FEV & FESP PTAT 2 Lecture Notes PDF

S- SOAP which is much worse and that might end Information will come from the pt. in HYPOTENSION” (Verbatim) Hypotension ○ Chief of complains (c/c) Low BP Comm...

S- SOAP which is much worse and that might end Information will come from the pt. in HYPOTENSION” (Verbatim) Hypotension ○ Chief of complains (c/c) Low BP Common complaint in cardiac cases: Check BP q 5 mins ○ CHEST PAIN/ PECTORALIS Give ACTIVE ANKLE PUMPS ANGINA ○ If not feasible, give passive Levine Sign ankle pumps although there are no studies supporting this. Referred pain of Chest pain: 1. Jaw (MC) 2. L shoulder (ulnar side) Ulnar kasi innervated si heart ni C4-T1 (Phrenic nn) Left because heart is shifted towards left Clenched fist at heart 3. Chest Indication of ischemic chest pain 4. Upper trapz Distress sign 5. Neck (LC) Type of chest pain 1. Ischemic cardiac pain (MI) Aka Myocardial Infarction Sudden onset Pain greater than 30 mins Not relieve by rest 2. Anginal pain (4 types) Looks like choking him/herself A. Chronic stable angina/ predictable Chest pain might be caused by angina Exercise Predictable since there is known Stress stimulus that can trigger the chest pain Emotions Stimuli: Exercise, stress, emotions Primary medication: NITROGLYCERIN First thing to do: Mode of administration: SUBLINGUAL ○ Give NTG (nitroglycerin) ○ So that medicine is absorbed B. Chronic Unstable Angina/ faster preinfarction/ progressive/ Crescendo Effects: Dilates aa/vein of the heart angina If chest pain persists after 5 mins of 1st NTG is not effective intake, give another tablet. If the pain CI: exercise so NO ANKLE PUMPS still persist after giving the 3RD Call for help (911) TABLET, call for help (911) Possible MI ADDITIONAL NOTES: ○ Start of MI “Wag itayo ang patient na may chest C. Nocturnal angina pain as it may result in venous pooling Chest pains while sleeping Fiona Erica Peji & Fhelomenarose Verzosa 1  ○ “Inatake sa pagtulog” Is the pt. Ambulatory? Could lead to CHF (Congestive Heart ○ Is the pt. Using assistive Failure) devices? If yes, what kind of D. Prinzmetal/ Variant angina assistive device? Spasm of the coronary aa (constriction) ○ Do pt. Need assistance to Mc in women than men ambulate? What kind of assist? ADDITIONAL NOTES: MYOCARDIAL Palpebra INFARCTION diaphoresis Minsan sx of MI also consist of: ○ Headache Under palpation+ additional infos ○ Vomiting Edema ○ Pallor ○ “Lulubog pag pinalpate:” ○ Dizziness Cool & Clammy Any symptoms that are similar to pregnant women Differential dx: HEARTBURN Palpitations/arrhythmia Abnormally fast heart beat Manifestation of heart condition Dyspnea SOB Manifestation of heart condition Under OI + additional infos Cyanosis Reference: ELSEVIER ○ Note that to check further for Syncope cyanosis you can do capillary Part of the Subjective blood refill test BUT THAT ○ Can be medical hx WILL BE PART OF THE Should be subjective for MRI and CT ASSESSMENT AND NOT OI scan 1-2 sec the color of nail Happens due to decrease O2 in brain bed should go back to Manifestation of heart condition normal Anginal scale 1001, 1002 (don’t count 0 No angina fast) ○ Check for toe, lips, nail bed 1+ Light, barely noticeable ○ Need for ECG ○ Manifestation of heart condition 2+ Moderate, bothersome (max na kayang itolerate) SWELLING ○ Note that if edema is present, 3+ Severe, very uncomfortable; pre swelling should also be (+) in infarction pain your OI 4+ Most severe pain ever experience; infarction pain Fiona Erica Peji & Fhelomenarose Verzosa 2 Dyspnea Scale In documentation, include why did you conclude that the patient 0 No dyspnea is sedentary or active +1 Mild, noticeable to pt. only Also take note that even though the pt.’s job is heavy like a +2 Mild also noticeable to PT construction worker– as long as the pt. is not allocating time to +3 Moderate