HEART

FAILURE/CORPULMONALE/SYSTEM
IC HTN
HEART FAILURE
 Heart fails to pump at a rate commensurate with the
requirements of the ,metabolizing tissues or is able to do so
only with an elevated diastolic filling pressure
Classification of HF: New York
Hear Association
 Class I patients have no limitation of physical activity

 Class II patients have slight limitation of physical activity

 Class III patients have marked limitation of physical

activity
 Class IV patients have symptoms even at rest and are
unable to carry on any physical activity without discomfort
Pathophysiology
 Insult with myocardial destruction

 Reduced cardiac output (systolic failure)

 Adaptations
 Frank starling mechanism: Increased preload

 Myocardial hypertrophy with/without chamber dilatation:

Increase mass of contactile tissue

 Activation of neurohumoral systems

 Release of NE by adrenergic cardiac nerves

 Activation of RAAS

 E/NE release, endothelin 1 & vasopressin-vasoconstriction

 This increases calcium afterload –augments myocardial

contractility and impairs relaxation (decreased lusitropy)-
Diastolic failure
 Calcium overload lead to arrhythmias

 Increased afterload and inotropy with impaired relaxation =

increased myocardial energy demand = further decrease in
CO
 Myocardial cell death ensue

 RAAS : salt and water retention= increased preload=

increased myocardial energy demand
 ANG II : hypertrophy
 Rate of myocyte turnover increases during pathologic stress

 In HF this mechanism become overwhelmed by a faster rate of myocyte

death

This leads to cardiac remodelling : Remodelling is molecular (ATP generation) ,

cellular(calcium handling) and interstitial changes manifesting as

Change in cavity D and mass (hypertrophyy and atrophy), geometry (wall

thickness & shape), fibrosis .

Remodelling: Genetic changes, Biochemical changes, molecular changes,

cellular changes, structural changes
 Activation of baroreceptors

 Atrial and Brain type natriuretic peptides (ANP & BNP)

rise – promote vasodilation and natriuresis
  Peripartum

 Congenital heart disease

Etiology
 Drugs
Underlying causes:
 Endocrine/rheumatologic
 Coronary artery disease disorders

 DM  Anaemia

 HTN  Polycythemia

 Valvular heart disease  Pulmonary hypertension

 Arrhythmias  PE / pulmonary valve stenosis

 Infections and inflammation  Pulmonary disease

 Neuromuscular disease
 Precipating causes

 Anaemia

 Obesity

 Fever
 Genetics
 Infection

 Medications : chemo/NSAID

 Uncontrolled HTN

 Arrhythmias

 Intense physical exertion

 Excess water/salt intake

Presentation
 Myopathy  Brethlessness

 Fatigue  Exertional dyspnoea

 Edema  Orthopnoea

 Palpitations  PND-may last upto 30 mins

unlike orthopnoea
 Chest pains
 Dyspnoea at rest
 Nocturia/ oliguria(late)
 Recumbency enhances CO  Acute pulmonary edema
 Confusion

 Anxiety

 Headaches

 Insomnia

 Night mares
Physical exam
 BP General inspection

 HR  Cyanosis

 RR  Sob

 Temps  Pallor

 Spo2  Malar flush edema

 Weight  Jaundice

 Oral thrush
 Hands

 Pallor

 Tar staining  Oslers nodes

 Xanthomata  Temperature

 Arachnodactyly –marfans  Capillary refill time <2secs

 FC  Radial pulse : radial radial delay:

COA, subclavian artery stenosis,
 Splinter haemorrhage
aortic dissection
 Jane way lesions  Blood pressure & pulse pressure
<20/>100mmhg
 Carotid pulse : auscultate
 JVP <3cm
 Hepatojugular reflux: @least 3cm
distance from the upper margin of
the baseline JVP to the mandible
angle
 Eyes :pallor, arcus, xanthelasma ,
Kayser-Fleischer rings –dark
rings encircling the iris (Wilsons
dse)
 Mouth

 Normally should not rise over 1-2

cardiac cycles. If sustained or >
4cm it’s a positive test
 Chest:  Posterior chest wall :scars

