CARDIOVASCULAR DISORDERS - MODULE 5

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136 Terms

1
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What are some examples of cardiovascular disorders?

  • angina and acute coronary syndrome

  • cardiac dysrhythmias / arrhythmias

  • other heart abnormalities

  • heart failure

  • shock

  • vascular disorders


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What is atherosclerosis?

  • disease of the tunica intima of the arteries

  • forms fibrous fatty lesions in large to medium sized arteries

    • including aorta, femoral, carotid, and coronary


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What does atherosclerosis result in?

  • increased wall thickness + decreased elasticity

  • reduced vessel radius leading to reduced flow rate

  • ischemia to organ / tissue


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What are the 5 sites of severe atherosclerosis?

  1. abdominal aorta + iliac arteries

  2. proximal coronary arteries

  3. thoracic aorta, femoral, and popliteal arteries

  4. internal carotid arteries

  5. vertebral, basilar, and mdidle cerebral arteries


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What is the etiology of atherosclerosis?

  • endothelial cell damage

  • possibly from:

    • hyperlipidemia

    • cigarette smoke

    • diabetes

    • immune mechanisms

    • turbulent blood flow


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What is the pathophysiology of atherosclerosis?

  1. increased endothelial permeability to plasma proteins and lipids

  2. monocyte migration into sub endothelial layers

  3. monocytes differentiate to macrophages, ingest lipid, and transform into lipid filled foam cells

  4. macrophages will release growth factors to proliferate smooth muscle, ROS, and more

  5. progressive tissue damage and plaque lesion growth will occur


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What are low density lipoproteins?

  • a transport version of lipids in blood

  • oxidized by ROS in plaques and then phagocytized by macrophages


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What are some predisposing risk factors for atherosclerosis?

  • elevated cholesterol which may be genetic

  • high blood pressure

  • obesity

  • diabetes

  • smoking

  • sedentary lifestyle


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What is common artery disease (CAD)?

  • ischemic heart disease cause

  • one third of all deaths in the west

  • nearly all elderly have a coronary impairment


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What is ischemic heart disesae (IHD)?

  • characterized by ischemia of the heart muscle

    • usually because of coronary artery disease


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What is the biology of the coronary arteries?

  • left (main) and right

  • originate from the aorta

  • main arteries on the surface

  • deeper branches penetrate the muscle


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What does the right coronary artery supply?

  • right ventricle

  • posterior regions of the heart


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What does the left coronary artery supply?

  • left ventricle

  • interventricular septum


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What is myocardial blood flow?

  • produces vasodilation or constriction of coronary blood vessels

  • run by two nervous mechanisms:

    • autonomic control which is parasympathetic through vagus nerve)

    • local autoregulatory control

  • coronary blood flow increases 3-4x during exercise


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How is the autoregulation control of myocardial blood flow controlled?

  • local factors

  • vasoactive mediators produce vasodilation or constriction of coronary vessels

    • to match metabolic / oxygen demands of cardiac muscle


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What happens to myocardial blood flow during ventricle contraction?

  • aka systole

  • muscle compresses muscle capillaries

  • reduces blood flow


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What happens to myocardial blood flow in CAD?

  • subendocardial muscle regions are damaged first because they have the most difficulty getting proper blood flow


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What makes myocardial blood flow a lifesaving value of collateral circulation?

  • anastomoses exist between smaller coronary arteries

  • anastomoses dilate within seconds during acute ischemia to provide an alternative path for blood


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What makes atherosclerosis a cause of IHD?

  1. cholesterol deposits under endothelium

  2. deposits get invaded by fibrous tissue

  3. deposits often become calcified which are atherosclerotic plaques

  4. plaques protrude into vessel lumens

  5. blocks blood flow

  6. first few cms of coronary arteries are common sites for atherosclerotic plaques

  7. a gradual hardening and narrowing of the coronary arteries can lead to angina pectoris and complete occlusion


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What is angina pectoris?

  • pains that occur from the sub sternal region of the chest to the jaw and down the arms


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What is stable angina?

  • intact plaque partially obstructs coronary arteries

  • pain is caused by physical exertion or emotional stress

    • myocardial blood flow cant respond to increased demand due to coronary artery narrowing

  • symptoms last less than 15 minutes and are relieved by GTN

  • causes transient myocardial ischemia with no necrosis


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What is unstable angina?

