Cardiopulmonary Week PDF

Cardiac Pathophysiology: Coronary Artery Disease Neeti Pathare, PT, MSPT, PhD  1. Understand the term coronary artery disease. 2. Identify the risk factors for coronary artery disease. 3. Recognize the disparity in gender with relati...

Cardiac Pathophysiology: Coronary Artery Disease Neeti Pathare, PT, MSPT, PhD  1. Understand the term coronary artery disease. 2. Identify the risk factors for coronary artery disease. 3. Recognize the disparity in gender with relation to coronary artery disease. 4. Describe the pathogenesis of coronary artery disease. 5. Detect the clinical presentation of coronary artery disease. Objectives 6. List the tools used for diagnosis of coronary artery disease.  Coronary Artery Disease (CAD) 1. Cardiovascular disease is considered the most https://www.ahajournals.org/statupdate common cause of death for both genders and people of most racial and ethnic groups in US 2. In the US, more than 1 in 3 adults have cardiovascular diseases 3. Nearly 40% of American adults had total cholesterol of 200 mg per deciliter or higher Coronary Artery Disease (CAD) https://watchlearnlive.heart.org/index.php?moduleSelect=corart 1. When the coronary arteries become narrowed or blocked, the areas of the heart muscle supplied by that artery do not receive enough oxygen and become ischemic and injured and infarction may result. 2. Also known as ischemic heart disease, coronary heart disease (CHD) Coronary Artery Disease (CAD) Deaths attributable to heart disease, United States, 1900–2018 From 2003 to 2013, the death rate from heart disease has fallen about 38 percent – but the burden and risk factors remain alarmingly high Virani SS, et al; on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2021 update: a report from the American Heart Association. Circulation. 2021;143:e254–e743. Coronary Artery Disease (CAD) http://www.framinghamheartstudy.org/ Identification of risk factors is crucial Framingham Study identified 10 risk factors Study begin in 1949. Harvard tracked > 5000 men and women over many years Risk Factors for CAD MODIFIABLE NON – MODIFIABLE Smoking Hypertension (HTN) Heredity Hypercholesterolemia Male Sex (Until Age 50 when women catch Physical Inactivity up due to menopause) DM (Controllable) Age Obesity Stress About half of Americans (47%) have at least one of these three risk factors Fryar CD, Chen T, Li X. Prevalence of Uncontrolled Risk Factors for Cardiovascular Disease: United States, 1999–2010[PDF-323K]. NCHS data brief, no 103. Hyattsville, MD: National Center for Health Statistics. 2012. American Heart Association’s My Life Check–Life’s Simple 7 Seven approaches to staying heart healthy: 1. be active 2. keep a healthy weight 3. learn about cholesterol 4. do not smoke or use smokeless tobacco 5. eat a heart-healthy diet 6. keep blood pressure healthy 7. learn about blood sugar and diabetes Physical Activity Risk Matrix Physical Activity and Risk Virani S. Circulation. Heart Disease and Stroke Statistics—2021 Update, Volume: 143, Issue: 8, Pages: e254-e743 yrs Trends in age-adjusted obesity prevalence Overweight/ Obesity Hypertension as a Risk factor for CAD Virani S. Circulation. Heart Disease and Stroke Statistics—2021 Update, Volume: 143, Issue: 8, Pages: e254-e743 Gender and CAD: Risk Factors Gender and CADM: Mortality Rates Cardiovascular disease (CVD) mortality trends for US males and females, 1980 to 2018. Virani S. Circulation. Heart Disease and Stroke Statistics—2021 Update, Volume: 143, Issue: 8, Pages: e254-e743 Coronary Artery Disease: Pathogenesis Hypercholesterolemia Atherosclerosis 1. It is primary risk factor for the 1. Triggered by trauma to the development of atherosclerosis intima of the arterial wall 2. Also affects cardiac 2. Primary cardiac risk factors: function independently high blood pressure and cigarette smoking 3. Elevated cholesterol levels 3. Characterized by thickening change the structure and and loss of elasticity of the arterial walls function of cell membranes  The exact mechanism by which the development of CAD is not known Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Infectious agents in initiating the inflammatory cascade are implicated In general, most current theories include the following major events in the Coronary Artery Disease: development of an atherosclerotic plaque: Pathogenesis Arterial wall damage occurs either from injury caused by harmful substances in the blood or by physical wear and tear as a result of high blood pressure. This injury to the blood vessel wall permits the infiltration of macromolecules (especially cholesterol) from blood through the damaged endothelium to the underlying smooth muscle cells. Naked collagen acts like flypaper for platelets, causing them to aggregate at the site of injury and plug up the wound. Once the platelets adhere, they also release chemicals that alter the structure of the blood vessel wall This can end up a swollen mound of platelets, muscle cells, and fibrous clots, a process called proliferation that obstructs the flow of blood through the vessel.  