cardiac pathophysiology Flashcards
what are the two essential mechanical functions of the heart
- eject blood into the arteries: systolic performance
- recieve blood from the veins: diastolic performance
what is systolic performance
- generation of high pressure sufficient for organ perfusion
- pulmonary artery and aorta
- ventricles during systole
what is diastolic performance
- maintenance of low pressure to avoid congestion
- atria and veins
- ventricles during diastole
what are the 5 determinants of cardiac output
- preload
- afterload
- contractility
- synergy
- heart rate
what is preload
- the stretch of the ventrile just before the onset of contraction (end-diastolic volume)
- achieving an optimal strech of the myocyte causes improved contractility
what is afterload
- the load against which the ventricles contracts
- resistance to the ejection of blood from the ventricle (myocardial wall stres)
- determined by: peripheral resistance (blood pressure) & heart size (chamber size/wall thickness)
blood pressure - pressure in order for blood to leave heart
what is myocardial contractility
- strength of the cardiac muscle contraction (systolic functioon)
- at the molecular level - it is a load-independent interaction between Ca2+ ions and the contractile proteins
what is synergy
atrio-ventricular synchrony
- atrial pump-priming funciton
- contribute roughly 25% of cardiac output
what is heart rate
cardiac output = stroke volume x HR
what is the modern concept of heart failure
- cardiac injury
- decreased cardiac output and decreased tissue perfusion
- “compensatory” responses
- Na+ and H2O retention, vasocontriction, cardiac and vascular remodeling
- congestion, inc afterload, early myocyte death
- cardiac injury (repeat cycle)
what are the frank-starling limitations
- flattened cardiac performance curve
- less improvement in performance for any given inc. in preload
- excessive preload -> congestive signs
what are the heart rate limitations
- inverse force-frequency relationship
- impaired diastolic filling due to elevated HR
what is cardiac hypertrophy
- one of the primary ways the heart responds to stress or disease
- pressure overload -> concentric hypertrophy
- volume overload -> eccentric hypertrophy
why does concentric hypertrophy occur?
- pressure overload = increased afterload
- increased afterload is the same as increased wall stress
- increase in P is offset by increase h (wall thickness), thus restoring normal wall stress
what are the limitations of myocardial hypertrophy
concentric
- excessive hypertrophy
- myocardial ischemia
- increased ventricular stiffness and poor diastolic relaxation
- arrhythmias
- diastolic heart failure
what are the limitations of myocardial hypertrophy
eccentric
- increased myocardial oxygen demand
- fibrosis, ventricular remodeling
what are endocrine responses
- the heart as a target of systemic endocrine substances
- catecholamines (SNS-NE)
- renin-angiotensin-aldosterone-system (RAAS)
- vasopressin (ADH)
- the heart produces natriuretic peptides
what triggers RAAS
- decreased renal perfusion due to low cardiac output
- renin release from the macula densa-juxtaglomerular cells (DCT)
how does angtiotensin II & aldoseterone work by trying to support circulation by increasing plasma volume and vasoconstriction
- fluid and Na+ retention in kidney
- increase ADH
- vasoconstriction of vascular smooth muscle
- increase thirst
- increase SNS/NE
- increase aldosterone
- myocardial hypertrophy
what are the short term effects of SNS activation
- increase HR
- vasocontriction
- increase contractility
- RAAS activation
- ADH release
what are the long term effects of SNS activation
- increase myocardial O2 demand
- increase afterload
- myocyte necrosis
- increase RAAS/ADH -> congestion
- arrhythmias
what is the natriuretic peptide system
- heart as endocrine organ
- increased plasma volume causes stretch or sress of myocardial tissue triggers production and release of natriuretic peptides
- atrial natriuretic peptide (ANP): B-type natriuretic peptide (BNP) -> elicits diuresis & vasodilation: counteracts the RAAS and SNS
what are the limits of natriuretic peptides
- diminished production by damaged heart tissue
- down-regulation of NPR-A (reduced beneficial biological effect)
- enhanced clearance of ANP/BNP
- NP system is overwhelmed by SNS and RAAS activity in later stages of heart disease
what are the clinical aspects of CHF: right vs left
- right: ascites, pleural effusion
- left: pulmonary edema (pleural effusion: cats)
- biventricular failure: both right and left CHF
what are the clinical aspects of low output heart failure
low cardiac output leads to hypotension and poor tissue perfusion: weakness, shock, collapse
what is preclinical vs symptomatic
- stage A: predisposed
- stage B: preclinical
- stage C: symptomatic
- stage D: end-stage
what are the clincial signs of congestion
- jugular distention, pulses
- abdominal distension, ascities
- anorexia, diarrhea, weight loss or gain
- cough, tachypnea
- dyspnea, increased effort
- orthopnea, cyanosis
- pulmonary edema (dogss, cats)
- pleural effusion (cats)
what are the clinical signs of low outout
- excersise intolerance
- weakness, fatigue
- collapse, syncope
