Patho Chap 12

Chapter 12

Cardiovascular System Disorders

Chapter Objectives

• Review of the Cardiovascular System

  • Located in the mediastinum, double-walled

• Explain the calculation of cardiac output and blood pressure

  • Cardiac Output: volume of blood ejected by a ventricle in 1 minute

  • Stroke volume: the volume pumped from one ventricle in one contraction

  • Blood pressure: the pressure of blood against the systemic arterial walls

    • Decreasing the diameter increases blood pressure: vasoconstriction

    • Vasodilation decreases blood pressure

      • All controlled by the vasomotor control and SNS

        •  SNS and epinephrine act at the beta-adrenergic receptors to increase the rate and contraction, elevated blood pressure

        •  SNS, epi and norepinephrine increase vasoconstriction by stimulating the alpha receptors in the arterioles of the skin, elevated blood pressure

        • ADH: increases water absorption, causes vasoconstriction

        • Aldosterone: increases blood volume

        • Rein-angiotensin-aldosterone causing vasoconstriction, increasing blood pressure

•  Define the pathways of impulse conduction in the human heart

  • Abnormal variations in the ECG: arrhythmias and dysrhythmias indicate acute problems like an infarction, systemic problems, electrolyte imbalances

  • Impulse Conduction

    • SA node pacemaker

    • Impulse spread through the atrial conduction: atriums contract

    • Impulses at AV node located at the septum

    • Slight delay before for the filling of the ventricles

    • Impulses continue to the ventricles terminal Purkinje network

• Depolarization=atrial contraction p wave

• Ventricular contraction & large wave of depolarization (QRS)

• T wave- repolarization of the ventricles 

•  Control of the heart: What controls the heart rate?

• Baroreceptors detect changes in blood pressure

• Cardiac center controls SNS and PNS response

• Sympathetic Nervous System=tachycardia increases heart rate

• Parasympathetic Nervous System =bradycardia, decreases heart rate

• The medulla of brain: cardiac control center

• Lubb-dub

  • Lubb closure of AV valves

  • Dub closure of the semilunar valves

  • Murmur defective valves, Ex. a hole in the septum of the heart

  • Pulse indicates heart rate

• Preload: mechanical state of the heart at the end of diastole with ventricles at max

• Afterload: force required to eject blood from ventricles (Determined by peripheral resistance)

• Diagnostic Tests: Describe common tests used to diagnose cardiovascular disease and myocardial infarction

  • ECG: useful in the initial diagnosis and monitoring of arrhythmia, MI, infection, and pericarditis

    • Noninvasive procedures illustrate the conduction activity of the heart

  • Auscultation: Detecting valvular abnormalities/shunts (Stethoscope)

  • Echocardiography: Records the image of the heart and valve moments (changes in heart structures)

  • Exercise stress test: Assessing general cardiovascular function

    • Checking for exercise-induced problems

  • Chest x-ray: Shows the shape and size of the heart

    •  Evidence for pulmonary congestion

  • Nuclear Imaging: Assesses the size of an infarct in the heart

    • Extent of myocardial perfusion and function

  • Tomographic: Illustrates various levels of a tissue mass

  • PET: CT scan of damaged tissue

  • Cardiac Catheterization: Passing a catheter through an appropriate blood vessel to visualize the inside of the heart, measure pressure, and blood flow to and from the heart

  • Angiography

  • Troponin & Myosin: serum levels of troponin the protein is released when there is cardiac damage + Myosin for muscle lesions

  • Doppler Studies: Microphone records the sounds of blood

  • Arterial blood gas:  Check current oxygen level and acid-base balance

• General Treatment Measures for Cardiac Disorders: Describe the measures used to treat cardiovascular disease, such as angina pectoris and myocardial infarction, including common drug and invasive treatments as well as lifestyle changes

  • Dietary Modification

  • Exercise

  • Cessation of smoking

  • Drugs:

    • Vasodilators 

    • Beta Blockers – Metoprolol or Atenolol

    • Calcium Channel blockers: decreases contractibility 

    • Digoxin – a cardiac glycoside, antiarrhythmic drug 

  • Antihypertensive drugs

    • Adrenergic-blocking

    • ACE inhibitors: 

