April May 2002
Pakistan Journal of Family Medicine
Clinical Features in CVS
Contents
Symptomology Dr Saleem Akhtar Rana Page no 3
Dyspnoea Dr Mahboob Ashraf 6
Oedema Dr Saleem Akhtar Rana 12
Chest Pain Dr Arshad Javaid Sh 16
Palpitations Dr Ehsan Assad 22
Cough,Hemoptysis,Cyanosis,Syncope,Pulmonary Oedema 25
Dr Saleem Akhtar Rana
Physical Examination on CVS patient 29
Dr Pervaiz Anwar Chaudhry
Expert on Editorial Board.
Dr Muhammad Asgher Sheikh
(Gold Medalist)
MBBS, DCP, Dip Card, FCPS-1
Cardiologist DHQ Hospital, Siddique Sadiq Hospital.
Importance of the History & Physical Examination
Specialized examination of cardiovascular system (Echo, ETT, Holter, Co-Angio, and Thalium) represents one of the triumphs of modern medicine. It provides a large portion of database required to establish the diagnosis of cardiac disease and to determine the extent of functional impairment of heart. However, their appropriate use is to supplement but not to supplant a careful history and clinical examination, which remains the cornerstone for the assessment of patients with cardiovascular disease. Obviously it is undesirable to subject patients to the un-necessary risks and expenses inherent in many specialized tests when a diagnosis can easily be made on the basis of an adequate clinical examination or when management will not be altered significantly as a result of these tests.
It must be appereciated that the history remains the richest source of information concerning the patients illness and secondly the physician’s attentive and thoughtful taking of a history establishes a bond with the patient that may be valuable later in securing the patient’s compliance in following a complex treatment plan, undergoing hospitalization for an intensive diagnostic work up or a hazardous operation and in some instances, accepting that heart disease is not present at all. Taking a careful history also permits physician to evaluate the result of diagnostic tests and to evaluate the impact of the disease on the various aspects of patient’s life.
Dr Muhammad Asgher Shiekh
****************
Editorial board is obliged to Dr M Asgher Sheikh for reviewing most of the material published in this issue. At least we are sure that material is correct and at the same time in proper order of importance. He has made many valuable alterations and additions in almost all articles.
Chapter One
Dr Saleem Akhtar Rana
Common Symptoms
Dyspnoea
Discomfort or severe pain in chest
Palpitations
Oedema
Less common Symptoms
Low cardiac output can cause following general symptoms.
Fatigue
Weakness
Impotence
Congestion in GIT and Liver (or CNS origin of some of GIT Symptoms) can produce following well-known symptoms.
Anorexia
Nausea
Fullness of abdomen
Cardiac Cachexia
Weight loss
Impairment of absorbtion from intestine
(Protein loosing enteropathy especially in RHF)
Congestive hepatomegaly
Jaundice /Other symptoms and signs of hepatic insufficiency
Decreased cardiac output May affact CNS circulation and cause following symptoms as symptoms of cardiac origin.
Paroxysmal dizziness
Presyncopy/ Syncopy
Confusion
Difficulty in concentration
Impairment of memory
Headache
Insomnia
Anxiety/Depression
During day venous return from extremities is not as good as during night due to gravity. Improved venous return during lying down i.e at night improves cardiac output. Leading to discarding of accumulated fluid, at nighttime. This scenario produces decreased output during day and increases urine output during the night.
Nocturia may contribute to insomnia.
Decreased urine output during day
Rheumatic fever may produce following symptoms.
Fever
Arthralgia
Peripheral arterial disease and deep vein thrombosis may give rise to following conditions.
Intermittent claudication
Leg pains at rest
Unilateral oedema at ankles or legs.
Cardiovascular patients present usually due to
Myocardial Ischaemia
Disturbance of pumping ability:
Problems in Contraction / relaxation of myocardium (Myocarditis)
Obstruction to blood flow
Abnormal rythem
Myocardial Ischaemia usually presents with chest discomfort. There are numerous descriptions and forms of this chest discomfort. Diagnostic difficulty lies in isolating cardiac etiology from non-cardiac ones. Most of the time’s cardiac pain needs to be defined on the basis of history only. Ischaemic heart disease may present as chest discomfort, heart failure, tachyarrythmias and sudden cardiac death.
Reduction of pumping ability leads to weakness and fatigability. Two symptoms we are prone to miss as symptoms of heart. Severe reduction leads to cyanosis, hypotension, syncope and elevated intravascular pressure behind the failing heart. The later leads to abnormal fluid accumulation, which in turn leads to dyspnoea, orthopnoea and systemic or pulmonary oedema.
Obstruction to blood flow as in valvular stenosis can cause symptoms resembling those in congestive heart failure.
Cardiac arrythmias develop usually suddenly and may cause palpitation, dyspnoea, hypotension, presyncope and syncope. These may disappear as suddenly as the sudden onset.
Significant percentage of CVS patients is asymptomatic. So any physical finding such as heart murmur, elevated arterial pressure, or and ECG abnormality, or abnormal silhouette on XRC should be investigated fully.
The diagnosis of myocardial ischaemia for chest discomfort is not good enough. To form therapeutic strategies and to calculate the prognosis in such patients we need to know the underlying anatomical abnormality and reason of such abnormality. Is it coronary atherosclerosis or aortic stenosis? Then is there another pathology present which exaggerates this problem of ischaemia?
Diagnosis shall define following aspects.
The underlying etiology: Is it congenital or infection or hypertensive or ischaemic in origin?
The anatomical extent: Which chamber or vavlve is involved? Are walls hypertrophied or dilated or infarced? Which valve is stenotic or regurgitant?
The Physiologic Distrubance: What is the status of myocardial function? How is the rythem? What is the extent of ischaemia at a certain level of activity? Is there any other physiologic disturbance of other systems? The kind of problem which can disturb the rythem or balance between supply of oxygen and demand.
Assessment of functional disability: Place the patient in the class of disability defined by New York Heart Association.
Family History
We know many cardiovascular problems cluster in families. Transmission is yet not localized but polygenic transmission seems to be the final answer. Following diseases are well known to be familial.
Essential Hypertension
Coronary Atherosclerosis
These two major killers may occur not only on the basis of genetic transmission but also on the basis of behaviour patterens such as excessive intake of salt, calories and cigarette smoking.
Mendelian transmission on single gene basis is exhibited in following diseases.
