OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

OUTLINE Common Cardiac Symptomatology B. Dyspnea A. C. Palpitations 1. Attributes of Pain D. Edema 2. Definitions E. 3. Chronic Recurrent Chest Pain Syndrome F. Syncope 4. Acute Chest Pain Syndrome II. Importance of History and PE 5. Case Discussion The lecture is similar from block B’s Lecture but we changed the formatting though kasing ang gulo nung topic.  So if mas naguluhan kayo sorry. Some changes: 1. All the symptomatology are now under common cardiac symptomatology. 2. Differentials for chest pain have been divided into chronic and acute.

I. COMMON CARDIAC SYMPTOMATOLOGY

 Symptoms: complaints of the patient (most common complaint: pain); Includes chest pain, dyspnea, palpitations, edema, cyanosis, syncope

 Signs: doctors’ objective findings and observations

A. CHEST PAIN

 Chest pain: most common but not exhaustive - can be caused by other factors such as hypertension

ATTRIBUTES OF PAIN (PPQRSTO)

 Provocative – what provokes/triggers the pain

o Is it precipitated by effort (exertional)?

o At what time does it appear? When you are trying to get up, moving the body, etc…

 Palliative – what relieves/palliates the pain

o Medications, therapy, etc…

 Quality – the nature of the pain

o Sharp, burning, pricking, stabbing, strangulating, oppressing, ache similar to muscle ache, etc.

 Region/Radiation – location (primary region where the pain is felt), central region, how wide the coverage is and where the pain radiates or is worst

o Central precordial pain  where does it radiate? Back? Leg?

o Hard to interview Filipinos – “doon, diyan” – vague descriptions of location

 Severity – intensity: mild, moderate, severe

o May use a scale from 0 to 10 (worst)

o Give open-ended questions

 Timing

o Onset – abrupt, worse at start, insidious, builds up/gradual Ian, Aca, Hannah UPCM 2016A: XVI, Walang 1 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

o Duration – how long does it last: few seconds, minutes, hours

o Frequency – once every month, once every 2 years, etc.; avoid using phrases such as rarely, sometimes

 Other associated symptoms – important to be able to identify the etiology

o Nausea and vomiting, cold sweats, palpitations, co-morbidities and other risk factors, etc.

o Always observe while you are examining (these might give you clues on the symptoms of the patient)

DEFINITIONS

From 2015 Block B:

 Spontaneous: comes and goes, not related to effort

 Rest: pain gradually subsides when the effort is eliminated

 Nitrates: coronary vasodilators; this as a palliative factor is characteristic of myocardial ischemia.

o Fastest acting- sublingual nitrates

 Diffuse: not more than one fingerbreadth

 Time: anything exceeding 20 minutes is associated with myocardial infarction

 Severe: acute coronary syndrome

CHRONIC RECURRENT CHEST PAIN SYNDROME DDX 1. CARDIAC ETIOLOGY: Classic AnginaA

 Fixed arterial stenosis causing symptoms, usually while exerting self

o Quality of chest pain of aortic stenosis is the same as that of angina

o Imbalance in myocardial oxygen demand outstripping the supply

▪ In anemics, the same amount of oxygen will be distributed to the tissues as normal if there is increase in Cardiac Output or if there is increase in Oxygen Extraction Rate in the tissues.

o American Heart Association (AHA): "a medical term for chest pain or discomfort due to coronary heart disease."

o Chronic angina- myocardial ischemia

o Nocturnal angina- provoked during sleep

o 2014: chest pain due to temporary myocardial ischemia, usually secondary to coronary atherosclerosis

o 2014 trans: Less than 15-20 minutes unstable coronary syndrome, if greater than 30 minutes, acute

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2. CARDIAC ETIOLOGY: Atypical Angina/Angina PectorisA

 the chest discomfort of myocardial ischemia is a visceral discomfort that is usually described as a heaviness, pressure, or squeezing (Harrison’s 17th Edition page 87).

o While at rest or while having atypical workload

Table 1. Differentiating the quality of angina

TYPICAL ATYPICAL DIABETICS FEATURES FEATURES

Heaviness Burning May have (vague ache in Stabbing paresthesia/ the chest) Pin Pricking change in Squeezing sensorium, will Constricting describe things Strangling differently builds up over time

A Coronary Artery Diseases (CAD)

 most common etiology for coronary insufficiency

 common symptom IS ANGINA. ANGINA is a symptom not a disease! (http://www.nhlbi.nih.gov/health/health-topics/topics/angina/)

 The aforementioned features are usually the basis for the determination of typical or atypical angina. In some references this is based on three classic signs:

o (1) substernal chest discomfort with a characteristic quality – pressure /squeezing/heaviness – an duration

o (2) provoked by exertion or emotional stress

o (3) relieved by rest or nitroglycerin.

o Typical angina if it has all these three signs and atypical if it has two.