 Scars  Auscultate lung fields

 Pectus  Sacral edema

 Visible pulsations  Abdomen

 Apex beat  Legs

 Heaves

 Thrills

 Auscultate 4 valve areas

Physical exam
 Depend with the stage  Central cyanosis

 Laboured breathing  Icterus

 Malnourished  Malar flush

 Visible pulsations of the eyes and  Diminished pulses , weak,

neck veins: In severe TR thready

 Low BP

 Ascites

 fever: cutaneous vasoconstriction

and impairment of heat loss
  Hepatomegally

 S3 gallop –occurs at the end of rapid

diastolic filling

 Pulsus alternans: variations in EDV

and impaired calcium handling
 Tachycardia
 Cardiomegally
 Diaphoresis
 Pulsus paradoxicus: Inadequate filling
 Cold extrimities of the heart
 Rales

 Wheezing

 Frothy blood tinged sputum

 Kussmaul sign – restrictive

cardiomyopathy
 Accentuated P2  Bloating

 Other murmurs  Constipation

 Cardiac cachexia esp RV failure:  Abdominal pains

Anorexia from hepatic &
intestinal congestion  Bloody stools
Framingham criteria for HF
Major Minor
 PND  Nocturnal cough
 Weight loss >4.5kg in 5/7 in  Dyspnoea on ordinary exertion
response to treatment
 Pleural effusion
 Neck vein distension

 Rales  Tachycardia >120

 Acute pulmonary edema  Hepatomegally

 HJR  Bilateral ankle edema

 S3 gallop

 CVP>16  2major
 Cardiomegally on radiography
 1 major + 2 minor
 Pulmonary edema
DDX
 AKI  PE

 Pneumonia  Pneumothorax

 Pulmonary edema

 Cirrhosis

 Pulmonary fibrosis

 MI

 Nephrotic syndrome
Workup
 NT-proBNP  Chest radiography

 Urea/E  TFT

 Glucose  Iron studies

 12 lead ECG  Ddimers

 ECHO  LFT

 CBC  Genetic testing: HCM(Vivian foe,

Miklos Feher),
DCM,ARVD/C(antonio Puerta)
Classification
 HFpEF LVEF >50%

 HFmrEF LVEF 40-49%

 HFrEF LVEF <40%

Pillar
 ACEi/ ARB/ARNI Angiotensin receptor-neprilysin
inhibitor
 MRA

 Beta blocker

 SGLT2i

Others
 Loop diuretics
 Sodium and water

 Aerobics
Corpulmonale
 Treat underlying pulmonary disease/oxygen

 Diuretics

 Vasodilators : Nifedipine –can lower pulmonary pressures

 Beta selective agonist: Bronchodilator and mucocilliary clearance

 Endothelin receptor blockers: Bosentan 62.5mg bd

 PDE5i : Primary PAH

 Theophylline 300-400mg od

 Warfarin
HYPERTENSION
2017 ACC/AHA
 Elevated BP 120-129/<80

 Stage 1 HTN 130-139/80-89

 Stage 2 HTN >140/>90mmhg

 ESC/ISH >140/>90 mmhg : Higher threshold

Kenya guidelines ESC/ISH
 Primary (90-95%): Variety of environmental or genetic
causes
 Secondary (2-10%) : Renal, vascular, endocrine causes
 DX
 Accurately measuring patients BP

 Focused medical history & PE

 Routine lab studies

Pathophysiology
 Complex involving interaction of genetic predisposition,
excess dietary salt intake, adrenergic tone, renal sodium
and water handling.
 In younger patients’ HTN may be associated with elevated
CO from volume and sodium retention and increased
adrenergic hyperactivity.
 As HTN is sustained vascular remodeling, constriction =
increased PVR
Etiology
 Primary

 Mental stress induces a DNA methylase which enhances

autonomic responsiveness
 Maternal water deprivation and protein restriction in
pregnancy increase Renin angiotensin expression in the
fetus
 Secondary
 Renal parenchymal & vascular disease:

 PKD

 CKD

 Urinary tract obstruction

 Renin producing tumor

 Liddle syndrome
 Increased activity of epithelial ENaC. Kidney Loss of K but retention of
too much Na & H2o

 Nephritic syndrome/glomerulonephritis
 COA Nsaids: inhibit COX 2.This Inhibit its
natriuretic effects-sodium retention
 Vasculitis
Inhibit vasodilating effects of PGE2/I2
 Collagen vascular disease
Brain tumor
 Steroids
Sleep apnoea
 Hyperaldosteronism
Intracranial hypertension
 Pheochromocytomas

