Two main Myocardial infarction complications
Arrhythmias + HF
What is HF
Complex clinical syndrome that involves inadequate pumping and/or filling of the heart. Impairs the ability of the heart to fill with blood at normal pressure or eject blood sufficient to fulfill oxygen needs
What is ejection fraction and normal %
Amount of blood ejected out of the left ventricle each time it contracts. Normal is 55-60%
HF with reduced ejection fraction = systolic failure - inability to contract properly = EF <40%
HF with preserved ejection fraction = diastolic failure - inability for ventricles to relax/fill - EF > 50%
Signs of acute decompensated HF, diagnosis of HF and HF complications
ADHF: anxious, cool/clammy, dyspnoea, hypo/hyperthermia, accessory muscle, frothy, crackles, rhonichi, Tachycardia
Diagnosis: symptoms, CXR, 12 lead ECG, echocardiogram,
HF complications: pleural effusion, dysrhythmias, renal failure
Left side heart failure patho
- L ventricle looses ability to generate enough pressure to eject blood. (Impaired contractility)
- Decreased in systolic function = reduced CO and tissue perfusion
- Compensation occurs to mange CO - activation of RAAS and SNS + cardiac remodelling (hypertrophy)
- Impaired blood flow = blood backs up into left atrium and pulmonary veins
- Increases hydrostatic pulmonary pressure = fluid shifts into pulmonary capillary beds into interstitium then alveoli = pulmonary congestion/oedema
Right side heart failure patho
- R) ventricle fails to contract effectively
- Increase resistance in pulmonary circulation = increases pressure in R ventricle to overcome this
- Lack of clearance leads to right atrial and right venous congestion into systemic circulation
- Systemic/peripheral oedema
Causes: cor pulmonale (R I gut hypertrophy caused by pulmonary disease), PE, L) HF
Clinical manifestions fo R) HF vs L) HF
R) HF: GIT congestion (poor absorption), venous portal congestion, JVD, sympathetic/peripheral oedema = pitting oedema, weight gain
L) HF: breathlessness when lying down/exertion, frothy cough (oedema), cyanosis, fatigue, crackles, dyspnoea, renal failure
Heart failure management
Goals: reduce morbidity/mortality
Non-pharm Management: treat underlying cause, monitor, educate, cardiac reheab, vital signs, urinary output
Pharmacological: diuretics, RAAS inhibitors (ACE inhibitors, angiotensin blocker), b-adrenergic blocker, vasodilator, positive intro-pic agents (digoxin)
What is digoxin MOA, adverse effects, nursing considerations
MOA: 1. prolongs the plateau phase of the cardiac action potential —> slowing ventricular contraction to allow more time for ventricular filling. 2. Increases the force of cardiac contractility = increases CO
Adverse: bradycardia/heart block, toxicity, N&V/diarrhoea
Nursing considerations:
- effect is enhanced by hypokalaemia, hypoxia, antibiotics
- use whole tablets not halves - might be displaced and therapeutic levels are close to toxic levels
What is an arrhythmia
A distribution in the hearts normal electrical condition
What are the characteristics of AFib and it’s causes
Characteristics: irregularly-irregular rhythm, variable ventricular rate, no p waves, undulating baseline
Causes: underlying cardiac/medical disease: HF/MI/CAD, thyrotoxicosis: alcohol intoxication, excess caffeine, electrolyte disturbance, idiopathic
Pathophysiology of AFib
- Abnormal electrical signalling - ok’ing all over atrium
- Quivering unco-ordinated atrial activity
- AV can’t filter number of signals coming from atria = inadequate emptying of the atria
- Ventricular rate increases due to signals passing through AV node
- Affects emptying of ventricles = reduce SV/CO
AFib goals and management
Goals: symptom control (reduce ventricular rate) and prevention thromboembolism
Management:
- Rate control: reduces ventricular rate to restore CO - slows conduction, beta blockers, calcium channel blockers, digoxin,
- Rhythm control: restore sinus rhythm - anti-dysrhythmic drug therapy/electrical cardio version, catheter ablation
- Anticoagulants: long term - reduce risk of ischemic stroke
Ventricular fibrillation characteristics and causes
Characteristics: ventricular rate > 300bpm, rhythm: extremely irregular, QRS irregular/unrecognisable, no p waves
Causes: MI/HF/cardiomyopathy, electric shock, electrolyte imbalance, acidosis, drug toxicity
VF pathophysiology and management
- Rapid disorganised ventricular rhythm causing ineffective contraction of the ventricles = quivering
- Ventricles suddenly attempt to contract at rates of up to 300-500, unable to contract in synchronised manner
- Immediate loss of CO
Management: CPR - DEFIB
Thrombus vs embolus
Thrombus: is a blood clot which is attached to a blood vessel
Embolus: is a moving clot
What is the Clotting cascade
Blood vessels protective inflammatory mechanism is to produce clots.
- Intrinsic/extrinsic pathways —> common pathway —> formation of factor Xa - when activated it converts prothrombin to thrombin.
- Fibrinogen and thrombin work together to form fibrin strands
- Activation of platelets assist in clotting process linked with fibrin strands
What is the action of antithrombin iii
Inhibits factor Xa = reduces the production of thrombin. inhibits thrombin from activating fibrinogen
Example of anti platelets and how do they work
Aspirin: irreversible inhibitor of the Cox 1/2 enzyme making cox enzymes inactive = which prevents the production of thromboxane A2 which prevents the mediation of platelet aggregation.
Clopidigrel/prasugreal: inhibits ADP-mediation of platelets
Tirofibran - blocks the final common pathway of platelet aggregation inhibiting glycoprotein iia/iib
Two main types of anticoagulants, their indication, MOA, adverse effects, route, nursing consideration, overdose management
- Heparin
- indication: slows growth (prophylaxis)
- MOA: binds to antithrombin iii which inhibits factor Xa - prolongs clotting time
- Adverse: haemorrhage
- Route: s/c or IV (inactivated oral)
- nursing consideration: monitor for signs of bleeding
- overdose management protamine - Warfarin
- indication: prevents thrombi (prophylaxis)
- MOA: interferes with synthesis of vitamin K - dependent clotting factor in liver
- Adverse: haemorrhage
- Route: oral
- nursing consideration: lots of drug interactions
- overdose management: fresh frozen plasma
What are examples of thrombolytic agent / MOA / adverse effects
Tenecteplase/alteplase (anything ending in -ase)
Moa: converts plasminogen into plasmin = plasmin breaks down the fibrin mesh clot to lyse the existing thrombi/emboli
Adverse: bleeding (systemic lysis of normal haemostasis plugs), allergies, hypotension, arrhythmia