 Angina symptoms resemble those of a heart attack. However, angina symptoms usually last only one to five minutes, while chest pain from a heart attack may last for hours. Angina symptoms normally diminish after resting or taking angina medications. Heart attack symptoms do not improve with rest, and angina medication will not reduce heart attack chest pain

 Angina (definition) – “chest pain caused by restricted blood flow to the heart (called ischemia). It often occurs when you are under emotional or physical stress, such as exercise. When the heart doesn't get enough oxygen from the coronary arteries, you feel a squeezing chest pain or pressure across your chest that usually goes away after you stop the activity. The most common cause of angina is hardening of the arteries (atherosclerosis).” (www.umm.edu)

Usual Distribution of Myocardial Ischemia

  Retrosternal chest pain

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 Central chest radiates to neck and jaw (angina dentis- dental pain); more commonly down the left arm (following dermatomal distribution)

 Can also radiate to right arm (for right coronary problems), epigastrium, or back.

 Dermatomal origin of heart involved (hence different areas of referred pain

 Tooth Ache and throat ache can also be a sign of MI – “up to the neck and into the jaw.

Figure 1. Usual Distribution of ischemic chest pain: dermatomal distribution of the heart *epigastrium: may suggest right coronary artery involvement

3. CARDIAC ETIOLOGY: Mitral Valve Prolapse

 An abnormal systolic ballooning of part of the mitral valve into the left atrium, resulting in a floppy leaky valve.

o Younger patients usually have this instead of coronary insufficiency

o Usually stays as it is, without hemodynamic deterioration of the valve or stroke

o 2-5% of people, especially the females  commonly seen in the clinics

o Not very life threatening, but is associated with mitral regurgitation in the United States.

Table 2. Chronic Recurrent Chest Pain Syndromes: Cardiac Differentials* Atypical Angina should be Mitral Valve Prolapse – Classic Angina distinguished from non- affects 5% of females cardiac chest pain** During effort/ exertion(e.g. Spontaneous/cold Spontaneous walking or during very hot or weather(mechanism is very cold weather); due to vasocontriction/ coronary P demand for oxygen (demand vasospasm = supply type of type) angina rather than demand type), pain at night

Rest / nitrates(diagnostic if chest Nitrates Spontaneous (can be P pain goes away in a few minutes) incapacitatingneed to use a B- blocker) Variable (TYPICAL: Squeezing, Variable(burning, pricking, Variable(diagnosis is based on constricting, pin pricking, stabbing pain; found in diabetics echocardiography) stabbing tightness, pressure, and the elderly; itis not life Q heaviness, strangling,vague threatening) chest discomfort) “basta mabigat” SEVERE: parang may hollow blocks sa chest Ian, Aca, Hannah UPCM 2016A: XVI, Walang 4 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

Atypical Angina should be Mitral Valve Prolapse – Classic Angina distinguished from non- affects 5% of females cardiac chest pain** Retrosternal/ precordial(diffuse Retrosternal (not typical ; maybe Left anterior, variable(can be R pain, more centrallylocated) different in location); especially under the breast) with diabetics, they usually present with atypical angina Mild to moderate*** (stable = Mild to moderate Mild – severe(not life threatening S same level of intensity for some but pain is incapacitating) time now) 1-30 min 1-30 mins Mins – hours T Typically <15-20 mins Maybe 2-3 mins If > 20 mins. = Myocardial Infarction (MI) Risk factors (i.e. Age: M>55/45*, Also w/ CSAP Young female(oftentimes the F>65/55*, 5 most common risk (Chronic Stable Angina Pectoris; complication is benign) factors: Smoking, DM, higher risk in diabetic patients hypertension, dyslipidemia, and in women, presence of at genetic predisposition) least 1 risk factor for coronary Associated factors: obesity, disease) O stress

*These are just common diseases (other diseases may present with similar pain/symptoms) **We should not dismiss the complaint just because it is atypical ***The Canadian Cardiovascular Society (CCS) grading of angina pectoris was described in the medical literature in 1976. This grading system of the severity of effort angina has been accepted throughout the world over the past 30 years.