 Oral contraceptives- usually

abates 6 monhs
 Drugs  Hyperthyroidism

 Cocaine  Hypercalcaemia

 Cyclosporine  Acromegally

 NSAID  Hyperparathyroidism

 EPO  Pregnancy

 Decongestants containing
ephedrine

 Nicotine
Causes of hypertensive emergencies
 Commonly unexplained in  COA
patients with chronic essential
hypertension  Preeclampsia/eclampsia

 Recreational drugs , abrupt  Postoperative htn

clonidine withdrawal

 Systemic sclerosis

 Pheo / cushing/
hyperaldosteronism

 Coccaine, amphetamine, Oral

contraceptives,
Presentation
Hx:  Thyroid disease

 OTC prescriptions containing  Etc

licorice

 Oral contraceptives

 Illicit drugs

 Ethanol

 Low exercise
PE
 Measure BPs  Palpate pripheral arteries
 over a period of several weeks
 Carotid bruits
 2-3 BP readings 1-2 mins apart
 Take in both arms and one leg  Thyroid enlargement
to avoid missing COA and
 Ausculate upper abdomen Renal
S/Clavian artery stenosis
artery bruits
 Rest for 5 mins
 Take in supine and sitting  Cardiac exam
positions
Workup
 Urinalysis  TFT

 FBS  24hr urinary metanephrines

 A1C  Plasma aldosterone

 UEC  Dexamethasone suppression test

 Ca2+  ECG/ECHO

 Lipid  CT MRI abdpelvis

 Cbc  Doppler flow u/s

 Serum GH: Elevated IGF-1, Brain

 Uric acid
MRI
Treatment
TREATMENT: Non Pharmacological
 Dietary changes  Weight loss: 5-10mmh/10kg loss

 Salt -8mmhg  Aerobic 4-9mmhg

 DASH: Rich in proteins, vegs,

low fat dairy products. 8-14mmhg

 Low levels of alcohol use: 2-

4mmhg

 >3drinks associated with htn

Pharmacologic
1st line agent Following MI

 ACEIs/ARBs  BB

 CCBs  ACEI

 Thiazide diuretics

CKD

 ACEI/ARB
HYPERTENSIVE EMERGENCY
 Elevated BP with acute HMOD

 Target organs: Retina, brain, heart, large aerteries, kidneys

 Iv therapy needed

 Malignant hypertension BP>200/120 associated with advanced

bilateral retinopathy: Papilledema must be present
 Hypertensive encephalopathy: Severe BP ass with lethargy,
seizures, cortical blindness and come
 Hypertensive thrombotic microangiopathy- ass with hemolysis or
thrombocytopaenia
 Associated with cerebral haemorrhage, acute stroke, acute coronay
syndrome, cardiogenic pulmonary edema , aortic aneurysm,
dissection, severe PET/Eclampsia
Resistant hypertension
 BP>140/90 despite treatment with atleast 3 drugs including
a diuretic in adequate doses and after exclusion of false
hypertension
 Nonadherence

 Volume overload: salt,low diuretics

 Associated conditions: Obesity, sleep apnoea, ethanol,

anxiety, chronic pain,
 Identifiable causes of htn

 Whitecoat

 Drug related: too low a dose, inapprpriate combination

 Drugs: NSAIDS, nasal decongestants

Hypertensive emergencies
 Acute ischaemic stroke and BP>220/>120: Reduce MAP
by 15% in 1 hr
 Ischaemic stroke with indication for thrombolysis &
BP>185/>110: 1hr MAP -15%
 Hypertensive encephalopathy: Immediate MAP -20-25%

 Acute haemorrhagic stroke & BP>180 : Reduce BP

immediately to 130-180mmhg for 1st 24hrs.
 Acute coronary event: immediate SBP<140
 Acute cardiogenic pulmonary edema: Immedite SBP<140:
Nitroprusside or nitroglycerine with loop diuretic
 Acute aortic dissection: Immediate BP <120 and HR <60:
Esmolol and Nitroprusside
 E/severe PET: Immediate BP <160/<105:Labetalo and Mg
s04