Sudden Death associated with prolonged QT interval.
Hypertrophic cardiomyopathy
Marfan syndrome
Natural History
Alert physician can delay or even prevent major catastrophies like extensive myocardial infarction or sudden death. For this physicians should be aware of risk factors in the history and routine examination of their patients. If physician takes the family history and finds clustering of infarction or atherosclerosis, he can order investigations immediately to rule our or rule in all known risk factors. On the basis of these findings interventions can be disigned to delay or prevent these killer deseases. If a physician picks up a murmur or routine examination he can again start calculating the future of such patients.
Chapter Two
Dyspnoea
By
This may be defined as udue awareness of respiratory effort or of need to increase this effort.
This is purely subjective feeling. Description of patient is no guide to the severity of condition. Some patient complains of dysnoea when capacity to exercise is normal while others do not complain even when abnormal respiratory effort is visible to others.
To guage the severity of problem, rate and depth of respiration, movement of ribs, extra respiratory muscles effort should be observed without the knowledge of patient. If patient becomes aware of observation then this can change the actual effort.
Normal rate is 16-20 in adults. It is faster in children and slower in the olds.
Tachypnea means increased respiratory rate.
Hyperpnoea means rapid and abnormally deep respiration.
Hyperventilation: Excessive breathing with or without the sensation of dyspnoea.
Orthopnoea: Dyspnoea when lying down, at least partially relieved in sitting or standing position.
Paroxysmal Nocturnal Dyspnoea (PND): This refers to the severe respiratory difficulty during sleep and which awakens patien from sleep. Partial relief is obtained when patient sits up.
Increased work of Breathing
Airways Obstruction e.g Asthma
Stiff Lungs e.g Pulmonary Fibrosis
Stiff chest Wall e.g Scoliosis
Pleural Cavity
filled
with air or fluid e.g
Pneumothorax or Pleural Effusion.
Decreased Neuromuscular
Power
e.g
Musculodystrophies, paralysis.
Increased drive to breathing
Chemical drive e.g Hypoxia,Acidosis
Neurologic drive e.g Fever
Increased Metobolism e.g Fever thyrotoxicosis.
Various Aspects of Dyspnoea
Mechanisms Producing
dyspnoea Increased work of Breathing Airways obstruction,
asthma,COPD Stiff Lungs:Pulm Fibrosis Stiff chest wall:Scoliosis Pleural cavity filled :Air,Fluid Increased drive to breath Chemical as in hypoxia acidosis Neurological:Fever Increased Metabolism:Fever and thyrotoxicosis Decreased muscular power Muscular dystrophies. Paralysis Classification of Dyspnoea based
upon time of onset Dramatically sudden onset
withen minutes Pneumothorax Asthma Pulmonary Oedema Inhaled F.B Pschogenic Acute onset ,withen hours Allergic alveolitis Asthma LVF Pneumonia Subacute onset ,withen days Pulmonary Effusion Bronchogenic Carcinoma Sub acute pulmonary infiltrations Slow onset withen months &
years. CCF
Pulmonary Embolism
Pulmonary Effusion Recurrent Pneumothorax Diffuse Pulmonary fibrosis Emphysema,Ch Bronchitis = COPD Neoplasms
Non Cardio-pulmonary causes of
Dyspnoea Obesity Anaemia Ankylosing Spondylitis Thyrotoxicosis D/D of Asthma and LVF Dyspnoea in both can develop over few hours. In asthma previous history of asthma is of
great help In patients of > 40 yrs of age first such
attack is rare in asthmatics and more probable in LVF In Lvf there may be findings in auscultation
of heart ECG and XRC is usually positive in LVF Asthmatics feel relief after cough and
expectoration of sputum. In LVF just sitting up from lying may g
ive relief.
Causes of Paroxysmal Nocturnal
Dyspnoea (PND) Mitral Stenosis Nocturnal attacks of asthma Sudden onset of Dyspnoea with
Chest Pain Acute Pulmonary Embolism Spontaneous Pneumothorax Inhalation of FB Acute Myocardial Infarction Dissecting Aneurysm Acute Pancreatitis Perforation of peptic ulcer. Dyspnoea with Haemoptysis Acute respiratory infections Bronchiectasis Lung Cancer Pulm TB M/S with LVh FB in respiratory airways. Dyspnoea with pleuritic Chest
pain Pneumonia Pulmonary Infarction Rib fracture Intermittent episodes of
Breathlessness Asthma Left ventricular Failure Psychosomatic Differentiation between cardiac
and Pulmonary Dyspnoea. In addition to history and examination
following investigations help. Measurement of respiratory function by
spirometery Echcardiography measuring ejection fraction at
rest and during exercise ETT ECG Arterial Gases
Xray Chest Dyspnoea in Acute Pulmonary Oedema. Breathlessness and agitation Skin is pale,drenched with sweat Sputume may be frothy, profuse and blood
tinged. Pulse is rapid if there is no heart block. Chest shows bubling rales and ronchi Gallop rythem may be present.
Dyspnoea of Gradual Onset (Over days to months)
This has entirely different list of differential diagnosis.
Pleural Effusion: Dyspnoea is accompanied by clearly defined following sings of pleural effusion.
An area in the chest where breath sounds and vocal fremitus is decreased or absent.
This area has stony dullness on percussion.
Small area above the area described above has increased breath sounds.
X-ray chest clinches the diagnosis.
Neoplasms Both primary and secondary infiltrations may cause dyspnoea, effusions, or collapse due to bronchial occlusion.
Diffuse Pulmonary Fibrosis: This causes dysnoea over months and years. This is most difficult to diagnose as clinical signs and symptoms are very mild for years on. Cyanosis and clubbing of fingers is present in general examination. Examination of chest may reveal restricted movements. Coarse rales are often present.
Congestive Heart Failure: Dyspnoea here progresses over monhts. It is always relateld with exertion. This is usually the earliest symptom in the coarse of development. JVP is raised. Cardiac murmurs may be present. X-ray Chest may clinch the diagnosis.
Chest pain in pulmonary embolism is usually crushing in nature. Examination reveals hypotension, cyanosis and a gallop rythem. Haemoptesis and tachycardia may be present. Initially there may not be any sign present in the chest. But later signs such as crepitations over the involved area, pleural friction rub, signs of effusion, start appearing as the cardiorespiratory compromise proceeds. Raised JVP and symptoms and signs of cardiac failure may develop later. Typical opacity appears in Xray chest.