Table 3. Canadian Cardiovascular Society Grading of Angina Pectoris Grade Description

Grade I Ordinary physical activity does not cause angi na, such as walking and climbing stairs. Angi na with strenuous or rapid or prolonged exertion at work or recreation. (least bothersome)

Grade I Slight limitation of ordinary activity. Walking I 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 the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions (provoked by more than usual to usual activities)

Grade I Marked limitation of ordinary physical activity. II Walking one or two blocks on the level and climbing o ne flight of stairs in normal conditions and at normal pace (provoked by less than usual activities)

Grade I Inability to carry on any physical activity with V out discomfort, anginal syndrome may be present at rest (dis abling or severe, pain at rest)

References:Campeau Lucien. Grading of angina pectoris. Circulation 1976;54:5223 http://www.ccs.ca/download/position_statements/ Grading%20of%20Angina.pdf

4. GI ETIOLOGY: ESOPHAGEAL, GASTRIC, BILIARY

Table 4. Chronic Recurrent Chest Pain Syndromes: GI differentials

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Esophageal Gastric Biliary

Acid Reflux Disease Gastric/Peptic Ulcer Gallbladder stones

P Feed (a common provoking factor), exercise, Fasting(or 2hrs after eating); Feeding (precipitated supine/lying down after a meal (due to reflux; e.g. peptic ulcer by high fat meals; especially if patient has hiatal hernia or weak spastic) GI sphincter; Gastroesophageal reflux: “HEARTBURN”)

P Drinking, proton pump inhibitors, antacids, Feeding, Rx (antacids: H2 Spontaneous,Rx(antis burping,(H2 blocker/proton pump inhibitors blockers, proton pump pasmodics, decrease acidity of gastric secretions) pain inhibitors) antiparasympathomim is due to acid going back to the esophagus, etic agents) SLN

Q Variable (burning, lower part of the chest; Variable (hunger- like pain; Colicky, crampy or angina-like) gnawing pain/discomfort) spastic/painful

R Substernal(may radiate to the epigastrium; Epigastrium/ lower sternum Right upper quadrant visceral ache) but can radiate to chest and shoulder

S Mild - severe Mild –moderate; severe(may Mild, severe imply persistence of a perforation if severe)

T 5-60 min (usually not relieved Hours(1.5 hrs or longer after a Min-hrs earlier) meal; antacids for immediate relief)

O Angina-like(esophageal spasms also Epigastric pain 4 F’s (risk factors of manifested but not relieved by nitrates) gallstones: fat, female, fertile, forty), nausea and vomiting

Your notes here: 

5. OTHER ETIOLOGY: PLEURAL, MSK, FUNCTIONAL

Table 5. Chronic Recurrent Chest Pain Syndromes: Other differentials Pleural (more diffuse) or Musculoskeletal (felt almost by Functional* (psychosomatic) Pulmonary (acute pericarditis, everyone unless sedentary) pneumonia)

P Respiration (deep breaths); Change in Position, upon Supratentorial; Stress: “all in the coughing; pleural application of pressure, upon head”  no organic basis; inflammation(acute pleuritis, motion; elicit tenderness; may be psychiatric (especially Borderline ) recurrent; may also be associated Personality) with P Analgesics (anti-inflammatory, Rest, Rx (analgesics and/or non- Relaxation; psychiatric intervention; narcotics) steroidals because it’s an extensive workup; deliberate thought inflammation) on diagnosisreally depends on history Q Variable (sharp, more localized Variable (dull muscle type Variable (but can be distressing pain) pain, depends on position and especially if unknown etiology) motion) R Variable (wherever pathology Variable Substernal is, esp. Left/ Right chest, back) S Mild – severe (unequal Mild – severe Mild – severe ; leaning on one side to protect the hurting area dependent if acute) T Variable(until inflammation Variable Hours abates) O Cough & fever (because Tietze’s Syndrome – acute Da Costa’s(soldier’s heart)– most inflammation involved), cough costochondritis; inflammation of severe; in soldiers sent to war  associated pain costal cartilages (costochondral patient with profound psycho and sternocostal junction), somatizations (loss of motivation, tenderness and sharp localized energy lack, chest pains, vague Ian, Aca, Hannah UPCM 2016A: XVI, Walang 6 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

Pleural (more diffuse) or Musculoskeletal (felt almost by Functional* (psychosomatic) Pulmonary (acute pericarditis, everyone unless sedentary) pneumonia)

pain (a few points in the chest) symptoms) - more common in females beyond -may require psychiatric care; forty; PE  evoke tenderness by circulatory neurastemia touching chest  pain *Functional aka supratentorial (it’s all in the mind”): but its symptoms is as real as those with organic symptoms Your notes here: 

Table 6. Chronic Recurrent Chest Pain Syndromes: Summary Differential Provocative Palliative T Other

Angina During effort Rest, sublingual nitrates Mins Coronary disease risk factors

Esophageal Feeding, exercise, Burping, drinking, SLN Mins Angina like supine position

GI Fasting Food, Antacids Mins Epigastric pain

Biliary Feeding Spontaneous, Rx Mins Crampy, colicky

Pleural, Pulmonary Respiration, cough Analgesics Var. Assoc.

with cough and

fever

Musculo-skeletal Position, motion, Analgesics, (muscle Var. Tietze’s syndrome pressure relaxants)

Functional Stress Relaxation Var. Da Costa’s syndrome

“Few modern doctors are equipped to recognize the subtle cases of angina, largely because they are ignorant of these details or unwilling to invest time in history taking…”“Of the million coronary angiograms done in 1993, 200,000 revealed normal coronary arteries…Had Levine’s teachings been heeded, few if any of the patients would have been subjected to such a costly and invasive procedure…” “Frequent reliance on a so-called work-up…Is testimony to lack of clinical skills…”

-Bernard Lown, MD (1985 Nobel Peace Prize)  Point of Emphasis: History and PE matter.

ACUTE CHEST PAIN SYNDROME DDX Table 7. Acute Chest Pain Syndromes Common Clinical Clues Causes

ACS: Acute MI* Prior angina, risk factors, ACS: >20minutes, crescendo Unstable Angina*

Dyspnea, clear fields (this is not Acute a pulmonary problem, it’s a vascular Pulmonary problem), Deep Vein Thrombosis is a Embolism* risk factors

Unequal phases- radial, brachial, Dissecting femoral aortic aneurysm* You can hear regurgitations

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Common Clinical Clues Causes

Pleuritic (aggravated when leaning Acute forward or taking deep breaths), Pericarditis central chest, anterior friction rub

Acute Pleuritic, cough Pneumonia

After alcohol, Acute Gastritis gnawing

Acute Nausea and After alcohol, Pancreatitis vomiting gallstones

Acute Jaundice Cholecystitis

Acute visceral problems Nausea, vomiting, cold sweat (abdomen)

*Three diseases associated with chest pain that would require immediate attention (life threatening). These “Big Three” diseases can be ruled out by CV angiogram (however relying on this test can make your mental capacities deteriorate (Maranon, 2011; basing from Lown) **Acute Coronary Syndrome (ACS): Acute MI and Unstable Angina. Unstable Angina is without necrosis (thus is diagnosed after MI is ruled out) ***Sometimes nausea and vomiting together with diffused pain can be a manifestation of acute MI (respect these symptoms!)

 Fixed obstruction kind can result to unstable angina.

o Intensity

o Frequency

o What provokes it

 Acute coronary syndrome – results from plaque rupture

o Necrosis is present in acute MI. Acute thrombosis occurs.

o Diagnostic of necrosis: Enzymes.

o Acute MI is ruled out if there is no evidence of myocardial necrosis, negative for EKG changes, and no characteristic pain. If enzyme tests negative, then it is unstable angina.

