Heart disease and failure Flashcards
Risk factors of CVD
High cholesterol High blood pressure Smoking Obesity Diabetes Age Family history Previous heart attack
Clinical manifestations of IHD
Development of atherosclerosis - fatty streak, lipid deposition, intimal fibrosis
Atherosclerotic plaque leads to an imbalance between myocardial oxygen supply and demand
Signs/symptoms
Asymptomatic
Stable angina
Acute coronary syndromes - unstable angina, NSTEMI, STEMI
Long term: HF, arrhythmias, sudden death
Typical angina
Substernal chest discomfort
Provoked by exertion
Relieved by rest/nitrates within minutes
What is an acute coronary syndrome
Unstable angina
Acute MIs
- you can tell if its MI by rise in troponin on blood test (not elevated in unstable angina)
Characterised by development of a thrombosis at the site of acute disruption
STEMI
ST elevation on ECG
Complete coronary occlusion
Need timely diagnosis
NSTEMI
ST depression, variable T wave
Incomplete coronary occlusion
ACS symptoms
Discomfort that lasts and radiates
Occurs with exertion and at rest
Not relieved by GTN
Breathlessness, nausea/vomiting, sweating/clamminess
Immediate assessment
Patient history
ECG
Physical exam
Then risk stratification and blood test (troponin)
Management of ACS
Antiplatelet therapy (aspirin, clopidogrel)
Anti-ischaemic therapy (nitrates)
Thrombolysis (if STEMI)
Secondary prevention (statin, ACE inhibitor, beta blocker, lifestyle)
Other causes of raised NSTEMI
Pneumonia, PE
Pericarditis, sepsis
Heart failure, uncontrolled tachyarrhythmias
High risk ACS patients
Elevated troponin Renal impairment Recurrent chest pain Changes on ECG Haemodynamic instability Major arrhythmias, HF Elderly
Cardiac output equation
CO = HR x SV
At rest: 70ml/kg/min
Stroke volume affected by contractility, preload and afterload
Low output heart failure
Systolic (iscahemic injury, pressure/volume overload)
Diastolic (hypertrophy, infiltrative disorders, constrictive pericarditis, restrictive cardiomyopathy)
High output heart failure
Caused by increased demand on CO
High demand for blood
Causes: anaemia, pregnancy, Pagets disease, sepsis, acromegaly, thyrotoxicosis
Cardiomyopathy
Dilated: 50% familial, or toxins, or systemic disease
Hypertrophic: familial
Restrictive - amyloid
Pathophysiology of heart failure
Reduced SV and CO -> compensatory mechanisms
Vasoconstriction, increased venous return -> enhanced contractility (starling law)
Results in augmented muscle mass
Activation of neurohormonal system (noradrenaline = increased heart rate; vasoconstriction, ANP, RAAS)
RAAS/compensation in heart failure
Vasoconstriction
Na and water retention
Excessive tachycardia
What does Left ventricular failure do to the kidneys
Decreased CO
Reduction in renal perfusion
Activation of RAAS
Increased blood volume
What does left ventricular failure do to the brain
Hypoxic encephalopathy Irritability Loss of attention Restlessness Stupor and coma
Effects of right sided heart failure
Liver and portal system (hepatomegaly, centrilobular necrosis, cardiac cirrhosis)
Spleen
Abdomen
Subcutaneous tissue (oedema
Pleural and pericardial space (effusions)
Biventricular failure
Due to same pathological process on each side of heart
Or left heart failure leads to volume overload and then right heart failure
Side effects of left ventricular failure
Pulmonary congestion and oedema
Heavy wet lungs - breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea
