Diseases Quiz 3 Flashcards
Circulatory Shock
Generalized
Severe reduction in blood supply to the body tissues –> metabolic needs are not met.
Arterial pressure usually low (even w/ compensatory mechanisms)
Severe shock –> inadequate brain blood flow leads to loss of consciousness w/ sudden onset. (syncope)
Sx: pallor, cold clammy skin, rapid HR, muscle weakness, venous constriction
Additional Compensatory Processes:
- Rapid, shallow breathing –> promotes VR via action of respiratory pump
- Increased renin release –> increased TPR via formation of angiotensin II
- Increased circulating levels of ADH –> increases TPR
- Increased circulating levels of epinephrine
- Reduced capillary hydrostatic pressure resulting from intense arteriolar constriction –> reabsorption
- Increased glycogenolysis in the liver (induced by epi and norepinephrine)
Progressive Shock: general CV situation progressively degenerates
Irreversible Shock: no intervention can halt the ultimate collapse of the CV system –> death
Cardiogenic shock
Cardiac pumping compromised –> decreased CO
Ex: severe arrhythmias, abrupt mitral malfunction, MI, coronary occlusions
Patient’s skin cold and clammy (intense vasoconstriction). Oxygen content high on swan-ganz (blood is rushing past tissues)
Hypovolemic shock
Depletion of body fluids –> decreased BV –> reduced cardiac filling –> reduced SV
Ex: hemorrhage (>20% of BV), fluid loss from severe burns, chronic diarrhea, prolonged vomiting
Patient’s skin cold and clammy (intense vasoconstriction). Oxygen content high on swan-ganz (blood is rushing past tissues)
Anaphylactic shock
Severe allergic reaction –> relase of histamine, prostaglandins, leukotrienes, bradykinin –> increased arteriolar vasodilation –> increased microvascular perm –> loss of venous tone –> decreased TPR and CO
Patient’s skin will be warm and pink (intense vasodilation). Oxygen content low on swan-ganz
Septic Shock
Severe vasodilation due to release of substances from infectious agenst
i.e. LPS –> NO synthase increased –> vasodilation
Patient’s skin will be warm and pink (intense vasodilation). Oxygen content low on swan-ganz
Neurogenic shock
Loss of vascular tone due to inhibition of normal tonic activity of sympathetic vasoconstictor nerves
Ex: deep anesthesia, reflex response to deep pain associated w/ trauma, vasovagal syncope.
Acute Coronary Syndrome
Unstable angina vs. MI
Caused by rupture of unstable plaque w/ partial or complete lumen occlusion by aggregated platelets/thrombosis.
MI
Complete thrombotic occlusion of an atherosclerotic coronary artery or hypotensive event superimposed on a partially occuled CA
> 30 min of complete ischemia = myocardial death
transmural infarciton: more likely STEMI
Extent of infarction depends on collateral circulation.
ACUTE sequelae:
Severe /unrelenting angina, acute congestive heart failure (CHF) with dyspnea (pulmonary edema/oxygen desaturation) cardiogenic shock, dysrhythmias, sudden death
Subacute sequale (several days - 2 weeks): Mural thrombosis/risk of embolism, left ventricular rupture = free wall, septal, or papillary muscle: fatal hemopericardium, acute VSD, or acutely flail/regurgitant mitral valve; peri-infarct pericarditis.
Chronic sequelae:
Left ventricular aneurysm; if infarct large enough or multiple infarcts = chronic CHF: LV ejection fraction usually
Cor pulmonale
Pure right sided hypertensive heart disease.
due to chronically increased pulmonary artery pressure from: -COPD
- interstitial fibrosing diseases. -Chronic hypoxia causing vasoconstriction (i.e. sleep apnea)
- Pulmonary vascular disease (primary pulmonary HTN or chronic recurrent thromboemboli)
Calcified Aortic Stenosis
Leading cause of valve replacement surgery along w/ mitral valve prolapse.