 Lethal

o Acute MI, Unstable Angina, Acute , Dissecting Aortic Aneurysm

 Unstable Angina

o more severe, more frequent, needs ICU confinement; crescendo angina (increasing intensity/ worsening pattern, unlike in classic and atypical angina), must monitor angina within the first month because it can “head south” to this

 Dissecting Aortic Aneurysm

o aorta tears; aortic insufficiency murmurs are heard on PE; the pain is more severe at the outset and it radiates to the back and the butt (depending on the extent of the aneurysm)

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o patients feel like they’re going to die (20% die at initial pain); unequal pulses depending on the levels of compromise of aortic branches

 Proximal aortic dissection

o manifests as chest pain

 Acute pulmonary embolism

o , clear lung fields (a problem of perfusion, not ventilation), oxygen desaturation/ , pleuritic, pulmonary hypertension- related, RV cannot compensate: Right . Pneumonia= ,

 Acute pericarditis- pericardial rub  Acute pneumonia

o febrile episode with pleuritic pain; inspiratory pleuritic rub

CASE DISCUSSION Case 2 “The pain usuallyCase occurs 1 “The patient is a 40F with during exertion but  In chestthis case: pain Doon exertion,not use endoscopy unless the patient does sometimes at rest or after usually after washing not respond to medications/ treatment fatty meals. It is relieved clothes…” by nitrates or rest or sometimesDiagno by belching…”Upper extremity effort (musculoskeletal sis pain); can also be due to angina BUT the Diagno multiple etiologies: biliary, esophageal,type of effort is important. sis atypical angina (Be open minded of other B. DYSPNEA possible etiologies. Do not Caveatbe limitedIn to angina, effort Definition: as light as Thewalking patient can is not necessarily in distress but is what is being discussed. ) cause the pain. sufferingThe kind offrom effort shortness will of breath characterize the pain. CaveatTWO MAINThe concept TYPES ofOF parsimony: DYSPNEA: simplest CARDIAC way AND to PULMONARYexplain (only one disease)

Table 8. Differentiating cardiac and pulmonary dyspnea Cardiac Pulmonary Usually from congestive heart failure or Obstructive pulmonary airway angina, but these do not include edema syndromes, e.g. asthma Progressive and occurs on exertion Progressive (chronic: COPD or end stage  Progressive: takes more effort at the outset, lung disease) On exertion then less and less in time until it occurs at rest episodic (bronchial asthma, which has  2015: RHD, MI or cardiomegaly reversible, intermittent causes) Late Immediate, can happen earlier on  unless in cases of acute mitral valve regurgitation Relieved by sitting orstanding Expectorate: PND** (Paroxysmal  reduction of central venous pooling  relieved by production & cough Nocturnal Dyspnea)  2015: when patient is supine, there is  2015:expectorating phlegm, blood “Cardiac Asthma” pulmonary congestion due to increased blood flow to the Cough Late symptom Early prominent symptom Ascending (from the feet up) Ascending(only in a R-sided failure or RV Edema Biventricular- from Left heart failure (CAD) heart failure from pulmonary hypertension “core pulmonare”) *To differentiate the different forms of dyspnea, be detailed as possible, since symptoms are similar for both the cardiac and pulmonary types

OTHER TYPES OF DYSPNEA SYNDROMES  Orthopnea - dyspnea when in supine; difficulty breathing in supine position, late sign  Paroxymal nocturnal dyspnea** - episodes of sudden dyspnea and orthopnea that awaken the patient from sleep, usually one or two hours after going to bed, “when you sleep, get up and you’re out of breath”  Trepopnea – dyspnea when lying on side/lateral decubitus position, can occur due to heart failure or pulmonary conditions or disease states

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– dyspnea when upright usually due to a diaphragmatic problem; differentials: hepatopulmonary syndrome due to pulmonary shunting, diaphragmatic mismatch  Treponea and Platypnea are issues with changing perfusion-ventilation ratios and congenital diaphragm problems  Non cardiac causes of dyspnea: Dyspnea may be caused by severe anemia and hypoxia, which are not exclusively cardiac or pulmonary causes

Caveat

“Doc, madali po akong mapagod…” Case 1 Diagnos easy fatigue vs. exertional dyspnea is difference in vernacular: tire easily (easy fatigue) versus out of breath (exertional dyspnea) Caveat Differentiate between pathologic and physiologic  Easy fatigue: effort intolerance due to low cardiac output  Exertionaldyspnea: congestive heart failure  Pathologic if the symptom is not age/… appropriate