Here patients have predisposing factors. Physician shall be on toes to pick up this condition whenever severe and sudden dyspnoea is associated with relevant symptoms like sudden & severe pain. Following factors are predisposing factors for pulmonary embolism.
Prolonged immobilization
Recent Trauma,
Surgery,
Contraceptive use
Recurrent Pulmonary Embolism: This may present most difficult diagnosis. Precipitating factors like DVT, Recent Embolism, use of conteraceptives etc should always sensitize the clinician. Pulmonary hypertension can develop from thrombo-embolism. In all unexplained cases this diagnosis is always on the cards. It can be arrested by use anticoagulants. Examination may reveal left parasternal border heave & second sound in pulmonary area. X ray chest may pick up areas of infarction if these is big enough. Right ventricular hypertrophy and strain may be picked up on ECG.Lung scan clinices the diagnosis where other investigations fail.
Chronic Brochitis: All features of chronic bronchitis like history of smoking wheezing chest, productive cough, periodicity in severity, Xray chest and negative cardiac investigations shall make the diagnosis easily.
Emphysema: Barrel shaped chest, non-responsive dyspnoea, typical xray chest is there to help ascribe dyspnoea to emphysema.
Congestive heart failure.
First compaint is usually of paroxysmal nocturnal dyspnoea. Then breathlessness on exertion appears. It may take days to months before patient seeks help for this partcicular symptom. Then orthopnoea becomes the next phase of severity. Dyspnoea even at rest is very close to the severity level of pulmonary oedema.
Pneumothorax.
There may be a history of sharp sudden chest pain felt on the affacted side. If pneumothorax is large enough to cause dyspnea then signs of mediastinal shift will be present.
Dyspnoea and Foreign Body inhalation.
History should not be negative unless patient is unable to speak or report. X ray chest shows inhaled foreign body.
Dyspnoea and Pneumonia Fever, chills, typical pleuritic chest pain, Cough with purulent sputum usually gives a straightforward diagnosis. Dyspnoea in-patients with chronic bronchitis may be quite severe. Signs of consolidation may be there.
Sudden Dyspnoea in Children: Usually it is due to inhalation of FB.Stridor may be present. Signs of lobar collapse may be present. XR chest is essential.
Psychogenic Dyspnoea: This is panic disorder of anxiety. Patient is breathing with fast rate. Breathing is usually shallow. Lot of anxiety is visible. Complaint of suffocation is there usually. Hyperventilation may lead to loss of CO2 causing tetany. If patient is coaxed to breath deeply on some excuse, such as for examination or made to breathe in a bag, capacity to breathe normally is intact. Chest has no signs. Total description does not fit into pattern of any organic disease. Dyspnoea is usually after exertion rather than during exertion.
Asthma
Chronic Bronchitits
Emphysema
Major airway obstruction e.g tumor
Persistent Cough, Purulent Sputum, Fever and Clubbing of Fingers.
Bronchiectasis
Chronic Bronchitis
Bronchogenic Carcinoma
Lung abcess
Pulmonary Koch’s
Pulmonary Fibrosis
Common Causes of Cyanosis
Severe pneumonia
Acute Asthma
LVF
Pulm Embolism
COPD
Pulmonary Fibrosis
Right to left cardiac shunt
LVF
Mitral Stenosis
Obstructive Lung disease
Rapidity of onset
Decide Duration of dyspnoea
Assess the severity
Any relation with postural changes
Any factors which aggreviate the problem or relieve this.
Response to bronchodilators or ace inhibitors or diuretics.
Any association with
Exertion
Sweating and cold and clamy skin
Chest pain: its site and characteristics.
Fever,cough,wheezing,sputum
Sneezing and skin allergies
Attacks of fits following numness around mouth
Past History:Any periodicity
Personal History: Smoking, work in cotton or mining or related industeries, keeps any pets.
Severe pneumothorax occuring abruptly is very suggestive of pneumothorax, pulmonary embolism, inhaled foreign body, or acute pulmonary oedema.
Chapter Three three
Oedema
Dr Saleem Akhtar Rana
Oedema is usually a late manifestation of CCF.It is never present independent of other symptoms of CCF.When the oedema is very great, it may affact the whole of the lower limbs, the genitalia, the abdominal and chest walls an even the face.ANASARCA.Ascites is later than gerneralized oedema whenever it is part of anasarca. Ascites can precede generalized oedema if right-sided faliure is present like in triscuspid valve disease or constrictive pericarditis. Pleural effusion is a frequent finding in CCF.It occurs relatively earlier than ascites. It can be sometimes the sole positive finding as far as fluid collection of CCF is concerned.
A thorough history should define oedema on following lines
Site:
Bilateral or unilateral
Generalised, Only ankles, Ankle and face, or in the sacral region if patient is confined to bed.
Change of site with change of posture,
Changes in the morning and in evening.
Duration.
Is it first timed in life or it has periodic history.
Accompanying symptoms:
Like colour of skin overlying the edematous tissues, pururitis or ulcer formation, and pain in oedematous tissues, blue coloring of nails, lips. Duration of blue coloration should be noted as since birth or few years after birth or later in life.
Other systemic symptoms like breathlessness, cough, fever etc.
Response to treatment.
Does it disappear with diuretic drugs? Patient can usually fill in on this aspect of previously used drugs. Does it change with posture?
. Examination should define
Pitting or non-pitting.
Any engorged vein on the same side. If so conduct a detailed examination for patency and integrity of veins.
Any change of colour of skin
Along with oedema are there any ulcers?
General examination, Chest, CVS & Abdomen should define corroborative positive findings.
Vasculitis accompanied by oedema
Common causes of bilateral oedema
CCF
CRF
Hepatic insufficiency
Nutritional deficiency.
Autoimmune mechanisms. It is actually vasculitis around ankles.
Local venous stasis
In all above-mentioned conditions except the last one it is always bilateral. Although in the very beginning it may be unilateral if there is some other local problem exists on this side, augmenting the causes somewhere else. Dirunal variation occurs in-patients who are well enough to walk around. It is more around the eyes in the morning and gathers around ankles by the evening. Patients in whom disease is advanced it may be present in all parts of body. In-patients who are bedridden oedema collects first in the sacral area.
Cardiac oedema is always pitting & bilateral oedema.