difficulty, but pt. Can still continue workout then pt. Is not considered active. +4 Severe difficulty, cannot continue 10. Familial Hx ADDITIONAL NOTES: HTN In Referred pain it should be around CHF upper trapz only because if back pain Valvular heart dse persist, (in documenting FMHx, it is not limited to these ○ Can be AORTIC ANEURYSM three but SHOULD be included since focus sa ○ Only until middle back (thoracic cardio) area) Congestive Heart failure Risk factors: Aka cardiac decompensation 1. Genetics: namamana yung condition Inability of the ventricles to contract that can lead to Heart Attack effectively 2. HTN 2 types of CHF: 3. Cigarette smoking 1. Left CHF (MC) Left ventricle is ineffective resulting in regurgitation of blood back to the LUNGS PULMONARY EDEMA Orthopnea = shortness of breath when lying down that's relieved by standing or sitting up Cerebral hypoxia - low O2 in brain 4. Hypercholesterol 2. Right CHF (N) values Right Ventricle is ineffective resulting in HDL - 60 mg/dl regurgitation of blood back to the LDL 100 mg/dl peRipherals Triglyceride 165 mg/dl Bipedal edema Cholesterol - 200 mg/dl Ascites (bloated) 5. Obesity Hepatomegaly > than 31 kg is at risk 6. Waist circumference Greater than 100 cm is at risk 7. Fasting blood glucose 8. BMI 9. Sedentary lifestyle Fiona Erica Peji & Fhelomenarose Verzosa 3 O = Objective Temporal Vital Signs External Carotid Baseline Brachial Since HTN is a risk factor Radial N BP = 110/70 mmhg Ulnar ADDITIONAL NOTES: Femoral OI and palpation should be part of Popliteal Objective Posterior tibial Pedal (dorsalis pedis) Types of HTN Under O2sat: Hypoxemia vs hypoxia 1. Primary HTN HYPOXIA HYPOXEMIA No identifiable cause Low O2 in tissue = Stroke Low O2 in blood 2. Secondary HTN Identifiable cause like: Low O2 in mm = necrotic ○ Arteriosclerosis Heart rate ○ Pregnancy Don't use thumb (kasi may own pulse) ○ Drugs 60-100 bpm That is why always ask 70 bpm avg if they are taking Kid: 70-170 bpm medications (HTN; Tachycardia (fast HR) controlled since keme) Bradycardia (slow HR) Hypotension Heart sounds Use compression stockings to promote venous return S1 (Normal) ○ Gravity results venous pooling Lub But fixing the problem in the heart Longer, Louder should be the top priority Lower in pitch N Pulse ox Marks the beginning of systole CLOSURE OF AV VALVES (tricuspid 98-100% & mitral) Pulse rate S2 (Normal) Dub Not louder than S1 Marks the end of systole CLOSURE OF SEMILUNAR VALVES (aortic & pulmonic) S3 (Abnormal) VenTHREEcular gallop Heard after S2, early diastole Left ventricle >> Left CHF Fiona Erica Peji & Fhelomenarose Verzosa 4 S4 (Abnormal) Pericardium 4TRIAL GALLOP Covering of the heart Heard after S1, late diastole Compose of 2 layers: MI 1. Fibrous HTN 2. Serous Heart auscultations LANDMARKS: 1. Aortic area - R 2nd ICS 2. Pulmonic area - L 2nd ICS 3. Tricuspid area - L 4th ICS 4. Mitral area - L 5th ICS, midclavicular 5. Erb’s pont - L 3rd ICS 1. Fibrous pericardium Outermost layer Composed of tough inelastic, dense irregular connective tissue Its open end is fused to the connective tissues of the blood vessels entering and leaving the heart. – Function: CARDIOVASCULAR ANAPHYSIO ○ Prevents overstretching of the Heart heart Shape ○ provides protection ○ Cone-shaped structure ○ anchors the heart in the ○ Relatively small same size as mediastinum closed fist 2. Serous pericardium Rest Innermost layer ○ Diaphragm Is a thinner, more delicate membrane Location that forms a double layer around the ○ mediastinum heart Orientation 2 layers of serous pericardium: ○ Apex: Anteriotly directed, Left, A. Parietal Layer of the serous (PSP) inferior (ALI) ○ outermost layer ○ Base: Posteriorly directed, B. Visceral layer of the serous (VSP) Right, Superior (PRS) ○ Aka the epicardium Landmarks ○ Innermost layer ○ Apex: L 5th ICS Pericardial fluid (PF) ○ Base: 2-3 costal cartilage Function: decreases friction in the heart N amount: 15 to 50 ml Fiona Erica Peji & Fhelomenarose Verzosa 5  Between the parietal & visceral layers of Forms most of the anterior surface of the the serous pericardium is a thin film of a heart lubricating serous fluid Inside RV contains a series of ridges ○ The space that contains PF is formed by raised bundles of cardiac mm kown as pericardial cavity fibers called “trabeculae carneae” Condition related to amount of PF Posterior surface (+) decrease PF - Pericardial friction rub Aka base surface (+) Increase PF - Cardiac tamponade Chamber: 1. Right atrium 2. Left atrium Forms most of the base of the heart Inferior surface Aka diaphragmatic surface Chamber: 1. Right Ventricle 2. Left Ventricle Chambers of the heart Surfaces of the heart 1. Anterior 2. Posterior 3. Inferior Anterior surface Aka Sternocostal surface Chambers in anterior surface includes: 1. R atrium Atrium: receiving chamber Receives blood from THREE veins Ventricle: pumping chamber ○ SVC 1. Right Atrium ○ IVC Describe as rough due to the presence of ○ Coronary sinus pectinate muscles in the inside of AVG thickness: 2-3 mm posterior wall of RA The insides of posterior and anterior Receives blood from THREE veins (aka walls of RA are different; openings) Ant wall of R atrium: rough due to ○ SVC presence of mm ridges “Pectinate mm”; ○ IVC Post wall of R atrium: smooth ○ Coronary sinus 2. R ventricle AVG thickness: 2-3 mm AVG thickness: 4-5 mm Fiona Erica Peji & Fhelomenarose Verzosa 6  2. Left Atrium Valves of the heart (+) pulmonary veins Function: prevents backflow of the ○ It receives blood from the lungs blood through FOUR pulmonary veins Atrioventricular valves (inlet valves) ○ Anterior wall of left atrium is ○ Right AV valve - tricuspid valve also smooth ○ Left AV valve - mitral/ bicuspid ○ Blood passses from left atrium valve into the left ventricle through Semilunar valves (outlet valves) the bicuspid valve ○ Right - pulmonic valve Interatrial Septum ○ Left - Aortic valve Divides the atrial region into a right atrium and left atrium Foramen ovale ○ Before birth, this structure allows most blood entering the righ tatrium pass into the left atrium (+) Fossa ovalis ○ Remnant of foramen ovale ○ Is formed by septum primum and septum secundum. Blood flow inside of the heart ○ Closed version ni foramen ovale (NORMAL) ○ Once the foramen closed after the first breath of the baby (yung iyak) 3. Ventricles (+) cardiac mm fiber (ridges) ○ Pectinate mm (+) papillary mm Trabeculae Carneae ○ Ridges and folds of the myocardium in the ventricles ○ Their contraction pulls on the chordae tendineae, preventing inversion of the mitral (bicuspid) and tricuspid valves towards the atrial chambers. Cordae Tendinae ○ are attached to the leaflets on to the ventricular side and prevent the cusps from swinging back into the atrial cavity during systole. (tortora) Fiona Erica Peji & Fhelomenarose Verzosa 7  The left side of the heart pumps oxygenated blood into the systemic circulation to all tissues of the body except the air sacs (alveoli) of the lungs. The right side of the heart pumps deoxygenated blood into the pulmonary circulation to the air sacs. (accdg to tortora, 15th ed) Branches of Aorta 2. Conduction system Autorhythmic fibers in the SA node, located in the right atrial wall (a), act as the heart’s pacemaker, initiating cardiac action potentials Autorhythmic fibers: (tortora, 15th ed, p.711) - An inherent and rhythmical electrical Heart Sounds activity is the reason for the heart’s lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers (auto-=self) because they are self-excitable. - repeatedly generate action potentials that trigger heart contractions 2 important fxn of Autorhythmic fibers Great Control Center of the Heart 1. act as a