Case 2 “Doc, hinihingal po ako kahit walang ginagawa, saka mayroon ho akong kaba, nahihilo ako, at nanlalamig, at lagi akong hinang-hina…” Diagnos syndrome is Caveat The case may appear non-specific but these signs are characteristic of hyperventilation syndrome, which may be a normal thing and would require patient to blow into rebreathing bag

 Dyspnea may be normal or abnormal depending upon the situation. Therefore, we need to elicit more information from the patient during the history taking. Remember that cardiac and pulmonary symptoms may always be present on exertion, orthopnea, PND, cough, and edema. Proper diagnosis entails a good history taking which involves the clear characterization of the symptoms and correct understanding of the patient’s descritption of cardio- pulmonary symptoms.

C. PALPITATION  Definition: Awareness/sensation of one’s heartbeat  Can be: o Singlet (skipped beats) o Rapid succession of palpitations (tachyarrhythmia) o How to differentiate? Ask the patient to tap on the table following the rhythm of his/her perceived heartbeat  Can develop during exercise  Not always tachycardia or bradycardia

Table 9. Differentiating functional and organic palpitations Functional Organic/ Pathologic Start Gradual Sudden End Gradual Sudden Trigger Stress None Rate <<100 >>100 (they can have supraventricular or ventricular tachycardias occurring and because of that, extremely rapid rate)

2015: although there are some bradycardic palpitations) Other Symptoms Anxiety (a little bit of tremulousness, stage fright) Chest tightness, shortness of * Many complain about this! breath, syncope

Caveat Case 1 “Doc, lagi po akong kinakabahan …” Diagno You can only come to a diagnosis if you ask the sis patient further. Ask: Ano pong ibig niyong sabiing kinakabahan?[Do not suggest an answer. If you Ian, Aca, Hannah UPCM 2016A: XVI, Walang 10 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

are prone to suggest, give multiple choices. Caveat Let the patient explain what s/he means

D. GENERALIZED EDEMA  characterized by an (abnormal) accumulation of water (actually an accumulationof salt, whichbringswaterwith it)  generally PAINLESS

Table 10. Differentiating the different types of edema Cause Description Renal Descending  Hypoalbuminic states: puffy eyelids (periorbital edema) and face, especially in nephrotic syndrome  Hypervolemia, acute renal failure  Two types: Acute renal failure and nephrotic syndrome Hepatic, systemic Centrifugal  Starts in the abdomen (ascites) due to portal hypertension  As secondary compensatory mechanism, you get it in your feet next Cardiac and Pulmonary Ascending (Dependent edema)  Feet first, bilateral then upward, may evolve to anasarca (generalized edema)  Heart failure (L&R for cardiac, R sided for pulmonary)

Caveat Case 1 “This 74F has been having bilateral ankle swelling for the past month, she can hardly walk…” Diagno Ankle Arthritis sis Caveat Check first if there is pain since arthritis and gout are usually painful. Edema is painless.

E. CYANOSIS  Definition: bluish color of the skin and mucous membranes resulting from an increased quantity of reduced hemoglobin (i.e., deoxygenated hemoglobin) or of hemoglobin derivatives (e.g., methemoglobin or sulfhemoglobin) in the small blood vessels of those tissues. (Harrison’s 18thed)  Common locations: in the mucous membranes (of the mouth), nail beds, conjunctivae   Pathophysiology: o Increase in the quantity of venous blood as a result of dilation of the venules and venous ends of the capillaries ~OR~ o Reduction in the saturation of arterial blood (SaO2) in the capillary blood o Leads to increase in the quantity of reduced hemoglobin in mucocutaneous vessels  Cyanosis becomes apparent when concencentrations of reduced hemoglobin in capillary blood exceeds 40g/L (4g/dL)  At least 5 grams per cell or greater (of desaturation): o It is the absolute, rather than the relative, quantity of reduced hemoglobin that is important in producing cyanosis (Harrison’s, 18th ed)  Thus, cyanosis is more appreciated in a polycythemic person rather than an anemic person Anemic patient w hemoglobin at 8, O2 saturation of 75% due to pulmonary disease  desaturation is ¼ of 8 = 2  not cyanotic because degree of deoxyhemoglobin is only 2 o Patient with hemoglobin of 16, 75% saturated  ¼ or 4 is not yet cyanotic (you need more desaturation for cyanosis to manifest)  It is easier to see desaturation or cyanosis… o In a polycythemic person o In fair skinned people than dark skinned (“skin color matters”) o Better detected in nail beds and malar prominences in fairer skinned persons o In mucous membranes than nail beds

