Cardiovascular Alterations: Hypertension & Thrombosis

Alterations in Cardiovascular Function

• Thrombus and thromboembolism are discussed regarding vein diseases.
• Hypertension and orthostatic hypotension are reviewed.
• Atherosclerosis, coronary artery disease, angina, and myocardial infarctions are examined.
• Pericardium disorders and an introduction to cardiomyopathies are furnished.

Thrombus and Thromboembolism

• Thrombus formation occurs in veins and factors promoting thrombosis include the Triad of Virchow:
  • Venous stasis occurs
  • Damage to venous endothelial
  • Hypercoagulable states
• Embolism occurs when a bolus of matter circulates in the bloodstream then lodges and obstructs blood flow.
• Treatment includes:
  • Anticoagulants like heparin and Coumadin
  • Thrombolytics like streptokinase and urokinase

Hypertension

• Consistent elevation of systemic arterial blood pressure occurs.
• Sustained systolic blood pressure is 130 mm Hg or greater or a diastolic pressure of 80 mm Hg or greater.
• Hypertension occurs because of increases in cardiac output or total peripheral resistance, or both.
  • Blood pressure/Hypertension = Cardiac output x Peripheral Resistance
  • Cardiac Output = Heart Rate x Stroke Volume

Primary Hypertension

• Primary hypertension is referred to as essential or idiopathic hypertension, it has no known cause.
• Proposed interactions of genetics and the environment mediated by neurohumoral effects may produce dysfunction of the sympathetic nervous system(SNS) and renin-angiotensin-aldosterone system (RAAS) and inflammation.
• 92-95% of those with hypertension have primary hypertension.
• Risk factors include:
  • Family history
  • Advancing age
  • Sex (Men are at greater risk than women before age 55, women at greater risk after 55)
  • Race (African Americans have 2x the risk)
  • Heavy alcohol consumption
  • Cigarette smoking
  • Obesity
  • High dietary sodium intake
  • Glucose intolerance

Pathophysiology of Primary Hypertension

• Genetics and environment can contribute to insulin resistance, inflammation, and dysfunction of the SNS, RAAS, adducin, and natriuretic hormones.
• Vasoconstriction and renal salt and water retention can occur.
• There can be increased peripheral resistance and increased blood volume
• Sustained hypertension occurs.

Secondary Hypertension

• Secondary hypertension is caused by a systemic disease that raises peripheral vascular resistance and/or cardiac output.
• Examples include:
  • Renal arterial stenosis
  • Pheochromocytoma
  • Hyperaldosteronism

Categories of Blood Pressure

• Normal systolic blood pressure is less than 120 mm Hg, diastolic, less than 80 mm Hg.
• Elevated systolic blood pressure is 120-129 mm Hg, diastolic, less than 80 mm Hg.
• High blood pressure(hypertension) stage 1 systolic blood pressure is 130-139 mm Hg, diastolic, 80-89 mm Hg.
• High blood pressure(hypertension) stage 2 systolic blood pressure is 140 or higher mm Hg, diastolic, 90 or higher mm Hg.
• Hypertensive crisis systolic blood pressure is higher than 180 mm Hg, diastolic, higher than 120 mm Hg.
• Measurement of blood pressure involves averaging two readings on at least two separate occasions.
• After 5 minutes of rest, with no smoking or caffeine intake in the past 30 minutes.

Hypertension Manifestations

• Early stages of hypertension have no clinical manifestations other than elevated blood pressure and is called silent disease
• Hypertensive crisis can occur which is rapidly progressive hypertension.
  • Systolic pressure is greater than 180 mm Hg and/or diastolic pressure is usually greater than 120 mm Hg.
  • It is life-threatening.

Complications of Persistent High Blood Pressure

• Brain: Stroke (CVA), intracerebral hemorrhage, and hypertensive encephalopathy(HA, altered LOC) can occur.
• Retina of the eye: Retinopathy can occur.
• Heart: Cardiovascular disease, heart failure and left ventricular hypertrophy can occur
• Kidneys: Chronic Renal Insufficiency and End Stage Renal Disease can occur
• Blood: Atherosclerosis which damages blood vessels and lead to artery narrowing

Hypertension Treatment

• Lifestyle modifications are recommended.
  • Reduce or eliminate risk factors
  • Restrict sodium intake to 2.4g/day, increase potassium intake, restrict saturated fat intake, and adjust calorie intake as required to maintain optimal weight.
  • Dietary approaches to stop hypertension (DASH)
• Stop smoking
• Exercise program that promotes endurance and relaxation
• Medications can be used to reduce hypertension.
  • Drugs that decrease heart rate include beta blockers, alpha-beta blockers, and alpha-2 stimulators
  • Drugs that decrease force of contraction include beta blockers and alpha-beta blockers
  • Drugs that decrease preload (systolic volume) include diuretics, ARBs, and selective aldosterone blockers
  • Drugs that decrease peripheral resistence include diuretics, calcium channel blockers, ARBs, ACE inhibitors, selective aldosterone blockers, alpha–beta blockers and alpha-2 stimulators
• Drugs decrease cardiac output by decreasing heart rate, decreasing force of contraction and decreasing preload
• Drugs can decrease peripheral resistence which decreases afterload
• Drugs that treat hypertension include Diuretics, calcium channel blockers, ARBs, ACE inhibitors, selective aldosterone blockers, Alpha-beta blockers and alpha-2 stimulators

Orthostatic Hypotension

• Decrease in the systolic and diastolic blood pressures on standing by 20 mm Hg or more and by 10 mm Hg or more, respectively.
• It is a lack of normal blood pressure compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation
• Classified as acute versus chronic orthostatic hypotension
• The clinical manifestation is fainting upon standing.
• Treatment includes:
  • Nonpharmacologic interventions of fluid and salt intake management, and thigh-high stockings.
  • Pharmacologic interventions with mineralocorticoids and vasoconstrictors

Atherosclerosis

• Thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall.
• Plaque develops.
• The process may occur anywhere throughout the body.
• It is the leading cause of coronary artery disease and cerebrovascular disease.
• Atherosclerotic plaques may lead to inadequate perfusion-> ischemia-> necrosis
• Risk factors include:
  • Nonmodifiable: Age, genetic disorders of lipid metabolism and family history of premature CAD
  • Modifiable: Smoking, obesity, HTN, hyperlipidemia, and DM
• Clinical manifestations depends on the organ affected.
• Symptoms and signs are the result of inadequate perfusion of tissues.
• It is treated by detecting and treatment to stabilize plaques
  • Exercise, controlling diet, stopping smoking
  • Controlling HTN, DM, and hyperlipidemia
• If atherosclerotic plaque ruptures, the goal becomes acute restoration of adequate blood flow.

Coronary Artery Disease (CAD)

• CAD constitutes any vascular disorder that narrows or occludes the coronary arteries,leading to myocardial ischemia.
• Atherosclerosis is the most common cause of CAD.
• Primary cause of heart disease in U.S.
• Modifiable risk factors include:
  • Dyslipidemia like high LDL and low HDL
  • Hypertension
  • Cigarette smoking
  • Diabetes mellitus and insulin resistance
  • Obesity and/or sedentary lifestyle
  • Atherogenic diet
• Nonmodifiable risk factors include:
  • Advanced age
  • Family history
  • Male gender or women after menopause

Coronary Artery Disease (CAD) Data

Angina Vs ACS

• NSTEMI is non ST elevated myocardial infarction. STEMI is ST elevated myocardial infarction
• Stable angina includes: plaque disruption, platelet aggregation, and thrombus.
• Acute coronary syndrome is either stable or unstable angina. | | Stable Angina | Unstable Angina NSTEMI | STEMI | | ------------- | ---------------------------------- | ------------------------------------------------------------ | ------------------------------------------ | | Manifestations| Predictable pain, Predictable relief | Progressive pain, minimal or no relief with conservative medical management | | | ECG/EKG | Normal ECG, ST depression, T wave inversion | | ST Segment elevation | | Biomakers | Negative Trops/CKMB | Postive Trops/CKMB | | | 1st Cardiac Procedures | Stress test (Either pharmacological or physical) | | PCI (percutaneous coronary intervention) | | 2nd Cardiac Procedures | Diagnostic Angiogram, possible interventional cath | PCI (percutaneous coronary intervention) | Coronary artery Bypass graft |
• Tx to remember:
  • MONA: Morphine, oxygen, nitroglycerine, aspirin

Importance of 12 Lead EKG

• Lateral leads: I, aVL, V5-V6
• Inferior leads: II,III,aVF
• Anterior/Septal Leads:: V1-V4
• LCx or Diagonal of LAD: Lateral
• RCA and/or LCx: Inferior
• LAD: Anterior/Septal Leads

Myocardial Infarctions

• NSTEMI is subendocardial infarction, meaning it is partial thickness.
• STEMI is transmural infarction, meaning it is full thickness.
• Ischemia results in a switch to anaerobic metabolism.
• Electrolyte imbalances occur.
• Catecholamines are released and Activation of RAAS occurs, and Angiotensin II is released The effects of the processes are peripheral vasoconstriction and fluid retention.
• Myocardial work increases, so myocyte contractility is exacerbated.
• Neurohormonal tissue is involved in myocardial remodeling which leads to hypertrophy due to growth factor for fibroblasts/scar tissue formation.
• Clinical manifestations include:
  • Severe chest pain
  • Radiation of pain to neck, jaw, back, left arm
  • Lightheadedness and dizziness
  • Atypical signs: indigestion, nausea, vomiting
  • Cool clammy skin
• TX and Complications:
  • Hospitalization and bed rest
  • Immediate administration ofO2, aspirin, and nitroglycerin
  • Morphine, Thrombolytics, Antithrombotic, Vasodilators
  • Percutaneous coronary intervention (PCI) and Surgery
• Complications include:
  • Dysrhythmias; Cardiogenic shock; Heart failure; and Pericarditis

Acute Pericarditis

• Acute inflammation of the pericardium.
• Most common causes are idiopathic or following a viral infection.
• Clinical manifestations includes fever, myalgias, and malaise, followed by the sudden onset of severe chest pain that is sharp, abrupt, pleuritic. Physical exam may reveal intermittent friction rub and ECG changes.
• Treated with rest, salicylates, and nonsteroidal anti-inflammatory drugs.

