Heart Failure [common causes, pathophysio, clinical features, stages]; Dx and treatment of secondary HTN Flashcards
Presentation that does not appear chronic or respond to trad treatments
Signs suggestive of Secondary HTN
- Resistant HTN
- Target organ damage disproportionate to degree of HTN [Stage 1 with CKD]
- Hypertensive Emergency
- Abrupt onset of HTN
- Onset < 30 years old
- Onset of diastolic HTN at > 65 years old
- Exacerbation of controlled HTN
- Drug-induced HTN
- Unprovoked or significant Hypokalemia
Causes of Secondary HTN based on age groups
< 40 year olds: Thyroid dysfunction; Fibromuscular dysplasia [predominantly Renal, Int carotid and vertebral arteries involved]; Renal parenchymal disease
40-64 year olds: Hyperaldosteronism; Thyroid dysfunction; Obstructive Sleep apnea
> 65 year olds: Renal artery stenosis
Essentially for Dx we try to discover the above causes of HTN
Dx methods to determine cause of Secondary HTN
Thyroid Dysfunction: [Hyperthyroidism]
- TSH levels [low]
- Free T4 levels [high]
Hyperaldosteronism: [Conn Syndrome]
- Plasma Aldosterone concentration [high]
- Plasma renin activity [low]
- Aldosterone-to-Renin ratio in morning blood sample [high]
FMD: [mainly effects small-to-medium arteries causing thickening and stenosis]
- HRCT
- DSA [Digital Subtraction Angiography]
- Duplex US/MRA/CTA for Renal artery Stenosis
Renal Parenchymal Diseases: [Glomerulonephritis; PKD; SLE; Renal tumours; Atrophic kidney]
- Renal US and Doppler
- RFTs
Obstructive Sleep apnea:
- Sleep studies
Pheochromocytoma:
- 24 hour urinary fractioned metanephrines [high]
- Plasma metanephrines [high]
Cushing Syndrome:
- Serum cortisol following low dose dexamethasone suppression test [high]
Urine drug screening:
- For psychostimulants and substance abuse causes of secondary HTN
Treatment options for Secondary HTN
In addition to Anti-hypertensive drugs, treating the underlying causes of HTN [pharmacological or surgical] will also help manage HTN or even cure it
3 Major causes of HF
- Hypertension
- Diabetes Mellitus
- Coronary Artery Disease
CV, Endocrine/Met, Pulm, Toxic, Genes
ALL Etiologies of HF
Cardiovascular causes:
- IHDs [CAD, MI]
- HTN
- Valvular heart disease
- Arrhythmias
- Myocarditis
- Hypertrophic Cardiomyopathy
- Restrictive Cardiomyopathy
Endocrine/Metabolic causes:
- Obesity
- Diabetes Mellitus
- Thyroid disease
- Renal disease
Pulmonary causes:
- COPD
- Pulmonary artery HTN
- Cor Pulmonale
Toxic causes:
- Chemotherapy
- Alcohol abuse
- Tobacco
- Cocaine, Methamphetamines
Others:
- Familial history or genetic
- Autoimmune like SLE, Giant cell arteritis
3 different ways to classify HF
- HF classified according to Left Ventricular Ejection Fraction
- HF classified by AHA/ACC through objective assessment of symptoms and clinical features
- HF classified by NYHA for symptomatic HF through assessment of physical activity limitation
HF classification based on LVEF
- HFpEF: preserved Ejection fraction with evidence of increasing LV filling pressures, reduced SV and normal/reduced EDV [LVEF >= 50%]
- HFrEF: reduced Ejection fraction <= 40%
- HFimpEF: previous HFrEF now showing improvement signs on followup [> 40% LVEF]
- HFmrEF: Mildly reduced Ejection fraction between 41%-49%
Signs of Increasing LV filling pressures - Increased Natriuretic peptide levels and hemodynamic measurements in LV
AHA/ACC classification of HF based on clinical features and symptoms
Stage A [at risk for HF]:
- Asymptomatic
- No Structural Heart disease or abnormal biomarkers
- Risk factors like HTN, DM, ASCVD, family history for cardiomyopathy present
Stage B [pre-HF]:
- Asymptomatic
- Presence of one or more of the below criteria
- Structural heart diease [Valvulopathy, reduced EF, ventricular hypertrophy
- Increased filling pressures
- Risk factors for HF + Increased BNP/Increased Troponins with no other plusable Ddx
Stage C:
- Symptomatic HF with signs of clinical features current or previous