by Saunders, an imprint of Elsevier, Inc. Copyright © 2015, 2009, 2003, 1998 Coronary Artery Disease: Pathogenesis Atherosclerosis begins with an injury to the endothelial lining of the artery (intimal layer) that makes the vessel permeable to circulating lipoproteins  https://www.cdc.gov/heartdisease/facts.htm How does an Infarct Occur? 1. Thrombus 2. Embolism 3. Rupture 4. Coronary Spasm Collateral Circulation AS CAD PROGRESSES VESSELS CAN THESE COLLATERAL VESSELS ALLOW A EXERCISE ENHANCES THE GROWTH OF GROW FROM OCCLUDED ARTERIES “BYPASS” TO MAINTAIN CIRCULATION THE COLLATERAL CIRCULATION THAT AND PREVENT/DELAY ISCHEMIA SUPPLIES BLOOD TO THE HEART Coronary Artery Disease: Clinical Manifestations Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. S/s: Critical deficit in By itself usually no Angina blood supply (~70- 75% symptoms blockage of lumen) pectoris, MI Coronary Artery Disease: Diagnosis Blood Cholesterol Coronary angiography Echocardiography Heart rate recovery after submaximal exercise  Cardiac Pathophysiology: Hypertension Neeti Pathare, PT, MSPT, PhD Objectives 1. Understand the term hypertension. 2. List the different categories of hypertension across the lifespan. 3. Identify the different types of hypertension. 4. Describe the pathogenesis and clinical manifestations of hypertension. Hypertension as a Risk factor for CAD Virani S. Circulation. Heart Disease and Stroke Statistics—2021 Update, Volume: 143, Issue: 8, Pages: e254-e743 Hypertension (Hypertensive Vascular Disease) Elsevier, Inc. Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Hypertension, or high blood pressure, is defined by the World Health Organization (WHO) as a persistent elevation of diastolic blood pressure, higher than 90 mm Hg, systolic blood pressure, higher than 140 mm Hg, or both measured on at least two separate occasions at least 2 weeks apart, i.e., sustained elevation of blood pressure.  Virani S. Circulation. Heart Disease and Stroke Statistics—2021 Update, Volume: 143, Issue: 8, Pages: e254-e743 Hypertension (Hypertensive Vascular Disease) Hypertension Classification in Children Normal < 90th percentile; 50th percentile is midpoint of the normal range imprint of Elsevier, Inc. Copyright © 2015, 2009, 2003, 1998 by Saunders, an th 90 — 95th percentile or if blood pressure is greater than Prehypertension 120/80 mm Hg (even if this figure is 99th percentile + 5 mm Hg  Hypertension Categories Is also known as idiopathic hypertension and accounts for 90% to Primary, or essential, hypertension 95% of all cases of hypertension Accounts for only 5% to 10% of cases Secondary hypertension and results from an identifiable cause. Is a syndrome of markedly elevated blood Malignant hypertension pressure (diastolic blood pressure of more than 125 mm Hg) with target organ damage. Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 7  Hypertension: Pathogeneis Blood pressure is regulated by two factors: Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. blood flow and peripheral vascular resistance. 2. Increased peripheral resistance as a result of the narrowing of the arterioles is the single most common characteristic of hypertension. 3. Constriction of the peripheral arterioles may be controlled by two mechanisms, each with several components: a. Sympathetic nervous system activity (autonomic regulation) b. Activation of the renin-angiotensin system https://www.heart.org/en/health-topics/high-blood-pressure/health-threats- from-high-blood-pressure Hypertension: Clinical Manifestations 1. Hypertension is frequently asymptomatic; this creates a significant health care risk for affected people. 2. When symptoms do occur, they may include headache. Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Cardiac Pathophysiology: Angina Pectoris Neeti Pathare, PT, MSPT, PhD Objectives 1. To define angina pectoris. 2. To describe the contributing factors for angina pectoris. 3. To recognize the clinical presentation of angina pectoris. 4. To compare the different types of angina pectoris. 5. To list the tools used for diagnosing angina pectoris. Angina Pectoris Angina is a symptom of ischemia usually brought on by an imbalance between cardiac workload and oxygen supply to myocardial tissue usually secondary to CAD Occurs when: Myocardial O2 Demand > Myocardial O2 Supply Very Serious and never a normal Symptom Increased oxygen needs of the heart, increased cardiac output, or reduced blood flow to the heart can cause angina. CAD accounts for 90% of all cases of angina. Angina Pectoris: Clinical Presentation 1. Chest Pain 2. Pressure on chest; squeezing, crushing 3. SOB; shortness of breath 4. Radiating Pain/Numbness and tingling: Jaw, Back, Arm; left side is classic, Neck 5. Typically starts in chest and radiates elsewhere OR it may originate in any of the above areas Angina Pectoris: Clinical Presentation a change in pattern or severity may indicate disease progression individual patients generally experience angina consistently VERY INDIVIDUAL! To distinguish between angina and musculoskeletal pain: musculoskeletal pain is reproducible and palpable  Angina Pectoris: Causes Typically precipitated by the “3 E’s” Cold weather Exercise/ Excessive Exertion vasoconstriction Emotions Eating Smoking Angina Pectoris is an indication of 1. Congestive heart failure (CHF) 2. Myocardial ischemia 3. Myocardial infarct (MI) 4. Mitral valve stenosis Types of Angina Angina associated with a set level of O2 demand Pts can usually predict when the pain will start Stable Angina (Predictable) Usually the same symptoms (type of pain) Relieved by Rest or Nitroglycerine Same symptoms as Stable but may occur without increase in workload Persists longer than usual; more intense Unstable Not relieved by rest and/or nitro Indication of CAD progression and need to be evaluated by MD Results from Coronary A. Spasm Unpredictable onset, occurs at odd times, eg. while sleeping Prinzmetal or Variant More common in women Not associated with exertion of exercise Predicting Stable Angina Rate Pressure Product (RPP) = HR (at onset of pain) x SBP (at onset of pain) Any time the pt. gets here, pt. will have Ex: 100 bpm x 140 = 140,000 symptoms Also called the point of ischemia Unstable Angina: Contributing Factors Increased levels of Epinephrine in Increased platelet Blood stream within 4 hours of activation Changes in the plaque waking  Typical angina at lower work loads Unstable Angina : Detection This type of Angina occurs to coronary artery spasm A. Stable B. Unstable C. Variant Angina: Diagnosis 1. History 2. Use of nitroglycerin relieves symptoms 1–2 minutes 3. Pharmacologic Stress test 4. Cardiac Catherization Angina Diagnosis: Cardiac Catheterization 1. A a fine catheter through femoral artery or brachial artery into the heart is passed 2. Measures all pressures (valves, cardiac output) 3. A contrast medium into chambers and arteries and filmed is injected 4. Allows to see blockages, flow of blood  Cardiac Pathophysiology: Myocardial Infarction Neeti Pathare, PT, MSPT, PhD  1. To define myocardial infarction. 2. To describe the pathogenesis of myocardial infarction. 3. To provide a timeline of pathophysiological changes in the myocardium following myocardial infarction. Objectives 4. To understand the classification of myocardial infarction. 5. To recognize the clinical presentation of myocardial infarction. 6. To compare the diagnostic tools for myocardial infarction. 7. To summarize the changes in key myocardial enzymes following myocardial infarction. Myocardial Infarction (MI) MI, also known as a heart attack is the development of ischemia with resultant necrosis of myocardial tissue. Actual necrosis of myocardium due to anoxia Eighty percent to 90% of MIs result from coronary thrombus at the site of a preexisting atherosclerotic stenosis. More frequently during early morning hours. Silent ischemia is highly prevalent among people with diabetes. Myocardial Infarction (MI): Pathogenesis 1. Plaque ruptures or sclerosed artery becomes Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. completely filled with thrombus. 2. Blood vessels get occluded by a clot 3. The most common site involved is the left ventricle Myocardial Infarction (MI): Pathogenesis Zone of ischemia 1. Next to the zone of hypoxic injury: reversible zone called the zone of ischemia Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Zone of injury 1. Immediately surrounding the area of infarction, less seriously damaged area of injury 2. This zone may return to normal within 2-3 weeks Zone of infarction 1. When the myocardium has been completely deprived of oxygen, cells die and the tissue becomes necrotic 2. The remaining heart muscle cells enlarge to compensate for the loss in heart pump function. 3. Formation of fibrous scar tissue is usually complete within 6–8 weeks.  4–10 days: Evolution MI: Pathogenesis of infarct Involved wall becomes 2–3 Months necrotic, Scar tissue 1st 6 hours weakened becomes firm, less Ischemia may be Activity vascular and pale reversible restricted to Vulnerability to w/thrombolytic light activity, complications agents exercise greatly decreased 18–24 hours: Inflammatory 6–8 Weeks response; intercellular enzyme release Necrotic tissue replaced by scar 1st 48 hours: High tissue vulnerability to arrhythmia Patients may begin aerobic After 1st 48 hours, conditioning at a if stable, ok to begin Phase more aggressive I Cardiac Rehab intensity MI : Classification Degree of wall How far does the damage extend into the heart involvement Location What artery involved and what area does it serve Size Uncomplicated or Complicated Types of MI – Degree of Wall Involvement Transmural Subendocardial (SEMI) Extends through the Epicardium, Myocardium, Heart mm. just under and Endocardium the Endocardial wall Full wall thickness Outer wall is spared That area becomes unable to contract  MI—Location of Infarction Area of Supplied Myocardium by Anterior Left coronary artery † Left anterior descending branch Posterior Right coronary artery Inferior Right coronary artery Determined by Left Main Occlusion Anteroseptal Left coronary artery Distribution of Left anterior descending branch Involved Artery Massive involvement of the Left Ventricle High Lateral Circumflex artery Left coronary artery Serious complications Diagonal branch for the heart to