CVS is designed to maintain effective perfusion of all organs according to their variable needs. This is mainly accomplished by maintaining cardiac output and local changes. Autonomic nervous system and hormones act in harmony towards this end. In failing heart these mechanisms try to adjust to changed hemodynamics. But after a certain borderline and after certain duration these mechanisms overshoot the compensatory role and become maladaptive. Maladaption not only contributes significanty to production of symptoms and signs but this also becomes a cuase to perpetuate the pathology.
In the formation of Oedema mainly two main pathways are involved.
Increased venous pressure.
Salt and water retention
Oedema is preceded by a gain in body weight of 3-5 kgs due to an increase in extracellular fluid. The oedema of cardiac origin is determined by the local factors like gravity.
Increased venous pressure: It is nearly always a factor in cardiac oedema but rarely the sole explanation. As retention of salt and water always antedates appearance of oedema. Hydrostatic pressure at arterial end of capillary is 30 mms of Hg.Colloidal pressure at this point is 25 mms of Hg.So this difference in both pressures is enough to force fluid outside the capillaries. At venous end of capillary the hydrostatic pressure falls greatly and it is only 12 mms of Hg.So here 25 mms of Hg of colloidal pressure is large enough to pull back the extracellular fluid in the capillaries. In CCF hydrostatic pressure at venous end is 25 mmgs, equal to that of colloids. Extracellular fluid is not reabsorbed effeiciently.
Salt and Water Retention: This is the result of multiple neuroendocrinal maladaptions. Renin angiotension-Aldosterone axis, secretion of ADH by Pitutary, Diminished sensitivity to atrial natriuretic peptide (ANP), and raised levels of many other natriuretic susbstances such as Endothelin-1, TumourNecrosis Factor are these players. Cumulative effect of these maladaptions is retention of salt and water. This increases the afterload so further complicating the heart failure. Players in the Vicious Circle.
Investigations
Rarely oedema is the only complaint. Usually there is a constellation of other symptoms like nocturnal dyspnoea, breathlessness, weakness, cough, or palpitation. History should point towards the possible causes. Heart, kidney liver and respiratory system shall be first investigated.
Urine: If there is no proteinuria one should feel quite assured that cause is not in kidneys. In CCF sometimes few RBCs are present. This is due to venous congestion of kidneys.
X-Ray Chest: This is one basic investigation in all cases of oedema. A rough guide to transverse diameter of heart can be judged. It should be less than 55 % of transverse diameter of ribcage at its largest point. Another guide is distribution of trasverse diameter of heart on both sides of midline. One third should be on right side and rest of the two third should be on left side under normal conditions. Upward divertion of vascular markings is first sign of increased venous pressure; later on it may progress to fluid in alveoli and may develop to pleural effusion.
ECG: When size of heart is normal on X-ray chest, it should not be sufficient to rule out heart, as cause of Oedema.There may be infarction of recent or late origin. This may compromise the heart function without producing any change in size on Xray. ECG should be able to decide or at least raise doubts on this account.
Echocadiography: This has become almost as routine an investigation as X-ray chest and ECG used to be few years ago. It is available easily. In Gujranwala it is available at two places. Echography should tell us size of all chambers, function of all valves, ejection fraction as an accurate index of systolic function. It can map the contraction of different walls of all chambers and with the help of echodoppler we can assess the diastolic function of heart. All these investigations should be competent enough to label heart as responsible for oedema or to exclude it as cause of oedema.
Difficulty arises when multiple etiologies are present. Cirrhosis of liver, CCF, Cor pulmonale and CRF are frequent partners of each other. Hypoproteinuria and salt + water accumaltion become very significant when cirrhosis of liver is present. In such cases it is almost impossible to judge accurately share of each pathology in causation of oedema. Estimation of liver and kidneys is quite in order if pyuria and casts in microscopic examination accompany proteinuria or there is billirubin or urobilinogen present in urine.
Anaemia shall always be kept in mind as possible cause of cardiomegaly. In CRF anaemia contributes significantly in the multiple abnormalities.
Drugs which may cause Generalized Oedema
Direct
Arterial/Arteriolar vasodilators
Minoxidil
Hydralazine
Clonidine
Guanethidine
Calcium Channel Blockers
Alpha adrenergic antagonists
Glucocorticoids
Anabolic steroids
Estrogen
Progesteron
Interleukin 2
OKT 3 monoclonal antibody
Cyclosporine
Growth Hormone
History, Examinatin, and laboratory findings
Of different types of Generalized Oedema
|
Organ System |
History |
Examinaion |
Lab findings
|
|
Cardiac |
Dyspnoea with exertion Orthopnea PND |
Elevated JVP Venticular gallop Cool extremities Cyanosis Small pulse pressure |
Elevated Urea nitrogen to creatinine ratio Elevated Uric acid Low Serum Sodium Liver enzymes may be elevated if liver is congested |
|
Hepatic |
Dyspnoea is not prominent finding until massive ascites is there.
|
Ascites is prominent JVP normal or low BP is low than in cardiac or renal causes. Signs of Liver failure |
Elevated or disturbed liver enzymes. Low serum albumin Hypokalaemia Respiratory Alkalosis Macrocytosis |
|
Renal |
Symptoms of CRF Dyspnoea not prominent untill heart failure and anaemia is there. |
Usually raised BP Uremic fetor Retinopathy Pericardial friction rub |
Albuminurea Hypoalbuminurea Anaemia Elevated Urea/Creatinine Hyperkalaemia Metabolic acidosis Hyperphosphatemia Hypocalcimia.
|
Diagnosis of Ischaemic Chest Pain
Whenever diagnosis of IHD is made it is mandatory to place patient in one of the following categories.
Unstable angina
Acute myocardial infarction
Diagnosis of Unstable angina means full assessment with ETT, Scan and angiography
Doctor shall not judge on affordability
In all doubtfull cases of IHD use follows tests more frequently. These are easily available
ETT
Cardiac Enzymes
Thallium scans
Angiography
Advantages of modern science shall reach patient. Doctor must propose an option. It is patient’s job to accept or not. Doctor shall not be a judge on affordability.
A life is at stake. Poorer is the patient; more preciouses are the life.
Different aspects of history of chest pain
Duration: Corelate duration with results of investigations. Longer is the duration; more probable is the positive result.
Site: Retrosternal left precordial area and epigastric sites are common for ischaemic pain.