Aging related atherosclerosis of aortic valve cusps w/ secondary nodular calcification producing severe ( age 65): association with CAD
Sx: angina, dyspnea, fatigue, syncope, hypertrophied LV, eventual CHF.
Rx: Aortic valve replacement +/- coronary re-vascularization
Cardiomyopathy
Intrinsic myocardial disease NOT associated w/ ischemic, valvular, hypertensive, or structural congenital heart disease.
Clinically divided into dilated, hypertrophic, or restrictive.
Causes include: genetic, myocarditis (i.e. viral), drug effects (alcohol, chemo), hemochromatosisi, and amyloidosis
Tamponade
Increased pericardial sac fluid critically compresses the heart
Many causes:
- effusion: from infx or non-infectious disease (CHF, neoplastic infiltrate, uremia)
- hemopaericardium: (ruptured MI, retrograde rupture of aortic dissection, or penetrating chest trauma)
Constrictive pericarditis:
Progressive pericardial space fibrosis which critically compresses the heart
Rhabdomyoma
Tumor found in children, usually w/ tuberous sclerosis.
Myxoma
Most common adult cardiac tumor. Usually left atrium.
Anemic Chest Pain
Severe anemia (Below 10 or 11) can cause angina due to ischemia especially when coupled with existing CAD.
Left Hypertensive Heart Disease
Systemic/arterial hypertension (chronic/long-standing) can cause:
- left ventricular hypertrophy (LVH) = increased LV wall thickness.
- in addition, hypertension is a risk factor for atherosclerotic CAD
- congestive left heart failure may result from:either systolic (low EF) or diastolic (preserved EF) failure: associated left atrial enlargement can cause atrial fibrillation
- sudden death may occur with LVH
- control of hypertension can reverse LVH
Right Hypertensive Heart Disease
RV failure: peripheral edema, elevated jugular venous pressure, congestive hepatomegaly, ascites
- commonly secondary to chronic left heart failure
- often due to chronic hypoxemic pulmonary disease (esp. COPD, chronic interstitial lung disease) or pulmonary hypertension = cor pulmonale
Note: Chronic hypoxemia states – induce pulmonary vasoconstriction/hypertension
Bicuspid aortic valve
1% of the population
Premature/accelerated AS due to flow abnormalities (often 6th decade symptoms): can be associated with aortopathy (aortic root dilatation/dissection): may cause severe AR in young adults
Mitral Valve Prolapse (MVP)
Most common cause of isolated sever mitral regurg in US requiring surgery.
Myxomatous degeneration/ballooning of mitral valve leaflets w/ elongation/thinning of chordae tendinae (+/- rupture of flail leaflets)
=systolic click murmur syndrome: 3% of U.S adults (usually incidental finding)
Artificial Heart valve complications
Thromboembolism (usually mechanical valves) - need lifelong anticoagulation
Infective endocarditis
Structural deterioration (esp. bioprosthetic valves) calcification and tearing
Intravascular hemolysis
Acute Aortic Regurgitation
typically due to:
- acute bacterial endocarditis
- acutely dilated aortic root secondary to aortic dissection
- traumatic rupture
Acute Mitral Regurgitation
Typically due to:
- papillary muscle/chordae rupture following AMI or chordae rupture in MVP patients = flail MV
- acute bacterial endocarditis
- blunt chest trauma
Dilated Cardiomyopathy
Dilation and impaired contractility of one or both ventricles
Typically associated w/:
-impaired systolic function, arrhythmias, SUDDEN DEATH
Causes: Genetic (20-50%), myocarditis, alcohol abuse, chemo, hemochromatosis, peripartum
Clinical: most commonly affects ages 20-50 w/ progressive symptoms.50% mortality within 2 years. Risk of mural thrombi w/ potential systemic embolism
Rx: LVAD, cardiac transplant.
Hypertrophic Cardiomyopathy
Increased LV wall thickness or mass NOT caused by pathological loading disorders.