perform its function! Apical Usually left coronary artery Left anterior branch Sometimes right coronary artery Posterior descending branch A Subendocardial MI is synonymous with a transmural MI A. True B. False  MI–Uncomplicated vs. Complicated Uncomplicated MI Complicated MI Small MI Large MI with one or more of the following “complications” No complications during recovery Arrythmias Usually fully recovery Conduction Disturbances with minimal decrease in cardiac function Heart failure Unstable angina Mechanical complications Cardiac arrest A complicated, acute myocardial infarction may be indicated by any of the following 1. angina following the MI 2. deconditioned response to activity 3. severe mitral regurgitation 4. associated pulmonary edema 5. All of the above Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Manifestations Clinical MI: MI: Clinical Manifestations Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. Symptoms do not always follow the classic pattern, especially in women 2. Two major symptoms in women are shortness of breath, sometimes occurring in the middle of the night, and chronic, unexplained fatigue 3. Postinfarction complications include arrhythmias, CHF, cardiogenic shock, pericarditis, rupture of the heart, thromboembolism, recurrent infarction, and sudden death Diagnosis and Prognosis: MI ECG Newer Markers Cardiac troponin I (TnI) and cardiac Echocardiogra troponin T (TnT) (regulatory proteins phy that help the heart muscle contract) Myocardial isoenzyme Newer biochemical TnT is quite specific: remains elevated markers 5 to 7 days after an MI and is a predictor Angiogram of cardiovascular mortality. Exercise Tolerance Test Diagnosis of MI Serial Enzymes CPK—MB; Isoenzyme of myocardial tissue 1. Elevated > 3% serum level 2. Elevated levels indicated death of myocardial tissue 3. Rises 3–4 hours after MI 4. Peaks at 33 hours after infarct 5. Levels return to normal in 3 days Diagnosis TEE and Angiogram Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. Transesophageal echocardiography (TEE), an ultrasonic technique that provides a clearer image of the heart, allowing for the identification of structural heart diseases 2. Angiogram A patient is undergoing tests in the hospital to evaluate for possible MI. Which of the following would be the definitive indicator for the diagnosis of MI: 1. ECG tracing revealed S–T segment changes 2. Physical examination revealed presence of substernal chest pain of a crushing nature 3. His serial blood enzyme levels are elevated over a 24–36 hour period 4. Administration of NTG failed to relieve chest pain  Cardiac Pathophysiology: Congestive Heart Failure Neeti Pathare, PT, MSPT, PhD  1. To define congestive heart failure (CHF). 2. To list the different types of CHF. Objectives 3. To describe the pathogenesis of CHF. 4. To compare left and right CHF as well as systolic and diastolic CHF. 5. To recognize the clinical presentation of CHF. 6. To explain the prognosis of CHF. 1. Represents a group of clinical manifestations caused by inadequate pump performance Congestive Heart Failure from either the cardiac valves or the myocardium 2. Heart unable to pump sufficient blood to supply the body’s needs 3. Backup of blood into the pulmonary veins and high pressure in the pulmonary capillaries -> pulmonary congestion and pulmonary hypertension 4. Right or left side or both sides 5. Chronic or Acute 6. Many cardiac conditions predispose individuals to CHF, but hypertension is one of the most prevalent.  CHF types CHF Systolic heart Heart failure with Left-sided heart Right-sided heart failure preserved failure failure caused by ejection fraction contractile or Diastolic Heart failure of the failure myocardium Pathogenesis: Left-sided CHF Contractility Goal is to This has limits ceases to increase maintain cardiac ventricular dilation based on Frank beyond a certain output Starling law point. Pathogenesis: First Compensatory Phase Pulmonary congestion Fluid seeping from Accumulation Actual flooding of the the distended of blood in air spaces of the blood vessels the lungs. lungs occurs Damming Pulmonary Edema of blood Pathogenesis: Second Compensatory Phase Ventricular Hypertrophy More pumping Increased Coronary arteries cannot HR increased Muscle Mass meet the oxygen Force of contraction Need for oxygen demands increased of the enlarged myocardium SNS response Angina Pathogenesis: Third Compensatory Phase Tissue Edema Kidneys retain water and sodium Expanded blood volume stress the comprised Activation Increased heart blood volume Renin Angiotensin Increased load System and burden The body initially attempts to compensate for a failing heart by 1. increasing vagal stimulation 2. an increase in heart rate 3. decreasing venous return that strengthens the hearts contraction 4. decreasing contractility to improve diastole  Pathogenesis Decompensated Compensated When the mechanisms backfire and further burden the heart All three mechanisms allow May range from mild to life threatening a normal cardiac output and be misunderstood for aging/deconditioning Pathogenesis Pathophysiologic mechanisms of congestive