    • Diuretics

  • Anticoagulants – blood thinners, reduce the risk of blood clot formation in coronary or systemic arteries

  • Cholesterol or Lipid-lowering drugs

•  Heart Disorders: Coronary Artery Disease, Ischemic Heart Disease, or Acute Coronary Syndrome

  • Differentiate between stable and unstable angina pectoris

    • Angina Pectoris (chest pain) causes deficit oxygen to the heart muscle, blood or oxygen supply to the myocardium is impaired, heart works way too hard and needs more oxygen

      • Causes: Atherosclerosis, arteriosclerosis, vasospasm, myocardial hypertrophy, severe anemia, respiratory disease

      •  Precipitating factors: running up the stairs, getting angry, respiratory infection

      • Signs and symptoms: tightness/pressure on the chest, Pallor, excessive sweating, nausea

      • Treatment: Coronary vasodilators nitroglycerin reduce systemic resistance

      • Subtype (Variant Angina-arterial spasms at rest)

    • Stable Pectoris - predictable pain upon exertion which subsides with rest- Better of the two

    • Unstable Pectoris- prolonged pain at rest and onset may precede with MI(High risk)

      • Treatment

        • Nitroglycerin

          • vasodilator

          • administer sublingual or spray?

• Myocardial Infarction: Discuss the pathophysiology of myocardial infarction

Treated with PTCA

• A heart attack, death of myocardial tissue because of ischemia 

  • Type 1- coronary artery totally obstructed, atherosclerosis, following is inflammation (Infarction may develop from thrombus, vasospasm, emboli)

    • Signs and Symptoms:

      • Sudden chest pain radiates to left arm

      • Pallor

      • Excessive sweating

      • Nausea

      • Low grade fever

    • Diagnostic tests:

      • Change in ECG

      • Serum enzymes and isoenzymes released from necrotic cells (CK-MB)

      • Serum levels of myosin and troponin elevated after the MI

      •  Serum electrolyte levels (potassium and sodium) hyperkalemia

      • Leukocytosis an elevated CRP and ESR – INFLAMMATION

      • Arterial blood gas measurements

      • Pulmonary artery pressure measurements

    • Treatments

      •  Analgesics for pain

      • Oxygen therapy

      • Anticoagulants to reduce clotting

      • Digoxin

      • Bypass surgery

      • Cardiac rehabilitation

      • Low dose of ASA

• Type 1 - Coronary Artery occluded

• Type 2 - Mismatch of blood supply and myocardial demand

• Type 3- sudden and fatal heart attack

• Type 4 & 5 MI induced from medical procedures 

• Cardiac Dysrhythmias (Arrhythmias): Recognize common arrhythmias and define cardiac arrest

  • SA Node Abnormalities: Pacemaker 

    • Bradycardia: stroke volume increased, reduced cardiac output, vagus nerve and PNS

    • Tachycardia: possibly reduced cardiac output, stimulation of sympathetic

    • Sick sinus syndrome; alternating between bradycardia and tachycardia, 

  • Atrial Conduction Abnormalities: most common dysrhythmia, digoxin slows AV node conduction

    • Premature atrial contractions: ectopic beats, extra contractions of the atrium from irritable atrial muscle cells, interfering with the timing of the beat 

    • Atrial flutter: rate 160-350 bpm ventricular rate is slower

    • Atrial fibrillation: a rate of than 350, no cardiac output, most common type of arrhythmia 

  • AV Node: Heart block when conduction is excessively delayed or stopped at the bundle of HIS, caused by ischemia or drugs

    • 1st degree: delay between the atrial and ventricular contraction

    • 2nd degree: missing ventricular contraction, longer delay

    • 3rd degree: no transmission of impulses from the atria to the ventricles causing syncope requires pacemaker

  • Ventricular Conduction Abnormalities

    • Bundle bunch block: interference with conduction in one of the bundle fibers either on the left or right side

