ICU - Cardiovascular CLINICAL FEATURES Symptoms 1. cardiac failure i. fatigue ii. syncope iii. dyspnoea, cough, haemoptysis iv. cyanosis v. peripheral oedema vi. abdominal distension & pain, nausea & vomiting 2. cardiac ischaemia i. pain ii. anxiety 3. arrhythmias i. palpitations ii. syncope Causes of Chest Pain 1. cardiac ischaemia | infarction pericarditis 2. oesophageal spasm, motility disorders functional or anatomical obstruction rupture / tear - Mallory-Weiss reflux, hiatal hernia 3. aortic dissection, aneurysmal stretching 4. thoracic wall pneumonia, pleurisy muscle tear / strain, chostochondritis, fractured ribs, tumour 5. vertebral spinal nerve entrapment / trauma, tumour Hepres zoster 6. abdominal disease acute cholecystitis 7. psychogenic ICU - Cardiovascular Causes of Syncope 1. autonomic vasovagal - micturition, defecation - tussive, deglutition - Valsalva carotid sinus syncope ANS dysfunction / neuropathy 2. cardiac AMI arrhythmia - prolonged QT syndrome - AV block - sick sinus syndrome - pacemaker related AS, HOCM atrial myxoma pulmonary - embolism - pulmonary stenosis - primary pulmonary hypertension 3. cerebral CVA, TIA subclavian steal syndrome epilepsy 4. metabolic hypocarbia, hypoglycaemia 5. psychiatric Clubbing described in four stages, 1. increased glossiness, cyanosis and prominence of the skin at the root of the nail 2. obliteration of the normal 15° angle at the base of the nail 3. increased concavity in both directions - "watch-glass" contour 4. hypertrophy of the soft tissue of the nail pulp, allowing the nail to float freely NB: may result from cellular hyperplasia 2° to platelet derived growth factor usually takes 1-2 months to develop 2 ICU - Cardiovascular Causes of Clubbing 1. pulmonary i. malignancy * bronchogenic carcinoma - pleural tumours - lymphoma, thymoma - very rarely with secondary lung tumours ii. vascular - AV malformations, hepatopulmonary syndrome iii. pyogenic - bronchiectasis, lung abscess, empyema 2. cardiac i. bacterial endocarditis ii. cyanotic congenital heart disease iii. thoracic aortic aneurysm 3. gastrointestinal i. hepatic - cirrhosis ii. colonic malignancy - adenocarcinoma inflammatory - ulcerative colitis, granulomatous colitis - polyposis coli 4. miscellaneous familial hyperthyroidism (acropachy), hyperparathyroidism syringomyelia 5. unilateral aneurysm of aorta, innominate or subclavian arteries apical lung carcinoma chronic shoulder dislocation 6. lower limb coarctation of the aorta Split Second HS 1. fixed - ASD 2. persistent with normal inspiratory widening RBBB › RV afterload - PS, pulmonary embolism 3. paradoxical spilt fi delayed LV ejection LBBB, RV pacemaker › LV afterload - AS, hypertension fl LV contractility - ischaemia, infarction 3 ICU - Cardiovascular NYHA Classification of Angina Class Symptoms Maximal VO 2 Class O asymptomatic1 Class I ordinary physical activity, such as walking or > 20 ml/kg/min climbing stairs, does not cause angina angina with strenuous or rapid prolonged exertion at work or recreation or with sexual relations Class II slight limitation of ordinary activity 16-20 ml/kg/min walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, or in cold, or in wind, or under emotional stress, or only during a few hours after awakening walking more than 2 blocks on the level, or more than 1 flight of stairs at a normal pace and in normal conditions Class III marked limitation of ordinary physical activity 10-15 ml/kg/min walking 1 or 2 blocks on the level and 1 flight of stairs at a normal pace and in normal conditions "comfortable at rest" Class IV inability to carry on any physical activity without < 10 ml/kg/min discomfort anginal syndrome may be present at rest 1 asymptomatic, but known presence of heart disease Causes of Autonomic Dysfunction 1. diabetes 2. alcoholism 3. chronic renal failure 4. drug induced - anticholinergics, a/b -blockers 5. familial dysautonomia - Riley-Day 6. Parkinsonism 7. rare causes tetanus porphyria, syringomyelia, amyloidosis hypokalaemia 4 ICU - Cardiovascular ACUTE MYOCARDIAL INFARCTION Incidence a. males ~ 3.5 : 1000 b. females ~ 1.0 : 1000 (age 20-65 yrs) NB: › risk ~ 5 fold with 2 major risk factors › risk ~ 8 fold with 3 factors (risk ~ 2x, x = factors) Aetiology a. atherosclerosis ~ 99% thrombotic occlusion > 95% of transmural AMI ~ 20-40% of subendocardial MI b. embolism thrombus, septic thrombus air, amniotic fluid c. coronary arteritis polyarteritis nodosa, SLE, RA, etc. Kawasaki's disease, Takayasu's disease d. coronary dissection - PTCA related e. aortic dissection 2° - aortitis, syphilis, Marfan's, trauma f. congenital coronary anomalies - LCA from PA, TGA g. myocardial hypertrophy & aortic stenosis h. severe trauma, electrocution i. severe hyperthermic syndromes j. prolonged cardiopulmonary bypass k. prolonged hypotension / hypovolaemia l. severe coronary artery spasm i. variant angina ii. nitrate workers iii. thyroid hormone excess iv. cocaine / amphetamine abusers 5 ICU - Cardiovascular Predisposing