heart failure Left-sided heart failure leads to pulmonary edema Right ventricular failure causes peripheral edema that is most prominent in the lower extremities CHF: Clinical manifestations; left–sided 1. Decreased Q (due to MI, decreased contractility) out of the LV 2. The RV is still pumping into the pulmonary system 3. Fluid overload in the lungs 4. Alveoli can get fluid instead of air 5. Inadequate gas exchange = Shortness of breath (SOB!) 6. Pulmonary symptoms predominate CHF: Clinical manifestations; right–sided 1. Decreased output into Pulmonary circulation 2. Blood still coming in from venous/system 3. Back up in the right atrium 4. Fluid fills up in the system 5. Usually found with left-sided failure CHF: Clinical manifestations Left Ventricular Failure Progressive dyspnea; exertional first Tachypnea Paroxysmal nocturnal dyspnea Diaphoresis Orthopnea Cerebral hypoxiaI Productive spasmodic cough Irritability Pulmonary edema Restlessness Extreme breathlessness Confusion Anxiety; associated with breathlessness Impaired memory Frothy pink sputum Sleep disturbances Nasal flaring Fatigue, exercise intolerance Accessory muscle use Muscular weakness Crackles; formerly called rales Renal changes CHF: Clinical manifestations Right Ventricular Failure Dependent edema; ankle or pretibial first Jugular vein distention Abdominal pain and distention Weight gain Right upper quadrant pain; liver congestion Cardiac cirrhosis Ascites Jaundice Anorexia, nausea Cyanosis (nail beds) Psychologic disturbances A patient in the clinic is a 69-year-old male with a history of 3 previous MIs over the last 10 years, all occurring in the left ventricle. The patient demonstrates cardiomegaly on radiograph. His functional work capacity is low. He has been in the maintenance phase of cardiac rehab at your facility. You note he has developed increasing SOB and ankle edema and has gained over 6 lbs. over the past week. You refer the patient to his physician and contact the physician’s office because you suspect the patient may be experiencing which of the following? A. MI B. Angina C. CHF Diastolic vs Systolic Heart Failure 1. “Diastolic HF : S/S of HF, preserved EF and abnormal diastolic function 2. Ventricular chamber is unable to accept an adequate volume of blood during diastole to maintain an appropriate stroke volume 3. Decrease in ventricular relaxation and/or an increase in ventricular stiffness 4. NYHA class II-IV Diagnosis: NT-proB-type Natriuretic Peptide (BNP) 1. Released in response to changes in pressure inside the heart Normal level With heart failure; unstable heart function < 74y 2. BNP levels are simple < 50y less than 125 pg/mL and objective measures Higher than 450 pg/mL of cardiac function. 75–99y > 50y less than 450 pg/mL Higher than 900 pg/mL 3. The high negative predictive value of BNP tests is particularly helpful for ruling out heart failure  Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Prognosis 1. Treatment of CHF remains difficult, and the prognosis is poor, even with advances in pharmacologic therapy 2. Other signs of poor prognosis include severe left ventricular dysfunction, severe symptoms and limitation of exercise capacity, secondary renal insufficiency, and elevated plasma catecholamine levels. A 60-year-old patient is undergoing tests in the hospital to evaluate for possible unstable CHF. Which of the following would be the definitive indicator? A. ECG tracing revealed S–T segment changes B. Physical examination revealed presence of substernal chest pain of a crushing nature C. His serial blood enzyme levels are elevated over a 24–36-hour period. D. BNP levels higher than normal age referenced values Cardiac Pathophysiology: Valvular Heart Disease Neeti Pathare, PT, MSPT, PhD  1. Identify the most common valvular conditions that might be seen by physical therapists. 2. Review the pathophysiology of the most Objectives common valvular conditions, and their implications for hemodynamics and for exercise. 3. Discuss the signs and symptoms associated with valvular conditions. Valvular Heart Disease Functional, Anatomic, eg, prolapse; congenital deformities; deformities caused by eg, stenosis, rheumatic fever, trauma, infection, insufficiency ischemia narrowing or constriction; valve cannot open fully Stenosis obstruction to blood flow, and the chamber behind the narrowed valve must produce extra work valve does not close properly Insufficiency; Regurgitation blood to flow back into the heart chamber the heart gradually dilates due to the increased work enlarged leaflets bulge backward into the atrium Prolapse affects the mitral or tricuspid valve Valvular Heart Disease Mitral Stenosis Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. Mitral stenosis is a sequela of rheumatic heart disease that primarily affects women. 