Prevalence at least 1 in 500
Most often IV septum is asymmetrically thickened
Impaired diastolic relaxation/filling. Limits CO and Increases LVEDP.
Sx: exertional dyspnea, myocardial ischemia, a fib, eventual ventricular failure w/ dilation. Ventricular arrhythmias and sudden death.
SUDDEN DEATH IN YOUNG (black) ATHLETES –> think Hank Gathers
Rx: Beta blockers, and occasionally partial septal ablation.
Primary / Essential Hypertension
Hypertension of unknown origin.
90% of HTN is this. Treat sx, not the cause.
Rx: Restrict salt intake
Lowers BP because of reduced requirement for water retention to osmotically balance the salt load
Diuretic therapy:
Inhibit renal tubular salt (and fluid) reabsorption
Beta Blockers:
Inhibit sympathetic influences on heart and renal renin release
ACE Inhibitors & Angiotensin II Receptor Blockers:
Block the effects of the renin-angiotensin system
Prominent Cricopharyngeus Muscle
May be asymptomatic or can interfere w/ normal swallowing.
“lump in the throat.”
Esophageal stricture
Secondary to GERD. Acid reflux inflames the esophageal lining causing scarring and subsequent constriction.
Achalasia
Senosis of Esophageal hiatus (LES). Causes dlation of esophagus, swallowing difficulty, weight loss, chest pain, heartburn
Aortic aneurysm
Usually occur in the ascending or descending aorta.
Sx: hoarsness (pressure on left recurrent laryngeal nerve), dysphagia (pressure on esophagus), and dyspnea (pressure on trachea, root of lung, and/or phrenic nerve)
Restrictive Cardiomyopathy
Much less common than dilated or hypertrophic CM.
Impaired ventricular filling.
Non-dilated/usually non-hypertophic ventricles
Causes: idiopathic/familial, amyloidosis, diabetic CM, sarcoid, chemo (anthracyclines)
Pheochromocytoma
NorEpi secreting tumor.
Can cause stress-induced CM.
Dx w/ increased Vanillymandelic aced (VMA) urine levels.
Syncope
Transient loss of consciousness secondary to cerebral hypoperfusion chacterized by rapid onset, short duration, and complete spontaneous recovery.
Classified as: Neurally (reflex) mediated, cardiogenic, autonomic dysfunction, and other.
Neurally mediated (reflex) syncope
Vasovagal - pain, fear, emotional stress, prolonged standing –> overwhelming psns response.
Situational - urination, defecation, coughing, sneezing, swallowing, exercise, weight lifting, otherst
Carotid sinus syncope - shaving, massage, etc.
Clues on hx: defecation, urination, or prolonged coughing, pain, fear, heat exposure
Cardiogenic
Arrhythmias, structural disease
Clues on hx: syncope during prone position, during exercise, palpitations, startling (long QT)
Autonomic dysfunction
Primary autonomic failure (lewy body disease, Parkinson’s disease.)
Secondary autonomic failuire
- diabetic neuropathy
- amyloid neuropathy
- spinal cord injury
Medications - antihypertensives, diuretics, tricyclic antidepressants, phenothiazines, others
Alcohol, exercise, post-prandial
Orthostatic hypotesnion
-diarrhea, hemorrhage, vomitting, adrenocortical insufficiency
Clues in history: standing quickly, prolonged standing, postprandial, heat exposure, following cessation of exercise
Stable Vtach
3 or more consecutive beats of ventricular origin (wide QRS) at a rate 100-200
Asymptomatic
Rx: Amiodarone –> plan for elective synchronized cardioversion.
Long term: Implantable cardioverter defibrillator, amiodarone, beta blockers
6 months w/o arrhythmia before driving.
Unstable Vtach
3 or more consecutive beats of ventricular origin (wide QRS) at a rate 100-200
Unstable - if sx (chest pain, dyspnea), hypotension (SBP 50 joules initially
Long term: Implantable cardioverter defibrillator, amiodarone, beta blockers
6 months w/o arrhythmia before driving.