    • Ventricular tachycardia: reduces the cardiac output because the filling time decreases

    • Ventricular fibrillation; ineffective in ejecting blood results in no cardiac output, the most dangerous, use of an AED

    • PVCs: additional beats from ventricles ectopic pacemaker

    • Paroxysmal supraventricular tachycardia: ectopic beat, episodes of fast beats, chambers don’t fill 

Treatment: antiarrhythmic 

• Cardiac Arrest: cessation of all heart activity, no contraction, no pulse, no cardiac output

• Congestive Heart Failure: The heart is unable to pump sufficient blood to meet the metabolic needs of the body, insufficiency of cardiac output 

• Left-Sided Congestive Heart Failure

  • Causes: infarction of the left side, aortic valve stenosis, hypertension, hyperthyroidism

  • Effects: decreased cardiac output, pulmonary congestion, pulmonary edema 

  • Signs and Symptoms

    • Dyspnea; difficulty breathing/orthopnea; difficulty breathing while lying down

    •  Cough producing phlegm that is white or pink

    • Paroxysmal nocturnal dyspnea: sudden attacks while they are asleep

• Right-Sided Congestive Heart Failure

  • Causes: infarction of the right side, pulmonary valve stenosis, pulmonary disease

  • Effects: systemic congestion, peripheral swelling edema

  • Signs and Symptoms:

    • Edema

    • Hepatomegaly

    • Splenomegaly

    • Ascites; a collection of fluid

    • Acute right side failure: enlarged neck veins

• Compensation

  • Tachycardia

  • vasoconstriction

  • oliguria 

• Cor Pulmonale - Pulmonary Hypertension from lung disease 

• Explain the circumstances and special considerations for young children with congestive   heart failure

  • Children with Congestive Heart  Failure

    • Usually secondary to congenital heart disease, feeding difficulties are the first sign with failure to gain weight, third heart sound present, enlarged heart with or without fluid, tripod position to play, flared nostrils, blood gas -> hypoxia

  • Heart Muscle Disease - Cardiomyopathy: in the presentation 

    • Dilated

    • Hypertrophic CMP

    • Restrictive CMP 

  •  Treatment of CHF

    • Reducing the workload of the heart

    • Prophylactic measures: vaccine

    • Maintaining diet

    • Vasoconstrictors/vasodilators

• Describe the pathophysiology of congenital heart disorders, particularly septal defects, shunts, patent ductus arteriosus, coarctation of the aorta, transposition of the great arteries, and tetralogy of Fallot 

  • Congenital Heart Defects:  Structural defects in the heart that develop during the first 8 weeks of embryonic life, multifactorial and combination of genetic (trisomy x) and environmental influences (fetal-alcohol syndrome), a major cause of death in the first year of life.

  • Signs and Symptoms of large cardiac anomaly

    •  Pallor/cyanosis

    • Tachycardia

    • Dyspnea

    • Clubbed fingers

    • Intolerance of cold weather and exercise

    • Delayed growth

  • Treatment: 

    • Surgical repair, palliative care

  • Septal defects: mixing of the oxygenated blood from pulmonary and systemic circulation

    • Atrial Septal Defect: left to right shunts; blood gets oxygenated again

    • More blood enters into the right side, and less blood into the tissue

    • Ventricular Septal Defect; right to left shunts 

  • Ductus Arteriosus 

  • Patent Ductus

  • Coarctation of the aorta: aorta and pulmonary artery are switched in positions 

-   Transposition of the great arteries

-   Tetralogy: most common cyanotic congenital heart condition, including four heart abnormalities. A right-to-left shunt is created causing the flow of unoxygenated blood to end up in the systemic circulation. Oxygen deficit

o   Pulmonary valve stenosis

o   VSD

o   Dextroposition of the aorta

o   Right ventricular hypertrophy

Valvular Disorders: Differentiate between valvular insufficiency  and valvular stenosis

Valvular Insufficiency- the valve cannot close properly  

Valvular Stenosis-narrowing of the valve

Mitral Valve - floppy valve causing backflow 

Mitral Valve Stenosis = pooling of blood leaking 

Inflammation and Infection of the Heart: Explain the pathophysiology of rheumatic heart disease, infectious endocarditis, myocarditis, and pericarditis