Table 11. DeoxyHb Concentration that cause Cyanosis DeoxyHb Concentration Normal 5 g/dl Met – Hbanemia (Abnormal Hb) 1.5 g/dl *congenital or acquired, from abnormal Hg or drugs (nitrates) *usually in toxic concentrations and hemoglobinopathies Sulf – Hb (Abnormal Hb) 0.5 g/dl  Met-Hb and Sulf-Hb arise from hemoglobin congenital problems and toxicities (nitrate poisoning)  Can be congenital or acquired

PATTERNS OF CYANOSIS: CENTRAL OR PERIPHERAL Table 12. Differentiating central and peripheral cyanosis Central Peripheral Ian, Aca, Hannah UPCM 2016A: XVI, Walang 11 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

Sir’s words: Sir’s words: Desaturated centrally Caused by something O2 saturation is low due in the periphery to a cardiac pulmonary (vasoconstriction, cold condition weather) The arterial blood has low There is oxygen level (hypoxemia vasoconstriction leading to arterial (demonstrated by oxygendesaturation from touching ice), arterial the aorta- venous occlusions, deoxyhemoglobin). hemostasis and arterial blood has normal Cyanosis is observed both oxygen level (normal in mucous membranes saturation) (mouth, lips, palpebral conjunctiva and But for some reason, especially under the cutaneous blood flow tongue) and nailbeds slows down and decreases, and the Happens with congenital tissues extract more heart disease, heart oxygen from the blood failure, There is an increase in venous deoxygenated blood in the capillaries, and only the nailbeds are cyanotic

This phenomenon can be attributed to:  Vasospasm (Raynaud’s phenomenon- characterized by the focal vasoconstricted state of the arteries), ex. Digital arteries  A thrombus, embolus or a normal response to a cold environment or anxiety  It could also be PDA: Patent Ductus Arteriosus – wherein the deoxygenated blood flows to the lower extremities (only the lower extremities are cyanotic, the upper extremities and oral mucosa look normal)  Polycythemic (with Hb<20) get cyanotic earlier than anemic.

Caveat Case 1 “The toes were cyanotic but her fingers were not…” Diagn Differential cyanosis from PDA osis Reverse PDA  There is a right to left shunting of blood past the subclavian artery, and the upper extremities are spared  Note that PDA is a left to right shunt Review: Patent Ductus Arteriosus  Ductus Arteriosus: Communication between the aorta and the pulmonary artery ligamentum arteriosum  Patent DA: The ductus arteriosus still persists as a vessel leading from the bifurcation of the pulmonary artery to the aorta just distal to the left subclavian artery instead of closing after birth In adult patients with PDA, pulmonary pressures are normal and a gradient and shunt from aorta to pulmonary artery persist throughout the cardiac cycle. Pulmonary pressure is 1/6 of the systemic circulation. Blood from the left heart goes upward (fingers), mixed blood goes downward (feet). Differential cyanosis from PDA o May be due to preferential shunting of blood to the feet via the patent ductus arteriosus (PDA). o Differential diagnosis include: . Diabetes and Eisenmenger syndrome- patients with a large communication between the two circulations at the aortopulmonary, ventricular or atrial levels and directional or predominantly right to left shunts because of high resistance and obstructive pulmonary hypertension . Severe pulmonary vascular disease results in reversal of flow through the ductus, unoxygenated blood is shunted to the descending aorta, and the toes, but not the fingers, become cyanotic and clubbed – termed differential cyanosis.

F. SYNCOPE  Syncope is the relatively abrupt loss of consciousness(2015: brief, seconds to a few minutes and due to decreased blood flow in the brain), with or without a short prodrome.  Presyncope dizziness  Some people develop syncope after dizziness  “Doc nahihilo ako”what type? Characterize and describe!