2. Mitral valve is thickened 3. Mitral valves opens in early diastole with a snap, audible on auscultation, and then closes slowly with a resultant murmur. Physiological Effects of Mitral Stenosis 1. Heart working harder Increased mm. mass = hypertrophy Increased O2 demand 2. Also…chamber does not fully empty Decreased EF, ejection fraction Decreased SV, stroke volume Decreased CO = Increased HR to compensate, increases demand Mitral Stenosis: Clinical Manifestations Moderate 1. Dyspnea and Fatigue 2. Left atrial pressure rises and mechanical obstruction of filling of the left ventricle reduces cardiac output Severe 1. Left atrial pressure is high enough to produce pulmonary venous congestion at rest and reduce cardiac output 2. Dyspnea, fatigue, and right ventricular failure  Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Mitral Valve Prolapse (MVP) 1. MVP is characterized by a slight variation in the shape or structure of the mitral (left atrioventricular) valve 2. The cause remains unknown, although there may be a genetic component 3. According to data from the Framingham Heart Study, MVP is not as prevalent as previously reported.  Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Mitral Valve Prolapse: Clinical Manifestations The most common triad of symptoms associated with MVP is profound fatigue that cannot be correlated with exercise or stress, palpitations, and dyspnea.  Valvular Incompetence or Insufficiency 1. Valves fail to close fully 2. Blood “regurgitates” back through the valve during contraction (systole) 3. Chamber in front and behind must bear extra load 4. Valve lesions are usually mixed, not pure 5. Classified according to predominant effect on the heart 6. Individuals often asymptomatic until condition is advanced  Aortic Stenosis Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. Disease of aging becoming more prevalent as our population ages 2. It is most commonly caused by progressive valvular calcification either superimposed on a congenitally bicuspid valve or, in the older adult, involving a previously normal valve following rheumatic fever. 3. Other risk factors for aortic stenosis same as those for heart disease; include obesity, a sedentary lifestyle, smoking, and high cholesterol.  Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. Aortic Stenosis: Clinical Manifestations 1. Characteristic sounds may be heard on auscultation, but cardiac output is maintained until the stenosis is severe and left ventricular failure, angina pectoris, or exertional syncope develops. 2. Adults with aortic stenosis who are asymptomatic have a normal life expectancy; they should receive prophylactic antibiotics against infective endocarditis. 3. The onset of angina, exercise-induced syncope, or cardiac failure indicates a poor prognostic outcome resulting in death. Aortic Regurgitation: Insufficiency Copyright © 2015, 2009, 2003, 1998 by Saunders, an imprint of Elsevier, Inc. 1. When cardiac systole ends, the aortic valve should completely prevent the flow of aortic blood back into the left ventricle. 2. A leakage during diastole is referred to as aortic regurgitation or aortic insufficiency 3. When aortic regurgitation develops gradually, the left ventricle compensates by both dilation and enough hypertrophy to maintain a normal wall thickness/cavity ratio, thereby preventing the development of symptoms. A leakage in valve during diastole is referred to A. Mitral stenosis B. Mitral insufficiency C. Aortic stenosis D. Aortic insufficiency Aortic Valve Lesions Aortic Stenosis Aortic Insufficiency LV is having blood back up LV working harder to when pumping into pump blood through this the aorta stenotic valve Aortic Valve Lesions Heart Compensates for Decreased SV/Cardiac Output Increased HR Increased Myocardial Work Ventricular Hypertrophy Eventually the ability of the LV to adapt is exceeded LV failure Q begins to fall off blood dams up behind failing ventricle > pulmonary edema high diastolic pressures prevent low systolic aortic pressures reduce subendocardial prefusion (stenosis) coronary blood flow (regurgitation) Signs/Symptoms of Valve Disease Initial Resting and exertional tachycardia Early Dyspnea on exertion (DOE) Later S/S BP falls as Q is unable to meet normal demands Dizziness, orthostatic hypotension, exertional syncope Recumbent position shifts fluid back to central circulation individual awakens suddenly gasping for breath paryxosysmal nocturnal dyspnea (PND) triggers "flash" pulmonary edema exercise may also bring on pulmonary edema ischemia and angina may occur in aortic valve diagnosis Initial S/S observed with Valvular conditions include A. Tachycardia B. Bradycardia C. Low resting BP D. Edema  Cardiac Pathophysiology: Congenital Heart Disease 1 Neeti Pathare, PT, MSPT, PhD  1. Identify the most common congenital heart defects that might be seen by physical therapists Objectives 2. Review the pathophysiology of the most common congenital heart defects and their implications for hemodynamics and for exercise 3. Discuss the signs and symptoms associated with congenital heart disease. Congenital Heart Disease Congenital heart disease (CHD) —CDC.gov is the most common birth defect worldwide and occurs in ~ 1 per 110 live births each year —Reller et al 2008 3 Epidemiology https://www.cdc.gov/ncbddd/heartdefects/data.html Lesions caused by abnormal fetal development The most common type of heart defect is a ventricular septal defect (VSD) ~ 1/4 