dyspnea Flashcards
dyspnea
the subjective experience of breathing discomfort (symptom) that consists of qualitatively distincl that vary in intesity
Synonyms- Breathlessness, shortness of breath, winded, cant catch breath , breathing is tight, suffocating, not getting enough oxygen/ air gasping
aspirin, atorvastatin, ramipril, hydrochlorothiazide
Aspirin- Secondary prevention of MI/stroke, irreversible of COX 1 and 2, antiplatelet effect block TX, Side effects- GI related
Atorvastatin- treatment of coronary artery disease, hypercholesterolemia, inhibition of HMGCoA reductase to decrease cholesterol biosynthesis, upregulation of LDL receptors to increase clearance of cholesterol from plasma, Side effect= muscle weakness
Ramipril- Treatment of hypertension, heart failure, Prevents formation of angiotensin 2, Effects- vasodilation, reverse remodeling of LVH, Sideeffects- cough, angioedema, hyperkalemia, orthostatec hypotension
HCTZ- treatment of hypertension, edema, associated with heart failure, hypercalciuria, inhibit NaCl transport in the distal convoluted tubule, effects- diuress, natriurisis, decrease BP, SEp hypokalemia, hypercuricemia, hyperglycemia
causes of dyspnea
Pulmonary- COPD or astham, infection (pneumonia, bronchitis), pneumothorax, Contusion, hemorrhage
Neuro/MSK- ALS myasthenia gravis, rib fracture, chest or spine deformity
Hematologic- Anemia, Pulmonary embolism
Upper airway- angioedema, anaphylaxis, pharyngeal infections, deep neck infections, Foreign body
Cardiaac- heart failure, MI, Arrythmia, Valvular disorder, Cardiac tamponade
Toxic/metabolic- metabolic acidosis, Poisonins (CO, salicylate)
Causes of heart failure
Other primary Cardiac causes- congenital lesions, valvular disease, arrythmias idiopathic
Preserved EF- Hypertension, Aging, Restrictive CM, Infiltrative (amyloidosis, sarcoidosis)
Reduced EF- Coronary artery disease/MI, Hypertension, Toxins (alcohol doxorubcin cocaine), Viral , idiopathic
High output failurep Anemia, thyrotoxicosis, nutritional (beri, beri), Dialysis fistula,
Pulmonary- cor pulmonale, COPD, ILD)
Ways of conceptualizing heart failure
Blood flow- forward flow issue- impaired oxygen delivery to vital organs. Backward flow issue- venous congestion of lungs, liver, kidney, mesentery
Evil humors- excessive adrenergic tone, ADH release, and RAA activation are initially protective but ultimately couterproductive
Pumo failure- impair contractility, systolic failure or HF rEF
Increased afterload in pulmonary or systemic circulaiton
Valvular incompetence leading to syndrome of heart failure,
Impaired relaxation- diastolic failure of myocardium, pericardial disease
Side- Right vs lef
Furosemide
most clinical manifestiations of HF result from excessive salt and water retention, Leads to inappropriate volume expansion of vascular and extravascular space
Treatment- furosemide loop diuretic, Excretion of 25% of filtered Na load through inhibition of the na k 2cl co transporter, impairs generation of a hypertonic interstitium
Types of vasodilators
venous- Nitrates, Decrease preload (LV end diastolic volume) Results in decreased wall stress with little effect on stroke volume
Mixed- ACEi, Angiotensin 2 inhbitors, Nitroprusside, Redices both preload and systemicvascular resistance (Afterload), results in increased stroke volume and decreased wall stress
Arterial- Hydralizine, Reduces afterload by decreasing systemic vascular resistance, results in increased stroke volume and decreased wall stress
Digoxins
Direct effects
Positive inotropic effect- Due to a direct effect to increase the contractile state of the myocardium, Increases stroke volume, Increases vagal tone (Slows heart rate)
Secondary Effect- Decreased heart rate, Arterial and venous dilation, decreased venous pressure
MOA- Postive inotropic effect due to inhibition of the Na K atpase, results in increased intracellular Na thereby decreasing driving force for ca extusion by Na Ca exchanger, indirectly results in increased intracellular concentration of Ca
K competets for binding of digoxin to the NA K ATPase
HFpEF treatments
Furosemide- treatment of peripheral or pulmonary edema, in excessive amounts can lead to dehydration and electrolyte depletion, Biggest risk ( hypokalemia, hyperuricemia at high doses, nephrotoxicity, and ototoxicity)
Beta blockers- may reduce myocardial oxygen demand by negatice chronotropy and inotropy, often useful for concomitant coronary artery disease, particularly in patiens with pervious AMI
Biggest risks- brady cardia, orthostasis
Orthostatic hypotension, postural hypotension, dizziness light headed or feeling faint
Common side effects of BB, vasodilators, also may be hypovolemia
Atrial fibrillaiton
Advancing age
CV causes and risk factors- hypertension, Coronary artery disease, Rheumatic heart disease, Non rheumatic valvular heart disease, cardiomyopathy
Others- thyrotoxicosis, Obstructive sleep apnea, Alcohol, Acute stressors
Causes of heart failure with AF
Other primary cardiac causes- congenital lesion, valvular disease, arrythmias, idiopathic
Preserved EF- HTN, Aging, restrictive CM, Infiltrative
Reduced EF- CAD, MI, HTN, Toxins, viral, idiopathic
High output failure- Anemia, thyrotoxicosis, nutritional
Pulmonary/vascular- Cor pulmonale, AV amlformation
Atrial fibrillation and heart failure a bidirectional association
Why patients with untreated AF develop HF: incomplete diastolic relaxation time, Sympathetic and R-A -A axis overactivation–> downregulation of receptors, oxidative stress and depletion of ATP
Why pts with HF develop AF- sympathetic overactivation, left atrial enlargement and stretch, mitral regurgitatation
Atrial fibrillation
Manage/ address other risk factors: HTN, CAD, Rheumatic heart disease, Non rheumatic valvular heart disease, cardiomyopathy
Treat other causes- Thyrotoxicosis, obstructive sleep apnea, Alcohol, Acute stressors
Treatment- control rate, convert to sinus rhythm, prevent stroke, improve symptoms, prevent / improve CHF
Calcium channel blockers
Neurons rely on N- and P-type Ca channels, skeletal muscle relies primarily on Cai, cardiac muscle requires Cainflux through L type Ca channels (contraction- fast response cells, upstroke of AP slow response cells)
Vascular smooth muscle requires Ca influx through L type Ca channels for contraction