Radiation: To neck, lower jaw, left shoulder, left arm and epigastrium is frequent sites.
Stable Angina: Should never be diagnosed if it not related with exertion.
Differential Diagnosis with APD, especially oesophagitis, can be ruled out on the basis of immediate response to antacids (1/2 Bottle) and withen day’s relief with PPIs.
Strong Family History
Smoking
Diabetes
Shall prompt a quick response even with doubtfull hitory and following investigations shall be ordered immediately
Lipid Profile
ETT
HbA1C to estimate the adequacy of diabetic therapy
ECG is no better enough to rule out IHD
All patients with strong family history shall have a baseline ECG at the age of 40.
Dr Arshad Javaid Sh
History plays major role in the diagnosis. Clinician can make an educated guess how to move further for signs and investigations. He can decide, only on the basis of history, how far he is going to rule out IHD.Chest pain may have its origin in the heart, lungs, mediastinum, ribcage and its appandages. This may be a reffered pain from neck, shoulders or upper abdominal viscera. History with detailed description of pain and associated symptoms should provide basis for diagnosis in most of the patients. Following characteristics can help to distinguish cardiac pain from other pains.
Location: Typical cardiac pain is centrally located in the chest. Pain only felt in the periphery of chest is rarely cardiac in origin.
Radiation: Cardiac pain especially when severe may radiate to the epigastrium, neck, jaw, and upper or even lower arms. Pain situated over left chest and radiating laterally may have various they cause including pleural or lung pains, chest injury or anxiety.
Provocative Factors: Anginal pain is precipitated by exertion or after heavy meals and is relieved by resting. In unstable angina similar pain may be brought on by minimal exertion or may also occur at rest. Pain associated with specific movement like bending, stretching or turning is likely to be musculoskeletal in origin. Some patients feel retrosternal pain after taking meals. This is especially so if they exert after meal. It is postprandial angina, which is difficult to differentiate from APD.
Duration of Pain: This is one of the major criteria to classify different types of ischaemic pain and to differentiate ischaemic from non-ischaemic pain, as this presentation will elaborate with each type of pain.
Character of Pain: Typical cardiac pain is dull, constricting or feeling of weight or heavyness. Patient may present with with feeling of discomfort and constricting sensation leading to breathlessness. Patients often use characteristic hand movements and gestures like open hand or clenched fist. Pleural pain is sharp in character, and catching in quality and iterrupts breathing, coughing or movement. Pericardial pain also changes with the posture.
Pattern of Onset: Sudden pain, which develops withen seconds, is usually of aortic dissection, pulmonary embolism or pneumothorax. Myocardial Infarction usually takes several minutes or even longer to develop to the climax. Anginal pain develops gradually in proportion to the intensity of exertion.
Associated Features: Profused sweating, nausea and vomiting is usually associated with severe pain of AMI, Aortic disection, pulmonary embolism etc. Breathlessness is associated with pulmonary oedema of AMI or respiratory causes of chest pain. Severe cough is characteristic of tracheitis, pneumonia or pulmonary oedema. Gasterointestinal symptoms will be seen in non-cardiac chest pain or oesophageal reflux, acid peptic disease, or in biliary disease.
Symptomatic Features in Differential Diagnosis.
Angina can be stable or unstable.
Stable Angina: Atheroscelotic narrowing of one or more coronary arteries is the most common cause of angina. Patient experiences pain, during physical activity, when oxygen demand of myocardium is not fullfilled due to coronary arteries obstruction. Conditions that may enhance angina include anaemia, thyroid dysfunction and tachycardia. Increased demands of oxygen, other than exertion or non-cardiac causes, may contribute to angina. Aortic stenosis and hypertrophic cardiomegaly are important in this respect.
Pain is neither momnentary nor sharp. Patient uses different words for pain like tightness, pressure, constriction, heaviness or weight on chest. Indigestion or a sensation of breathlessness can also be the discription.
Duration of pain is usually between 2-10 minutes. It is rarely longer or shorter.
Severity of pain is moderate in intensity.
Location is usually retrosternal. It radiates very widely across the chest, to one or both arms, to neck, to the back of chest, to lower jaw or even to the epigastrium. Rarely these sites may be the only site affacted.
Onset of pain is usually precipitated by physical or emotional or both types of stresses. It is likely to occur after meals, exposure to cold wind or walking uphill or upstairs.
Sulblingual nitroglycerin usually relieves pain withen 3 minutes in majority of patients. Failure to do so means that either it is not angina or it is unstable angina or AMI.
Severity of pain has been graded by
Canadian Society of CVS in following categories.
Angina on sternous activity but not on ordinary activity.
Slight limitation of ordinary activity.
Marked limitation of ordinary activity
Inability to carry out any activity without discomfort or presence of pain even at rest.
It can be localised by a finger.
The duration is consistently less than 30 seconds.
Nature of pain is sticking, or stabbing or throbbing.
It occurs exclusively at rest.
This is defined as angina of recent onset or stable angina, which has increased, severity or frequency, or duration or which occurs at rest.
Here pain usually develops without any precipitating factor like exertion, i.e, at rest.
Such pain lasting for less than 30 minutes is usually unstable angina and if it lasts for more than 30 minutes than it is usually AMI.Serial ECGs and cardiac enzyme measurement is required to establish the diagnosis of AMI.
Pain is commonly quite severe and is typically crushing, pressing, burning and aching type.
Duration of pain is longer than half an hour and may be several hours.
Location is typically retrosternal but may be in precordium or in other locations. This commonly radiates to thorax, lower jaw, shoulder and arms. It is usually transmitted to left shoulder and around.
Symptoms of dyspnoea, profused cold sweating and indigestion usually accompany the pain.
Sometimes attack of AMI is painless but there will be non-specific gasterointestinal symptoms. Patient may appear cold, pale and cyanotic and in quite distress.
Pain of AMI does not respond to nitrates.
Pericarditic Pain
This pain is usually sharp and related to inspiration resembling pleuritic pain.
Lying flat, twisting or swallowing increase pain or coughing and deep inspirationIt is relieved by sitting upright or leaning forward.
Pain is usually central but may radiate into neck and back and left side of chest, shoulder or even the abdomen.
Pain persists for hours or days depending upon etiology.
Development of pericardial effusion usually lessens the severity.
This usually occurs in hypertensives of 40 –70 years of age.