- Structural heart disease present
- Improvement of HF symptoms DOES NOT change the staging of patient [Stage C patient always remains Stage C]
Stage D [Advanced HF]:
- Symptoms that disrupt daily life with frequent hospitalization despite proper guided medical therapy for HF
NYHA classification of HF based on physical activity limitation in Symptomatic/Stage C/D HF patients
Class I:
- No limitations in physical activity
- No symptoms of HF
Class II:
- Mild symptoms and slight limitations in ordinary physical activity
- No symptoms at rest
Class III:
- Marked limitations in physical activty
- Less-than-ordinary activity causes symptoms
- Comfortable only at rest
Class IV:
- Severe limitations
- Symptoms during any form of physical activity
- Symptoms at rest
HFrEF, HFpEF, Left-sided HF, Right-sided HF
Basic Pathophysio of HF
Reduction in Cardiac Output causing Heart Failure can be due to Increase in Afterload, Increase in Preload or Decrease in Ventricular Contractility
HFrEF:
- Reduced contractility [causing increased EDV, ESV and decreased LVEF]
- AKA Systolic ventricular dysfunction
- Damage to myocytes [IHD], arrhythmias and high output condition can lead to this type of HF
HFpEF:
- Decrease in ventricular compliance [causing increased LVEDP, decreased EDV but LVEF remains above 50%]
- AKA Diastolic ventricular dysfunction
- Increase in LV stiffness [long standing HTN], Outflow obstruction [Aortic stenosis], Impaired relaxation of ventricles [tamponades, constrictive pericarditis] can lead to this type of HF
Left-sided HF:
- Increased LV Afterload - Arterial HTN, Aortic Stenosis leading to reduced CO
- Increased LV Preload - Aortic Regurgitation leading to increased EDV reducing CO
Right-Sided HF:
- Increased RV Afterload - Pulmonary arterial HTN
- Increased RV Preload - Pulmonary valve regurgitation, left-right shunting
Consequences of Decompensated HF
When compensatory mechanisms get exhausted or not effective enough
Forward Failure:
- Decreased CO
- Decreased Organ perfusion [Hypotension]
- Organ dysfunction [Renal especially, activating RAAS creating a Vicious cycle] and End-organ damage
Backward Failure:
- LV blood pooling - Backflow into Pulmonary circulation - Cardiogenic Pulmonary edema and Dyspnea - Pulmonary Artery pressure increase from blood backflow and congestion
- RV blood pooling from Pulmonary Artery HTN - Backflow into venous systems - Venous congestions [Liver and stomach] and Peripheral edema
- Nutmeg Liver
HF is characterized by reduced CO leading to venous congestions and poor systemic perfusion
Basics about Compensatory mechanisms employed by body to counter HF and reduction in CO
- Increased Adrenergic activity [Increased HR, BP and contractility]
- Increased RAAS activity [Systemic vasoconstriction causing increased Afterload, Increased Preload via increased absorption of sodium and water in nephrons]
- Secretion of Natriuretic peptides [Systemic vasodilation and increased Diuresis]
General, Left sided, Right sided
Clinical Features of Heart Failure
General Symptoms:
- Nocturia [Supine position improves renal vasoconstriction and CO]
- Fatigue
- Tachycardia and various Arrhythmias [Increase in sympathetic tone and long standing HF causing remodelling]
- S3/S4 gallop rhythm
- Pulsus alternans [alternating strong and weak pulses]
- Cachexia
Left-Sided HF:
- Pulmonary congestion [Dyspnea, Pulmonary edema, Orthopnea, Paroxysmal Nocturnal Dyspnea, Cardiac asthma]
- Audible bilateral basilar rales on auscultation
- Laterally displaced apex beat
- Coolness and palor of lower extremities
Right-Sided HF:
- Peripheral pitting edema
- Abd pain
- Jaundice
- Nausea
- Jugular Venous distention
- Kussmal sign [Jugular vein distention during inspiration]
- Hepatosplenomegaly [causing cirrhosis or ascites]
- Hepatojugular reflex [external manual pressure on liver - RV overload from venous return - jugular vein distention]