pacemaker 1. Autonomic Nervous System (ANS) 2. forms the cardiac conduction system The conduction system ensures that the chambers of the heart contract in a coordinated manner. Fiona Erica Peji & Fhelomenarose Verzosa 8  1. SA node Natural pacemaker: autorhythmic fibers in the Cardiac excitation normally begins in SA node would initiate an AP about every 0.6 the sinoatrial (SA) node second, or 100 times per minute located in the right atrial wall just inferior and lateral to the opening of the Summary: SVC SA node cells do not have a stable resting potential, but repeatedly depolarize The spontaneous depolarization is called pacemaker potential: triggers action potential Each action potential from the SA node Coronary Artery - BS of the Heart propagates throughout both atria via gap junctions in the intercalated discs of atrial muscle fibers. Following the action potential, the two atria contract at the same time. 2. AV node By conducting along atrial muscle fibers, the action potential reaches the atrioventricular (AV) node located in the interatrial septum, just anterior to the opening of the coronary sinus action potential slows considerably as a result of various differences in cell structure in the AV node This delay provides time for the atria to empty their blood into the ventricles. 3. Atrioventricular (AV) bundle aka bundle of His only site where action potentials can conduct from the atria to the ventricles 4. Right and Left bundle branches extend through the interventricular Cardiac Action Potential septum toward the apex of the heart 5. Purkinje fibers rapidly conduct the AP beginning at the apex of the heart upward to the remainder of the ventricular myocardium ventricles contract, pushing the blood upward toward the semilunar valves Fiona Erica Peji & Fhelomenarose Verzosa 9 (Action potential in a ventricular contractile Hemodynamics fiber. The resting membrane potential is about Systolic – Highest arterial pressure −90 mV.) (_mmHg) Diastolic – Lowest arterial pressure (_mmHg) Pulse Pressure – Difference between the systolic and diastolic (SBP – DBP) End Diastolic Volume – Amount of blood left after diastole (ventricular relaxation) ○ Normal – 120ml – preload – (initial stretching of the heart) End Systolic Volume - Amount of Skeletal muscle vs. Heart muscle blood left after systole (ventricular contraction) ○ Normal – 50ml Stroke Volume – Amount of blood pumped by ventricles per contraction ○ Normal – 70ml Cardiac Output – Amount of blood pumped by ventricles per minute Cardiac Cycle ○ Normal – 4-6L Pumping action of the Heart Mean Arterial Pressure – Arterial Diastole: Ventricular relaxation pressure with respect to time Systole: Ventricular contraction ○ DBP + 1/3 PP ECG Reading Normal electrocardiogram (ECG). P wave = atrial depolarization; QRS complex = onset of ventricular depolarization; T wave = ventricular repolarization. Fiona Erica Peji & Fhelomenarose Verzosa 10  The analysis of an ECG involves measuring time spans between waves, known as intervals or segments. The P–Q interval measures the time from the start of the P wave to the beginning of the QRS complex, indicating the conduction time from atrial to ventricular excitation. ○ Lengthening of this interval can occur due to scar tissue from conditions like coronary artery disease. The S–T segment, from the end of the S wave to the start of the T wave, reflects the depolarization of ventricular contractile fibers ○ can be elevated in acute myocardial infarction or depressed with insufficient oxygen The Q–T interval, from the start of the QRS complex to the end of the T wave, represents the duration of ventricular depolarization and repolarization ○ can be prolonged by myocardial damage, ischemia, or conduction issues Fiona Erica Peji & Fhelomenarose Verzosa 11 Fiona Erica Peji & Fhelomenarose Verzosa 12