Week 6

Question 1

Two main Myocardial infarction complications

Answer 1

Arrhythmias + HF

Question 2

What is HF

Answer 2

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

Question 3

What is ejection fraction and normal %

Answer 3

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%

Question 4

Signs of acute decompensated HF, diagnosis of HF and HF complications

Answer 4

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

Question 5

Left side heart failure patho

Answer 5

1. L ventricle looses ability to generate enough pressure to eject blood. (Impaired contractility)
2. Decreased in systolic function = reduced CO and tissue perfusion
3. Compensation occurs to mange CO - activation of RAAS and SNS + cardiac remodelling (hypertrophy)
4. Impaired blood flow = blood backs up into left atrium and pulmonary veins
5. Increases hydrostatic pulmonary pressure = fluid shifts into pulmonary capillary beds into interstitium then alveoli = pulmonary congestion/oedema

Question 6

Right side heart failure patho

Answer 6

1. R) ventricle fails to contract effectively
2. Increase resistance in pulmonary circulation = increases pressure in R ventricle to overcome this
3. Lack of clearance leads to right atrial and right venous congestion into systemic circulation
4. Systemic/peripheral oedema

Causes: cor pulmonale (R I gut hypertrophy caused by pulmonary disease), PE, L) HF

Question 7

Clinical manifestions fo R) HF vs L) HF

Answer 7

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

Question 8

Heart failure management

Answer 8

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)

Question 9

What is digoxin MOA, adverse effects, nursing considerations

Answer 9

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

Question 10

What is an arrhythmia

Answer 10

A distribution in the hearts normal electrical condition

Question 11

What are the characteristics of AFib and it’s causes

Answer 11

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

Question 12

Pathophysiology of AFib

Answer 12

1. Abnormal electrical signalling - ok’ing all over atrium
2. Quivering unco-ordinated atrial activity
3. AV can’t filter number of signals coming from atria = inadequate emptying of the atria
4. Ventricular rate increases due to signals passing through AV node
5. Affects emptying of ventricles = reduce SV/CO

Question 13

AFib goals and management

Answer 13

Goals: symptom control (reduce ventricular rate) and prevention thromboembolism

Management:

1. Rate control: reduces ventricular rate to restore CO - slows conduction, beta blockers, calcium channel blockers, digoxin,
2. Rhythm control: restore sinus rhythm - anti-dysrhythmic drug therapy/electrical cardio version, catheter ablation
3. Anticoagulants: long term - reduce risk of ischemic stroke

Question 14

Ventricular fibrillation characteristics and causes

Answer 14

Characteristics: ventricular rate > 300bpm, rhythm: extremely irregular, QRS irregular/unrecognisable, no p waves

Causes: MI/HF/cardiomyopathy, electric shock, electrolyte imbalance, acidosis, drug toxicity

Question 15

VF pathophysiology and management

Answer 15

1. Rapid disorganised ventricular rhythm causing ineffective contraction of the ventricles = quivering
2. Ventricles suddenly attempt to contract at rates of up to 300-500, unable to contract in synchronised manner
3. Immediate loss of CO

Management: CPR - DEFIB

Question 16

Thrombus vs embolus

Answer 16

Thrombus: is a blood clot which is attached to a blood vessel
Embolus: is a moving clot

Question 17

What is the Clotting cascade

Answer 17

Blood vessels protective inflammatory mechanism is to produce clots.

1. Intrinsic/extrinsic pathways —> common pathway —> formation of factor Xa - when activated it converts prothrombin to thrombin.
2. Fibrinogen and thrombin work together to form fibrin strands
3. Activation of platelets assist in clotting process linked with fibrin strands

Question 18

What is the action of antithrombin iii

Answer 18

Inhibits factor Xa = reduces the production of thrombin. inhibits thrombin from activating fibrinogen

Question 19

Example of anti platelets and how do they work

Answer 19

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

Question 20

Two main types of anticoagulants, their indication, MOA, adverse effects, route, nursing consideration, overdose management

Answer 20

1. 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
2. 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

Question 21

What are examples of thrombolytic agent / MOA / adverse effects

Answer 21

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