaluate what the priorities are
Administer beta blockers to Slow the HR, lower the BP and reduce the force of contraction
COLDSPA to ax pain, severity, pattern and hx. Administer nitrates - GTN, to relieve angina and ioncrease blood flow
Daily weighs to ax baseline and ax if interventions are working. Administer Diuretics [frusomide] to ^ sodium and water exrection by kidneys to assist with fluid overload
IF APPLICABLE: Administer antiplatelet [ASPIRIN] to prevent platelet aggregation and emerging/subsequent thrombosis, which impedes blood flow