  • plaque surfaces are disrupted which lead to small thromboses (temporary ischemia)

  • chest pain is spontaneous, sudden, and unpredictable

  • pain lasts longer than 20 minutes, is more severe, and GTN doesnt help

  • ischemia effects are temporary with no necrosis

  • may predict myocardial infection


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What treatments are used for unstable angina?

  • oxygen

  • aspirin to reduce clotting

  • nitrates

  • morphine


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What is acute coronary syndrome (ACS)?

  • represents a spectrum of ischemic heart diseases

    • ranges from unstable angina to myocardial infarction


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What are the signs and symptoms of acute coronary syndrome?

  • pain lasts longer than 20 minutes

  • pain can increase in severity

  • unstable angina can have history as a risk factor

  • GTN doesnt relieve symptoms

  • most cases of unstable angina have recovery and temporary effects


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What is myocardial infarction?

  • develops if there is no recovery after unstable angina

  • immediate result of complete coronary occlusion

  • blood flow stops in vessels past the occlusion

  • produces acute ischemia in the myocardium

  • areas of affected myocardium are infarcted


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What does myocardial infection prognosis depend on?

  • the degree of msucle damage


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What is the STEMI classification of myocardial infection?

  • the clot lodges permanently in the vessel and the entire myocardium thickness becomes ischemic

  • associated with the ST segment elevation on the ECG

  • serious and requires immediate emergency intervention


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What is the Non STEMI classification of myocardial infection?

  • thrombus can disintegrate before complete tissue necrosis

  • only the subendocardium is affected

  • associated with ST depression and then T wave inversion


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What are the general manifestations of acute coronary syndrome?

  • fast onset

  • severe and crushing pain that is substernal and radiates to the left arm, neck, or jaw

  • fatigue and weakness

  • tachycardia, restlessness, anxiety, and feelings of doom

  • pale, cool, and moist skin

  • gastrointestinal problems


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How does a decreased cardiac output lead to death in myocardial infection?

  • pumping is reduced

  • can be exacerbated by systolic stretch

    • dead muscle is forced outward by pressure

  • heart failure and peripheral ischemia occurs

  • aka cardiogenic shock


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How does the fibrillation of the ventricles lead to death in myocardial infection?

  • main cause of death in STEMI

  • most serious cardiac arrhythmia

  • cardiac output is zero

    • due to abnormal electrical impulses and conduction pathways in damaged myocardium

  • dangerous in 1st 10 mins and after 1 hour


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How does the rupture of the infarcted area lead to death in myocardial infection?

  • can occur several days after an infarction bc of muscle fiber necrosis and heart wall stretching

  • systolic stretch increases and causes heart rupture

  • can be assessed by cardiac imaging to monitor the stretch


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What immediate care options help with ACS management?

  • anticoagulant therapy from aspirin or platelet inhibitors

  • nitroglycerin

  • beta blockers to slow HR and lengthen diastole

  • oxygen therapy

  • morphine for pain

  • bed rest

  • 12 lead ECG

  • ECG monitoring


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What is the importance of absolute body rest for ACS management?

  • prevents cellular death and lowers injury from ischemia

  • reduces collateral circulation that may be assisting damaged muscle during recovery


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What is the importance of pain relief for ACS management?

  • relief is important for comfort

  • lower pain = increased stress = increased cardiac output = increased heart workload


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What is the pathway of electrical conduction in the heart?

  1. SA node for action potential

  2. atria contract and travels to AV node

  3. travels down interventricular septum through the AV bundle of His

  4. splits into left and right bundle branches

  5. ends at the purkinje fibres to supply ventricular myocardium


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What does a normal ECG look like?

  • P wave reads atria depolarization

  • QRS complex reads ventricle depolarization

  • T wave reads ventricle repolarization


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What are the 4 types of normal ECGs?

  1. normal sinus rhythm (normal)

  2. tachycardia (fast)

  3. bradycardia (slow)

  4. sinus arrhythmia during respiration (irregular)


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What are dysrhytmias or arrhythmias?

  • can be missed or rapid beats

  • can be serious disturbances that impair the heart’s pumping ability

  • caused by;

    • abnormal impulse generation rate of SA node

    • abnormal impulse conduction


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What are atrial conduction abnormalities?

  • most common

  • can be asymptomatic because ventricular filling is not dependent on atrial contraction

  • e.g. atrial fibrilltion (400-600 bpm)


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What is atrial fibrillation?

  • disorganized and irregular atrial rhythm with irregular ventricular rhythm

  • sites within the atria generate their own impulses

  • causes pooling of blood in atria

  • treated by anticoagulants to prevent emboli


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What are the atrioventricular node abnormalities?