Pain is very severe, unbearable having sharp tearing or ripping across quality. Pain is like that of AMI accompanied by profuse sweating and dyspnoea but with no ECG changes unless coronary ostium is involved. Large and frequent doses of morphine are required to relieve pain.
Location of pain co-relates with the site of intimal rupture.
When pain is above aortic valve pain is in ant chest
When rupture is distal to left of sub-clavian artery pain is reffered to back.
In abdominal Aortic Dissection pain is in epigastrium.
Non Cardiac Chest Pains
M/Skeletal structures of nech, shoulder and thorax are common sources of chest pain. Ant/Posterior chest pain or both may result from involvements of roots of cervical and upper thoracic spine by osteoartheritis, disc lesions or deformaties.
The pain usually occurs at night.
Fatigue incorrect posture, and movement of involved segments but not the movement of body as a whole precipitate pain.
Cough and sneezing increase the pain.
Pain may last for hours at time.
Rest, analgesics often provide relief, and local heat & postural exercises may help.
Here the pain originates from the swelling of costo-chondral or costo-sternal areas or both. The pain is usually well localized but may radiate across the chest and over to arms.
Tenderness on palpation over the involved articulations is the clue to diagnosis.
This can be with or without hiatus hernia. This can closely simulate anginal pain.
Pain is substernal and may radiate to left arm and lower jaw.
Overeating, alcohal intake, and highly seasoned foods increase pain, by bending forward and lying flat. Patient may regurgitate gastric contents.
The pain is usually relieved by assuming an upright position and by ingestion of antacids.
Pain is indistinguishable from that of myocardial ischaemia.
Glyceral nitrates may relieve pain.
Pain is most often felt retrosternally.
Difficulty in swallowing both liquid and solid Amy occurs.
Diagnosis can be made by radiographic studies with barium.
Here patient feels tightness as a result of anxiety. Pain is not relieved untill anxiety disappears. Sometimes development of chest pain leads to such anxiety those hyperventilation results. There is no constant relationship with exertion. Duration of pain is variable and it may last for seconds, hours or days. A statement that pain is coming from heart is almost a giveaway for the diagnosis of psychogenic pain.
Next Issues.
Editorial board is planning to bring out next issues on different aspects of cardiology.Following are the topics.
Non ivasive and invasive investigations
Paediatric Cardiology
Heart Failure / Cor Pulmonale
Atheroscelosis / Diseases of Aorta
Hypertension
Ishchaemic Heart Disease
Arrythmias
Valvular Heart Disease
Rheumatic Fever/Congenital heart disease in the adult
Cardiomyopathies/ Myocarditis
Pericardial Disease
Cardiac Emergencies
Peripheral Vascular Diseases.
Let us join hands together in writing these issues and in the process learning from each other and authorities.It is going to be a good experience.Give us a ring.
Chapter Five
Palpitations
Dr Ehsan Assad
MBBS, Post Graduate Course in medicine (Edinburgh)
Physician Ehsan Hospital Noshehra Road, Gujranwala.
Many many definitions are available. My definition is this. These can be simply defined as an unpleasant awareness of the forceful beating of the heart, caused by a change in heart’s rate/rythem/force of contractions or only a feeling at conscious level due to aleterations in autonomic feedback due to affactive disorders.
Patient uses different descriptive words to explain his conditions. These words are of diagnostic value. Following Words are used.
Jumping or Skipping of a beat or series of beats = Extracystoles (premature ventricular contractions)
Abrupt onset and abrupt stopping of racing = Paroxysmal tachycardias.
Fluttering = Atrial flutter or fibrilation (here patient may say that his heart beat is quite chaotic)
Racing = All conditions where rate is high but regular
Ponding = Usually increased heart rate and high output conditions.
Occasionally you may feel light-headedness or short of breath or tightness in the chest when you have palpitations. But usually there is no othe symptom.
The feeling is normal when there is real increase in rate/rythem or force of contrations. Examples are exercise, Pregnancy, sudden emotional outburst etc. Some individuals wake up from sleep with palpitations, especially when they are lying on left side.
Emotional status as in anxiety/panic disorder, depression and other affactive disorders. Here rate/rythem and force of contractions is normal or only a sinus tachycardia (with all other normal cardiac parameters). Patient just becomes awares of heartbeat.
Organic diseases outside the heart increasing heart rate/rythem and force of contrations. Following are the examples.
Anaemia
Anxiety
Thyroid disease
Hypoglycaemia
Pheochromocytoma
Fevers.
Overuse of stimulants e.g coffee, tea soda, nicotine, decongestants, medicines for flu & common cold, antidepressants, Thyroxine, vasodilators, antiasthmatics like ventolin, bricanil, aminophylline etc.
Cardiac diseases giving rise to irregular or abnormal heart rate.
Decide which type of following two main groups of palpitations is the problem.
Palpitations not associated with cardiac conditions
Palpitations associated with cardiac conditions. These may further be classified as those associated with arrythmias or those not associated with arrythmias.
Cardiac conditions, which can present as palpitation, are followings.
Mitral valve prolapse: Usually anxious young female are patients. Echography picks up the abnormality. No intervention is usually advised if cardiac function is not compromised. This is usually not compromised.
In following condition examination of CVS and history leave no doubt that patient should have further investigations like echocardiography, X-ray chest, ECG etc. These usually label the patient appropriately.
Aortic Regurgitations (AR):
Aortic Stenosis (AS): .
PDA:
VSD
ASD
Marked cardiomegaly
Acute LVF
Tricuspid insufficiency
Pericarditis
Prosthetic valves
Pacemakers
Tachyarrythmias
At flutter and fibrilation
Ventricular tachycardia
Bradycardia
Most common cardiac cause of palpitations is cardiac arrythmias including premature ventricular contractions; paroxysmal and non-paroxysmal tachycardias and marked bradycardias are the most common causes of palpitations.
Approach towards patient of Palpitations.