Pericardial Effusion

• Accumulation of fluid occurs in the pericardial cavity.
• Manifestations include distant/muffled heart sounds, dyspnea, and dull chest pain.
• A complication is Cardiac Tamponade.
• Treatment is pericardiocentesis.

Cardiac Tamponade

• A condition when rapid fluid accumulation with resulting increased intrapericardial pressures impairs diastolic filling and reduces cardiac output (CO). Caused by:
  • LIFE THREATENING compression
  • Rapid blood or fluid buildup in the pericardium
  • Clinical Manifestation of Systemic and pulmonary hypoperfusion
    • Dyspnea, tachypnea, tachycardia, hypotension
    • Jugular vein distension
    • Pulsus paradoxus
  • Dx: imaging/ history
  • Tx: pericardiocentesis & treatment of underlying cause

Introduction to Cardiomyopathies

• A diverse group of diseases affecting the myocardium of the heart.
• May be caused by hereditary issues or caused by another disease.
• Remodeling of the myocardium occurs, which impacts either diastolic or systolic function.
• 3 Major Types:
  • Dilated
  • Hypertrophic
  • Restrictive

Dilated Cardiomyopathy

• Dilated globular shape of the heart, particularly in the left ventricle, leads to systolic dysfunction.
• Causes unknown
• Clinical manifestations includes dyspnea, fatigue, and edema.
• Treatment has a focus on reducing blood volume and increases contractility.

Hypertrophic Cardiomyopathy

• Can be Hypertrophic obstructive cardiomyopathy or cause due to hypertension/valvular issues.
• Hypertrophy happens as the myocytes attempt to compensate for increased myocardial workload.
• Causing Diastolic Dysfunction

Restrictive Cardiomyopathy

• Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole.
• Idiopathically or manifestation of other disease process.

Heart Failure

• A pathophysiologic condition in which the heart cannot generate adequate cardiac output, resulting in inadequate perfusion of tissues.
• Classifications include:
• Left vs. Right Heart Failure (Systolic or diastolic)
• Low vs. High-Output HF

Heart Failure

• Myocardial dysfunction due to myocardial infarction, ischemic heart disease, hypertension, or other conditions.
• Activation of RAAS system retains Sodium and water through vasopressin, endothelin, and cytokines causing ventricular remodeled that impairs contractility

Heart Failure - Left Sided

Distinguished as systolic heart failure, reduced EF, or diastolic heart failure.

• Contractile heart tissue impairment reduces EF.
• Decreased compliance and relaxation of the left ventricle is present Characteristics:
  • Dyspnea, possible fatigue, cough, and pulmonary edema
  • Pulmonary edema causing possible oliguria and abnormal sounds due to decreased urine output
  • The inability of adequate circulation to perfuse

Heart Failure -- Right Sided

• Inability of right ventricle to provide adequate blood flow at a normal venous pressure.
• Can result from Left vs pulmonary disase
• Characteristics include Peripherial edema.
• The manifestation of upper QUAD discomformity
• Physical findings for jugular distension.

Heart Failure Diagnosis

• Laboratory examinations can include: - Basic labs Comprehensive metabolic panel - Cardiac specific natriuretic peptides like ANP and BNP - EKG Pulmonary artery catheterization
• NP: Quantifies the severity through volume or pressure in ANP, BNP and LV:Syst/ Dias+ Rv to valvular disfunction

Heart Failure Treatment

• May vary and depend on which form of heart failure patient may have.
• Some medications used in treatment include:
  • Diuretics
  • ACEI , ARBS and Aldosterone antagonists
  • Beta Blockers
  • Inotropic agents
  • Direct acting pulmonary vasodilators
• Other surgical interventions of implantable defibrillators, pacemakers.

Classification of Heart Failure

• Class 1: No limitations of heart failure
• Class 2: Slight limitation of ordinary physical
• Class 3: Marked limitation of physical activity but comfortable at rest
• Class 4: Severe limitations and symptoms even as rest

High Output Failure

• It occurs when the heart cannot supply adequate blood flow and nutrients to the body despite having normal or elevated myocardial contractility.
• Underlying issues include anemia, beriberi, sepsis, thyroid issues

Shock Overview

• Shock is a state of acute circulatory failure that includes inadequate tissue perfusion. -- This results cellular hypoxia with an imbalance in oxygen demands
  • Causing metabolic switch
  • The inflammtory result causes lactic Generation
  • Common types includes altered mental state and weak feelers

Types of Shock

• Classified as an imbalance between symathetic and parsympatic stimulation - Hypovolemic: fluid volume - Cardiogenic: heart failure - Neurogenic: muscle - Anaphylactic: immune - Septic: Infection

Multiple Organ Dysfunction

• It is a progressive syndrome of the organ systems resuting from uncontrolled inflammation which show through respritory, renal, cardiac and nuerologic manifestations.