  • heart block occurs

  • partial and slower conduction (first and second degree)

  • lack of conduction (third degree)

  • cardiac output is reduced a lot


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What is heart block?

  • occurs when conduction is delayed or stopped at the AV node or bundle of His

    • not all atrial beats get to the ventricles


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What are the ventricular conduction abnormalities?

  • ventricular fibrillation

    • no ventricle contraction

    • cant eject blood

    • leads to death within minutes if not treated


46
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What is asystole?

  • no electrical heart activity

  • heartbeat absence

  • aka flatlined heart


47
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What is the pericarditis heart disorder?

  • acute pericardium inflammation causing pain and fever

  • caused by infection, surgery, etc

  • idiopathic

  • treated by relieving symptoms with anti inflammatory drugs


48
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What is the cardiomyopathy heart disorder?

  • affects the myocardium itself

  • many idiopathic cases

  • some genetic

  • some acquired as a result of inflammtion

  • can be dilated or hypertrophic


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What is dilated cardiomyopathy?

  • increased ventricular volume from stretched muscle causing impaired systolic function

  • can be inherited, from infection, chemotherapy, or idiopathic

  • manifestations include dyspnea, orthopnea, and reduced exercise capacity

  • common cause of heart failure and the need for transplants


50
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What is hypertrophic cardiomyopathy?

  • septum thickening that decreases left ventricle size and blocks blood outflow

  • most common cardiomyopathy type

  • inherited

  • mostly asymptomatic

    • symptoms can include angina, dyspnea, and reduced exercise capacity


51
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What is the broken heart syndrome?

  • left ventricle changes shape after intense emotional and physical stress

  • is temporary and recovers within 2 months


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What is the valvular dysfunction heart disorder?

  • congenital or acquireed

    • rheumatic heart disease is most common acquired cause

  • affects aortic and mitral valves

  • stenosis and incompetent / regurgitant valve disruptions occur

  • murmurs occur from abnormal blood flow


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What is the stenosis disruption in valvular dysfunction?

  • narrowing of the valve opening

  • causes turbulent flow and enlargement of emptying chambers


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What is the incompetent / regurgitant valve disruption in valvular dysfunction?

  • permits backflow of blood


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What is heart failure?

  • heart is unable to generate a sufficient cardiac output

  • this can cause insufficient tissue perfusion or increased pulmonary capillary pressures OR BOTH

  • common causes are CAD, valvular disease, and cardiomyopathies

  • common in people ages 65+


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How is cardiac output calculated?

  • stroke volume x heart rate

    • stroke volume depends on preload, afterload, and myocardial contractility


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What is preload?

  • volume of blood in the ventricle after diastole

  • determined by:

    • blood entering the ventricle during diastole

    • blood in ventricle after systole

    • the frank starling law of the heart


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What is the frank starling law of the heart?

  • the more stretched the ventricle wall, the greater contraction force

    • e.g. the more blood in the ventricles, the stronger the contraction


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What is the afterload?

  • resistance to ejection of blood from the left ventricle

  • peripheral vascular resistance is a good afterload indicator


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What is inotropy or contractility?

  • contraction force of a muscle

  • ability of the actin and myosin of the heart muscle to interact and shorten against a load

  • increases cardiac output

  • independent of pre and afterload


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What else can increase contractility?

  • ventricular hypertrophy

  • myocardial infarction


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What are the risk factors for heart failure?

  • ischemic heart disease

  • hypertension

  • type 2 diabetes mellitus

  • obesity

  • old age

  • lack of exercise

  • smoking


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What is systolic heart failure?

  • myocardial contracility is impaired which leads to an ejection fraction decrease

  • caused by:

    • decreased contractility

    • volume overload (e.g. valvular incompetence)

    • pressure overload (e.g. hypertension)

  • more blood in ventricle after contraction increases pre load

    • leads to pulmonary or peripheral edema


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What is diastolic heart failure?

  • impaired diastolic relaxation in the left ventricle

    • causing less blood to enter the ventricle

  • causes include:

    • pericardial effusion: decreased ventricular expansion

    • hypertrophic cardiomyopathy: increased wall thickness and reduced chamber size

    • myocardial ischemia: delayed diastolic relaxation

  • results in pulmonary edema

  • may occur alone or with systolic heart failure

  • accounts for 35–55% of LHF cases


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What is left heart failure (LHF)?

