Heart Failure / APO Flashcards
Define heart failure
A complex clinical syndrome with typical signs and symptoms that generally occur on exertion, or at rest (particularly when recumbent).
Secondary to abnormality of cardiac structure or function that impairs ability of the heart to fill at normal pressures or eject blood in sufficient volumes to meet metabolic demands.
Outline the functional classifications of heart failure
Class 1:
No limitations
Ordinary physical activity.
Does not cause fatigue, dyspnoea or palpitations
Class 2:
Mild CHF
Slight limitations on physical activity.
Ordinary physical activity results in fatigue, palpitations, dyspnoea or angina
Class 3:
Moderate CHF
Marked limitation on physical activity.
Less than ordinary physical activities leads to symptoms
Class 4:
Severe CHF
Unable to carry out any physical activity with discomfort.
Symptoms of CHF at rest.
Explain the classification of heart failure according to left ventricular ejection fraction
Heart Failure with Reduced Ejection Fraction:
- symptoms +/- signs of HF
and
- LVEF <50%
reduced LV function and CO, leads to decreased organ perfusion, cardiac remodeling and dysfunction
Heart Failure with Preserved Ejection Fraction:
-Symptoms +/- signs of HF
and
-LVEF <50%
and
- Evidence of structural heart disease (LV hypertrophy and LA enlargement)
and/or
- Diastolic disfunction with high filling pressures
pathophys unclear - coronary microvasculature inflammation causes hypertrophy and fibrosis –> increased afterload due to arterial stiffening
Define:
Preload
Afterload
Contractility
Preload:
The amount of stretch at the end of ventricular filling (diastole)
Afterload:
The pressure that the heart must work against to eject blood during systole
Contractility:
The ability to produce force during contraction with degrees of binding between different types of tissue
Discuss the pathophysiology of heart failure
Preload increases.
Compensatory mechanisms work up to a point.
Stretching of the myocardium leads to dysfunction and decreased contractility.
Afterload increases due to increased peripheral vascular resistance, Resistance to ventricular emptying increases workload on the L ventricle causing hypertrophy.
Increased LV workload causes compensatory mechanisms of catecholamines and angiotensin 2 which increase PVR.
Increased myocyte O2 demands and ventricular remodeling decreases contractility, therefore CO and tissue perfusion.
Discuss the compensatory mechanisms for CHF
SNS activation:
Decreased SV and CP cause increased SNS activation –> catecholamine release –> alpha 1 receptor increases afterload –> beta 1 receptor increases HR –: increased myocardial contractility
Neurohormonal response:
CO falls –> decreased blood flow to kidneys (decreased GFR) –> RAAS activated –> decreased cerebral perfusion pressure –> production of endothelin (vasoconstricts) –> inflammatory markers released
Discuss the difference between acute and chronic heart failure
Acute heart failure:
Sudden onset with no compensatory mechanisms (eg: pulmonary oedema, cardiogenic shock)
Chronic heart failure:
Hypervolaemia
Sodium and water retention
Structural changes to heart chambers - Dx for a period of time (minimum 3 months)
Describe the investigations undertaken to diagnose heart failure
ECG
- LV hypertrophy and LAD
CXR
Biochemistry
Haematology
Discuss the management, including pharmacology, of acute heart failure
- O2 therapy for SpO2 <94%
- Avoid opioids
- NIPPV if congested, SpO2 <94% and tachypnoic despite O2
- Consider intubation if fatigue, hypercapnia, decreased RR and GCS
- Diuretics (IV) in signs of congestion for symptomatic relief if adequate BP
Favour loop diuretics 20-40mg - Vasodialators if BP >90mmHg
- Inotropes only if hypoperfused and refractory congestion
Discuss the management, including pharmacology, of chronic heart failure
Triple therapy:
- ACE inhibitor
- beta-blocker
- MRA
Non pharmalogical:
- Collaborative care of GP, heart failure nurses, cardiologist
- Self management - educating pt’s/families
- Fluid restriction, daily weight
- Sliding scale diuretics based on weight
- Exercise training
- Single chamber pacemaker
-
Symptoms of HF
- Dyspnoea
- Fatigue
- Palpitations
- Nocturnal cough
- Wheeze
- Confusion
- Dizziness/syncope
- Chest pain
- Abdo bloating
- Anorexia
Signs of HF
-Cardiac dysfunction Tachycardia - Tachypnoea Third heart sound Murmor Displaced apex beat - Reduced end organ perfusion - Congestion Increased JVP, hepatic enlargement Peripheral oedema Crackles Pleural effusion Ascites - Weight gain >2kg/week - Weight loss
Define APO
An abnormal accumulation of fluid in the interstitial fluid and alveoli of the lung.
Fluid impairs gas exchange and lung compliance.
*mortality is associated with heart failure rather than APO
Pathophysiology of cardiogenic APO
Occurs when decreased CO despite increased systemic vascular resistance
Blood returning to the L atrium exceeds that leaving the LV, increase in pulmonary venous pressure.
Causes capillary hydrostatic pressure in the lungs to exceed oncotic pressure of the blood, leading to a let filtration of protein poor fluid out of the capillaries
Pathophysiology of non-cardiogenic APO
Pathological process acting directly or indirectly on pulmonary vascular permeability.
Proteins leak from capillaries increasing the interstitial oncotic pressure so that it exceeds that of the blood and fluid is subsequently drawn from the capillaries
Eg:
High output states
- septicaemia, anaemia, thyrotoxicosis
Systemic increase of vascular permeability
- pancreatitis, eclampsia, DIC, burns
Toxins/environmental
- immersion/submersion, toxic inhalation, decompression illness
Other
- head injury, drugs, PE