of children born with CHD require intervention in the first year of life ~ 95% of babies born with a non-critical CHD and ~69% with critical CHDs are expected to survive to 18 years of age At least 15% of CHDs are associated with genetic conditions About 20% to 30% of people with a CHD have other physical problems or developmental or cognitive disorder 4 Living with CHD Improved survival rate # adults living with CHDs is at least equal to, if not greater than, # children living with CHDs —CDC.gov Moons P et al 2010 5  6 Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session of the CV system Development Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session Idiopathic 7 Medications taken by mother Smoking by mother Genetics Etiology Classification of Lesions: Acyanotic/Left to Right Shunt Blood shunted from (L) Oxygenated side (R) Blood bypass the systemic circulation Decreased Cardiac Output: Compensation: Increased HR Increased Venous Return from shunted blood Increased preload = Increased contractility; heart working harder Leads to failure Example: Ventricular/Atrial Septal Defect  Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session Classification of Lesions: Acyanotic/Left to Right Shunt 1. Atrial Septal Defect 2. Ventricular Septal Defect 3. Patent Ductus Arteriosus 4. Atrioventricular Septal Defect 5. Coarctation of the Aorta Classification of Lesions: Cyanotic/Right to Left Shunt 1. Blood passes from (R) (L) without being oxygenated 2. Bypass the pulmonary circulation 3. Cyanotic Babies… no O2 10 Classification of Lesions: Cyanotic/Right to Left Shunt Cardiopulmonary Educators session Hillegass E (2016) Pediatric Cardiovascular PT. PT 1. Tetralogy of Fallot 2. Hypoplastic Left Heart Syndrome 3. Transposition of Great Arteries 4. Tricuspid Atresia 5. Pulmonary Atresia 6. Truncus Arteriosus 7. Total Anomalous Pulmonary Venous Return 11 What type of shunt is more serious? A. Left to Right B. Right to Left Classification of Lesions: Stenosis 1. Valve 2. Great vessel 3. Example: Coarctation of Aorta  Stenotic Lesions: Coarctation of Aorta 1. Narrowing of the Aorta itself; early within the Aorta; not the valve 2. LV hypertrophy  Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session Stenotic Lesions: Coarctation of Aorta Signs/Symptoms 1. May have extremely high BPs and cause aortic aneurysm, brain hemorrhage, stroke and heart failure as well as CAD. 2. Usually undergo repair by age 10 Implications for Physical Therapy 1. BP monitoring is essential 2. Ventricular changes remain for a lifetime therefore these individuals are at risk for HF Stenotic Lesions: Congenital Aortic or Pulmonary Stenosis Pulmonary stenosis Narrowing of the pulmonary valve RV hypertrophy May need to be opened with pulmonary valvuloplasty Less gas exchange: shortness of breath, less exercise tolerance Stenotic Lesions Aortic stenosis Narrowing of the aortic valve LV hypertrophy Surgery: surgery or widening of valve with valvuloplasty Less cardiac output, syncope These patients are at high risk for sudden death Education on syncope Typically, ASD causes what type of shunt A. Left to Right B. Right to Left Cardiac Pathophysiology: Congenital Heart Disease 2 Neeti Pathare, PT, MSPT, PhD  1. Identify the most common congenital heart defects that might be seen by physical therapists. 2. Review the pathophysiology Objectives of the most common congenital heart defects, and their implications for hemodynamics and for exercise. 3. Discuss the signs and symptoms associated with congenital heart disease.  Patent Ductus Arteriosus/Patent Foramen Ovale 1. Problem: Fetal circulation that persists in newborns 2. Fetal Life a. Blood bypasses the pulmonary circulation b. Fetus gets blood from the placenta and this is routed to the Right atrium (RA) LA LV c. This occurs due to i. Foramen Ovale; Passage in the atrial septum, R L ii. Ductus Arteriosis; connects Pulm a. and aorta 4 Patent Foramen Ovale/Atrial Septal Defect Opening between Pressure is higher on Atriums fails to the (L) so blood flow close from (L) (R) Bypassing Decreased Cardiac systemic Output circulation Can close spontaneously Patent Ductus Arteriosus/Patent Foramen Ovale When newborns take a Blood that gets into breath at birth, lungs Foramen Ovale closes Before birth, the Aorta is just inflate, fluid is taken out immediately lungs are and blood begins functionally and flowing in to flow into the filled with fluid the path of least anatomically 2–3 pulmonary circulation; resistance less pressure here than months later systemic if FO and DA do not DA closes functionally within Creates a left close, or remain patent, the first 15–72 hours in to right shunt response to increased arterial oxygenated blood is re oxygen saturation. Anatomical routed through pulm circ closure occurs by 2–3 weeks in most term neonates Patent Ductus Arteriosus DA does not close Blood flows into the path of least resistance Pulmonary ® side Bypass of systemic circulation Decreased Cardiac Output (L) (R) Shunt Can close on own, close with meds or needs to be surgically closed Ductus arteriosus connects Pulmonary artery and Pulmonary vein