  • congestive heart failure

    • can be systolic, diastolic, or both

  • decreased cardiac output from the left ventricle to systemic circulation

  • blood backs up into the left heart and lungs

    • increasing pulmonary venous pressure

    • causing fluid to enter lung tissue

    • resulting in pulmonary edema


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What is right heart failure (RHF)?

  • right ventricle is unable to move deoxygenated blood from the systemic circulation into the pulmonary circulation

  • increased systemic venous pressure causes peripheral edema

  • swelling occurs in the lower limbs because of gravity

  • organ congestion causes hepatomegaly (enlarged liver) and ascites (abdominal fluid buildup)

  • severe cases can cause distended jugular veins

    • visible buging neck veins even when standing


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What are the causes of right heart failure (RHF)?

  • left heart failure (most common)

    • increased pulmonary pressure causes blood to back up into the right ventricle

    • causing the right ventricle to dilate and fail

  • cor pulmonale (lung disease)

    • lung diseases increase pulmonary pressure, leading to RHF

    • e.g., COPD, cystic fibrosis, ARDS

  • right heart problems

    • conditions that weaken right heart contraction

    • e.g., MI, cardiomyopathy, valvular disease


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How does sympathetic nervous system activation compensate for heart failure?

  • activates to increase blood pressure and cardiac output

  • increases heart rate and contraction strength

  • puts more strain on the weakened heart


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How does RAAS activation compensate for heart failure?

  • decreased cardiac output reduces kidney blood flow

    • activating RAAS and releasing ADH

  • vasoconstriction

    • increases afterload

  • increased blood volume

    • increases preload

  • both increase strain on the weakened heart


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What is the RAAS system?

  • renin angiotensin aldosterone system


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How does hypertrophy affect the heart during heart failure?

  • thickened ventricular walls

    • increased muscle fiber width

    • may increase ischemia

  • thinned ventricular walls

    • increased muscle fiber length

    • causing ventricular dilation and weaker contractions


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What are the symptoms of heart failure?

  • dyspnea: shortness of breath

  • orthopnea: difficulty breathing when lying down, relieved by sitting up (LHF)

  • fatigue

  • edema: swelling, mainly in lower limbs (weight gain)

  • decreased urine output


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What are the treatments for heart failure?

  • main goal is to decrease preload and afterload

  • salt restriction

  • weight management

  • diuretics to remove excess fluid

  • digitalis to improve stroke volume

  • beta blockers

  • O2 therapy


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What is circulatory shock?

  • sudden failure of circulation to supply enough blood to the body

  • causes cellular hypoxia

  • has many causes and symptoms

  • can lead to organ failure and death if untreated


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What are the clinical manifestations of shock?

  • symptoms vary depending on the type of shock

  • may feel sick, weak, cold, hot, dizzy, confused, afraid, thirsty, or short of breath

  • hypotension: low blood pressure (MAP below 60 mmHg)

    • normal MAP: 70–110 mmHg

  • increased respiratory rate: faster breathing


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What are the cellular effects of shock?

  • decreased oxygen delivery causing cells to switch to anaerobic respiration

    • producing much less ATP

  • decreased ATP causing sodium/potassium pumps to work poorly

    • disrupting Na+, K+, and Ca2+ balance

    • affecting nervous and muscular systems

  • positive feedback mechanisms worsening shock and increasing its severity


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What is positive feedback loop #1 in shock?

  • increased sodium entering cells, causing water to follow

  • water moving from blood vessels into tissues

    • decreasing blood volume and blood pressure

  • decreased blood volume further reducing tissue perfusion (blood flow) and worsening shock


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What is positive feedback loop #2 in shock?

  • decreased ATP and cell swelling causing cell membrane damage

    • releasing lysosomal enzymes

  • lysosomal enzymes damaging surrounding tissues

    • triggering inflammation and further tissue damage

  • increased tissue damage impairing cellular metabolism

    • reducing ATP production and worsening shock


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What is the positive feedback loop #3 in shock?

  • increased acidity decreasing hemoglobin's affinity for oxygen

    • causing more oxygen to be released and worsening tissue hypoxia when blood flow is poor

  • severe damage to vital organs causing shock to become irreversible

    • involving cell membrane damage, lysosomal enzyme leakage, and ATP depletion


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What is cardiogenic shock?

  • decreased cardiac output despite having enough blood volume

    • caused by decreased contractility, increased preload, and/or increased afterload

  • most commonly occurring after MI

    • other causes are possible


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What are the compensatory mechanisms in cardiogenic shock?