Factors a. smoking++ - › [COHb] - vasoconstriction - accelerated atherosclerosis - › lipids and platelet adhesiveness - › incidence of sudden death and MI b. hypertension++ c. hyperlipidaemia++ - high cholesterol:HDL ratio d. family history * type 2 hypercholesterolaemia e. diabetes mellitus f. obesity g. gender - males > females h. age i. lifestyle factors Aggravating Factors a. anaemia b. hypoxaemia c. tachycardia / hypertension d. surgery, trauma e. thyroid disease f. pulmonary embolism g. chronic lung disease Clinical Presentation a. silent AMI ~ 25% in Framingham study b. chest pain c. atypical pain d. syncope / arrhythmias e. LV failure / acute pulmonary oedema f. hypotension / cardiogenic shock g. peripheral emboli from mural thrombus h. sudden death ~ 25% of sudden deaths at PM due to acute MI - AMI or sudden death fi 1st presentation of CAD in ‡ 50% - vast majority 2° to VF 6 ICU - Cardiovascular Clinical Signs a. fever - commences in 1st 24 hours, lasting up to 1 week £ 38°C b. CCF c. tachycardia ~ 25% of anterior MI d. bradycardia ~ 50% of inferior MI e. pericardial friction rub ~ 10-15% not a C/I to anticoagulation f. signs of cardiogenic shock if present Time Course of Infarction NB: irreversible myocardial necrosis occurs ~ 60 minutes after "no flow" coronary thrombosis is demonstrated in ‡ 90% of acute MI a. EM changes ~ 15 min b. light microscope changes ~ 6 hrs c. macroscopic changes ~ 24 hrs d. commencement of healing ~ 2 wks e. fibrotic scar ~ 6 wks fi period of greatest irritability Anatomical Relationships a. RCA - inferior - posterior - SA & AV nodes (85-90%) b. LCA - anterior - septum c. circumflex - anterolateral 7 ICU - Cardiovascular Diagnosis a. history and examination - most important b. ECG fi sensitivity ~ 73 % (LBBB see below) specificity ~ 95% ST elevation ‡ 1 mm fi ‡ 2 adjacent limb leads ‡ 2 mm fi ‡ 2 adjacent precordial leads LIGW states ‡ 1 mm fi ‡ 2 limb leads, or V 4-5-6 ‡ 2 mm fi ‡ 2 V 1-2-3 ± T wave inversion pathological Q waves - usually > 3 hrs, maximal by 12 hrs - appear earlier with thrombolysis new LBBB c. cardiac enzymes i. CK (MB) - › 8-24 / fl 48-72 hrs > 15% CK-MB fi highly specific myocardium contains ~ 20% MB / 80% MM bands acute myocarditis may produce elevation angina & pericarditis do not result in elevation plasma CK-MB > 4% & > 10 IU/l fi sensitivity ~ 98% specificity ~ 95% absolute elevation gives crude estimate of infarct size & prognosis earlier peak and clearance with thrombolysis may remain elevated with large MI's or delayed excretion ii. LDH (LDH ) - › 24-48 hrs / fl 7-14 days 1 - LD :LD ratio reversal fi "LD flip" 1 2 ~ 75% sensitivity ~ 97% specificity iii. cardiac troponin T - › 3-4 hrs / fl 6 days - sensitivity / specificity cf. CK-MB d. radioisotope scans i. Tc99m fi hot spots at 1-10 days ii. Th201 fi cold spots e. gated blood pool scan - regional wall motion abnormalities - papillary muscle dysfunction - ejection fraction f. coronary angiography - usually in assessment for CABG g. echocardiography - regional wall motion abnormalities - papillary muscle dysfunction - ejection fraction - pericardial effusions - valvular, papillary muscle function 8 ICU - Cardiovascular h. CXR * best indicator of degree of LVF - not helpful in early diagnosis i. nonspecific changes i. › ESR - at 48 hrs, maximal at 5 days ii. › BSL iii. › WCC < 15-20,000 / µl - may persist for 7-10 days iv. › urea & myoglobin AMI & LBBB data from the GUSTO I trial factors independently predictive of AMI with LBBB, 1. ST elevation concordant with QRS > 1 mm 5 pts (OR ~ 25:1) 2. ST depression in V > 1 mm 3 pts (OR ~ 6:1) 1-2-3 3. ST elevation discordant with QRS > 5 mm 2 pts (OR ~ 4:1) Sgarbossa et al NEJM 1996 used point score ‡ 3 pts for treatment fi a. sensitivity ~ 40% b. specificity ~ 96% CPK Asymptomatic Elevation a. factitious - haemolysis - laboratory error b. physiological - newborn - post-partum - post-exercise c. cardiac origin - traumatic contusion - silent AMI d. skeletal muscle - trauma, surgery - alcoholic myopathy - Duchene's muscular dystrophy (female carrier) - hypothyroidism e. MH susceptible patients, i. family history of MH ii. inherited and congenital myopathies iii. Duchene's muscular dystrophy iv. King-Denborough syndrome v. skeletal deformities vi. ? myotonia 9 ICU - Cardiovascular Treatment - Aims 1. relief of symptoms 2. limitation of infarct size 3. prevention of reinfarction 4. detection and treatment of complications i. arrhythmias - responsible for ~ 40% of post-MI deaths ii. CCF - acute pulmonary oedema, hypoxaemia - acidaemia, hypoperfusion iii. CVA iv. cardiac rupture or septal perforation v. acute valvular dysfunction vi. ventricular aneurysm vii. Dressler's syndrome - pericarditis, friction rub, fever ± pneumonitis - rare, occuring at weeks to months 5. rehabilitation Options: Contemporary Management AJM 1995 1. initial stabilization 2. acute reperfusion measures 3. anti-platelet and antithrombin agents 4. other pharmacotherapy 5. elective coronary revasulcarization 10