TableIan, Aca,13. Types Hannah of Dizziness UPCM 2016A: XVI, Walang 12 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

Types and causes of cardiogenic syncope Vertigo Disequilibrium Syncope/ Near Syncope sensation less than vertigo, passing out  Stokes-Adams/ cardiac (syncope)- sudden cessation of of may be ear problems/ (2015: near cardiac function and effective CO, complete heart block; spinning vestibular or the CNS/ faintness, about bradycardia(from complete heart block)causing loss of or the central connections in to pass out, consciousness room is the brain (2015: light  Vasovagal/Common faint- aka neurocardiogenic spinning sense of imbalance; headedness), syncope(2015: Neurologic cause with prodrome(flashes of mild kind of vertigo; metabolic light, weakness and cold clammy sweat), more benign; problem with sometimes interaction of cardiac mechanoreceptors as well as para- proprioceptors, (hypoglycemia and sympathetic receptors; vasodepressor or inhibitor. Can stereognosis; … but that’s not be prevented because there are warning signs) unsteady gait) our topic since this is cardio) Table 14. Qualities of syncope Stokes Adams Vasovagal(the common faint e.g. in the heat)

Onset Sudden With short prodrome (stomachache, dimming of vision, lightheadedness); close to hyperventilation; position dependent, aka common faint

End Asymptomatic, (2015: no post ictus, Usually no post ictus (post seizure) except for a few pt has no memory of occurrence) brief jerks sometimes

Duration Seconds (or else the patient will be Minutes to hours, relieved by lying down (blood goes dead) to head)

Table 15. Other Causes of Syncope-like Episodes (DDx) Absence seizures Situational(2015: pre- and post-ictal stages, weak and sleepy upon revival, non convulsive seizures) Cough syncope Situational (2015: benign and common in elderly, loss of consciousness after coughing bout due to increased vagal stimulation) Post micturition Situational (2015: benign syndrome and common in elderly, pt is woken up by an urge to urinate and losses consciousness upon micturition) Carotid sinus Passing out when shaving hypersensitivity (2015: when the patient turns his heador wears a tight collared shirt) Hyperventilation 2015: Due to syndrome leading to loss of consciousness Hypoglycemia 2015: through intake of oral hypoglycemics such as glibenclamide, metformin, insulin and comistamil Caveat:

Case 1 Doc, nahihilopo ako… then loses consciousness Diagnosis Trauma Caveat Determine the differentials (this patient had trauma (head injury)) Temporal order is important (hitting head then getting up and fainting vs fainting and then falling and hitting head)

II. IMPORTANCE OF HISTORY AND PE Table 16. Importance of Hx and PE Crombie, 1963 History and PE accounts for 88% of patient diagnosis Hampton, 1975 History=82% PE= 9% Saundler, 1980 History=56% PE= 15% Sapira, 1990 History=90% PE= 9% Ian, Aca, Hannah UPCM 2016A: XVI, Walang 13 of Kapantay! 14 OS 213: Cardiovascular System LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE Exam 1 | Dr. Donato Marañon | September 24, 2012

 Looking at the more recent values, we can see that we can still arrive at a diagnosis with history and PE. Between the two, history is important!  Remember the importance of history taking (and PE) so we can prove this guy wrong: "Doctors pour drugs of which they know little, to cure diseases of which they know less, into human beings of whom they know nothing". – Voltaire

END OF TRANSCRIPTION Ian: Hi block A! One last module, then SEMBREAK na! Yehey! :) Aca: Aca: Heaven in a wild flower. Also, I’m currently in a post-Awkward (season 2) high. Matty please, please be the one! [cc: DOMS] They won’t get to read this, but happy happy birthday to my beloved batchmate, Blessie! I love you, sis  Also to the sizzling hot and awesome Patrick (super miss na kita ) and lastly, belated happy birthday to one of the sausage masters, Lee! Kevin, awesome job, man. Sexy mo! Hi sisses and brods, AFTG! XVI: Walang Kapantay! Hi you! ” Hannah: Kamustamus Kalabasa naman sa minigreetings?! Hahaha! Sorry guys! We did our best but we guess our best was the best. (vangagaboomboomangpakalakapeg!)

Ian, Aca, Hannah UPCM 2016A: XVI, Walang 14 of Kapantay! 14