  • decreased blood pressure triggering compensatory mechanisms

    • increasing epinephrine release

    • activating RAAS

  • increased oxygen and nutrient demand placing more strain on the heart

    • further weakening the heart's ability to pump blood


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What is the prognosis of cardiogenic shock?

  • often difficult to treat

  • high mortality rate

    • 70% according to your notes (rates vary with treatment and severity)


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What is hypovolemic shock?

  • decreased blood volume causing inadequate circulation

  • caused by significant fluid loss

    • hemorrhage (blood loss)

    • burns (plasma loss)

    • diarrhea or diuresis (fluid loss)

  • begins developing when blood volume decreases by about 20%


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What are the compensatory mechanisms in hypovolemic shock?

  • increased HR and vasoconstriction helping maintain blood pressure

  • interstitial fluid moving into the bloodstream

  • liver and spleen releasing stored blood

  • RAAS and ADH activation helping retain fluid

  • continued fluid loss causing these mechanisms to fail


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What is the treatment for hypovolemic shock?

  • rapid fluid replacement to restore blood volume

  • controlling the cause of fluid loss


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What is distributive shock?

  • massive vasodilation causing blood vessels to widen

    • blood volume stays the same, but has more space to fill

  • decreased blood pressure reducing blood flow and nutrient delivery to cells


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What are the 3 types of distributive shock?

  • neurogenic shock

  • anaphylactic shock

  • septic shock


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What is neurogenic shock?

  • massive vasodilation caused by:

    • increased parasympathetic NS activity

    • decreased sympathetic NS activity

  • causes:

    • spinal cord or medulla injury

    • anesthetic agents

    • severe pain

  • rare and usually temporary


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What is anaphylactic shock?

  • type I hypersensitivity reaction

  • mast cells release histamine, causing:

    • massive vasodilation and increased vascular permeability

    • blood pooling in peripheral vessels and tissue edema

  • smooth muscle constriction causing:

    • laryngospasm and bronchospasm

    • diarrhea


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What is the onset and treatment of anaphylactic shock?

  • sudden onset that can lead to death within minutes

  • treatment: intramuscular epinephrine

    • causes vasoconstriction to increase blood pressure

    • reverses airway constriction to improve breathing


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What is septic shock?

  • most common type of vasodilatory shock

  • severe infection causing an overwhelming inflammatory response

    • triggered by microorganisms or their toxins

  • common cause of death in intensive care units


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How does septic shock differ from other types of shock?

  • warm and flushed skin due to widespread vasodilation

  • other types of shock often cause vasoconstriction

    • reducing blood flow to the skin, making it cold and pale


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What is obstructive shock?

  • mechanical blockage preventing normal blood flow through the central circulation

    • affecting major veins, heart, or lungs

  • increased right heart pressure

  • decreased cardiac output due to blocked blood flow

  • sometimes grouped under cardiogenic shock


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What are the causes of obstructive shock?

  • pulmonary embolism (most common)

  • cardiac tamponade (fluid compressing the heart)

  • pneumothorax (collapsed lung)


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What are the treatments for shock?

  • removing the underlying cause

  • IV fluids to increase blood volume

  • vasopressors to increase vasoconstriction

  • supplemental oxygen

  • positive feedback loops making treatment difficult once established


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What are the effects of atherosclerosis in medium sized arteries?

  • vessel occlusion causing ischemia and infarction

    • coronary arteries lead to heart attack

    • cerebral arterie lead to stroke

  • CAD caused by atherosclerosis is the major cause of myocardial ischemia


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What are the effects of atherosclerosis in peripheral arteries?

  • peripheral artery disease (PAD) causing obstruction of peripheral arteries

  • leading to significant pain and disability

  • common in diabetics


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What are the effects of atherosclerosis in large arteries?

  • thrombus formation

    • may lead to hypertension or emboli

  • weakening of vessel walls

    • may lead to aneurysms

  • commonly affecting large vessels such as the aorta


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How is atherosclerosis managed?

  • reducing risk factors and preventing plaque progression

    • when artery obstruction has not become acute

  • lifestyle changes

    • exercise

    • quitting smoking

  • controlling hypertension

  • reducing LDL through diet or medications


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What is hypertension?

  • consistently elevated systemic arterial blood pressure

    • systolic BP > 130 mmHg or diastolic BP > 80 mmHg

  • increased risk of:

    • myocardial infarction

    • kidney disease

    • stroke