Rheumatic Heart Disease: Acute systemic inflammatory condition that appears after an untreated infection caused by the hemolytic group A beta streptococcus.

o   Preceding infection: upper respiratory infection, tonsilitis, pharyngitis or strep throat

o   Antibodies form and create connective tissues in the skin, joints, and heart = inflammation

o   Pericarditis: inflammation of the outer layer impairing filling

o   Myocarditis: lesions in the heart muscle Aschoff bodies

o   Endocarditis: valves have warts affecting the blood flow, creating stenosis (verrucae)

o   Causing rheumatic heart disease

o   Signs and Symptoms:

•   Low-grade fever

• Leukocytoiss

•  Malaise, fatigue

• Tachycardia

• Anorexia

• Pain

o   Diagnostic: elevated levels of antibody levels

o   Treatment: penicillin V, anti-inflammatory agents, valve replacement

Infective Endocarditis; Subacute type and Acute type

Subacute: defective heart valves by low virulence microorganisms (S. Viridans)

Acute: defective heart valves by high virulence microorganism (S. Aureus)

o   Patho: microorganisms invade entering through general circulation creating vegetation in the valves: masses of fibrin strands and platelets

loosely 

o   Pieces may break off forming septic emboli

o   Etiology:

·  Predisposing conditions

·  Invasive procedures increasing risk of infection

o   Diagnosis: hearing many heart murmurs

Pericarditis: Acute or chronic and secondary

Acute: simple inflammation of the pericardium, causing chest pain and rough friction

Fluid could accumulate in the pericardial sac compressing the heart

Chronic: formation of adhesions limiting heart movement

o   Etiology: Acute: secondary to MI, open heart surgery, RF, systemic lupus, cancer renal failure, Chronic: radiation and tuberculosis

o   Signs/Symptoms: tachycardia, chest pain, dyspnea, distended neck veins, painful heartbeats

o   Treatment: fluid must be aspirated

Arterial Disorders: Describe the pathophysiology of primary, secondary, and malignant hypertension and hypertension’s effects on body system, Describe the development of hypertensive heart disease

Primary Hypertension/ Essential: idiopathic, more common, hardened area=higher pressure 

Secondary Hypertension: results from renal or endocrine disease, a benign tumor (pheochromocytoma benign SNS tumor) 

Malignant Hypertension: emergency extremely high blood pressure, uncontrollable

o   Patho: increased vasoconstriction can decrease blood flow to the kidneys and trigger even more vasoconstrictors

o   Decreasing blood flow: ischemia and necrosis

o   Etiology/pre-disposing factors: Age, men, race, diet high sodium intake

o   Signs/Symptoms: fatigue, malaise, morning headache, kidney issues, retinopathy, cardiomegaly, left ventricular hypertrophy

o   Treatment: Lifestyle changes, diuretics depending on  serum levels of sodium, vasodilators

Cardiomyopathy

 Discuss the pathophysiology of cardiomyopathy and identify its different types

Shock: Define shock and its effects on the body

Shock: decreased circulating blood volume leading to hypoxia and severe lack of tissue perfusion, poor oxygenation

Patho: decrease blood volume, blood pressure drops, less cardiac output, less oxygen

Compensation:

o   SNS stimulated=increased heart rate tachycardia

o   Renin released = increase blood volume

o   Increased secretion of ADH = vasoconstriction

o   Acidosis: increase respiration

Decompensation: if the shock is not reversed quickly

o   Acute renal failure

o   ARDS; shock lung

o   Hepatic failure

o   Paralytic

o   Depression of cardiac function

o   Multiorgan failure

Etiology:

Hypovolemic Shock: loss of blood or loss of plasma

Cardiogenic Shock: cardiac impairment such as acute infarction of the left ventricle

Vasogenic Shock: blood relocated within the system

Anaphylactic shock: systemic vasodilation and increased capillary permeability

Septic shock: Vasodilation owing to severe infection