A. True B. False Ventricular Septal Defect MOST COMMON defect An opening is present in the interventricular or interatrial septum Due to higher left ventricular or left atrial pressures gradient is from left to right side of heart Ventricular Septal Defect Oxygenated blood in the Increased preload on the ® ventricular hypertrophy LV is shunted back to the right side – ® side has (R) side of the heart to work harder may fail For every LV contraction blood is going to aorta Decreased cardiac output Pulmonary hypertension and back to RV Implications for Physical Therapy Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session Need to assess HR, BP and SpO2 responses to activity Watch for signs R heart failure VSD and ASD especially: Low EF possibly, and more Right sided heart problems, including may have Pulmonary Hypertension VSD: May need to utilize significant supplemental oxygen If surgical repair: Will need annual assessment Tetralogy of Fallot 1. Aorta originates from RV or overrides the IV Septum 2. VSD a. (R) (L) Shunt 3. Pulmonary a. Stenosis a. Less blood getting O2 b. Increases pressures on ® = Encourages shunt to (L) 4. RV Hypertrophy 12 Tetralogy of Fallot 1. Aorta originates from RV or overrides the IV Septum 2. VSD a. (R) (L) Shunt 3. Pulmonary a. Stenosis a. Less blood getting O2 b. Increases pressures on ® = Encourages shunt to (L) 4. RV Hypertrophy 13 Tetralogy of Fallot Blood enters aorta from both ventricles; mixing of oxygenated and deoxygenated blood (R) (L) shunt of non-O2 blood into systemic circulation Biggest problems are with low O2 levels : Cyanosis! Seriousness of situation depends on amount of pulmonary stenosis. Usually have surgery early to repair pulmonary stenosis and VSD Tetralogy of Fallot causes what type of shunt A. Left to Right B. Right to Left Secondary Conditions with Cardiac Issues Hillegass E (2016) Pediatric Cardiovascular PT. PT Cardiopulmonary Educators session 1. Downs: several defects 2. VATER: vertebral, anus, tracheoesophageal, radial and renal 3. Marfan: connective tissue disease: aortic aneurysm 4. Aortic and mitral valve issues 5. Williams: Associated with supravalvular aortic and pulmonic stenosis 6. Fetal Alcohol Syndrome — facial dysmorphology, VSD, pulmonary valve stenosis, PDA 7. DiGeorge — multiple cardiac abnormalities 17 Other diagnoses with decreased activity Cerebral Palsy Duchenne’s Spina Bifida Spinal Atrophy cdc.gov Cardiac Pathophysiology: Peripheral Arterial Disease Neeti Pathare, PT, MSPT, PhD Objectives 1. Define peripheral vascular disease (PVD) and peripheral arterial disease (PAD). 2. Review the pathophysiology of PAD. 3. Discuss the clinical manifestations of PAD. 4. Identify the surgical procedures used for PAD. Peripheral Vascular Disease 1. PVD is a broader, more encompassing grouping of disorders of both the arterial and venous blood vessels, whereas peripheral arterial disease (PAD) only refers to arterial blood vessels. 2. PVD typically affects the legs more often than the arms, but upper extremity involvement is not uncommon. Copyright © 2017 by Elsevier, Inc. All rights reserved. Peripheral Arterial Disease PAD is referred to as atherosclerotic occlusive disease (AOD) Atherosclerosis is the underlying cause of occlusive disease. Atheromatous plaque obstruction of large or medium-sized arteries supplying blood to the extremities PAD correlates most strongly with cigarette smoking and either diabetes or impaired glucose tolerance. Other risk factors include male gender, hypertension, low levels of HDL cholesterol, and high levels of triglycerides, etc. Copyright © 2017 by Elsevier, Inc. All rights reserved. Arterial Thrombosis and Embolism 1. Occlusive diseases may be complicated by arterial thrombosis and embolism. 2. Chronic, incomplete arterial obstruction usually results in the development of collateral vessels before complete occlusion threatens circulation to the extremity. 3. Signs and symptoms of pain, numbness, coldness, tingling or changes in sensation, skin changes (pallor, mottling), weakness, and muscle spasm occur in the extremity distal to the block. Copyright © 2017 by Elsevier, Inc. All rights reserved. 5 Clinical Manifestations (PAD) 1. In peripheral vessels, claudication symptoms appear when the diameter of the vessel narrows by 50%. 2. The distance a person can walk before the onset of pain indicates the degree of circulatory inadequacy (e.g., two blocks or more is mild; one block is moderate; one half block or less is severe). 3. The primary symptom may only be a sense of weakness or tiredness in these same areas; both the pain and weakness or fatigue are relieved by rest. Copyright © 2017 by Elsevier, Inc. All rights reserved. 6 Copyright © 2017 by Elsevier, Inc. All rights reserved. Ankle Brachial Index The ankle/brachial index (ABI) is a measure Useful in documenting the need for and of arterial perfusion benefit of a prescriptive exercise program. Angioplasty Medical Illustration Copyright © 2022 Nucleus Medical Media. All rights reserved external link. Bypass Surgery Medical Illustration Copyright © 2022 Nucleus Medical Media. All rights reserved external link.