Pulse Heart sounds & Co ordination with History
Shall point towards or
rule out General Examination shall
pick up Fever Goitere Anaemia Normal pulse
Normal Heart Sounds during an
episode of Palpitation should point towards Anxiety States or menopause Increased pulse rate during sleep (to be counted
by another person) should suggest. If suspicion of cardiac origin of palpitation is
still their then order ECG & X-Ray Chest, & Echocardiography
Examination of
Premature ventricular contractions (Ectopics) Sinus Tachycardia Atrial Flutter Atrial Fibrilation Aortic Regurgitations (AR) Aortic Stenosis (AS) PDA VSD ASD Marked cardiomegaly Acute LVF Tricuspid insufficiency Pericarditis Prosthetic valves Pacemakers Tachyarrythmias At flutter and fibrilation Ventricular tachycardia Bradycardia
Thyroid
function tests
Holter’s Monitering remains the last
resort to diagnose hidden pathologies of cardiac origin
Chapter Six
Cough, Haemoptysis
Cyanosis, Syncope
Pulmonary Oedema
Dr Saleem Akhtar Rana
Cough
Congestive heart failure may be associated with cough. It may be due to interstitial and peribronchial oedema. All coughs associated with dyspnoea should be investigated keeping in mind diagnosis of asthma and congestive heart failure. Character of sputum is almost same in both. Prominence of hilar shadows, especially in children, is typical batwing pattern in congestion due to heart failure. Murmurs in children/adults shall direct towards valvular heart disease. Many patients are on ATT while fever; X-ray picture and blood tinges sputum is due to congestive heart failure.
A non-productive cough may be associated with the use of ACE Inhibitors in 5-20 % of users. Onset is usually withen one week of using the drug but can be delayed upto 6 months. Mechanism may be due to accumulation of bradykinin or substance P, both of which are degraded by this ACE.
Cough due to ACE inhibitors never goes away. There is no adaptation. Many patients keep on having these agents on their prescriptions only because they are changing their physicians rapidly. No single physician has enough time to ascribe cough due to these.
Haemoptysis
Coughing out blood is not uncommon in-patients of heart disease. Several mechanisms are involved. Examination of sputum may tell which mechanism is involved. Usually three types of haemoptysis.
Frank haemoptysis, coughing up pure blood is seen in mitral stenosis. It is due to rupture of bronchial or pulmonary veins and may also be due to pulmonary infarction.
In infections like pneumonia sputum is rusty and purulent.
In pulmonary oedema pink, frothy, blood tinged sputum may be seen.
Beware that patients with heart disease may have other pathologies such as tuberculosis, or bronchiectasis or bronchial neoplasia.
Syncope
Definition: It is a transient loss of consciousness during standing posture, rarely during sitting and never when patient is lying or walking. The onset is annouced by sense of weakness, yawning or sighing, sweating and and feeling of nausea and sinking of heart. Before patient can actually comprehend these feelings he falls down and looses his consciousness. This loss of consciousness is only for few seconds or a minute or two. In severe attack, face is pale, pupils are dilated, respiration is slow and heart rate is diminished to the extent that sometimes-radial pulse can not be felt although carotid pulsation is felt.
Mechanism: This is due to inadequate blood supply to brain. Cerebral blood supply depends upon
Cardiac output
Arterial blood pressure
Resistance of cerebral circulation.
Cerebral arteries are not much affacted by autonomic system but these are dilated by carbon dioxide. Cardiac output is decreased by many ways. In emotional etiology main reasone is pooling of blood in arteries of muscles due to autonomic disturbances. In cardiac etiogies obviously cardiac output is decreased due to multiple aspects of cardiac function.
Types:
Emotional situations: Commonest cause is often a response to painful emotions. Simple faint is due to vaso-motor or vasodepressor reflexes. In addition to emotions blood loss, debility after infections and intense pain may contribute to this reflex loss of consciousness.
Syncope in Arrythmias: If heart is too fast (>180/m) there is not enough time for ventricular filling. So cardiac output comes out. With it cerebral blood supply is compromised. If it happens suddenly then patient drops unconscious.
Adams-Stokes Attacks: Brief episode of cardiac arrest leads to sudden decrease in cardiac output. Examples are asystole or ventricular fibrilation. This happens most often in-patients with heart block. Frequently arrythmias are superimposed on heart block. After loosing consciousness cardiac output is restored usually withen 10-15 seconds. If attacks last longer than consciousness is accompanied by flushing as blood starts flowing in dilated blood vessels. Dilatation is due to hypoxia during attack.
Syncope of Exertion: This is most common in Aortic Stenosis as heart is unable to maintain sufficient cardiac output in face of increased demads of exercise. These patients of Aortic Stenosis are also prone to get heart blocks and arrythmias.
Carotic Sinus Syncope: This occurs in old persons when light pressure on carotid sinus reduces heart rate to the extent that cardiac output is compromised.
Postural Syncope: When a normal individual stands up, pooling of blood in the legs is prevented by arteriolar and venous constriction in addition to increased heart rate. Persons in whom autonomic system is disturbed as in Diabetes Mellitus these mechanisms of adjustment of cardiac output are not available so pooling occurs in leg muscles and syncope occurs. This is so in some o/w normal old persons. Some antihypertensives which affact autonomic system also produce postural syncope.
Micturation Syncope: In some adult patients with nocturia conscious is lost immediately after emptying U-Bladder.This is more common after excessive alcohal consumption. This is usually due to reflex action after release of bladder pressure.
8-10. Massive Pulmonary Embolism, AMI and mitral valve obstruction as in atrial myxoma.
Cyanosis
Cyanosis is more a sign rather than a symptom. It is often noticed by onlookers rather the patient when he is exposed to exercise or cold wind. This discoloration is due to reduced haemoglobin in superficial capillaries and venules. Amount has to exceed 5 gms/dl. So in severe anaemia Hb may not be in sufficient amount to cause cyanosis although all other requirements are there.
Central Cyanois is defined when etiology lies in the central organs i.e heart and/or lungs. Arterial blood can not be properly oxidated. Rarely it may be due to use of certain drugs.
Peripheral Cyanosis is said to be present when peripheral tissues extract unusually large amouts of oxygen. This happens when insufficient blood flow is present in these tissues ethier due to low output or due to cold.
Differentiation between these two types is usually not difficult. In peripheral cyanosis skin is cold and cyanoses while warm mucous membranes as of tongue are normal. Peripheral cyanosis can be abolished when cyanosed areas are warmed. In central cyanosis arterial blood is not properly oxigenated and PO2 is less than 85 %.
Pulmonary Oedema
Increase in pulmonary venous pressure leading to egogrgement of pulmonary vasculature is the basis of dyspnoea in-patients of congestive heart failure. This results into
Decreased lung compliance
Increased resistance of small airways.
Increased lymphatic circulation.
Mild Tachypnea
Net gain of fluid in extravascular space i.e-interstitial oedema.
When above mentioned problems become more severe, pulmonary venous pressure rises further, capicity of lymphatic circulation is overwhelmed and if continued for longer and longer duration following course of events leads to full blown clinical situation known as pulmonary oedema.
Tachypnea increases
Gas exchange deteriotes further
Kerley B lines on X ray
Loss of distinct vascular margins
Capillary endothelium intercellular junctions widen
Allow passage of macromolecules in the interstitial spaces
Further elevation in intravascular pressure disrupts the tight junctions between alveolar lining cells, alveolar oedema results.
Alveolar spaces contain fluid, which contains RBCs & maromolecules (Proteins).
Further deterioation in cardiac function alveolar – capillary membrane further disrupts and alveolar space and airways are flooded with this fluid.
Clinical Picture of full blown Pulmonary Oedema
Patient is anxious, perspires freely, respiratory effort is visible to onlookers. Bilateral wet rales and ronchi are present on examination. Chest radiograph shows bilateral lung hazzyness with more density in hilar regions.
Further Progress of Patient: Gas exchange is more severely compromises with worsening hypoxia. Without effective intervention progressive acidemia, hypercapnia, and respriatory arrest occurs. Management must be on emergency basis. Oxygen shall be given immediately for immediate relief and drug treatment should be targeted to reduce pulmonary venous pressure.
Other types of pulmonary oedema.
Increased venous pulmonary pressure is not the only etiology known. There are many condition where fluid collects in alveolar spaces. Following brief description is given just to complete the list of etiologies of Pulmonary Oedema.
Classification of Pulmonary Oedem Based upon Mechanisms involved. Imbalance of Starling Forces Altered alveolar-capillary membrance
permeability Lymphatic Insufficiency Unknown or incomlpletely understood mechanism. Imbalance of starling forces A- Increased pulmonary pressure Increased pressure without left ventricular
failure,e.g Mitral stenosis Secondary to LVF Secondary to increased pulmonary arterial
pressure B- Decreased Plasma Oncotic Pressure Hypoalbuminaemia C- Increased negativity of
interstitial pressure likes rapied removal of pneumothorax
with applied negative pressure. Altered alveolar-capillary membrance
permeability Infectitous Pneumonia Inhaled toxins. Circulation toxins like venom or entotoxins. Aspiration of acid gastric contents Acute radiation pneumonitis DIC Hypersensitivity Pneumonitis Shock
Chapter Seven
Physical Examinatin
Of
Cardiovascular System
Dr Parvez Anwar Chaudhary
MBBS, DTCD,
Saeed Hospital, Commissioner Road, Gujranwala
Hosp No: Tel no 250013,250015, Mobile 0300 8641115
A thorough examination is certainly much better in furnishing the information than all investigations combined. Art of picking up physical signs can make the difference between good physician and not so good a physician. Physical examination is an important determinant in making a diagnosis in following diseases. Echography can easily confirm the diagnosis.
Mitral valve prolapse
Congestive heart failure
Cardiac tamponade
Hypertension
Mitral stenosis
Chronic mitral regurgitation
Chronic aortic regurgitation
Tricuspid regurgitation
Aortic Stenosis
Acute pulmonary hypertension
Chronic pulmonary hypertension
High-output states
Atrial septal defect
Anginal syndrome
General Examination:
Following points must be looked in GPE.
Anaemia
Cyanosis
Clubbing of fingers
Splinter haemmorrages under nails,
Osler’s nodes
Xanthelasma and tendon xanthomat
In Eyes fundoscopy is essential in all CVS patients.
Examination of abdomen: Slenomegaly, hepatomegaly and ascites must be ruled out.
It consists of meticulous examination of arterial & venous pulses, blood pressure
Recording, palpation of precordeum, attentive auscultation and auscultation of chest.
The following characteristics of arterial pulses should be taken note of.
Rate
Rythem
Amplitude
Character of wave form
These pulses are detected by gently pressing the vessel wall against some solid structure usually bone. Following are main sites and pulses, which are examined. Please note this aspect of examination is not complete till both sides are examined and compared.
Radial Against the head of radius.
Brachial Against humerus in antecubital fossa.
Carotid Against the transverse processes of cervical vertebrae.
Femoral Midway between the iliac crest and pubic ramus
Popliteal Difficult to palpate. Feel in popliteal fossa.
Post tibial 1 cm behind the medial malleolus of tibia
Dorsal Pedis against the tarsal bone.
Normal rate is 60-90 beats /minute.
Bradycardia: Less than 60/m. Following are the common causes.
Sinus bradycardia
Junctional rythem or heart block
Drugs like beta blockers or digitalis
Increased vagal tone.
Increased intracranial pressure.
Myxedema
Hypothermia
Trained athletes.
Tachycardia: more than 90/m. Followings are the common causes.
Emotion
Exercise
Thyrotoxicosis
Fever
Tension
Anxiety
Decide whether regular or irregular
The pulse of atrial fibrilation is completely irregular.
An occasional irregular beat in O/W regular rythem is due to ectopic beat.
It depends upon pulse pressure i.e difference between systolic and diastolic pressures.
Small volume: It is seen in
Low stroke volume
Peripheral vasoconstriction
Shock Syndrome
Mitral stenosis
Pericardial Constriction
Pericardial temponade
Anacrotic Pusle is seen in aortic stenosis. It is small in volume but duration is prolonged and has slow upstroke. Upstoke is the feeling your fingers convey to you about the amplitude of pulse waveform. In simple words force of pulse.
Collapsing or water hammer Pulse is slow volume but it has rapid upstoke and rapid desent. It is seen in PDA, Large AV communication and Aortic Regurgitation (AR).
Pulses Bisferiens is a pulse of moderate or large volume in which double beat can be felt. It is a sign of combination of aortic stenosis and aortic regurgitation but not diagnostic.
Large Volume: associated with large stroke volume.
Aortic Regurgitation
Anaemia
Pregnancy
Thyrotoxicosis
Pulsus Paradoxus is an accentuation of physiological fall in peak arterial pressure of 5-10 mms during inspiration. This is seen in
Pericardial Effusion
Asthma
COPD
Obstructive lung disease.
Pulsus Alternans shows regularly spaced beats of alternate large and small volumes. For example in LVF.